CIP SEMINARS

Basic Learning Material

for Students of Mental Health

GOVT. OF INDIA
CENTRAL INSTITUTE OF PSYCHIATRY,
RANCHI
2011
 LIST OF CONTENTS
Pages
CHAPTER -I:
GENERAL PHYSICAL EXAMINATION 1-13
CHAPTER -II:
EXAMINATION OF CARDIO VASCULAR SYSTEM 14-28
CHAPTER -III:
EXAMINATION OF RESPIRATORY SYSTEM 29-54
CHAPTER-IV:
EXAMINATION OF GASTROINTESTINAL SYSTEM 55-81
CHAPTER-V:
DISORDERS OF HIGHER MENTAL FUNCTIONS 82-100
CHAPTER -VI:
EXAMINATION OF CRANIAL NERVES 101-132
CHAPTER -VII:
EXAXMINATION OF MOTOR AND SENSORY SYSTEM 133-156
CHAPTER-VIII:
EXAMINATION OF AUTONOMIC NERVOUS SYSTEM 157-170
CHAPTER -IX:
PHENOMENOLOGY AND PSYCHOPATHOLOGY 171-176
CHAPTER-X:
DISORDERS OF PERCEPTION 177-192
CHAPTER-XI:
DISORDERS OF THOUGHT 193-213
CHAPTER -XII:
DISORDERS OF SPEECH AND LANGUAGE 214-232
CHAPTER-XIII:
DISORDERS OF MEMORY 233-262
CHAPTER -XIV:
DISORDERS OF EMOTION 263-286
CHAPTER-XV:
DISORDERS OF EXPERIENCE OF SELF AND CONSCIOUSNESS 287-321
CHAPTER-XVI:
MOTOR DISORDERS 322-349
CHAPTER-XVII:
BASICS OF PSYCHOLOGICAL ASSESSMENT 350-383
CHAPTER-XVIII:
BASICS OF PSYCHOTHERAPY 384-408
CHAPTER –I
 GENERAL PHYSICAL EXAMINATION

The aim of first consultation is to diagnose and understand the nature of patient’s
perception of the problem. There might be difficulties while eliciting the symptoms and signs
due to differences in educational level, variety of cultural and ethnic backgrounds and social
issues. To overcome it the examiner requires experience, knowledge of people and ability
to strike up a relationship with very different individuals. If the patient does not wish to
discuss certain topics or to be examined fully, it should be respected (Swash & Glynn,
2007).

What is the need to do a physical examination?

Age-adjusted annual death rates from all causes among psychiatric patients are 2-4 times
higher than in the general population (Harris & Barraclough,1998),with a higher rate of
physical disorder across the entire range of mental disorders. It has been reported that
between 6 and 20% of patients with physical illness are misdiagnosed as having mental
disorder (Koranyi, 1979; Koran et al, 1989). This discrepancy may be due to the fact that
patients who are mentally disturbed may be unable to give a clear account of their
symptoms, even in the presence of a life-threatening disorder (Kampmeier, 1977). Studies
have shown that, in many cases, physical diseases will not be diagnosed and treated when
a patient is admitted to a psychiatric unit (Felker et al, 1996; Moos & Mertens, 1996), which
has potentially serious implications for patient’s overall health, delaying recovery and
increasing length of stay. Consequently an important aspect of psychiatric evaluation is
differentiating organic disease from ‘functional’ psychiatric disorders. A competent
assessment of patient’s physical health also helps to tailor drug use and reduce the risk of
side-effects. Additionally, it gives a clear baseline for comparison, should a patient’s
physical state change, thus informing the clinician of the severity of the effect of drug and of
the need for action.

Barriers to overcome
Many psychiatrists have not used a stethoscope, let alone done a physical examination, for
many years. Past surveys reported that most psychiatrists did not examine their patients
routinely and that a third had little confidence in their ability to do so (McIntyre & Romano,
1977), or believed that it should be done by a physician other than a psychiatrist (Victoroff
et al, 1979). There is little evidence to show that the situation has changed.

How to proceed with the examination?

The first step is to check whether you have the right patient, following which the address
and the age is checked. Make it clear that you hear what the patient wants to say first. It is
a good idea to get at least some of the information at the beginning. After obtaining the
relevant points in history one proceeds to the examination.

PURPOSE OF GENERAL PHYSICAL EXAMINATION:

1. It will provide confidence to the patient which makes further examination easier.

1
2. It will provide information which leads us to guess what further physical findings we could
get from a particular system.
3. It will lead us to which system we will be dealing first (because one should start
examination in a manner that is relevant to the patient’s symptoms and general survey)
(Swash & Glynn, 2007).

PREREQUISITES FOR GOOD PHYSICAL EXAMINATION:

1. Patient needs to be supportive.
2. Room should be quiet, contended and illuminated.
3. Patient and doctor should be comfortable with each other.
4. Patient should be relaxed and reassured by explaining the procedure.
5. Privacy should be maintained.
6. Examination should be done as softly as possible, without exposing unreasonably.
7. Female attendant should accompany male doctor while examining a female
patient especially during urogenital or rectal examination.
8. One may postpone a routine examination and perform only the minimum needed
for a provisional diagnosis and management, if patient is severely ill (Swash &
Glynn, 2007).

COMPONENTS OF A GENERAL PHYSICAL EXAMINATION:

Handshake and introduction Breasts

Posture (physical attitude) Axillae (lymph glands)
Gait Temperature
General appearance Pulse
Facial appearance Respiration
Skin Nutrition
Hands Height & Weight
Feet Obesity
Neck Hydration

Handshake and introduction: Patient should be greeted in a friendly but skilled manner.
Introduce yourself and shake hands. Diagnostic clues include:-
1. Handedness and hemiparesis can be assessed while shaking hands.
2. Cold and sweaty hands are suggestive of anxiety.
3. Cold and dry hands are suggestive of Raynaud’s phenomenon.
4. Hot and sweaty hands are suggestive of Hyperthyroidism.
5. Large, fleshy, sweaty hands are suggestive of Acromegaly.
6. Dry, coarse hands are suggestive of regular water exposure( OCD), manual occupation,
hypothyroidism.
7. Delayed relaxation of grip is suggestive of Myotonic dystrophy.
8. Deformed hands/fingers are suggestive of Dupuytren’s contracture, Rheumatoid
arthritis.
9. Movements: a) Tremors can be seen in anxiety, hyperthyroidism, alcohol withdrawal,
salbutamol therapy.

2
 b) Involuntary movements are usually seen in extrapyramidal system
diseases.
c) Twitching & myoclonic jerks can be seen in uraemia.
10. Nails: a) Seperation of nail from nailbed (onycholysis) with pitting is seen in psoriasis.
b) Transverse groove (Beau’s line) is seen in any severe systemic illness
disturbing growth of nail matrix.
c) Spoon shaped depression of nail is seen in koilonychias of iron deficiency.
d) Red streaks (splinter hemorrhage) are seen in trauma, infective
endocarditis.
e) Nail fold erythema is seen in SLE.
f) Nail breaks easily in cases of detergent exposure, iron deficiency,
hypothyroidism.
11. Clubbing: It can be confirmed:
(a) Initially by loss of normal obtuse angle b/w nail and nailbed &
increased nailbed fluctuation.
(b) Later stages by increased nail curvature (both longitudinal and lateral)
& increased bulk of soft tissues over terminal phalanges.
 How to look for clubbing:
1. See nail bed angle by looking across the nail. It is either lost or exceeds 180
degrees.
2. Schamroth’s window test—viewed from the side, in normal nails, when both thumb
nails are placed in Opposition, there is a lozenge shaped gap. In clubbing it is decreased.
3. Both thumbs are placed under the pulp of terminal phalynxtry to move the nail
within the nail bed using your Index fingers---feel something ‘spongy’nail bed fluctuation
present.
4. View the finger laterallySee the nail curvature and bulk of soft tissues over
terminal phalanges (drum-stick appearance).
 Conditions in which clubbing is seen:
(a) Cardiac diseases (Fallot’s tetrology, bacterial endocarditis).
(b) Lung infections(empyema, tuberculosis, bronchiectasis).
(c) Neoplasia (bronchial CA, mesothelioma).
(d) Ulcerative colitis & chron’s disease.
(e) Genetic (familial) (Cerio,2007 and Devereux & Douglas,2006).
12. Epitrochlear glands: Support the patient’s left wrist with your right hand, grasp the
patient’s partially flexed elbow with your left palm; now with your left thumb palpate the
epitrochlear glands. Likewise examine right glands with your right thumb (Bewan &
Gawkrodger, 2006).

Posture: The position or attitude constantly assumed by a patient at rest or in motion is

referred to as posture.
The various postures seen in clinical practice are:
Postures seen when the patient is standing/sitting:
a) Vertical line seen in standing posture, when viewed from side, is a good posture.

3
 b) Standing posture, when it assumes a S-shaped curve, when viewed from side, is a
poor posture.
c) Asthenic posture: Normal curves of the spine are exaggerated. Seen in debility,
wasting, and in senility.
d) Parkinsonian posture: Universally flexed posture.
e) Lordotic posture: Exaggerated lumbar lordosis, seen in muscular dystrophy and
bilateral hip problems.
f) Cerebellar posture: Patient stands with his feet wide apart, and is unable to maintain a
steady posture when standing with both his feet placed close together. Patient is ataxic on
sitting (truncal ataxia) when the vermis of the cerebellum is involved.
g) Posture in ankylosing spondylitis: Loss of lumbar lordosis, with an exaggeration of
upper thoracic kyphosis.
h) Catatonic posture: Patient maintains a particular posture of the body or limb for hours
together, seen commonly in schizophrenia.
2. Postures seen when the patient is lying down:
a) Decerebrate posture: Extension of elbows and wrists, with pronation of arms is seen. It
suggests a lesion at brainstem level.
b) Decorticate posture: Flexion of elbows and wrists, with supination of arms is seen. It
suggests severe bilateral hemispherical damage above the midbrain.
c) Hemiplegic posture: Patient lies on his back, with the cheek on the affected side
blowing out with each expiration. The affected upper limb lies flaccidly by his side, and the
affected lower limb is externally rotated.
d) Opisthotonus: Patient is arched up like a bow, with his heel and occiput in contact with
the bed.
It is seen in tetanus and strychnine poisoning.
e) Lateral decubitus posture with curled up limbs to minimize the stretching of meninges,
is seen with meningitis or meningism.
f) Patient sitting up and holding on to a support before him, in order to fix his shoulders,
and having dyspnoea, suggests a diagnosis of bronchial asthma.
h) Patient lying down still and (i) Clutching his chest---anginal chest pain.
(ii) Shallow breathing, with minimal or no movement of
anterior abdominal wall peritonitis.
i) Patient rolling about in his bed from side to side and (i) Cjutching his chest---Myocardial
infarction.
(ii) Holding upper abdomen---Biliary colic.
j) Patient sitting up and bending forwards may be seen in pericarditis, peritonitis.
h) Prone posture: may be due to abdominal aortic aneurism which may erode on the
vertebrae in the supine posture and cause back pain.

Gait: Gait is best observed as the patient walks into the consulting room. Then repeat it
with feet exposed and without shoes or slippers. Some common patterns:
1. Parkinsonian gait---stooped, small rapid steps, decreased arm swing, distal pill-
rolling tremor.
2. Cerebellar gait---unsteady(drunken), irregular, wide base.
4
 3. Hemiplegic gait---circumduction of leg, inability to flex leg and dorsiflex foot
against gravity.
4. Sensory ataxic gait---cerebellar gait+stamping stepping.

General appearance: Note general appearances while talking.

1. Does the patient look well, mildly ill, or severely ill and therefore in need of urgent
attention?
2. Any immediate and obvious clues,e.g.obesity, plethora, breathlessness.
3. Skin tattoos—in our set up one can suspect drug addiction, personality disorder, mania,
blood born viral infections,e.g.hepatitis,etc.
4. Is the body proportionate i.e Height= fingertip to fingertip measurement of outstretched
arms e.g.achondroplasia characterized by dwarfism, stocky body and very short legs;
hypopituitarism in adulthood looks dwarfed with an unusually youthful appearance; in
acromegaly coarsened features and large jaws, feet and hands.
5. Signs of malnutrition such as wasting, apathy, anemia and skin changes.
6. Is the patient neglected? Elderly patients with dirty clothes and urinary soiling---severe
physical disease, immobility, dementia.
7.Sounds: Dysarthria---speech articulation problems,e.g.bulbar palsy(consonant
pronounciation), Cerebellar(scanning, robotic); Dysphonia---impaired control of
airflow,e.g.laryngeal papilloma, Laryngitis, Singer’s nodules; Dysphasias---speech &
language problem; Cleft palate; Severe hypothyroidism(low pitched, slow, deliberate and
laboured); crowing noise of stridor(inspiratory sound) in foreign body or tumor of respiratory
tract ; musical wheezing(expiratory sound) in asthma, COPD.
Facial appearance: Patients with deliberate self-harm may cover their face. Poverty of
expression is seen in parkinsonism; startle expression in hyperthyroidism; down head,
poverty of expression and poor eye-contact in depression; apathy, pale and puffy skin in
hypothyroidism; prominent forehead in acromegaly, chronic hydrocephalus, rickets,
thalasemia; Unilateral absence of wrinkling of forehead in Bell’s palsy and bilateral absence
of wrinkling in myotonic dystrophy and in hyperthyroidism(Jeffroy’s sign). Pallor, icterus and
cyanosis are also noted.

Pallor: It depends on thickness, quality of skin and amount & quality of blood in capillaries.
It may be:-
a) Temporary: Generalized---shock, LVF; localized---following cold exposure.
b) Persistent: Generalized---person with thick or opaque skin hypopituitarism, severe
anemia; Localized---Raynaud’s disease.
Best place for checking anemia is mucous membrane of mouth and conjunctiva. Ask the
patient to look straight while you will pull the lower eyelid down to expose the palpebral
conjunctiva. Ask the patient to open the mouth and pull the tip of the tongue in different
directions to see the mucous membrane of the mouth. See if it is pale in natural light.
Pernicious anemia may yield lemon-yellow tint due to combination of mild jaundice and
anaemia. The degree of pallor of mucous membrane is only a rough guide to the severity of
anaemia, it should be corroborated with Hb % estimation (Ogilvie & Evans, 1997). A Hb

5
level of 10-11gm% has been defined as early anaemia and <10gm% as marked anaemia
(Park,2007).

Icterus: It is yellowish discolouration of skin, sclera, and mucous membrane due to

hyperbilirubinemia. Level of bilirubin >/=50 umol/L is needed for clinical detection. Examine
the patient always in day light.
Ask the patient to look down while you will pull the upper eyelid to expose the sclera.
Ask the patient to open the mouth and pull the tip of the tongue inwards to see the
undersurface of the tongue and floor of the mouth. The colour may be dark olive-green in
obstructive jaundice.

Cyanosis: Bluish discolouration of skin and mucous membranes due to increased reduced
hemoglobin in superficial blood vessels.
Central cyanosis: Reversed shunting PDA, pulmonary oedemaarterial
hypoxiacyanosis of lips, tongue and mucous membranes of mouth.
Peripheral cyanosis: Cold exposure, heart failure, mitral stenosiscutaneous
vasoconstriction Cyanosis of hands, feet and all the central sites.

CHARACTERISTIC TYPES OF FACIES:

1. Acromegalic facies: Prominent lower jaw, coarse features, large nose, lips, ears,
prominent forehead and cheek bones and widespread teeth.
2. Cushing’s syndrome: Rounded ‘moon face’ with excessive hair growth.
3. Hypothyroid face: Puffy face with a dull expression with swollen eyelids and loss of hair
over eyebrows.
4. Hyperthyroid face: Anxious look with widely opened eyes with the upper and lower
limbus seen, associated with infrequent blinking and absence of wrinkling of the forehead.
5. Leonine facies: seen in leprosy, and shows thickening of the skin and ear lobes with a
flattened nasal bridge and loss of hair over lateral aspect of eyebrows and eyelashes
(madarosis).
6. Myasthenic facies: Bilateral ptosis with outward deviation of eyes, wrinkling of forehead
and partially opened mouth.
8. Congenital pulmonary stenosis: A broad face with eyes set wide apart (moon face).
9. Face in COPD: Anxious look with bluish discolouration of lips, tip of nose, ear lobes and
breathing out through pursed lips.
10. Face in scleroderma: Skin over the face is taut and shiny. Patient finds difficulty in
opening his mouth or to smile (microstomia).
11. Face in SLE: seen predominantly in women. There is butterfly rash seen over the face
encompassing the upper cheeks and the nasal bridge.
12. Parkinsonian face: Immobile, fixed and expressionless face with infrequent blinking of
eyes (normal=20 per minute). On closing the eyes, fluttering of the eyelids is seen
(blepharoclonus). In postencephalitic parkinsonism, oculogyric crisis may be seen. A jaw
tremor may be seen.
13. Bell’s palsy: Absence of wrinkling of forehead on the side of the lesion, along with
inability to close the eyes, and on attempting to do so the eyeball is seen to move upwards
6
and outwards (Bell’s phenonmenon). There is also loss of the naso-labial fold on the side of
the lesion and deviation of angle of mouth to the opposite healthy side on smiling.
14. Cirrhotic facies: Sunken cheeks and eyes with malar prominence and presence of
bilaterally enlarged parotid glands (especially in cirrhosis secondary to alcoholism).
15. Tabetic facies: Partial ptosis with wrinkling of forehead and unequal, small, irregular
pupils.
16. Cretinoid face: Face is pale and has a stupid and dull look. Nose is broad and flattened.
Lips are thick and separated by a large and fissured protruding tongue. Presence of
prominent medial epicanthal folds and low set ears.

Skin: Complexion depends on thickness, quality of skin and amount & quality of blood (oxy
Hb, red Hb, melanin, carotene, etc) in the capillaries. Some unusual skin colour:-
1. Colour: yellow-brownish tingeuraemia, brownish-blackclofazamine, bluish-
greyamiodarone, slate-gray (after prolonged use, in sun exposed areas)less potent
antipsychotics like phenothiazine (CPZ) or TCA like imipramine.
2. Photosensitivitypimozide.
3. Brown pigmentation in skin creases, recent scars, bony prominences, and mucous
membranes of mouth and lipsAddison’s disease.
4. Blotchy pigmentation of cheeks (cloasma)pregnancy & OCPs.
5. Plethoric complexionPolycythaemia, Cushing’s syndrome.
6. Transient pink flushingperimenopausal.
7. Greyish-brown Haemochromatosis,’bronzed diabetes’.
8. Finely dappled (more in covered parts)chronic arsenic poisoning.
9. Plethoric and rounded face (moon face) Cushing’s syndrome.
10. Skin eruptions: Ask the patient to undress to his underclothes, use a hand lens, wear
gloves if the skin is broken and look for distribution, variation, composition and pattern of
arrangement (configuration).
Examination sequence: Stand back and look for skin abnormalityassess the
distribution and colourassess size, shape of each lesionpalpate any lesion for
consistency.
Distribution: Symmetricalinternal causation; asymmetricalexternal causation;
centripetalchickenpox,Pityriasis rosea; centrifugalerythema nodosum; flexoratopic
eczema; extensorpsoriasis; swelling of eyelids with heliotrope erythema without
scalingdermatomyositis; swelling of eyelids without redness & scalingacute nephritis,
trichinosis (Cerio R,2007).
11. Subcutaneous nodules: It may be due to gouty tophi (helix of ear, finger pulps),
rheumatoid nodule (bony prominences like ulna), vascular nodule of SLE, xanthomatous
deposit, cysticercosis, etc. Heberden’s & Bouchard’s nodule (osteoarthritis) are seen at DIP
& PIP joints respectively (D’Cruz,2007).
12. Petechiae: A hemorrhagic punctuate spot 1-2mm dia. Multiple petechiae on legs and
conjunctivae often due to vasculitis.
13. Vitiligo: Patches of white and darkly pigmented skin due to complete absence of
melanocyte, autoimmune origin.

7
14. Spider naevi: Hemangiomata with bright-red central feeding arterioles and radiating
capillaries in the upper half of the bodyliver disease, OCP, pregnancy.
15. Hair loss (alopecia): Diffusemale pattern hair loss, hypothyroidism, hypopituitarism,
iron deficiency; localized non-scarring alopeciaalopecia areata (circumscribed);
scarring alopeciaburns, herpes zoster, lichen planus,SLE; loss of secondary sexual
hairold age, cirrhosis, hypopituitarism.
16. Swellings: Inspect the swelling—colour, overlying skin. Measure skin temperature with
dorsum of your hand. See any tenderness. Define the site, size, shape and record
diagrammatically. Feel for any pulsation. Assess the consistency, surface texture and
margin. Try to pick up the overlying skin to assess fixity. Try to move the swelling in
different plane to assess the fixity to deeper structures. Look for fluctuation by compressing
the swelling on one side and feel if a bulge is created in the opposite side. Confirm it in two
planes. Auscultate for bruits andother sounds. Transilluminate, to see if swelling can
transmit light through it.
17. Injuries and scars: Specific callositiesmanual worker; Transverse linear multiple
wounds over flexor surface of Forearmdeliberate self-harm (CerioR,2007 and Bevan&
Gawkrodger,2006).

Feet: The feet must be uncovered.

1. Peripheral vascular diseaseshiny skin, feeble or absent dorsalis pedis & posterior tibial
pulses, pallor on passive elevation of feet.
2. Diabetic peripheral neuropathypainless deep ulcers on the soles.
3. Oedema: Swelling of the tissue due to increased interstitial fluid.
Postural oedemalower limbs (healthy person sitting for long), paralysed limb (back of
thighs), lumbosacral area(bed-ridden,immobile patient).
Localized oedemalymphatic obstruction (usually in legs,external genitalia, female
breast), inflammation(accompanied with redness, heat and pain),allergy(red,itchy but
painless).
Angio-edemarapid swelling of the face,lips and mouth.
Generalized oedemanutritional and fluid overloads (diseases of heart, kidney and
liver).
Cardinal sign:Apply firm pressure with your fingers or thumb for few seconds (best place
for cardiac oedema is over medial malleolus and sacrum)release itpitting of the
skinpersists for several minutes.
Myxoedema and chronic oedema do not pit on pressure.
4. Deformities:
(a)Genu varum: Rickets, osteomalacia, osteitis deformans (Paget disease), achondroplasia.
(b)Genu valgum: Congenital, rickets.
(c)Rocker bottom feet: trisomy-18 (Edward’s syndrome).
(d)Pes cavus (Claw foot): Familial, Freidreich’s ataxia, syringomyelia,
anterior poliomyelitis.
5. Heel pad thickness: It is the distance measured in a X-ray film of the patient’s foot taken
laterally from the lower most point of the calcaneum to the lower most point of the heel pad
8
soft tissue shadow. It is increased when >23mm in females, & >21mm in males. Causes (of
increase) include: acromegaly, myxoedema, obesity, infection or injury to heel, phenytoin
therapy.

Neck: Neck should be inspected and palpated.

1. Neck veins: Cardiac function=rt.atrial pressure=int.jugular pressure(ext.jugular vein is
prone to kinking).
Position the patient reclining supine at 45 degree by resting the back of the head on the
pillow in a good light (neck muscles must be relaxed)from the right side look at the
neckidentify int.jugular pulsation deep to the sternocleidomastoid musclepress firmly
over the centre of the abdomen for few seconds (after explaining the patient)increase of
JVP(a diffuse pulsation, not the vein itself) by 2-3 cm (abdomino-jugular reflex).
Causes of elevated JVP: CHF, corpulmonale, pulmonary embolism, tamponade,
constrictive pericarditis, SVC obstruction.
2. Cervical glands:Patient is in sitting position. From behind (anterior triangle)submental,
submandibular, Preauricular, tonsillar, supraclavicular, deep cervical glands. Palpate deeply
with index fingerscalene nodes.
From behind (posterior triangle)posterior auricular and occipital nodes (Bevan&
Gawkrodger,2006).
3. Lymph glands: Lymph glands are often palpable normally in submandibular, axillae and
groin (</=0.5 cm in diameter ;soft,rubbery in consistency;non-tender and freely moving are
characteristics of normal glands).
Inspect any visible lymphadenopathy, palpate one side at a time with fingers of one
hand, compare with other side ; assess size,consistency,tenderness,fixity to any structures.
Examine the inguinal & popliteal glands with the patient lying down. Palpate just below the
inguinal ligament for horizontal chain. Then over the vertical chain along the line of
saphenous vein. Use both hands to palpate popliteal fossa with knee flexed and limb
muscles relaxed (Cerio R,2007 and Bevan& Gawkrodger,2006).
4. Thyroid gland: It is normally palpable in about 50% of females and 25% of males. Ask the
patient to extend his neck slightlyfrom front inspect area below the cricoids cartilage. Ask
to take sip of water,extend the neck and swallowlook for upward move of the glandnote
its contour and any asymmetry. Stand behind the patient. Place your hands gently on the
front of the patient’s slightly extended neck with your index finger just touching area below
the cricoids cartilage. Now drag the index finger down and laterally to feel lateral lobes with
inferior borders. Ask the patient to swallow a sip of waterfeel the gland. Note the size,
shape and consistency of any goiter, presence of thrill. Measure any discrete nodule.
Auscultate with stethoscope for any bruit.

Breasts:Patient is in sitting position. Explain the procedure and purposethe breast should
be exposedassess asymmetry, visible mass, distortion (dimpling) of skin, nipple
discharge, ulceration, oedema, erythema of the skin (peau d’ orange),axillary lymph node
enlargement, oedema of the arm. Now patient in near supine position with pillows beneath
the head and arms raised and hands behind her headexaminer palpates the breast
between the flat of the hand and the chest wall posteriorly. Normal lobular consistency
9
becomes palpable after menopause. Palpation should be in 4 quadrants and axillary tail.
Now use thumb and fore-finger to define any suspected mass in relation to size,
consistency, fixation, relation to the nipple (Swash & Glynn,2007).

Axillae(axillary glands): Patient is in sitting position. From the front (a) left axillasupport
the patient’s left wrist with your left hand, keep the patient’s left forearm on your right
forearmnow palpate the left axilla with your right fingers. (b) right axilla support the
patient’s right wrist and forearm with your right hand now palpate the right axilla with your
left fingers. Gently place your finger tips into the vault of axilla and then draw them
downwards to feel the medial, anterior and posterior axillary wall in turn (Ogilvie & Evans,
1997).

Temperature: It can be measured from mouth, rectum or axilla. Rectum is the best site for
core temperature (Swash & Glynn,2007).Rectal temp.>oral temp. by 0.5 degree
celcius>axillary temp. by 0.5 degree celcius. Before using thermometer wash it with
antiseptic or cold water, mercury should be shaken down. Axilla is not recommended as a
site for reliable measurement. Oral temp. may be taken from undersurface of tongue with
lips closed. For childrenin the fold of groin with thigh flexedusually it should be kept for
one minute.Max. normal oral temperature: At 6.00 AM is 37.0 C (98.6 F), at 6.00 PM is 37.6
C (99.6 F).Febrile: Above 37.8 C (100 F).
Hyperpyrexia: Above 41 C (106 F).Causespontine hemorrhage,rheumatic fever,
meningococcal meningitis,septicemia, cerebral malaria, heat stroke, NMS, serotonin
syndrome, thyrotoxicosis.
Hypothermia: Less than 35 C (95 F).
Fever with relative bradycardia: typhoid
fever,meningitis,influenza,brucellosis,leptospirosis,drug induced.
Fever with exanthems: chicken pox(rash on first day), measles(rash on 4th day),
typhoid(rash on 7th day).
Continuous fever:temp. fluctuation does not exceed 0.6 C and never touches
baseline,e.g. lobar pneumonia Infective endocarditis, enteric fever.
Remittent fever: temp. fluctuation exceeds 0.6 C and never touches baseline.
Intermittent fever: elevated temp. touches baseline in between. In hectic or septic
type,diurnal variation is extremely large,as occurs in septicemia. Quotidian fever is a hectic
fever occurring daily.
Relapsing fever: febrile episodes are separated by normal temp. for >one day,e.g.
Borrelia infection.
(a) tertian fever: plasmodium.vivax, ovale, falciparum.
(b) quartan fever: plasmodium malariae.
(c) pel-ebstein fever: hodgkin’s and other lymphomas(fever for 3-10
days f/b an afebrile period of 3-10 days).
(d) saddle back fever: dengue fever(fever for 2-3 days followed by
afebrile period of 2 days and again fever for 2-3 days).

Pulse:
10
1. Place 3 middle fingers over right wrist lateral to the flexor carpi radialis tendon (radial
pulse). Assess rate (by counting 30 secs and multiply by 2), rhythm and volume.
2. To detect the collapsing pulse (i.e. early peak, followed by rapid decent in pulse pressure
producing collapsing sensation, seen in severe aortic regurgitation)raise patient’s arm
and feel across the pulse with your pads of fingers.
3. Now palpate left radial pulse. Simultaneously palpate bothnote any difference.
4. Use your left thumb (for right brachial artery and vice versa) and palpate brachial artery
in the antecubital fossa medial to biceps tendon while supporting the arm with your left
fingers.
5. Palpate the carotid pulse with patient lying on a bed, between the larynx and anterior
border of the sternocleidomastoid muscle using your left thumb for right carotid and vice
versa. Now ask to hold the breath and auscultate for bruits over both carotids (Northridge,
Gruet et a land Bradbury, 2006).

Respiration: Observe the chest movements while feeling the pulse, and count the
respiration per minute.
Normal rate in adults is 14-18 per minute (Swash & Glynn, 2007).

Nutrition: In PEM due to oedema, weight is not reliable indicator. Muscle mass-wasting of
temporalis muscle (gaunt appearance), limb muscles are thin; dry, cracked skin, loss of
body and scalp hair and poor wound healing; subcutaneous fat is atrophic.
Harpenden caliper-triceps (most commonly used, between acromian and olecranon
in vertical plane with arm hanging relaxed by the side of the body), biceps, infrascapular
region. In adults</=10mm (male) or </=13mm (female) is suggestive of moderate depletion.
Quetlet index: Body mass index= Weight in kgs/ Height in (metres).
Weight loss (BMI</=18.5, underweight)hyperthyroidism, IDDM, hypopituitarism,
addison’s disease,anorexia nervosa.

Height & Weight: Both for immediate use (e.g. drug dose estimation) and for future
reference.
Disproportionately low weight with increased appetite suggests thyrotoxicosis and
diabetes mellitus.
Obesity: BMI>/=30obesity (most commonly used) and BMI=20-30overweight.
Simple obesityenergy intake/expenditure imbalance.
Geneticnon-mendelian inheritance.
Social and psychological factors (related to diet and excersise).
Drugspsychotropics.
Primary hypothyroidism.
Cushing’s syndrome (truncal obesity with proximal thinning of limbs).
Hypothalamic lesion.

Assessment of hydration: (a)Skin turgor: Gently pinch a fold of skin on the neck or
anterior chest wallhold it for few secondsrelease it. (b)Pulse rate and supine/erect
blood pressure.
11
Features Mild dehydration Moderate dehydration
Appearance Thirsty,alert,restless Drowsy,cold,sweaty
Radial pulse (N) rate & volume Rapid & feeble
B.P (N) <80mmHg/unrecordable
Skin turgor Retracts immediately Retracts very
slowly(>2secs)
Tongue Moist Very dry
Urine flow (N) Little/none
(Park , 2007)

Odours: Excessive body odour occurs in: very elderly, demented; alcohol or drug misuse;
physical disability.
Some diagnostic odours are: (a) Stale mousy smell on breathliver failure (fetor
hepaticus).
(b) Sweetness of breathdiabetes, starvation or ketoacidosis. (c) Fishy smellbacterial
vaginosis.
(d) Halitosis (bad breath)gingivitis,stomatitis,atrophic rhinitis,bronchiectasis,gastrocolic
fistula.

References

Beven, J.S., Gawkrodger, D.J .( 2006) General examination & Examination of skin,hair and
nail. In: Douglas G,Nicol F, Robertson C, eds. Mackeod’s Clinical Examination (11th
edition). London: Elsevier, Churchill Livingstone,:40-62, 65-76.
Biswas,P.S & V.K.Sinha, (2009), General Physical Examination, Journal Club, Central
Institute Of Psychiatry.
Cerio, R.( 2007) skin, nails and hair. In: Swash M, Glynn M, eds. Hutchison’s Clinical
Methods (22nd edition). Londonm,W.B.Saunders,:pp251-262.
D’Cruz D. (2007) Locomotor system. In: Swash M, Glynn M, eds. Hutchison’s Clinical
Methods (22nd edition). London: W.B.Saunders,;pp156-157.
Felker,B.,Yazell, J.J; Short,D.(1996) Mortality and medical comorbidity among psychiatric
patients: a review Psychiatric Services, 47, 1356-1363.
Harris, E.C. & Barraclough, B. (1998) Excess mortality of mental disorder.British Journal of
Psychiatry, 173, 11-55.
Korayni, E.K. (1979) Morbidity and rate of undiagnosed physical illness in a psychiatric
clinical population Archives of General Psychiatry, 36, 414-419.
Koran,L.M.,Sox,H.C.,Marton,K.L.et al (1989) Medical evaluation of psychiatric patients.
Archives of General Psychiatry, 46, 733-740.
Kampmeier, R.H. (1977) Diagnosis and treatment of physical disease in mentally ill. Annals
of Internal Medicine87, 637-645.
Moos,R.H.& Mertens,J.R.(1996) Pattern of diagnosis, comorbidities, and treatment in late-
middle-aged and older affective disorder patients: comparison of mental health and medical
sectors. Journal of American Geriatric Society, 44, 682-688.

12
McIntyre,J.S. & Romano,J.(1977) Is there a stethoscope in the house (and is it used)?
Archives of General Psychiatry, 34, 1147-1157.
McAuley J, Swash M. (2007) Nervous system. In: Swash M, Glynn M, eds. Hutchison’s
Clinical Methods (22nd edition). London:W.B.Saunders,;227-228.
Monson J P and Drake W(2007). Endocrine disorder. In: Swash M, Glynn M, eds.
Hutchison’s Clinical Methods (22nd edition). London:W.B.Saunders,;272-276.
Northridge D,Grubb N and Bradbury A (2006).The Cardiovascular system.In:Douglas G,
Nicol F, Robertson C, eds.Mackeod’s Clinical Examination (11th edition). London: Elsevier,
Churchill Livingstone,:90-97.
Park(2007). Park’s textbook of preventive and social medicine (19th edition). Banarsidas
Bhanot Publishers, Jabalpur, India,: 493 & 184.
Swain P. (2007) The gastrointestinal tract and abdomen. In: Swash M, Glynn M, eds.
Hutchison’s Clinical Methods (22nd edition). London:W.B.Saunders,:133.
Swash M & Glynn M. (2007) Patient and doctor: General principles of history taking. In:
Swash M, Glynn M, eds. Hutchison’s Clinical Methods (22nd edition).
London:W.B.Saunders,:1-12.
Swash M & Glynn M. (2007) Physical examination: General principles. In: Swash M, Glynn
M, eds. Hutchison’s Clinical Methods (22nd edition). London:W.B.Saunders,:14-18.
Timmis A. (2007) The cardiac examination. In: Swash M, Glynn M, eds. Hutchison’s Clinical
Methods (22nd edition). London:W.B.Saunders,;77-78.
Victoroff,V.M.,Mantel Jnr,S.J.,Bailetti,A.,et al (1979) Physical examination in psychiatric
practice in Ohio Hospital and Community Psychiatry, 30, 536-540.

13
CHAPTER –II
 EXAMINATION OF CARDIOVASCULAR SYSTEM

Examination of cardiovascular system (CVS) includes examination of cardia,

peripheral arteries and venous system.

SURFACE ANATOMY OF HEART (Timmis, 2007)

Heart is situated obliquely in the chest and two third of it lies to the left of the
midline. The right ventricle forms a greater portion of the front of heart and its inferior
margin forms the lower border of heart which extends from the lateral border of the
sternum at the level of seventh costal cartilage to the apex. The left ventricle is seen
at a narrow strip in the front and it forms the apex. Left border extends from apex to
the left second inter costal space within the parasternal line. A greater part of the left
atrium is situated posteriorly and the left auricular appendage reaches the highest
point in the thorax and is situated just behind the second inter costal space. The right
atrium forms the right cardiac border. The boundary can be drawn in the form of a
curved line joining the two points on the right lateral border of sternum at the level of
union of third and seventh costal cartilage.

EXAMINATION OF CVS:
1. General observation
2. Specific observation
 Arterial Pulse:- Rate, Rhythm, Character, Volume
 Blood Pressure
 Neck veins
 Precordium:- Inspection, Palpation, Auscultation

General observation:
 Carefully look at the patient's general appearance and assess whether
patient is sitting comfortably in the bed or not.
 Chest wall deformities such as pectus excavatum should be noted. Large
ventricular or aortic aneurysms may cause visible pulsations. Superior vena
caval obstruction is associated with prominent venous collaterals on the
chest wall. Prominent venous collaterals around the shoulder occur in axillary
or subclavian vein obstruction. Note the patient's colour - pale, cyanosed,
grey, or sweaty. In mitral stenosis, cyanosis over the malar area produces
characteristic mitral facies. The hands and the face can reveal important
signs of cardiac disease. The presence of finger clubbing in association with
central cyanosis suggests there is a right to left shunt at the intracardiac or
intrapulmonary levels. In patients with infective endocarditis- finger clubbing
and splenomegaly may be present. Microvascular embolic phenomenon may
be manifested by splinter hemorrhages in the nail beds of fingers and toes
and small petechial hemorrhages in the conjunctiva. The ‘classic’
manifestations of endocardits like Osler’s nodes (tender erythematous
nodules in the pulps of fingers), Janeway lesions (painless erythematous
lesions on the palms) and Roth’s spots (erythematous lesions in the optic
fundi) are now rarely seen. Coldness of extremities is an important sign of
reduced cardiac output in patients with severe heart failure. Pyrexia may

14
 occur in infective endocarditis and first three days after myocardial infarction.
Subcutaneous oedema which pits on digital pressure is a feature of
congestive heart failure.

Common symptoms of cardiac disease:

Source:- The Cardiovascular system, Mcleod’s Clinical Examination, 2007.

Specific observation:

ARTERIAL PULSE:
The arterial pulses are detected by gently compressing the vessel against
some firm underlying structure usually bone. The radial pulse is found at the wrist,
lateral to the flexor carpi radialis tendon. Use this to assess pulse rate and rhythm.
The brachial pulse is found in the antecubital fossa medial to the biceps tendon. The
carotid pulse is most easily palpable at the angle of the jaw, anterior to the
sternocleidomastoid muscle. Palpate the larger brachial and carotid arteries for a
more reliable assessment of pulse volume and character than is given by the radial
pulse.

Examination sequence (Northridge et al., 2007)

Radial pulses
 Place your three middle fingers over the right radial pulse.
 Use the pads of your fingers to assess the rate, rhythm and volume. The
patient forearm should be slightly pronated and wrist slightly flexed.
 Count the pulse usually for entire one minute or in cases of emergency for 30
seconds and multiply by 2 to obtain the pulse rate in beats per minute
(b.p.m.).

15
  Now palpate the left radial pulse. If either pulse feels diminished in volume,
confirm any difference by simultaneous palpation.
Brachial pulses
 Use your thumb (right thumb for right arm and vice versa) with your fingers
cupped round the back of the elbow
 Feel medial to the tendon of the biceps muscle to find the pulse and assess
its character.

Carotid pulses
 Palpate the carotid pulse with the patient lying on a bed or couch
 Never compress both carotid arteries simultaneously.
 Use your left thumb for the right carotid pulse and vice versa.
 Place the tip of your thumb between the larynx and the anterior border of the
sternocleidomastoid muscle.
 Press your thumb gently backwards to feel the pulse.
 Listen for bruits over both carotid arteries using the diaphragm of your
stethoscope while the patient holds his breath.

Pulse Rate:
A normal adult resting pulse rate is between 60-100 b.p.m. Bradycardia is a
pulse rate of < 60 b.p.m. and tachycardia > 100 b.p.m. These are arbitrary definitions
and one should assess the heart rate in the context of the clinical situation. A pulse
rate of 50 b.p.m. may be normal in a fit young person, whereas a pulse rate of 65
b.p.m. may be slow in acute heart failure. Pulse rate should not be counted
immediately placing fingers upon the pulse, but when any tachycardia due to
nervousness in patient has subsided and patient has resumed its normal rate.
A normal cardiac rhythm is called sinus rhythm because it arises from the
sinoatrial node. Sinus rhythm seldom produces a complete regular pulse because
the heart speeds up during inspiration and slows at the beginning of expiration in
response to changes in vagus nerve activity. This sinus arrhythmia is most obvious
in children, young adults and athletes.

Causes of fast and slow pulse rate:

16
Pulse Rhythm:
Decide whether the rhythm is regular or irregular. If it is irregular, decide if it is
completely irregular, whether irregularity has a recurring pattern or whether an
otherwise regular rthym is occasionally interrupted by some slight irregularities.
Atrial fibrillation causes a chaotic ventricular rhythm leading to a pulse which
is completely irregular in timing and of variable volume. Untreated atrial fibrillation
usually produces a rapid ventricular rate during which the interval between
successive ventricular contractions may be too short to allow proper filling. This can
produce a considerable pulse deficit. When the ventricular response to atrial
fibrillation is rapid, assess the heart rate by listening at the apex or from an ECG. If
atrial fibrillation occurs in the absence of structural cardiac disease, it is important to
check for thyrotoxicosis and alcohol as potential causes (Swash, 1997).

ECG strip showing atrial fibrilation

Causes of irregular pulse:

17
Pulse Character:
Character is the impression of the pulse waveform obtained. Character or
form of arterial pulse wave is best studied by the palpation of carotid pulse. It is not
usually possible to detect slight variation from the normal but in certain cases the
character of the arterial pulse is detectably abnormal. Some of the important pulse
characters are as follows:
1. Slow rising pulse (Anacrotic pulse): A slow-rising pulse has a gradual
upstroke to the pulse waveform and a reduced peak that occurs late in systole. It is a
feature of severe aortic stenosis. (Swash, 1997)

Slow rising pulse

2. Collapsing pulse (Water-hammer pulse)(Swash, 1997)Pulse with a rapid
upstroke and descent characteristically occurs in aortic regurgitation. The rapid
descent is due to first, the diastolic run off into left ventricle or secondly, the rapid run
off to the periphery because of a low systemic vascular resistance. It is exaggerated
by raising the patient's arm well above the level of the heart. This is also found with
PDA, ruptured sinus of valsalva or large arteriovenous malformation(AVM).
3. Bisferiens pulse, (Swash, 1997) which occurs with mixed aortic stenosis
and regurgitation, has two systolic peaks separated by a distinct midsystolic dip.
4. Pulsus Alternans (Swash, 1997) is rare and describes a beat-to-beat
variation in pulse volume in the presence of a regular rhythm. It occurs in advanced
heart failure and is often initially detected when measuring the blood pressure.

Pulsus alternans

5. Pulsus paradoxus is a pulse that increases in volume on expiration and

decreases in volume in inspiration. This variation occurs in health but is not normally
easy to detect. This variation in pulse pressure is abnormal if it is exaggerated to the
point that it is clinically detectable. It occurs with severe airways obstruction e.g.
acute asthma, because of extreme changes in intrathoracic pressure, and in
pericardial tamponade due to a large pericardial effusion. Pulsus paradoxus is best
assessed by measuring the difference in systolic blood pressure during inspiration
and expiration. A difference > 15 mmHg is pathological.

18
Pulse Volume:
Volume is the movement imparted to the fingers and reflects the pulse
pressure - the difference between systolic and diastolic blood pressure. A large
volume pulse may be due to aortic regurgitation, or a high cardiac output state.
Exercise, emotion, heat and pregnancy are physiological factors causing
vasodilatation and increased cardiac output, which also occurs with fever,
thyrotoxicosis, anaemia, peripheral arteriovenous shunts and Paget's disease of
bone. A low volume pulse is associated with reduced stroke volume due to heart
failure, or peripheral vascular disease. The pulse may be thin and 'thready' in
hypovolemia due to haemorrhage or dehydration.

BLOOD PRESSURE
Blood pressure is usually measured using a sphygmomanometer cuff
wrapped round the upper arm. Use the correct size of cuff(of width at least 40% of
the arm circumference); an undersized cuff leads to overestimation of blood
pressure. A bladder length of 30-35 cm and width of 12 cm is suitable for most adults
but if the Velcro fastening 'tears' while pumping up, use a larger sized cuff.
Examination sequence (Northridge et al, 2007)
 Rest the patient for five minutes
 In ambulant patients, measurements are normally made with the patient
seated. Either arm can be used.
 Support the patient's arm comfortably at about heart level.
 Apply the cuff to the upper arm, with the lower border more than 2.5 cm
above the cubital fossa. The manometer is placed so as to be at the same
level as the cuff on the patient’s arm and observer’s eye.
 Palpate the brachial pulse.
 Inflate the cuff until the pulse is impalpable. Note the pressure on the
manometer. This is a rough estimate of systolic pressure.
 Now inflate the cuff another 30 mmHg and listen through the stethoscope
over the brachial artery. Five phases of Korotkoff sounds are heard as the
cuff is deflated:
Phase 1: the first appearance of the sounds marking systolic pressure
Phase 2 and 3: increasingly loud sounds
Phase4: abrupt muffling of sounds
Phase5: disappearance of the sounds.
 Record the pressure at which the sounds completely disappear as diastolic
pressure (Phase 5). Occasionally muffled sounds persist and do not

19
 disappear, in which case the point of muffling (Phase 4) is the best guide to
the diastolic pressure.

Normal findings:
Normal systolic pressure in healthy adult is 100-140mmHg and average
diastolic pressure is 60-90mmHg. In children it is closer to lower end of the scale and
in elderly it reaches or even exceeds the higher figures. The difference between the
systolic and diastolic pressures- the pulse pressure- is 30-60mmHg.
Blood pressure varies with excitement, stress and environment. Repeated
measurements, made on separate occasions, in a stress-free environment, are
required to diagnose hypertension. In some patients simply measuring blood
pressure can cause it to rise - so-called 'white coat' hypertension.

Common abnormalities
Hypertension is defined as a systolic blood pressure of > 140 mmHg and/or a
diastolic pressure of > 90 mmHg. It is common and its prevalence increases with
age. Hypertension has no specific symptoms but, untreated, can lead to death or
morbidity from heart failure, cerebrovascular accident or renal failure.
It is a major risk factor for coronary heart disease and atrial fibrillation. Clinical
assessment of the hypertensive patient has four aims:
 to identify any underlying cause
 to assess the severity of the problem, as this dictates treatment
 to identify end-organ damage (cardiac, renal and retinal)
 to assess risk of cardiovascular disease in the context of other risk factors
Essential or primary hypertension is a diagnosis of exclusion. Hypertension is often
familial, and is commonly associated with obesity and alcohol abuse. A cause of
hypertension (secondary hypertension) is identified in < 15% of patients, most of
whom are < 40 years.

NECK VEINS:

JUGULAR VENOUS PRESSURE AND WAVEFORM:

Anatomy
There are no valves between the right atrium and the internal jugular vein.
The degree of distension of this vein is therefore dictated by the right atrial pressure,
and the venous waveform provides information about cardiac function. The internal
jugular vein enters the neck behind the mastoid process. It runs deep to the
sternocleidomastoid muscle before entering the thorax between the sternal and
clavicular heads and can only be examined when the neck muscles are relaxed.
When the pressure in the internal jugular vein is elevated one can see a diffuse
pulsation, although not the vein itself.
The external jugular vein is more superficial and prominent. Do not examine
this routinely because it is prone to kinking and partial obstruction as it traverses the
deep fascia of the neck.

20
Normal findings

Jugular venous pressure (JVP).

Mean right atrial pressure is normally < 7 mmHg (9 cmH2O). Since the sternal
angle is approximately 5 cm above the right atrium the normal jugular venous pulse
should extend not more than 4 cm above the sternal angle. When a healthy subject
sits upright the pulse is hidden behind the clavicle and sternum. When the patient
reclines at 45° the upper limit of the JVP is at the level of the clavicle. If one cannot
see the JVP, press firmly over the centre of the abdomen for a few seconds after
explaining to the patient what you are about to do. This increases venous return to
the heart, transiently increasing right atrial pressure and the height of the jugular
venous pulse by 2-3 cm (abdominojugular reflux). The normal waveform has two
peaks per cardiac cycle, which helps distinguish it from the carotid arterial pulse. The
first peak ('a' wave) coincides with right atrial contraction and occurs just before the
first heart sound. The second peak ('v' wave) is caused by atrial filling during
ventricular systole when the tricuspid valve is closed. A third peak, the 'c' wave, is a
transmitted pulsation from the carotid artery and is rarely visible.
Normally the JVP falls with inspiration because the fall in intrathoracic
pressure is transmitted to the right atrium. Identification of the JVP waveform is
difficult and requires experience.

Examination sequence(Northridge et al, 2007)

 Position the patient reclining supine at 45° in good light.

 Ensure that the neck muscles are relaxed by resting the back of the head on
a pillow.
 Look across the neck from the right side of the patient.
 Identify the internal jugular pulsation (if necessary use the abdominojugular
reflux).
 Estimate the vertical height in centimeters between the top of the venous
pulsation and the sternal angle to give the venous pressure.
 If necessary, readjust the position of the patient until the waveform is clearly
visible.
 Identify the timing and form of the pulsation and note any abnormality.

21
Common abnormalities

The commonest cause of an elevated JVP is heart failure. It is also elevated

in other disorders characterized by fluid overload, e.g. renal failure, hepatic failure, IV
fluid administration. Mechanical obstruction of the superior vena cava and massive
pulmonary embolism can cause the JVP to be so high that it is not seen in the semi-
recumbent position. With superior vena caval obstruction the JVP is elevated and
non-pulsatile. Pericardial constriction causes a specific respiratory pattern of
elevation in which there is a paradoxical rise on inspiration (Küssmaul's sign).

THE PRECORDIUM
INSPECTION AND PALPATION:
Chest deformities can affect the rest of the examination. Pectus excavatum
(posterior displacement of the lower sternum) and pectus carinatum ('pigeon chest')
may displace the heart and affect palpation and auscultation. A midline sternotomy
scar usually indicates previous coronary bypass surgery or valve replacement. A left
submammary scar is usually the result of a surgical mitral valvotomy. Infraclavicular
scars are seen after pacemaker implantation, and the bulge of the pacemaker may
be obvious in thin subjects.
The apex beat is normally found in the 5th left intercostal space (the space
below the 5th rib) medial to the midclavicular line. Count the rib spaces down from
the sternal angle - which is at the junction of the sternum and second rib. The
midclavicular line is halfway between the suprasternal notch and the
acromioclavicular joint. A normal apical impulse briefly lifts the palpating fingers and
is localized. In overweight or muscular subjects the apex beat may be impalpable. It
may also be impalpable in patients with asthma or emphysema because the chest is
hyperinflated. Occasionally, the heart may be on the right (dextrocardia).

Examination sequence
 Inspect the precordium with the patient sitting at a 45° angle with shoulders
horizontal. Look for surgical scars, visible pulsations and chest deformity.
 Lay your whole hand flat over the precordium to obtain a general impression
of cardiac activity.
 Locate the apex beat by laying your fingers on the chest parallel to the rib
spaces ; if you cannot feel it, ask the patient to roll onto the left side
 Assess the character of the apex beat and its position.
 Feel for the right ventricle using the heel of your hand applied firmly to the
left parasternal position.
 Ask the patient to hold his breath in expiration.
 Palpate for thrills at the apex and both sides of the sternum.
 If you hear a murmur, feel again for a thrill using the flat of your fingers while
the patient is in the optimum position.
.
Displacement of the apex beat.
The apex may be displaced laterally in subjects with chest deformity, or because of
mediastinal shift secondary to a large pleural effusion, tension pneumothorax (away
from the affected side) or pneumonectomy or lung collapse (towards the affected

22
side). In these situations the trachea may also be deviated. Left ventricular dilatation
causes the apex beat to be diffusely displaced inferiorly and laterally.

Character of the apical impulse.

A heave is a palpable impulse that feels as though it 'lifts' your hand from the
patient's chest. Conditions that cause left ventricular hypertrophy, such as
hypertension and aortic stenosis, produce a forceful apical impulse that is not
significantly displaced. This thrusting apical 'heave' is quite different from the diffuse
impulse of left ventricular dilatation. A pulsation over the left parasternal area (right
ventricular heave) is usually abnormal in adults and indicative of right ventricular
hypertrophy or dilatation, e.g. in pulmonary hypertension. The 'tapping' apex beat
found in mitral stenosis represents a palpable first heart sound, and is not usually
displaced.
A double apical impulse is characteristic of hypertrophic obstructive cardiomyopathy.
A thrill is a palpable murmur and feels rather like placing your hand on a purring cat.
The most common thrill is that of aortic stenosis which may be palpable at the apex,
the lower sternum, or in the neck. The thrill caused by a ventricular septal defect is
best felt at the left sternal edge. Diastolic thrills are very rare.
PERCUSSION:
Percussion of the heart is seldom carried out, adds little to the clinical assessment
and has to be superseded by the chest X-ray and echocardiogram.

AUSCULTATION:
Auscultation requires a stethoscope equipped with a bell and a diaphragm. The bell
emphasizes low-pitched sounds such as the murmur of mitral stenosis. The
diaphragm filters out these sounds and helps to identify high-pitched sounds such as
normal heart sounds and most systolic murmurs. The earpieces of the stethoscope
should fit comfortably. The tubing should be about 25 cm long and thick enough to
reduce external sound. Make sure the room is quiet when auscultating.
Normal heart valves make a sound when they close (lub-dub) but not when they
open. One must know the surface anatomy of the heart to understand how and
where the sounds and murmurs radiate and basic cardiac physiology to appreciate
their timings.
Use a regular routine for auscultation. Listen first at the apex and identify the two
heart sounds. Simultaneously feel the carotid pulse with your thumb to time the
sounds and murmurs. The first heart sound precedes the carotid pulsation, the
second sound follows it.
Identify and describe the following:
 the first and second heart sounds
 extra heart sounds (third and fourth heard in diastole)
 additional sounds, e.g. clicks and snaps
 pericardial rubs
 murmurs in systole and/or diastole.
AUSCULTATORY AREAS (Alagappan, 2007)
Certain areas of the precordium are customarily named according to the valve from
which murmurs arise:
 Mitral area corresponds to the apex beat.
 Tricuspid area lies just to the left of the lower sternum
 Aortic area is to the right of the sternum in the second intercostals space
 Pulmonary area is to the left of the sternum in the second intercostals space.

23
  Erb’s area (second aortic area) corresponds to third intercostals space close
to sternum.
 Gibson’s area corresponds to the left first intercostal space close to sternum.
PDA murmur is best heard over this area (Gibson’s murmur).

Normal findings
The first heart sound (S1) is caused by the closure of the mitral and tricuspid
valves at onset of ventricular systole. It is best heard at the apex.

The second heart sound (S2) is caused by closure of the pulmonary and
aortic valves at the end of ventricular systole and is best heard at the left sternal
edge. It is louder and higher pitched than the first sound, and normally the aortic
component is louder than the pulmonary one.
Physiological splitting of the second heart sound occurs because contraction
of the left ventricle slightly precedes that of the right ventricle so that the pulmonary
valve closes after the aortic valve. This splitting increases at end-inspiration because
the increased venous filling of the right ventricle further delays pulmonary valve
closure. This separation disappears on expiration. Splitting of the second sound is
best heard at the left sternal edge using the diaphragm. On auscultation, the clinician
hears 'lub d/dub' (inspiration) 'lub-dub' (expiration). Normal and pathological splitting
of the second heart sound.
A third heart sound (S3) is a low-pitched early diastolic sound best heard with
the bell at the apex. It coincides with rapid ventricular filling immediately after
opening of the atrioventricular valves. A third heart sound is therefore heard after the
second as 'lub-dub-dum'. A third heart sound is a normal finding in children, young
adults and during pregnancy.
Examination sequence (Northridge et al, 2007)
 Explain that you wish to examine the chest and ask the patient to remove his
clothing above the waist.
 With the patient lying at approximately 45° to the horizontal, listen over the
precordium at the base of the heart, apex, and upper left and right sternal edges
with both bell and diaphragm. Also listen over the carotid arteries and the axilla.
 At each site identify the first and second heart sounds and assess their character
and intensity; note any splitting of the second heart sound.
 Concentrate in turn on systole (the interval between S1 and S2) and diastole (the
interval between the S2 and S1). Listen for added sounds and then for murmurs.
 Roll the patient on to the left side. Listen at the apex using light pressure with the
bell, to detect the mid-diastolic and presystolic murmur of mitral stenosis .
 Sit the patient up and forwards, and ask the patient to breathe out fully and then
hold his breath.
 Listen over the right second intercostal space and over the left sternal edge with
the diaphragm for the murmur of aortic incompetence.
Note the character and intensity of any murmur heard.

Common abnormalities (Northridge et al, 2007)

First heart sound.
In mitral stenosis the intensity of the first heart sound is often increased due to the
elevated left atrial pressure .

24
Second heart sound.
The aortic component of the second heart sound is sometimes quiet or absent in
calcific aortic stenosis and may be reduced in aortic incompetence. The aortic
component is loud in systemic hypertension, and the pulmonary component is
increased in pulmonary hypertension.

Abnormalities of intensity of first heart sound:

Source The Cardiovascular system, Mcleod’s Clinical Examination

Abnormalities of the intensity of second heart sound:

Source The Cardiovascular system, Mcleod’s Clinical Examination

Causes of third heart sound:

Source The Cardiovascular system, Mcleod’s Clinical Examination

25
Heart murmurs
These are caused by turbulent flow of blood within the heart and great vessels.
Occasionally the turbulence is caused by increased flow through a normal valve
usually aortic or pulmonary producing an innocent murmur. Heart murmurs are
characterized by loudness, quality, location and timing.
The loudness of a murmur reflects the degree of turbulence. This relates to the
volume and velocity of flow and not the severity of cardiac lesions. Loudness is
graded on a scale of 1-6. 1 means barely audible and 6 denotes audible even
without application of the stethoscope to the chest wall.
The quality of a murmur relates to its frequency and is described as low, medium or
high pitched. Location of a murmur on the chest wall depends on its site of origin and
has lead to the description of four valve areas. Murmurs are timed according to the
phase of systole or diastole during which they are audible. Systolic murmurs are
classified as mid-systolic, pan-systolic and late-systolic. Diastolic murmurs are either
early diastolic mid diastolic or pre-systolic in timing. While as continuous murmurs
are audible throughout the cardiac cycle. The murmurs are thus described with
respect to timing whether it is systolic or diastolic, duration, character and pitch,
intensity, location and radiation.
Frictions rubs and venous hums
Friction rub occurs in pericarditis, it is best heard in maintained expiration with the
patient leaning forward, as high pitched scratching noise audible during any part of
the cardiac cycle and at any part of precordium.
A continuous venous hum at the base of the heart reflects hyperkinetic jugular
venous flow.
Cardiac Investigations
ELECTROCARDIOGRAM (ECG): (Ogilvie & Evans, 1997)
ECG records the electrical activity of heart at the skin surface. The main areas in
which the ECG can prove useful are:
 Analysis of abnormal rhythms
 Detection and localization of the changes in the myocardium due to coronary
artery disease
 Detection of hypertrophy of the walls of the atria and ventricles
 Detection of changes in the electrical activity due to the pericardial disease
 Detection of changes in the electrical activity of the heart consequent on
general metabolic changes.
The standard 12-lead ECG uses recordings made from six precordial electrodes (V1-
V6) and six different recordings from the limb electrodes (left arm, right arm and left
leg). The right leg electrode is used as a reference.
The ECG is ordinarily recorded on a special graph paper which is divided into 1mm
square grid like boxes. Since the ECG paper speed is generally 25mm/sec, the
smallest (1mm) horizontal divisions correspond to 0.04 (40msec) with heavier lines
at interval of 0.20 sec (200msec). There are four major ECG intervals: R-R, P-R,
QRS, and QT intervals.
The PR interval measures the time (normally 120-200msec) between atrial and
ventricular depolarization which includes the physiological delay imposed by
stimulation of cells in the AV junction area. This includes usually 3-5 small squares
and is measured from the beginning of p wave to the start of QRS complex.
The QRS interval (100-110msec or less) reflects the duration of ventricular
depolarization. This usually includes three small squares.

26
The QT interval includes both ventricular depolarization and repolarization times and
varies inversely with the heart rate and is calculated on ECG trace as a time from the
beginning of the QRS complex to the end of the T wave. A rate related (corrected)
QT interval (QTc) can be calculated as Qtc= QT/√RR and normally is <0.44sec.
The heart rate can be readily computed from the inter-beat interval (RR) by dividing
the number of large time units between consecutive R waves multiplied by 300 or the
number of small units (.04sec) multiplied by 1500.
ECG is most commonly used in psychiatry to assess the side effects of psychotropic
medications. Drugs like ziprasidone, thioridazine are associated with prolongation of
QTc interval and is associated with torsades de pointes, arrhythmias, and sudden
cardiac death. So an initial ECG should be done before starting these drugs.
Tricyclic antidepressants are often associated with prolongation of PR, QT, and QRS
intervals along with ST and T wave abnormalities. Lithium therapy can cause benign
reversible T wave changes.

Chest X-ray
The chest X-ray is important in the investigation of heart disease. An enlarged heart,
as judged by the cardiothoracic ratio (maximum diameter is less than half the internal
transthoracic diameter), is a common feature of valvular heart disease and heart
failure. In heart failure this is often accompanied by distension of the upper lobe
pulmonary veins, diffuse shadowing within the lungs due to pulmonary oedema and
the finding of Kerley B lines (horizontal engorged lymphatics at the periphery of the
lower lobes).

27
Common cardiac investigations:

Source: The Cardiovascular system, Mcleod’s Clinical Examination.

REFERENCES:

1. Algappan, R. Cardiovascular sysem. In: Algappan, R. Practical of Medicine.

Jaypee Brothers, Medical Publisher, Pvt. Ltd. New Delhi, 2007:75-189.

2. Hussain, M. M. ,Munda, S.K.(2009). Examination of cardiovascular system.

(2009). Physical club, central institute of psychiatry, Kanke, Ranchi.

3. Northridge, D., Grubb, N., Bradbury, A.2007 The cardiovascular system. In:
Douglas, G., Nicol, F., Robertson, C. Eds. Mecleod’s Clinical examination
(11th edition) London: Elsevier, Churchil Livingstone, : 79-121.

4. Ogilvie, C., Evans, C.C. (1997). Chamberlain’s symptoms and signs in

medicine. 12th Edition. Butterworth-Heinemann international edition.

5. Swash, M. Cardiovascular system. In: Swash, M. Hutchinson’s Clinical

Method (20th edition). London: W.B. Saunder, 1997:165-205.

6. Timmis, A. Cardiovascular system. In: Swash, M., Glynn, M. eds. Hutchinson’s

Clinical Method (22nd edition). London: W.B. Saunders, 2007:72-116.

28
CHAPTER –III
 RESPIRATORY SYSTEM EXAMINATION

INTRODUCTION

Diseases of the respiratory system account for up to a third of deaths in most

countries and a major proportion of visits to the doctor and time away from work or
school. They commonly occur in densely populated places (Moore-Gillon, 2007).
A thorough clinical history and examination are fundamental to respiratory
medicine. For many common respiratory disorders a detailed history, careful
examination, chest radiograph and simple tests of ventilatory function are sufficient
to make the diagnosis (Devereux & Douglas, 2006).
Personal History: Stress on the following points during history taking
Occupation: e.g.
– Silicosis may be complicated by pulmonary T.B.
– Asbestosis may be complicated by mesothelioma
Ask about the following:
-Duration of exposure: several years needed for pneumoconiosis.
-Adherence to safety measures as wearing special masks.
 Special Habits smoking cigarettes.

Past History

 Attack or disease similar to the present one: e.g. – Asthma recurrent

pneumonia
 Allergic disorders: eczema, urticaria , angioedema and hay fever.
 Acute abdominal conditions.
 Admission in any hospital before and why?
 Bilharziasis: bilharzial cor-pulmonale.
 Chest injuries and operations.
 Other Surgical procedures.

Coma, convulsions ….may predispose to aspiration and lung abscess.

Cardiac disease and history of rheumatic fever.
Diabetes mellitus.
Hypertension .Cough may result from ACE inhibitors.
Tuberculosis and history of admission to a chest hospital for the treatment of
T.B, medicines, duration of the treatment and adherence to it.

Previous radiological examination if any so that we can compare with the

current radiograph.

Family and Social history if any

 Similar condition in the family.

 History of tuberculosis.
 History of allergy as eczema and hay fever.
 History of diabetes mellitus.

29
ANATOMY
The respiratory system includes upper and lower respiratory tracts.
The upper airway includes the nose, mouth, larynx, trachea and lower respiratory
tract includes the two lungs. The left lung is smaller than the right lung, containing
approximately 45% of the surface area available for gas exchange, because of the
presence of the heart within the left thoracic cavity. The right lung is made up of
three lobes (upper ,middle and lower lobes) and the left lung has two lobes (upper
and lower) ( Devereux & Douglas, 2009).
The lungs are well protected within the thoracic cage. The bifurcation of trachea
corresponds in front with the lower border of the manubrium sterni, i.e., with the
Louis angle and behind with the inter vertebral disc between the fourth and fifth
thoracic vertebra. The ribs are best counted downwards from the second coastal
cartilage.
This cartilage articulates with the sternum at the extremity of the angle of
Louis, which is a transverse bony ridge at the junction of the body of the sternum and
the manubrium sterni and which is easily felt beneath the skin.
A line from the second thoracic spine to the sixth rib in the mammary line
corresponds to the upper border of the lower lobe (major inter lobar fissure). On the
right side a horizontal line from the sternum at the level of the fourth costal cartilage,
drawn to meet the line of the major inter lobar fissure, marks the boundary between
the upper and middle lobes (minor inter lobar fissure) (Moore-Gillon , 2007).

COMMON SYMPTOMS
The mode of onset, duration , progression and predominance of symptoms vary
according to the cause .The six principal symptoms of respiratory disease are;
• Cough
• Expectoration(Sputum production)
• Haemoptysis
• Chest pain
• Dyspnoea (Breathlessness)
• Added sounds (wheeze, crackles).
Other symptoms of importance in chest disease:

1- Symptoms of mediastinal syndrome as dysphagia and hoarseness of

voice.

2- Symptoms of toxemia as night fever, night sweats, loss of appetite and

weight as in T.B.

3- Symptoms of RVF as lower limb edema and pain in the right upper quadrant
of the abdomen (due to congested tender liver).

4- Fever as in upper and lower respiratory tract infections.

Finally any other symptoms related to other systems.

30
COUGH
Cough is a forced expulsive manoeuvre against an initially closed glottis, causing a
characteristic sound and it is the most common symptom of respiratory tract
diseases (Devereux & Douglas, 2009). Cough is usually an involuntary reflex but
may be a voluntary act. Cough may be classified according to the duration. Acute if it
is less than 3 weeks and chronic if it is more than 8 weeks. Most of the acute
episodes are self-limiting and usually caused by infections and most common one is
viral .If the cough is acute then thinks of allergies and infections. If it is chronic think
in line of interstitial lung disease. Ask about the duration, time, aggravating and
relieving factors. Is it associated with sputum production or not. Use of drugs like
ACE inhibitors for hypertension. Ask regarding smoking. Did you ever smoke? How
many bidis or cigarettes per day. Is there any period of abstinent from smoking? If he
smoked the pipe, try to get them to quantify tobacco use in ounces per week (Moore-
Gillon, 2007).

Causes of cough (Devereux & Douglas, 2009).

Acute cough Normal chest X-ray Abnormal chest X-ray
Viral respiratory tract Pneumonia infection, Inhaled foreign body,
(<3weeks) Bacterial infection, Acute extrinsic allergic
Inhaled foreign body, alveolitis
Inhalation of irritant, dusts
/fumes

Chronic cough GORD Asthma Lung tumor, Tuberculosis,

(>8weeks) Rhinitis/sinusitis, Intrinsic lung disease,
Cigarette smoking, Bronchiectasis
Drugs especially, ACE
inhibitors, Irritant dusts or
fumes, Postviral bronchial,
hyper-reactivity

Other causes include (Devereux & Douglas, 2006)

Sinuses Infection
Infection

Larynx, trachea, large airways Tumours

Benign malignant, primary,
secondary
Aspiration
Gastro-oesophageal reflux
Foreign body
Irritant dusts

Small airways Asthma

Alveoli Post-viral airway reactivity

Chronic bronchitis (COPD)
Bronchiectasis
Bronchiolitis
Irritant dusts
Drugs, e.g. angiotensin-converting enzyme
Inhibitors
Infection: Pneumonia, tuberculosis
Alveolitis
Left ventricular failure
Irritant dusts

31
The sound of the cough and the circumstances in which it occurs may be helpful in
making the diagnosis.
Sound of the cough (Devereux & Douglas, 2009)
A feeble non-explosive ‘bovine’ cough with hoarseness- respiratory muscle
weakness, lung cancer invading the left recurrent laryngeal nerve with resultant
paralysis of the left vocal cord.
Harsh, barking or painful cough associated with hoarseness and stridor-
laryngeal inflammation.
A moist cough usually indicates secretions in the upper and larger airways
and occurs in bronchial infection and bronchiectasis.
A persistent moist ‘smoker’s’ cough first thing in the morning is typical of
chronic bronchitis. Any change in the pattern of this cough may indicate the
development of lung cancer.
A dry centrally painful and non-productive cough is a feature of tracheitis and
pneumonia.
A paroxysmal dry cough in patients with asthma may follow a viral respiratory
infection and last several months.
A chronic dry cough is common in interstitial disease, e.g. cryptogenic
fibrosing alveolitis.

Circumstances of the cough (Devereux & Douglas, 2009)

A nocturnal cough causing sleep disturbance is a common symptom of asthma.
Occult gastro-oesophageal reflux is a common cause of daytime cough, as is chronic
sinus disease with associated postnasal drip.
Angiotensin-converting enzyme inhibitors used to treat left ventricular failure
and hypertension may cause a dry cough, particularly in women. Coughing during
and after swallowing liquids suggests neuromuscular disease of the oropharynx.
Occupational asthma and exposure to dusts and fumes are a recognized cause of
chronic cough that typically lessens during weekends and holidays.
‘Red flag’ symptoms associated with cough that should prompt a chest X-ray
Haemoptysis, Breathlessness ,Fever ,Chest pain ,Weight loss.

SPUTUM PRODUCTION
Expectorated respiratory secretions are known as sputum or phlegm and
need to be specifically asked about. Patients may find it difficult to discuss sputum
production because of a natural reluctance, and it may be regularly swallowed.
There are four main types of sputum (G Devereux & G Douglas, 2009).
Type Appearance Cause
1. Serous Clear Watery Acute pulmonary oedema
Alveolar cell cancer
Frothy, Pink Chronic bronchitis/COPD
2. Mucoid Clear, grey Asthma

White, viscid Bronchopulmonary inf

3. Purulent Yellow, Pneumonia
Bronchiectasis
Green Cystic Fibrosis
Lung abscess

4. Rusty Rusty red Pneumococcal pneumonia

Amount
Ask how many teaspoons of sputum are coughed up each day. Statements by
patients that they cough up small (a teaspoonful) or large (a teacupful) amounts of
sputum are usually helpful (Devereux & Douglas, 2006).

32
Colour
Clear or mucoid sputum is produced by patients with COPD without active
infection.
Yellowish sputum is found in acute lower respiratory tract infection (live
neutrophils) and also in asthma (eosinophils).
Green sputum (dead neutrophils) indicates chronic infection as in
exacerbations of COPD, bronchiectasis. In the early stages of pneumococcal
pneumonia sputum may be of a characteristic rusty red color as pneumonic
inflammation passes through the red hepatization phase. In coal miners with
pneumoconiosis the rupture of necrotic areas of pulmonary fibrosis can result in the
expectoration of black sputum (melanoptysis) (Devereux & Douglas, 2006).
Purulent sputum is green because of lysed neutrophils which release the
green pigmented enzyme verdoperoxidase.

Taste or smell
‘Foul’ or ‘vile-tasting’ or -smelling sputum suggests anaerobic bacterial
infection and can occur in bronchiectasis, lung abscess and empyema. In
bronchiectasis a change of sputum taste may indicate an infective exacerbation
(Devereux & Douglas, 2006).
Solid material
In asthma and allergic bronchopulmonary aspergillosis viscid secretions can
accumulate in airways. When these are coughed up they appear as ‘worm-like’
structures that are casts of the bronchi. Other recognizable solid matter sometimes
coughed up includes necrotic tumour and inhaled foreign bodies such as food, teeth
and tablets (Devereux & Douglas, 2009).

HAEMOPTYSIS
Haemoptysis means coughing up of blood in the sputum. It may induces
anxiety in many patients because of its association with lung cancer. It is important
to determine whether the blood has been coughed up from the respiratory tract,
been vomited from the upper gastrointestinal tract or has suddenly appeared in the
mouth without coughing suggesting a nasopharyngeal origin. Haemoptysis is an
important symptom and can de life threatening. It should always be investigated
(Devereux & Douglas 2009).

DIAGNOSIS OF HAEMOPTYSIS AND HAEMATEMESIS

(Colin Ogilvie, Christopher C .Evans 1997)

HAEMOPTYSIS HAEMATEMESIS

1. Cough precedes haemorrhage 1. Nausea and vomiting precedes haemorrhage

2. Blood frothy from admixture with air 2. Generally airless
3. Sputum BRIGHT RED in colour and may 3. Blood often altered in colour b admixture with
be stained for many days gastric contents usually DARK RED or BROWN
4. History suggests respiratory 4. Previous history of indigestion
disease 5. Confirmed by GASTROSCOPY
5. Confirmed by BRONCHOSCOPY

33
Amount and appearance
Patients usually describe whether the haemoptysis is a small or large amount of pure
blood. Streaking of clear sputum with blood or the presence of blood clots in the
sputum for more than a week is suggestive of lung cancer. Haemoptysis with
purulent sputum suggests an infective cause such as bronchiectasis. Diffuse staining
of sputum with blood (pink froth) can occur in acute pulmonary oedema. Coughing
up large amounts of pure blood is fortunately rare but potentially life-threatening; the
most frequent causes are bronchiectasis, tuberculosis, and lung cancer. Less
frequent causes include pulmonary infarction, lung abscess, mycetoma , cystic
fibrosis aorto-bronchial fistula and Wegener’s granulomatosis (Devereux & Douglas,
2009).

Duration and frequency

Haemoptysis occurring intermittently for a few years usually in association with a
respiratory tract infection occurs in bronchiectasis. Daily haemoptysis for a week or
more is a common symptom of lung cancer, other causes include tuberculosis and
lung abscess. Single episode of haemoptysis may need immediate investigation if
they are very large or associated with symptoms, e.g. pleuritic chest pain and
breathlessness suggesting pulmonary thromboembolism and infarction (Devereux &
Douglas, 2009).

CHEST PAIN
Chest pain can originate from the pleura, the chest wall, and mediastinal
structures. The lungs are not a source of pain because of their exclusive autonomic
innervations. A careful history of chest pain should include site, radiation, mode of
onset, duration, severity, and aggravating/relieving factors including the effects
of breathing and movement (Devereux & Douglas, 2009).

Pleural pain
Pleuritic pain is typically sharp, stabbing and always intensified by inspiration
or coughing. Irritation of the parietal pleura of the upper six ribs is perceived as a
localized pain, whereas irritation of the parietal pleura overlying the central
diaphragm innervated by the phrenic nerve is referred to the neck or shoulder tip.
The lower six intercostal nerves innervate the parietal pleura of the lower ribs and
the outer diaphragm, and hence pain from these sites may be referred to the upper
abdomen (Devereux & Douglas, 2009).

Chest wall pain

Pain originating from the chest wall may indicate respiatory or
musculoskeletal disease. Generalized feeling of chest tightness or diffuse pain
suggests-asthma or COPD. Localized pain after vigorous coughing or direct trauma -
rib fractures or intercostal muscle injury.
Chest pain in a thoracic dermatomal distribution- Prevesicular herpes zoster
and intercostal nerve root compression.
Typically dull, aching or gnawing in nature ,unreIated to respiration,
progressively worsening and eventually disrupting sleep- Malignant chest wall pain
due to lung cancer ,mesothelioma or rib metastases (Devereux & Douglas,2009).
Mediastinal pain
Mediastinal pain is typically central, retrosternal and unrelated to respiration
or cough. However pain originating from the tracheobronchial tree due to infection or

34
inhalation of irritant dusts is typically retrosternal with a raw burning character and is
greatly worsened by cough.
A dull aching retrosternal pain that progresses to disturb sleep can be a
feature of malignancy invading mediastinal lymph nodes or enlarging thymoma.
Massive pulmonary thromboembolism sufficient to induce an acute increase
in right ventricular pressure may produce central chest pain identical to myocardial
ischaemia (Devereux & Douglas, 2009).

BREATHLESSNESS
Breathlessness (dyspnoea) is an undue awareness of breathing. It is a natural
consequence of strenuous physical exercise. A careful history of breathlessness
covers mode of onset, duration, progression, variation, aggravating or relieving
factors, severity and associated symptoms.
Ask what situations or activities bring on breathlessness as this may provide
clues as to the likely cause. Left ventricular failure and respiratory muscle weakness
commonly present with breathlessness when lying flat (orthopnoea). Orthopnoea can
be a feature of any severe lung disease. Breathlessness that wakes the patient from
sleep is typical of asthma and left ventricular failure (paroxysmal nocturnal dyspnoea
or PND). Patients with asthma are typically awakened between 3 and 5 a.m. and
have associated wheezing. Breathlessness that is worst first thing on waking in the
morning is more typical of COPD and may settle after coughing up sputum
(Devereux & Douglas, 2009).

Breathlessness: modes of onset , duration and progression

Minutes
 Pulmonary thromboembolism Asthma
Pneumothorax Inhaled foreign body
Acute LVF
Hours to days
 Pneumonia Asthma
 Exacerbation of COPD
Weeks to months
Anaemia Respiratory neuromuscular
Pleural effusion disorders
Months to years
COPD Pulmonary fibrosis
Pulmonary TB
Severity
It is important to determine the severity of breathlessness and the restrictions
it imposes on a patients everyday activities.
With milder degrees of breathlessness, ask about breathlessness during
work, carrying loads, heavy exertion, walking up hills or walking with contemporaries.
Breathlessness while walking on the flat, up gentle inclines, and stairs usually
indicates a more severe degree of breathlessness. Severely breathless patients are
dyspnoeic at rest, walking around the house, getting washed, while dressing, eating
or doing light housework (Devereux & Douglas. 2006).

35
Severity of breathlessness: Medical research council (MCR) classification
(Devereux & Douglas, 2009).
Grade 1 Breathless when hurrying on the level or walking up a slight
hill.
Grade 2 Breathless when walking with people of own age or on level
ground.
Grade 3 Has to stop because of breathlessness when walking on
level ground at own pace.

ADDED SOUNDS
Crackles
Interrupted non-musical sounds are called crackles. The terms rales and
crepitations should be abandoned. Crackles usually result from loss of stability of
peripheral airways, which collapse on expiration. With high inspiratory pressures air
enters rapidly into these distal airways with abrupt opening of alveoli and small
bronchi, producing the characteristic crackling noise.
Note when crackles occur within the respiratory cycle. Early inspiratory
crackles suggest small airways disease and can occur in bronchiolitis. In pulmonary
oedema crackles occur in mid-inspiration. Fine late inspiratory crackles, which sound
similar to rubbing hair between the fingers, are characteristic of pulmonary fibrosis.
Crackles may also be heard when air bubbles through secretions in major bronchi,
dilated bronchi as in bronchiectasis or in pulmonary cavities. These crackles sound
coarse, have a gurgling quality and change with coughing if the secretions are
dislodged. Crackles throughout inspiration and expiration are characteristic of
bronchiectasis.

Causes (Devereux & Douglas, 2009)

Phase of inspiration Cause

Early Small airways disease as in bronchiolitis

Middle Pulmonary oedema

Late Pulmonary fibrosis (fine)

Pulmonary oedema (medium)
Bronchial secretions in COPD,
pneumonia, etc. (coarse) lung abscess ,
tubercular lung cavities (coarse)

Biphasic bronchiesctasis (coarse)

Wheeze
Wheezes have a musical quality and should be timed in relation to the
respiratory cycle. The term, ronchus, should be abandoned. The sound is due to
continuous oscillation of opposing airway walls and implies airway narrowing.
Wheeze tends to be louder on expiration because airways normally dilate during
inspiration and narrows on expiration. Inspiratory wheeze therefore implies severe
airway narrowing. High-pitched wheeze arises from smaller airways and has a

36
whistling quality, while low- pitched wheeze originates from larger bronchi. However,
wheeze alone is a poor guide to the severity of airflow obstruction. In severe airways
obstruction wheeze may be absent because of reduced airflow producing ‘silent
chest’.
Wheeze is characteristic of asthma and COPD. A fixed bronchial obstruction,
most commonly due to lung cancer, may cause localized wheeze with a single
musical note that does not clear on coughing. It is very important to distinguish
wheeze from inspiratory stridor. Stridor is a harsh, rasping or croaking noise heard
on inspiration, which may be aggravated by coughing. Common causes are foreign
body or tumour partially occluding the larynx, trachea or a main bronchus. If you
suspect stridor ask the patient to cough and then breathe deeply in and out with the
mouth wide open. Listen carefully close to the patient’s mouth. Always investigate
stridor (Devereux & Douglas, 2009).

APNOEA
Apnoea is usually defined as involuntary absence of breathing for 10 seconds
or more: Patients with suspected sleep apnoea or hypopnoea syndrome are
commonly referred to respiratory specialists. Apnoea may also be voluntary or can
alternate with periods of hyperventilation as seen in Cheyne-Stokes breathing.

Respiratory system examination

Preparation for Examination: Client and Environment
Adequate respiratory examination requires a warm, well-lighted, quite room.
In addition to a adequate room lighting, a mechanism for supplementary lighting is
essential to aid in close inspection of specific areas.
Introduce yourself to the patient and ask for the permission to examine him. Ask
the patient to get on the bed. You may need to help him. Ask the patient to remove
all the garments covering chest and arms. Privacy is important because of the need
to examine the entire chest area.
Female clients may wish to have a gown or towel to cover their breasts while the
posterior thorax is being examined. Female attendant (chaperon) should be there
while examining female patient. Female clients can use a towel or gown to cover
their breasts when the posterior and lateral portions of the chest are being examined.
Arrange the patient so that his chest is at 45 degree to the horizontal (Cox, 2006).
The examination of the respiratory system generally is done in the traditional
sequence-Inspection, Palpation, Percusssion and Auscultation.

GENERAL EXAMINATION:
Examination of the respiratory system is incomplete without a simultaneous
general assessment. Points to be noted in general assessment are Physique, voice,
breathlessness, clubbing, cyanosis or pallor, intercostal recession, use of accessory
repiratory muscles, venous pulses and Lymph nodes.
INSPECTION
Inspection is performed to 1) measure and assess the pattern of respirations and 2)
assess the skin and the overall configuration, symmetry and integrity of the thorax.
Features to note in assessing the shape of the chest (Moore-Gillon, 2007)

Kyphosis
Scoliosis
Flattening

37
Over-inflation
Measurements of the chest (Moore-Gillon , 2007)
Rate of respiration
Rhythm of respiration
Chest expansion
Symmetry

A. Inspect both hands for clubbing, peripheral cyanosis, tremor, muscle

wasting, and tar staining.
How to examine (Cox, 2006)
1. Instruct the patient, that you are going to ‘examine his hands and fingers’.
2. Lift the patient’s right hand up to a few inches.
3. Bend down so that your eyes are at the same level as the patient’s hand and
look at the patient’s hand and look at the patient’s fingers from the sides.
4. Focus on one finger, the right middle is best, and look at the nail bed angle.
5. Decide if the angle is lost or preserved.
6. Next, examine other fingers on the right hand and then the left hand.

B. Inspect face for swelling and underneath tongue for cyanosis.

How to examine (Cox, 2006)
1. Briefly look at the face, is the face abnormally swollen? Is it plethoric or
cyanosed?
2. If you think the face might be swollen, then look at external jugular vein. Is it
distended and is it pulsating? Look at the chest wall and neck for any distended
veins?
The combination of a swollen face with a distended non-pusatile external jugular vein
suggests Superior Vena Caval (SVC) obstruction and prominent chest wall veins
lend support to the diagnosis.

C. Inspect right internal jugular vein for jugular venous pressure. Check for
hepatojugular reflux.
How to examine (Cox, 2006)
The vein is usually examined with the patient at 45 degree. This is because of the
following.
1. The normal maximum right atrial pressure is 7 cm water.
2. With the patient sitting straight up, the venous pulsation are normally too deep
in the chest to be seen.
3. With the patient lying flat the vein is always full and there is no visible
pulsation
4. With the patient at 45 degree, the venous pulsations are normally at the level
of the clavicle between the heads of sternocleidomastoid. They may or may
not be visible here. In a patient with elevated venous pressure, the pulsation
is seen high up in the neck.
If the jugular venous pressure is extremely elevated, the top of the
pulsation may be above the neck and so not visible. In such patients, the
internal jugular vein is better observed with the patient sitting up straight.

38
D. Inspect front of chest from foot end of the bed, assessing breathing pattern,
chest shape and movements.
How to examine (Cox, 2006)
1. Walk confidently to the end of the bed.
2. Explain to the patient. ‘I now want to have thorough look at your chest’.
For female patient if appropriate add, ‘could you please remove the
towel?’
3. Stand and look carefully at the patient’s chest.
4. Certain abnormalities will be obvious such as pursed lip breathing, the
presence of the chest drain, a depressed or prominent sternum, and
kyphoscoliosis.
5. Go through a checklist in your mind.
a) Is the patent’s breathing pattern is normal? If not, decide
what is abnormal. Is the patient’s breathing become deeper
and deeper before ceasing for a period (suggesting Cheyne-
Strokes respiration)?
b) Are they using their accessory muscles? Sometimes, pursed
lip breathing and accessory muscles will go together.
c) Is the chest shape normal? If not, does the chest look barrel
shaped?
d) Are their prominent chest wall veins (suggesting SVC
obstruction)?
e) Look at the neck. Is there swelling of the neck (suggesting
subcutaneous emphysema)?
f) Next, ask the patient to take a deep breath in and out
through their mouth. Show the patient what you want them to
do: ‘Please take deep breath in and out ….like this’.
g) As the patent breathes, watch the chest carefully and
concentrate whether one side is moving more than the other.
Force yourself to decide whether both sides move equally or
if there is difference.
h) Then ask the patient to repeat their deep breath in and out. If
your opinion remains unchanged this part of the examination
is complete.

E. Inspect front of chest and neck close up.

How to examine (Cox, 2006)
1. Go back to the left-hand side of the patient’s bed.
2. If there were any possible radiotherapy patches, inspect for small tattoo
marks, which are often over the irradiated skin.
3. Inspect for prominent chest wall vein suggesting SVC obstruction.
4. Look for a chest drain scar over the second intercostal space in the mid-
clavicular line.
5. Ask the patient to lift up right arm and look in the axilla for a chest drain scar
in the fourth, fifth and sixth intercostal spaces in the mid axillary line. Do the
same for left axilla.

39
F. Inspect the back of the chest assessing movementmovements, chest shape,
shape and other
visible abnormalities.
How to examine (Cox, 2006)
1. Stand behind the patient and inspect back of the chest.
2. Certain abnormalities will be obvious such as kyphoscoliosis, thoracotomy
scar, or a plaster over a cchest drain or aspiration site.
3. Inspect carefully for marks at the base of the lungs suggesting recent chest drain
or aspiration.
4. Next, ask the patient to take a deep breath in and then out through their
mouth.
5. As the patient breathes, watch the chest carefully and concentrate on
If one sidee is moving more than the other. A Asymmetrical expansion suggests
unilateral disease.
6. Then, ask the patient to repeat their deep breath in and out. If your opinion
remains unchanged, this part o of the examination is complete.
7. If you are unsure gett your patient to continue breathing until you are.
Abnormalities in the shape of the chest (Devereux & Douglas, 2009)
Increase in anteroposterior diameter.
When the antero-posterior
posterior diameter is increased compared with the lateral
diameter, the chest is described as ‘barrel shaped’. This is associated with lung
hyperinflation as seen in patients with severe COPD
COPD, Kyphosis and scoliosis.
Kyphosis is an exaggerated anterior curvature of the spine and scoliosis is
lateral curvature. Kyphoscoliosis
Kyphoscoliosis involving both deformities may be idiopathic or
secondary to childhood poliomyelitis or spinal tuberculosis. Such deformity can be
grossly disfiguring and disabling in otherwise healthy individuals.

40
Pectus carinatum (pigeon chest)
This is a localized prominence of the sternum and adjacent costal cartilages
often accompanied by indrawing of the ribs to form symmetrical horizontal grooves
(‘Harrison’s sulci’) above the costal margin. These deformities result from lung
hyperinflation with repeated vigorous contractions of the diaphragm while the bony
thorax is still in a pliable prepubertal state. It is most often caused by severe and
poorly controlled childhood asthma but can occur in osteomalacia and rickets.
Pectus excavatum (funnel chest)
This is a developmental deformity with localized depression of the lower end
of the sternum or, less commonly, depression of the whole length of the sternum.
The patient is usually asymptomatic but may express concern about the appearance
of the deformity. In severe cases the heart is displaced to the left and the ventilatory
capacity is reduced.

BREATHING PATTERNS
Condition Description Causes

Eupnea Normal breathing rate and

pattern
Tachypnea Increased respiratory rate Fever, anxiety, exercise,
shock
Bradypnea Decreased respiratory rate Sleep, drugs, metabolic
syndrome, head injury,
stroke
Apnea Absence of breathing Deceased patient, head
injury, stroke.
Hyperpnea Normal rate, but deep Emotional stress, diabetic
respirations ketoacidosis.
Cheyne Stokes Gradual increase and Increased intracranial
decrease in respirations pressure, brain stem
with periods of apnea injury.
Biot’s Rapid, deep Spinal meningitis, many
respirations(gasps) with CNS causes, head injury.
short pauses between sets
Kussmaul’s Tachypnea and hyperpnea Renal failure, metabolic
acidosis, diabetic
ketoacidosis.
Apneustic Prolonged inspiratory Lesions in brainstem.
phase
shortened expiratory
phase

PALPATION
Palpation is performed to 1) further assess abnormalities suggested by the
health history or by observation, such as tenderness, pulsations, masses or skin
lesions 2) assess the skin and subcutaneous structures 3) assess thoracic
expansion 4)assess tactile vocal fremitus and 5)assess tracheal position.

41
Points to note on palpation of the chest (Moore-Gillon, 2007)
• Swelling
• Pain and tenderness
• Tracheal position
• Cardiac impulse
• Asymmetry
• Tactile vocal fremitus (TVF)

A. Palpate right radial pulse for pulse rate and rhythm and consider if
bounding. Then check respiratory rate.
How to examine (Cox, 2006)
In the respiratory system, the aim is to assess rate and the rhythm and consider
whether the pulse is large volume (‘bounding’). The respiratory rate is one of the few
signs that can be altered voluntarily. If the patient realize you are watching their
chest closely, they find it very diff
difficult to ignore and tend to breath self--consciously.
Thus a little duplicity is required.
1. Having assessed the patient’s pulse, continue to give the impression that you are
examining it.
2. While doing this, inspect the patient’s breath in and out and count them over 30s
(10 s is too short).
Palpation of trachea.

How to examine (Cox, 2006)

1. Keep the patient positioned at 45 degree with their neck relaxed against the
pillow.
2. Say the patient something like like, I need to feel your windpipe. It is little
uncomfortable but I will try to be gentle.’
3. Then using your right index finger, gently palpate
alpate the patient’s neck about 2
cm superior to the suprasternal notch in the mid line.
4. You will feel a resistance there. If you move your finger 0.5 cm. to the right or
left, the resistance is more difficult to palpate. The resistance is the ttrachea.

42
 5. Palpate the space either side to get a feel for whether trachea is central.
6. Decide whether trachea is central or it is displaced to one side.
Tracheal deviation (Devereux & Douglas, 2009)
Towards the side of the lung lesion
• Upper lobe or lung collapse
• Upper lobe fibrosis
• Pneumonectomy
Away from the side of the lung lesion
• Tension pneumothorax
• Massive pleural effusion
Upper mediastinal mass
• Retrosternal goitre
• Lymphoma
• Lung cancer
B. Palpate the precordium for apex beat position, axillary lymph nodes, and if
suspected, tender areas and subcutaneous emphysema.
How to examine (Cox, 2006)
1. Ask the patient ‘is front of your chest painful or tender?’
2. If the answer is ‘yes’ ask for permission to examine. ‘Do you mind if I examine
the painful or tender areas?’ If permission is granted gently palpate the painful
spot. Can you elicit tenderness? Is the painful or tender spot within a hard
bony area suggesting rib injury?
3. If you have previously observed chest or neck swelling suggestive of
subcutaneous emphysemas, gently palpate the area, if subcutaneous
emphysema is present you will feel crackling sensation under the hand.
4. Palpate the apex beat position-palpate the cardiac impulse around the fifth
intercostal space in the mid-clavicular line. Always wait for 10 seconds then
once you found an apical pulsation, feel a little further down and out to see if it
is still palpable. Continue until it is no longer palpable. Go back to the furthest
point down and out at which you felt the cardiac impulse. This is the apex beat.
5. To examine for axillary lymph nodes, the patient needs to abduct their arms:
‘please lift your right arm out to the side….do mind if I check in your armpit for
glands?’
6. If the muscle and tendons around the axilla are tense, it is very difficult to
palpate nodes so take the weight of the patient’s right arm by holding it at the
elbow with your left arm (to allow the shoulder muscles to relax).
7. Using the palmer aspects of the fingers of your right hand, palpate in the
sequence the medial, anterior, lateral, posterior and apical aspects of the
axilla. Do you feel any round masses?
8. If so, palpate these specifically with the tips of your fingers to get a clear idea
of size and consistency.
9. Then do the same for the left axilla- this time using your right arm to support
the patient’s arm and left hand to palpate for nodes.
Deviation of the cardiac apex beat indicates shift of the lower
mediastinum. Displacement of the cardiac impulse without deviation of the
trachea is usually due to left ventricular enlargement but can also occur in
scoliosis, kyphoscoliosis, or severe pectus excavatum. The cardiac apex beat
may be difficult to localize in obesity, pericardial effusion, poor left ventricular
function or patients with lung hyperinflation as in COPD. The heave of right

43
 ventricular hypertrophy, found in severe pulmonary hypertension is best felt at
the left sternal edge (Devereux & Douglas, 2009).
C. Palpate for chest expansion anteriorly, comparing both sides.
How to examine (Cox, 2006)
Front of the chest
1. Your examination of the precordium should have identified any area of
tenderness- be careful of these.
2. Ask the patient to breath in and then out and to hold their breath in expiration
(so that the subsequent expansion will be maximal).
3. Then having warned the patient, place your hands firmly on the chest wall
with fingers gripping their sides (the lower rib cage).
4. Bring your thumb together to meet in the midline around the inferior part of the
sternum but not touching the chest. Exactly where you grip the patient’s side
will vary according to the patient’s size but essentially you grip in the position
that allows you to bring your thumb together to meet the mid-line.
5. Ask the patient to take a deep breath in and watch your thumb. If one thumb
moves less than the other, this indicates reduced expansion on that side.
6. Chest expansion can be easily recorded with a tape measure around the
chest at about the level of the nipples. Normal expansion is 5-8 cm (Moore-
Gillon, 2007).
Reduced expansion on one side indicates abnormality on that side, e.g. pleural
effusion, lung or lobar collapse, pneumothorax and unilateral fibrosis. Bilateral
reduction in chest wall movement is common in advanced COPD and diffuse
pulmonary fibrosis (Devereux & Douglas, 2009).

D. Change the patient’s position to facilitate examination of the neck and

the back of the chest. How to examine (Cox, 2006)
1. Ask the patient to sit forward. The ideal position is arms crossed — so that the
scapulae are rotated laterally. However, patients may have difficulty
maintaining this position. A more comfortable alternative is for the patient to
sit with their hands on their knees.
2. Explain that you now wish to examine their neck and the back of their chest.
3. Remove pillow and let down the headrest of the bed to allow easy access to
the patient’s back.
4. If need, ask the patient to shuffle down the bed to give you more room behind
him.
5. Check that the patient is comfortable — they will need to stay in this position
for a few minutes.
Back of the chest
1. First concentrate on the lower lobes. The same procedure is followed as for
the front of the chest, this time with the doctor standing behind the patient.
2. Ask the patient to breath in and then out and to hold their breath in expiration.
3. To assess lower lobes,
1. Place your hands firmly on the chest wall with fingers gripping their
Sides (the lower rib cage) and bring your thumb together to meet in the
mid line around the lower thoracic spine but not touching the chest.
2. Ask the patient to take a deep breath in and watch your thumb. If one
thumb moves less than the other- indicating reduced expansion on that
side.
3. To assess upper lobes.

44
 Do the same this time higher up with thumb meeting around T3 level.
E. Examine the neck for enlarged lymph nodes.
As for the axillary nodes, it is important for the muscles to be as relaxed as possible
to facilitate palpation of any neck nodes. Also, it is better (less painful) if in general
you use the flats of the palmer aspects of your fingers and only use the tips of your
fingers where necessary to get a better feel.
1. Stand behind the patient.
2. Ask the patient to flex their head slightly (so that the neck muscles are
relaxed).
3. If you palpate any lumps, ascertain their approximate size, consistency (firm
or hard), where they are discrete or fused together, and whether they are
attached to underlying structures.
4. Supraclavicular
a) Using your index, middle, and ring fingers together gently palpate both
supraclavicular fossae.
b) Use the tips of your index fingers to palpate space between the two
heads of sternocleidomastoid.
5. Sternocleidomastoid.
1. It is best to examine the two sides separately — avoiding potential
bilateral palpation of the carotid sinus, which may cause fainting.
2. Use your right index, middle, and ring fingers together to slowly
palpate up the right sternocleidomastoid to the angle of the jaw.
3. Use your left hand to do the same on the patient’s left side.
6. Submandibular
1. Here, we have to use the tips of our fingers. Use index, middle, and
ring fingers together to palpate both sides simultaneously.
2. Palpate under the angle of the jaw.
3. Work your way forward on both sides to meet at the chin.

PERCUSSION:
Points to note on percussion of the chest (Moore-Gillon, 2007)

45
 •Resonance
•Dullness
• Pain and tenderness
A. Percuss front of chest and in the axillae, comparing the two sides.
How to examine: the basic technique (Cox, 2006)
There are two different techniques — a normal technique for percussing over the
chest wall in general and a modified technique for over the clavicle.
Percussion over the chest wall
1. Place your left hand palm down on the chest wall.
2. Align your fingers with the ribs so that your middle finger is between ribs.
3. Spread your finger slightly apart.
4. Press your left middle finger firmly against the chest wall,
5. Now, hold right hand extended at the wrist with middle metacarpophalangeal
joint slightly flexed, so that distal phalanx is roughly at right angles to the
hand.
6. Now hyperextend the wrist further in preparation to strike your left middle
finger.
7. Then, briskly flex the wrist and use pad of your right middle finger to strike
the dorsum of the middle phalanx of the left middle finger.
8. Remove percussing finger immediately.
9. With same motion of the right hand, strike the left middle finger for a second
time, again removing the percussing finger quickly. (second strike is
nonessential and merely provides confirmation of your first attempt; if you
are confident striking once, this is acceptable).
10. While doing the same listen to noise made and sense the feeling of the two
fingers meeting— percussion note is both heard and felt.
Percussion over clavicle
For percussing the clavicle, only the right hand is used. The same technique
is applied except that the pad of the right middle finger strike the clavicle directly
rather than the left middle finger. This can be painful for the patient, so gentle
percussion is needed.
The aim of the chest percussion is to compare right and left side of the chest.
There are three normal percussion sounds or sensations.
1. Dull — occurs over solid organs such as liver.
2. Resonant — occurs over the lung.
3. Tympanic — occurs over the abdomen.
The resonance over the lung is present to approximately the sixth rib anteriorly, the
eight rib in the axilla, and tenth rib posteriorly. There is usually liver and cardiac
dullness anteriorly.
How to examine (Cox, 2006)
Front of the chest and axillae
The patient should remain at 45 degree, supported by pillows.
1. First, percuss the patient’s right clavicle over its medial third (only the medial
third overlies lung tissue).
2. Next percuss left clavicle using the same force, comparing the noise and
sensation — is one side duller than the other?
3. Now percuss the chest wall anteriorly: upper right, upper left, middle right,
middle left, lower right, lower left using the same force and comparing the
sides as you go. In female patients, their breast may make the percussion
note dull and percussion more difficult.

46
 4. Ask the patient to abduct their right arm and then percuss the right upper
axilla and compare with the left upper axilla; next percuss the right and then
left lower axillae.
5. If at any point you think there might be a difference but are unsure, repeat the
percussion in that area.

Back of the chest

1. The patient should be sitting up and percussion performed with the doctor
standing slightly behind him
2. Percuss the chest wall posteriorly: upper right, upper left, middle right, middle
left, lower right, lower left, always using the same force and comparing the
side as you go.
Pneumothorax produces a hyperresonant note. Percussion over solid structures
such as the liver, heart or a consolidated area of lung produces a dull note. Find
the upper level of liver dullness by percussing down the anterior wall of the right
chest. Normally in adults the upper level of liver dullness is at the level of 5th rib
in the midclavicular line. Resonance below this is a sign of hyperinflation as
occurs in COPD or severe asthma. The area of cardiac dullness present on the
left anterior chest may be decreased when the lungs are hyperinflated.
Percussion over a fluid-filled area, such as a pleural effusion, produces an
extremely dull note, known as ‘stony dull’. Basal dullness due to elevation of the
diaphragm is easily confused with pleural fluid.
Percussion note
Type Detected Over
Resonant Normal lung
Hyperresonant Pneumothorax
Dull Pulmonary consolidation
Pulmonary collapse
Stony dull Severe pulmonary fibrosis
Pleural effusion
Haemothorax

B. Assess tactile vocal fremitus at the front of the chest and in the axillae,
comparing the two sides.
How to examine (Cox, 2006)
You should already have established if there are any tender areas — if so you
may need to modify your examination to avoid these areas.
Front of the chest and axillae
1. Assess TVF at the apices
1. The vibration over the clavicle is used to assess apical TVF.
2. Place the ulnar border of your right hand on the patient’s right clavicle.
3. Ask the patient to say ‘ninety nine’. Whilst they are speaking, concentrate on
the vibration transmitted to your right hand.
4. Next, place the ulnar border of your right hand on the patient’s left clavicle,
asks the patient to say ‘ninety-nine’, and again assess the vibration
transmitted to your right hand .Note that the vibration is same on both sides in
normal subjects.
5. If you are not sure, recheck.
2. Assess TVF of the upper lobes

47
 1. Place the ulnar border of your right hand over the top of the right side of the
patient’s chest.
2. Ask the patient to say ‘ninety —nine’ concentrating on the vibration
transmitted to your right hand.
3. Do the same on the patient’s left side and consider if the two sides are equal.
4. If you are not sure, recheck.
3. Assess TVF of lateral aspects of the lungs
1. Ask the patient to abduct their right arm: ‘please lift your right arm out to the
side... Do you mind if I feel in your armpit (again)’.
2. Place the ulnar border of your right hand on the medial aspects of the
patient’s right axilla.
3. Ask the patient to say ‘ninety —nine’ concentrating on the vibration
transmitted to your hand.
4. Do the same for left axilla, again comparing the two sides.
Back of the chest
You should be standing behind the patient.
1. Assess TVF of the upper lobes
Place the ulnar border of your right hand over the top of the right side of the patient’s
chest and repeat as for the front, comparing both sides.
2. Assess TVF of the lower lobes
Place the ulnar border of your right hand over the lower aspects of the right side of
the patient’s chest and repeat as above, comparing both sides.
A. AUSCULTATION
Following points to be noted on auscultation of the chest (Moore-Gillon, 2007)
• Vesicular breath sounds
• Bronchial breath sounds
• Vocal resonance
-bronchophony
-whisphering pectoriloquy
-aegophony
Added sounds
Pleural rub
Wheezes
Crackles

A. Auscultate over the front of the chest and in the axillae, comparing the two
sides.
Chest auscultation is performed with the stethoscope. There is no consensus
on whether the bell or the diaphragm should be used. The case for the bell is strong:
in theory it should be better for hearing breath sounds as these are mostly low
pitched; skin or hairs being stretched under the diaphragm may create unwanted
artifact. However, these issues seem to be little practical importance and it is
common practice to auscultate using the diaphragm apart from the lung apices
where good contact with the diaphragm is difficult and the bell is used.
1. Place the diaphragm on the chest wall.
2. Ask the patient to breath in and out through their mouth deeply and quite fast —
respiratory rate about 30 beat per minute.
3. Listen to the sounds generated.
Bear in mind that too much deep breathing may make the patient dizzy or even
collapse (hyperventilation).

48
The normal breath sounds over the chest wall are called ‘vesicular’. The quality of
these sounds is soft. Their origins not completely understood. The inspiratory sound
is thought to be due to air turbulence within the small air-way and alveoli. Thus the
intensity of the sound gradually increased through inspiration as more and more air
reaches to the alveoli. The initial part of the expiratory sound is initially due to air
flowing out of the alveoli. Once, these have emptied, the sounds heard originates in
the large airway — further away from the stethoscope — so that the noise become
quieter in the second half of the expiration, fading away to become inaudible.

How to examine (Cox, 2006)

Front of the chest axillae
1. Place the diaphragm of your stethoscope over the patient’s chest starting just
below the right clavicle.
2. Ask the patient to breathe in deep and fast through the mouth. Demonstrate
this to the patient.
3. After each breath move your stethoscope to the next site, comparing both
sides. You may need to encourage the patient to keep breathing by saying
‘in... out... in.. out...’
4. Decide on the intensity and the character of the breath sounds and the
presence and absence of added sounds as you go.
5. If you suspect an abnormality, listen longer in that area and confirm whether
the finding is there or not. If so determine its nature (abnormality may be quite
localized so the abnormal sounds are heard only over a small area).
6. Finally, use your bell to listen to the right and left apices alternatively.
Back of the chest
1. Stand behind the patient
2. Use the diaphragm
3. Ausculate over the chest: upper right, upper left, middle right, middle left,
lower left lower right.
Normal breath sounds
Normal breath sounds heard at the chest wall are caused by turbulent flow in
large airways. When heard through a stethoscope these normal breath sounds have
a rustling quality and are said to be ‘vesicular’. The larynx makes little contribution in
quiet breathing but may accentuate the noise in deep respiration. The pattern and
intensity of breath sounds reflect regional ventilation. In the normal upright lung,
breath sounds are loudest at the apex in early inspiration and at the bases in mid-
inspiration. During expiration, normal breath sounds rapidly fade because of
decreasing airflow. In their passage through normal lungs the intensity and
frequency of the sounds are decreased since normal lung parenchyma transmits
sounds poorly.
Bronchial breathing
Bronchial breathing is characterized by breath sounds that are high-pitched with a
hollow or blowing quality similar to those heard over the trachea and larynx during
tidal breathing. The breath sounds are of similar length and intensity in both
inspiration and expiration and have a characteristic pause between. Bronchial breath
sounds are found whenever normal lung tissue is replaced by uniformly conducting
tissue, whether through consolidation, fibrosis or collapse and the relevant major
bronchus is patent. The presence of bronchial breathing is confirmed by finding
whispering pectoriloquy. Vocal resonance is also increased over consolidated lung,
which readily transmits sound.

49
Bronchial breathing and whispering pectoriloquy are heard most commonly over
areas of pulmonary consolidation but can sometimes be heard over areas of
collapse or dense fibrosis if the underlying major bronchus is patent. The presence
of bronchial breathing, therefore, tends to exclude the possibility of an obstructing
lung cancer. Both may also be heard at the top of a pleural effusion.
Causes of bronchial breath sounds
Common
• Lung consolidation (pneumonia)
Uncommon
• Localized pulmonary fibrosis
• At the top of a pleural effusion
• Collapsed lung (where the underlying major bronchus is patent)
Causes of diminished vesicular breathing
Reduced conduction
• Obesity/thick chest wall
• Pleural effusion or thickening
• Pneumothorax
Reduced air flow
• Generalized, e.g. COPD
• Localized, e.g. collapsed lung due to occluding lung cancer
B. Assess vocal resonance at the front of the chest and in the axillae,
comparing the two sides.

How to examine (Cox, 2006)

Front of the chest and axillae
1. Assess VR at the apices
1. Place the bell of the stethoscope over the patient’s right supraclavicular
fossa.
2. Ask the patient to say ‘ninety - nine’, then ‘e’ for aegophony and ask the
patient to whisper 1, 2, 3 for whispering pectoriloquy.
3. When they are speaking concentrate on the sound coming through the
stethoscope. Next, place the bell of the stethoscope over the patient’s left
supraclavicular fossa.
4. Repeat the same procedure as mentioned above.
5. Assess is the sound same on both sides or not.
6. If you are not sure recheck.
2. Assess VR of the upper lobes
1. Place the diaphragm of your stethoscope over the top of the right side
of the patient’s chest.
2. Ask the patient to say ‘ninety — nine’ then ‘e’ for aegophony and ask
the patient to whisper 1, 2, 3 for whispering pectoriloquy, concentrating
on the sound transmitted through the stethoscope.
3. Do the same on the patient’s left side and consider if the sides are
equal.
3. Assess VR over lateral aspects of the lungs
1. Ask the patient to abduct their right arm: ‘please lift your right arm out
to the side... ask the permission to examine.
2. Place the diaphragm of your stethoscope on the medial aspect of the
patient s right axilla

50
 3. Ask the patient to say ninety - nine then ‘e’ for aegophony and ask the
patient to whisper 1,2,3, for whispering pectoriloquy, concentrating on
the sound transmitted through the stethoscope
4. Do the same for the left axilla, again comparing both the sides.
Back of the chest
1. Stand behind the patient.
2. Use the diaphragm.
3. Assess vocal resonance over the chest: upper right, upper left, middle right,
middle left, and lower left, lower right.

FINDINGS OF COMMON RESPIRATORY DISEASES:

Disorder Inspection Palpation Percussion Auscultation

Hyperinflation, Impaired
Prolonged
Bronchial asthma use of expansion, Hyperresonance,
expiration,
(acute attack) accessory decreased low diaphragms
wheezes
muscles fremitus
Absent
Pneumothorax Lag on affected Absent Hyperresonant or
breath
(complete) side fremitus tympanitic
sounds
Decreased
fremitus,
trachea
Absent
Pleural effusion Lag on affected and heart Dullness or
breath
(large) side shifted flatness
sounds
toward
affected
side
Decreased
fremitus,
trachea
Absent
Atelectasis(lobar Lag on affected and heart Dullness or
breath
obstruction) side shifted flatness
sounds
toward
affected
side

COMMON RESPIRATORY INVESTIGATIONS

Chest X-ray
The chest X-ray is an important extension of the clinical examination.
particularly in patients with respiratory symptoms and those with unexplained fever.
The standard chest X-ray is a posteroanterior (PA) view taken with the film against
the front of the chest and the X-ray source 2 m behind the patient. In an
anteroposterior film the X-ray source is in front of the patient, which tends to enlarge
anterior structures such as the heart.
Interpretation of a chest X-ray requires knowledge of anatomy and pathology
and appreciation of normal appearances. A lateral film provides additional
information about the nature and site of the pulmonary, pleural or mediastinal
abnormality. A systematic approach is the most useful way of interpretation
(Devereux & Douglas, 2009).

51
 • Check name, date and orientation of the film - anteroposterior films are
usually marked as such; otherwise assume posteroanterior.
• Lung fields: should be of equal translucency. Identify the horizontal fissure
running from the right hilum to the 6th rib in the axillary line.
• Lung apices; look specifically for masses, cavitation, consolidation, etc.
above and behind the clavicles.
• Trachea: confirm this is central, midway between the ends of the clavicles.
Look for paratracheal masses, retrosternal goitre, etc.
• Heart: check the heart is of normal shape and the maximum diameter is less
than half the internal transthoracic diameter (cardiothoracic ratio). Look specifically
for any retrocardiac masses.
• Hila: the left hilum should be higher than the right. Compare the shape and
density of the two hila - both should appear concave laterally: A convex appearance
suggests a mass or lymphadenopathy
• Diaphragm: the right hemidihphragrm should be higher than the left. The
anterior end of the 6th rib should cross the mid-diaphragm. If this does not reach,
then hyperinflation is present.
• Costophrenic angles: these should be well-defined, acute angles. Loss of
one or both suggests pleural fluid or pleural thickening.
• Soft tissues: note the presence of both breast shadows in female patients.
Look around the chest wall for any soft tissue masses or subcutaneous emphysema,
etc.
• Bones: step closer to the film and look at the ribs, scapulae and vertebrae.
Look for fractures at the edges of each bone.
Spirometry
• Dynamic lung volumes are measured by inhaling to total lung capacity and
then exhaling into a spirometer with maximal effort to residual volume. The volume
exhaled-in the first second and the total volume exhaled is known as the forced
expiratory volume in 1 second (FEV1) and the forced vital capacity (FVC). Normal
predictive values for FEV1 and FVC are available and are influenced by age, gender,
height and race. In normal young and middle-aged adults the FEV1/FVC ratio is
usually greater than 75%, while in the elderly the ratio is usually 70-75%. A reduction
in the FEV1/FVC ratio indicates airway obstruction. The severity of obstruction is
represented by the absolute FEV1 expressed as a percentage of the predicted
.Airway obstruction that reverses with inhaled beta 2 agonist or a trial of oral steroid
over 5 days or more (an absolute increase in FEV1 >200 ml, that is> 15% of
baseline) favours a diagnosis of asthma over COPD.
In interstitial lung disorders such as cryptogenic fibrosing alveolitis pulmonary
sarcoidosis or extrinsic allergic alveolitis there is a decrease in FVC with
preservation of FEV1/FVC ratio, a restrictive defect (Devereux & Douglas, 2009).

Respiratory system examination at a glance (Devereux & Douglas, 2009)

1) Note the patient’s general appearance and demeanour.
2) Observe the respiratory rate and pattern of breathing, look for use of
accessory muscles.
3) Listen for hoarseness and stridor.
4) Look for central cyanosis of the lips and tongue.
5) Measure the blood pressure.
6) Examine the skin for rashes and nodules.
7) Examine the hands for finger clubbing, peripheral cyanosis and tremor.

52
 8) Examine the neck for raised JVP and cervical lymphadenopathy.
9) Inspect the chest front and back for abnormalities of shape and scars.
10) Feel the trachea and cardiac apex beat for evidence of mediastinal shift.
11) Percuss the chest front and back for areas of dullness or hyper-Resonance.
12) Listen to the chest front and back for altered breath sounds and added
sounds.

Key points to be remembered in respiratory system are

(Devereux & Douglas, 2009)
a) Night-time wakening with cough and wheeze is characteristic of poorly
controlled asthma.
b) Always consider an occupational cause in adult-onset asthma.
c) Consider sleep apnoea in patients who snore and have day time
sleepiness. Ask specifically about driving and occupational risks.
d) Chronic cough with a normal chest X-ray is usually caused by smoking,
sinusitis, GERD, asthma or ACE inhibitors.
e) Patients with severe COPD may lose weight.
f) Respiratory rate, blood pressure and mental state are important markers of
pneumonia severity.
g) Always investigate haemoptysis in a smoker with a chest X-ray and, if
appropriate, bronchoscopy .
h) ‘Bovine cough’ or superior vena caval obstruction in a patient with lung
cancer indicates that the tumor is inoperable.
i) Bronchial breathing is unlikely in lung cancer.
j) Distinguish stridor from wheeze, and always investigate its cause.
k) Pulmonary thromboembolism usually occurs in the absence of clinical signs
of deep vein thrombosis.
l) Local chest wall tenderness occurs in costochondritis, rib fracture and
pulmonary infarction.
m) Always perform pleural biopsy on initial aspiration of an undiagnosed
pleural effusion.
n) In patients with suspected pulmonary tuberculosis, arrange urgent sputum
examination by auramine (screening) and Ziehl-Neelsen staining .If
positive, the patient should be isolated and treated, and the disease
notified.

References:

1) Devereux, G. & Douglas, G. (2009) The respiratory system. In: Douglas, G.,
Nicol, F., Robertson, C., (Eds.), Macleod’s clinical examination, Elsevier,
Churchill Livingstone, London. pp. 153-182

2) Moore-Gillon, J. (2007) Respiratory system. In: Swash, M., Glynn, M., (Eds.),
Hutchinson’s Clinical Methods, pp. 55-69, W.B. Saunders, London.
3) Cox, L., T. (2006) Respiratory system. In: Cox, L., T. & Roper, T., A., (Eds.),
Clinical skills, pp. 76-120, Oxford University Press, Oxford.

53
4) Ogilvie, C. & Evans, C., C. (1997), chamberlain’s symptoms and signs in clinical
medicine. An Introduction to Medical Diagnosis, PP. 103-130.

54
CHAPTER-IV
 EXAMINATION OF GASTROINTESTINAL SYSTEM
INTRODUCTION

Gastroenterology, perhaps more than any other specialty, has to approach the patient as a
whole and not as isolated systems. Many gastrointestinal (GI) illnesses have extra-intestinal
or extra-hepatic manifestations affecting the nervous system, skin or joints. Conversely,
many non-GI conditions, such as thyroid, adrenal and cardiovascular diseases, may
present with symptoms referable to the GI tract. This underlines the importance of a
systematic history and clinical examination prior to investigation and diagnosis.

THE CARDINAL SYMPTOMS OF G.I. SYSTEM

 Anorexia (loss of appetite)

 Dysphagia, odynophagia: toothache, bleeding gum, dentures
 Nausea, vomiting, retching, hiccough (singultus)
 Heartburn (pyrosis), water brash (salivary hypersecretion) and regurgitation
 (Effortless appearance of gastric contents in mouth)
 Jaundice
 Pain abdomen (including biliary colic)
 Haematemesis
 Bleeding per rectum and melaena
 Alteration in bowel habit: diarrhea or constipation, mucus in stool
 Swelling in the abdomen, distension of the abdomen or mass in the abdomen
 Wind or flatulence (belching or flatus)
 Loss of weight
 Edema
 Urinary symptoms

1. ANOREXIA

Anorexia is loss of appetite. It hints important pathology in upper gastrointestinal

and liver diseases including malignancy and hepatitis but does not specifically indicate
gastrointestinal disease. Weight loss (<3 kg in 6 months) without any other symptoms,
usually does not indicate underlying disease. Weight loss with normal, or even increased,
calorie intake, occur in type I diabetes mellitus, hyperthyroidism, malabsorption, and fever.
Very rapid weight loss (> 0.5 kg/day) invariably indicates fluid loss, and causes include
diuretic therapy, severe diarrhoea, vomiting, heat illness or seven burns. Weight loss is

55
common in malignancies of liver and pancreas, but is a late feature of colon cancer. When
severe it is called cancer cachexia (Cox and Roper, 2006).

2. DYSPEPSIA
Indigestion is a commonly used term for ill-defined symptoms arising from the upper
gastrointestinal tract that includes epigastric pain, heartburn, distension, nausea or an acid
feeling occurring after eating or drinking. It is associated with gastro-oesophageal reflux
disease, peptic ulcer disease and non-ulcer or functional dyspepsia. Dyspepsia is very
common, affects up to 80% of the population at some time in their lives. Pain which is
worse with an empty stomach and eased by eating is the classical peptic ulcer description.
This is sometimes so localized that the patient indicates single spot where the pain occurs;
the 'finger pointing' sign. 'Fat intolerance' is common to all causes of dyspepsia and does
not specifically suggest gall bladder disease (Cox and Roper, 2006).

3. DYSPHAGIA
Dysphagia is difficulty in swallowing. Dysphagia may be caused by disorders
affecting any part of following structures:
- mouth (painful ulcers, mouth or throat infections, ill-fitting dentures)
- brain stem (cerebrovascular accidents, bulbar palsy)
- oesophagus (benign stricture, cancer).
An oesophageal or upper gastric carcinoma presents with dysphagia for solids,
progressing to liquids. Neurological dysphagia resulting from bulbar or pseudobulbar
palsies is typically worse for liquids than for solids, and may be accompanied by choking,
spluttering and regurgitation of fluid from the nose. Neuromuscular dysphagia or
oesophageal dysmotility, most often presents in middle-age. It is worse for solids and may
be helped by liquids and sitting upright.
Achalasia, when the lower oesophageal sphincter fails to relax normally, leads to
progressive oesophageal dilatation above the sphincter.

Oesophageal dysmotility may be associated with oesophageal spasm and central

chest pain which may be confused with cardiac pain. 'Mechanical' dysphagia is often due to
oesophageal stricture. When associated with weight loss, a short history, and no heartburn,
suspect oesophageal cancer. Longstanding dysphagia without weight loss but
56
accompanied by heartburn is more likely to be due to a benign peptic stricture.
Odynophagia is pain on swallowing often precipitated by drinking hot liquids. It may be
present with or without dysphagia and is often an indication of active esophageal ulceration
from peptic oesophagitis or esophageal candidiasis (Cox and Roper, 2006).

4. NAUSEA AND VOMITING

Nausea is the sensation of feeling sick. Vomiting is the expulsion of gastric contents
via the mouth. It is a neurogenic response triggered by chemoreceptors in the brainstem or
reflexly through irritation of the stomach. It consists of a phase of nausea, hypersalivation,
pallor, sweating and hyperventilation.
Find out if vomiting is associated with abdominal pain or discomfort suggesting upper
GI disorders, drugs the patient is taking, projectile vomiting of large volumes, bile-stained
(green) vomit, acute or chronic, effortless or not, quantity, content, contain blood or not, any
antecedent food intake (Cox and Roper, 2006).

5. HEARTBURN AND OTHER REFLUX SYMPTOMS

It is the acid reflux from the stomach into the esophagus, causes a hot, burning
retrosternal discomfort which radiates upwards. Most common cause is gastro-oesophageal
reflux disease. It is often accompanied by acid reflux due to regurgitation of acid producing
a sour taste in the mouth. The burning quality and upward radiation of heartburn and its
occurrence on lying flat or bending forward help to differentiate it from retrosternal chest
pain originating from the heart. Water brash is the sudden appearance of excessive saliva
in the mouth due to reflex salivation and suggests gastro-oesophageal reflux disease.
Patient should be asked for accompanying nausea, waterbrash, aggravation by spicy food,
by lying flat, response with antacids (Cox and Roper, 2006).

6. JAUNDICE
Jaundice is a yellowish discoloration of the skin, sclerae and mucous membranes
and is due to hyperbilirubinaemia. Jaundice maybe:
- Prehepatic (e.g. haemolysis)
- Hepatocellular (e.g. hepatitis, hereditary liver enzyme deficiencies)
- Obstructive (e.g. biliary obstruction due to gallstones, cancer of the head of the
pancreas or drug-induced cholestasis)

57
Patient with jaundice should be asked for duration, colour of stool and urine associated
itching or pain, any recent blood transfusion and current drug history (Cox and Roper,
2006).

7. ABDOMINAL PAIN
It is a common symptom of gastrointestinal disease. When patient complains of pain,
look for the site, intensity, character, radiation, duration and frequency, together with
aggravating and relieving factors.

Analysis of abdominal pain (Cox and Roper, 2006):

Disorder
Peptic ulcer Biliary colic Acute Renal colic
pancreatitis
Main site Epigastric Epigastrium/right Epigastrium/left Loin
hypochondrium hypochondrium
Radiation Into the back Beneath right Into the back Into genitalia/inner
scapula May become thigh
Right shoulder tip generalized
Character Gnawing Constant Constant Constant with small
fluctuations
Severity Mild to Severe Severe Severe
moderate
Duration ½-2 h 4-24 h > 24 h 4-24 h
Frequency Remission for Unpredictable - Unpredictable - Usually a discrete
and weeks/months can enumerate can enumerate episode
Periodicity attacks attacks
Special Nocturnal After heavy Following
times of Especially drinking periods of
Occurrence when hungry, dehydration
e.g. between
meals
Aggravating Stress, spicy Unable to eat Alcohol
factors foods, alcohol, during bouts of Unable to eat
smoking, pain during bouts of
aspirin pain
Relieving Food, Eased by sitting
factors antacids, upright
vomiting
Associated Family history, Restlessness, Vomiting, Restlessness,
phenomena GI bleeding, vomiting, jaundice, vomiting,
perforation jaundice paralytic ileus haematuria, dysuria
Causes Helicobacter Gallstones (bile Gallstones, Dehydration,
pylori- salt disorders, drugs, e.g. hyperuricaemia,
associated obesity, diuretics, alcohol hypercalcaemia
gastritis haemolytic Hypercalcaemia
anaemia)
58
 Sites of acute abdominal pain and
related

Pain from foregut structures (stomach, pancreas, liver and biliary system) is
localized above the umbilicus. Pain due to small intestinal obstruction, is felt around the
umbilicus (periumbilical). If the parietal peritoneum is involved, the pain will localize to that
area, e.g. right iliac fossa pain in acute appendicitis and in Crohn's disease of the terminal
ileum.
Colonic pain is characteristically felt below the umbilicus, e.g. pain in the left iliac
fossa from diverticular disease of the sigmoid colon. Pain from the hepatic flexure can be
located in the right hypochondrium.
Pain from the pancreas is usually felt in the midline and radiates through to the back.
The pain of renal colic classically radiates from the flank into the groin
In young males, unilateral testicular pain strongly suggests torsion of the testis rather
than epididymo-orchitis. In women one must consider possible gynaecological causes such
as ruptured ovarian cyst, pelvic inflammatory disease or an ectopic pregnancy. In patients,
with acute right iliac fossa pain, always consider appendicitis (Swash, 2002).

Nature of pain
Is the pain constant or colicky? Constant pain usually arises from a solid organ, e.g.
pancreatitis. Colicky pain lasts for a short period of time (seconds or minutes), eases off

59
and then returns. Colicky pain comes from hollow structures, e.g. small or large bowel
usually in association with obstruction. Biliary and renal 'colic' are misnamed, as the pain
resulting from a stone obstructing the bile duct or ureter builds to a peak over several hours
before declining (Cox and Roper, 2006).

Speed of onset
Sudden onset of abdominal pain, severe in intensity, which progresses rapidly and
become generalized in site and constant in nature, is suggestive of perforation of a hollow
viscus, a ruptured abdominal aortic aneurysm of mesenteric infarction. Torsion of an organ
causes rapid onset of abdominal pain as it occludes the blood supply. A slower onset and
progression of abdominal pain over hours or days suggests inflammatory disorders, e.g.
acute cholecystitis, appendicitis or diverticular disease (Cox and Roper, 2006).

8. HAEMATEMESIS
Haematemesis i.e. vomiting of blood, results from bleeding in the upper GI tract
above the duodenojejunal flexure. The blood is degraded by gastric pepsin, it turns black,
when vomited it looks like ground coffee. In case of bleeding from oesophageal varices,
fresh blood wells up in the mouth rather than being actively vomited. Upper gastrointestinal
bleeding often results in melaena, the passage of altered blood per rectum. To gauge the
severity of the bleed, ask about symptoms suggesting hypovolaemia.
Peptic ulcer is a common cause of upper gastrointestinal bleeding. However, 25% of
bleeding peptic ulcers presents without a previous history of dyspepsia, and this proportion
is higher in the elderly and patients taking non-steroidal anti-inflammatory drugs. Ask
patients about recent ingestion of aspirin, non-steroidal anti-inflammatory drugs and
alcohol.

Excessive alcohol ingestion may cause haematemesis:

- directly by acute alcoholic gastritis or alcohol-induced vomiting leading to a Mallory-
Weiss tear.
- Indirectly by the development of liver cirrhosis causing portal hypertension and
bleeding esophageal varices (Swash, 2002).

60
9. RECTAL BLEEDING AND MELAENA
Fresh rectal bleeding indicates a disorder in the anal canal, rectum or colon. Blood
may be mixed with the stool, may coat the surface of otherwise normal stool, or may be
seen on the toilet paper or in the pan. Melaena is the passage of black, tarry stool with a
characteristic odour signifying blood loss in the upper gastrointestinal tract. Occasionally,
with a particularly brisk or severe upper gastrointestinal bleed, blood may pass through the
intestine unaltered causing fresh rectal bleeding. Such a brisk bleed will be accompanied by
other features associated with severe blood loss such as shock.
Patient should be asked whether the blood loss is severe, is there any dizziness,
colour of passed blood, mixed with mucus, blood mixed with motion or any dripping after
passage of stool, pain on defaecation (Cox and Roper, 2006).

10. ALTERED BOWEL HABIT – DIARRHOEA, CONSTIPATION

Normal bowel movement frequency can be from three times each day to once
every three days. Diarrhoea is the frequent passage of loose stools. Constipation is the
infrequent passage of hard stools. Clarify what patients mean when they say they have a
change in bowel habit. When they say diarrhoea do they mean a change in stool
consistency from solid to liquid, or increased frequency of defecation, urgency of defecation
or all three? With constipation, ask if they mean they are moving their bowels less
frequently than usual, or if defecation is difficult because the stool is hard.
Constipation can result from:
- a delay in delivery of stools round the colon to the rectum, due to impaired motility
(e.g. irritable bowel syndrome) or physical obstruction (e.g. colorectal cancer).
- Impaired rectal sensation resulting in lack of awareness that the rectum is full, thus
preventing the normal 'call to stool'.
- anorectal dysfunction preventing normal defecation despite appropriate signals.
Diarrhoea may be of high or low volume. High-volume diarrhea (> 200 g stool/day or > 11
per day) occurs when the water content of the stool is increased. High-volume diarrhoea is
divided into:
- Secretory, due to intestinal inflammation, e.g. viral or bacterial infection, ulcerative
colitis or crohn's disease
- Osmotic, due to malabsorption, drugs or motility disorders. Osmotic diarrhoea stops
if the patient fasts but secretory diarrhoea persists (Cox and Roper, 2006).

61
11. ABDOMINAL DISTENSION
The principal causes of abdominal distension are the five Fs: fat, flatus, faeces, fluid,
and fetus. Ascites is accumulation of fluid in the peritoneal cavity.
Bloating is fluctuating abdominal distension which usually develops during the day
and resolves overnight. It is particularly common in women and is rarely due to organic
disease. It usually occurs with other symptoms of irritable bowel syndrome (Cox and Roper,
2006).

12. WIND AND FLATULENCE

Patients may call repeated belching, excessive or offensive rectal flatus, abdominal
distension and borborygmi (audible bowel sounds) 'wind'. Ask the patient to describe what
is being experienced. Belching may result from air swallowing (aerophagy) and is usually of
no major significance. It may indicate anxiety, but sometimes occurs in an attempt to relieve
abdominal pain or discomfort, and accompanies gastro-oesophageal reflux disease.
The normal volume of flatus passed per rectum varies from 200-2000 ml per day.
Excessive flatus is particularly troublesome in lactase deficiency and intestinal
malabsorption. The inability to pass flatus is a feature of intestinal obstruction. Borborygmi
result from the movement of fluid and gas along the bowel. Though usually just a source of
embarrassment, it may indicate small bowel obstruction or dysmotility (Cox and Roper,
2006).

13. OEDEMA
Accumulation of excessive amount of tissue fluid in the subcutaneous tissue or serous
cavity due to increase in extravascular component of the extracelluar fluid volume.

THE HISTORY
1. PRESENTING COMPLAINT
Gastrointestinal symptoms are very common and often caused by functional
dyspepsia and irritable bowel syndrome. The patient may want relief from symptoms, or
reassurance that there is no serious underlying cause for the symptoms. Always investigate
'alarm symptoms' such as excessive weight loss or gastrointestinal bleeding (Kundu, 2005).

62
2. PAST HISTORY
History of a similar problem may suggest the diagnosis, e.g. a bleeding peptic ulcer
or inflammatory bowel disease. Always ask about previous abdominal surgery (Kundu,
2005).

3. DRUG HISTORY
Ask about all prescribed medications, over-the-counter medicines, and 'alternative'
medications. Almost any drug can affect the gastrointestinal tract. Aspirin and NSAIDs can
cause dyspepsia, gastric erosions or peptic ulcers, opioid analgesia cause nausea/vomiting
and constipation, antibiotics can cause diarrhoea (with or without Clostridium difficile
infection pseudomembranous colitis) and many drugs can cause hepatotoxicity. Selective
serotonin reuptake inhibitor antidepressants often cause nausea initially (Kundu, 2005).

4. FAMILY HISTORY
Many gastrointestinal conditions, including gallstones, dyspepsia, irritable bowel
syndrome and diverticular disease are so common that a positive family history is not
helpful. For some conditions a family history is relevant. For example, colorectal cancer in a
first-degree relative < 50 years old increases the risk of colorectal cancer and polyps.
Inflammatory bowel disease is more common in patients with a positive family history
(Kundu, 2005).

5. DIETARY HISTORY
Many patients assume that their symptoms are diet related. Diets lacking in fruit,
vegetables and fiber increase the risk of colonic cancer and diverticular disease. Patients
with diarrhoea due to lactose intolerance report worsening of their symptoms after eating
dairy produce. True gluten enteropathy occurs in coeliac disease. Smokers are at increased
risk of many gastrointestinal diseases, including oesophageal cancer, colorectal cancer and
peptic ulcer.
Many gastrointestinal disorders, particularly irritable bowel syndrome and dys!epsia,
are functional; that is, no physical abnormality can be found and the conditions may be
linked to the stresses of modem life. Ask about potential sources of stress including work,
home circumstances, relationships and finance as well as symptoms of anxiety and
depression (Kundu, 2005).

63
EXAMINATION OF THE ABDOMEN:
GENERAL EXAMINATION (Swash, 2002; Macgilchrist and Park, 2007):
 Nutritional state: The assessment of nutritional state is important in patients with GI
disease. Record the height, weight, waist circumference and calculate the patient's body-
mass index (It is derived from the formula Weight (in kg)/Height (in meter2)). Note if obesity
is truncal or generalized. Loose skin folds signify recent weight loss. Pallor, particularly on
the conjunctivae and palmar creases, may indicate anaemia. Look for tissue stigmata of
iron deficiency including koilonychias (spoon-shaped nails), angular cheilitis (painful hacks
at the comers of the mouth) and atrophic glossitis (pale, smooth tongue).The tongue has a
beefy, raw appearance in folate and vitamin B12deficiency.

 Hands: Inspect both hands for signs of chronic liver disease for example clubbing,
palmar erythema, Dupuytren's contracture, spider naevi.

Palmar erythema is a redness of the palms. The redness is concentrated on the

thenar eminence, the hypothenar eminence and the pulp of fingers, with the centre of the
palm being spared. Best is to compare your own palms to appreciate the difference.

Spider naevi (isolated telangiectatic lesions found on the upper trunk, arms and face
which characteristically fill from a central feeding vessel) signify chronic liver disease. This
must be demonstrated by blanching it. Pressing once on the central blob and very quick
removal of your finger shows that blood rushes back and the red spider legs reappear.

Dupuytren's contracture is thickening and shortening of the palmar fascia, results

in flexion deformities, particularly of the little and ring fingers. Running the fingers over this
region is a good way of making the diagnosis.

Clubbing, gastrointestinal causes include cirrhosis, inflammatory bowel disease and

amyloidosis.

Leukonychia (white nails) are a sign of hypoalbuminaemia due to liver disease,

malabsorption, protein malnutrition or nephrotic syndrome.

64
 Flapping Tremor (asterixis) has to be looked for in liver failure. Ask the patient to
extend their arms and cock their wrists back and spread their fingers. If liver failure is
present the hands should start flapping rhythmically.

 Face, eyes and lips: Inspect the face for xanthelasmata, spider naevi, inspect the eyes for
jaundice and conjunctivae for anaemia.

 Palpation of the neck: Palpate the neck for cervical lymph nodes, particularly the left
supraclavicular region. An enlarged lymph node here may be caused by spread from
gastrointestinal cancer. This node is often called virchow's node and referred as troisier's
sign. This area is readily felt with fingertips with patient lying flat (Swash, 2002).

INSPECTION (Swash, 2002; Macgilchrist and Park, 2007):

 How to examine:
- Examine the patient in good light and warm surroundings.
- The patient should be lying supine with arms loosely by his /her sides, the head and
neck supported by pillows.
- Use extra pillows to support a patient with severe kyphosis.
- Do not ask a patient with severe breathlessness to lie flat.
- Stand on right side of the patient, explain the procedure. Ask the patient to remove
his clothes so that there is complete exposure from the xiphisternum to the pubis.
- Leave the chest and legs covered (Swash, 2002).

 Normal appearance:
The abdomen is normally flat or slightly scaphoid and symmetrical. At rest, respiration is
principally diaphragmatic and the abdominal wall moves out with inspiration. The umbilicus
is usually inverted.

Skin: In marked distension of abdomen, the skin is smooth and shiny. Striae atrophica or
gravidarum are white or pink linear marks on abdominal skin, these are mostly stretch
marks and indicate a recent decrease in girth of abdomen. Wide purple striae are
characteristic of cushing’s syndrome and excessive steroid treatment.

65
Hair: Secondary sexual hair appears at puberty. Cirrhosis in the male may produce a
female distribution of body hair.

Visible veins: Abnormally prominent veins on the abdominal wall signify portal
hypertension or vena caval obstruction. In portal hypertension this results from the
recanalization of the umbilical vein along the falciform ligament. Distended veins around
umbilicus are not common known as, the 'caput medusa’, other signs include splenomegaly
and ascites more typically the umbilicus appears distended by blood. It should not be
confused with an umbilical hernia where the umbilicus is everted, distended, has a palpable
cough impulse and does not appear vascular. Dilated tortuous veins which all flow upwards
are collateral veins due to obstruction of the inferior vena cava. Rarely, obstruction of the
superior vena cava will give rise to similar distended abdominal veins which all flow
downwards.

Collaterals in IVC obstruction

Collaterals in IVC obstruction

66
How to examine

First look at the distribution of the veins. Work out the direction of blood flow. In portal
hypertension the blood flow is away from umbilicus and in IVCO the flow is upwards.
To determine the blood flow, one needs to press on a vein with the index finger of one
hand. Place the index finger of the other hand next to it and milk out of the vein by sliding
your finger about 3-5 cm. in any direction. Lift up the finger of the milking hand and if the
vein refills, then the blood flow is opposite to the direction of milking. If you lift up the milking
finger and the vein does not distend then the blood flow is in the direction of milking and is
being dammed back by your non-milking finger.

Testing of direction of venous flow

Pigmentation: Linea nigra seen in midline, below umbilicus is a sign of pregnancy.

Erythema-ab-igne is a brown mottled pigmentation produced due to constant application of
heat. It is a sign that the patient is experiencing severe pain, such as from chronic
pancreatitis.

Distension/swelling: If abdomen is distended, look whether the distension is generalized

or caused by a localized mass. Localized swelling, e.g. due to massive enlargement of liver
or spleen, is seen as asymmetry when you look at the patient from the foot of the bed.

Scars and stomas: Note for any surgical scars and clarify what they were for. Generally an
appendicectomy scar lies diagonally in the right iliac fossa, the Pfannenstiel incision, a
horizontal suprapubic scar, is used for gynaecological surgery, a right subcostal incision is
given for an open cholecystectomy while a bilateral subcostal scar with a vertical extension
to the xiphisternum - known as a 'Mercedes-Benz' scar for obvious reasons - is the result of
liver surgery.

67
 Any midline scar may develop an incisional hernia. This is palpable as a defect in the
abdominal wall musculature and is more obvious if the patient raises the head from the bed
or coughs. A similar appearance of midline swelling in the absence of a seal is due to
divarification of the rectus sheath. Stomas may be present: usually an ileostomy is situated
in the right iliac fossa; a transverse colostomy in the left hypochondrium; and a sigmoid
colostomy in the left iliac fossa.

Groin: Inspect groins, penis and scrotum, look for any swelling and inflamation, note
whether both testes are in normal position.

PALPATION OF THE ABDOMEN (Swash, 2002; Macgilchrist and Park, 2007):

 Different methods for palpation

1) Conventional or classical method eg. Palpation of liver.
2) Hooking method, used in palpation of spleen.
3) Dipping method, palpation in presence of ascites.
4) Bimanual palpation-palpation of kidney.
 How to examine:
- Ensure that your hands are warm. If the patient is in a low bed, sit on, or kneel
beside the bed on the patient's right side.
- Ask the patient to place his arms alongside his body to help relax the abdominal wall.
- Placing a pillow under the patient's knees may also help by allowing flexion of the
hips.
- Ask the patient to breathe slightly deeply with mouth open.
- Ask the patient to show you where he feels pain before you start, and to report any
tenderness as you examine him.
- Begin with gentle superficial examination of the whole abdomen. If the patient has
abdominal pain, start away from the site of maximal pain and move in a systematic
manner through the nine regions of the abdomen.
- Use your right hand, keeping it flat and in contact with the abdominal wall, and avoid
using your finger tips. As you palpate, watch the patient's face for any sign of
discomfort.
- Palpate lightly in each region in turn, and then repeat this palpating deeply.

68
 - If patient is not yet relax, can be asked to flex the hips and knees.
- At times deep palpation is needed, it is a good practice to use both hands one above
the other. While the upper hand put more pressure, the lower hand remains passive
to receive more information about the structures deep to this hand.

The abnormalities are either tenderness and/or masses:

Tenderness
Discomfort during palpation is accompanied by resistance to palpation and varies widely in
severity. Apparent tenderness in several areas with minimal pressure may be due to
generalized peritonitis, or due to patient anxiety. Severe pain with no tenderness on deep
palpation, or where the tenderness disappears when the patient is distracted, suggests
non-organic pathology. If the whole peritoneal cavity is inflamed there will be generalized
peritonitis and the muscles of the anterior abdominal wall will be held rigid (board-like
rigidity). The anterior abdominal wall does not move with respiration and breathing
becomes increasingly thoracic.
'Rebound' tenderness is a sensitive sign of intra-abdominal disease but not a reliable
indicator of peritoneal irritation. Gently press your hand in, and then rapidly remove it. The
patient shows more discomfort as your hand is released. Ask the patient to cough, or gently
percuss the abdomen and note tenderness. More localized but severe tenderness may
indicate localized peritonitis. The site of the tenderness is important, e.g. tenderness in the
epigastrium suggests peptic ulcer; in the right hypochondrium, cholecystitis and in the right
iliac fossa, appendicitis.
Palpable mass
Normally, no masses are palpable in the abdomen, but there are exceptions to this rule in
thin patients:
• The liver edge may be felt below the right costal margin
• The aorta may be palpable as a pulsatile swelling above the umbilicus
• The lower pole of the right kidney may be palpable in the right flank
• The sigmoid colon may be palpable in the left iliac fossa, if loaded with faeces
• A full bladder is palpable as a mass in the suprapubic region arising out of the
pelvis
• A foetus in the later months of pregnancy.

69
When you feel a mass, decide if it is due to enlargement of an abdominal organ, or a
separate mass. If latter, is it simply palpable faeces in a constipated patient, or is it
pathological. Palpable faeces can usually be indented with your examining finger. If the
mass or lump seems superficial it may be within the anterior abdominal wall rather than the
abdominal cavity. Ask the patient to tense the abdominal muscles by lifting the head; an
abdominal wall mass will still be palpable, whereas a deep mass will not. In particular
describe its site, size, surface, shape, consistency and whether it moves on respiration. A
swelling that is hard, irregular in outline and nodular is likely to be malignant. A regular,
round, smooth, tense swelling is likely to be cystic. A solid, ill defined and tender mass is
suggestive of inflammatory lesion, eg crohn’s disease. Swellings in the liver, spleen,
kidneys, gall bladder and distal stomach show down ward movement during inspiration.
See if it is fixed or mobile. When fixed it signifies, a mass of retroperitoneal origin.
Assess whether it is bimanually palpable. A pulsatile mass palpable in the upper abdomen
may be normal aortic pulsation in thin people, a gastric or pancreatic tumour transmitting
underlying aortic pulsation, or an aortic aneurysm.
Palpating for enlarged organs
LIVER
Hepatic enlargement can result from chronic parenchymal liver disease from any
cause. Enlargement due to metastatic tumour deposits is hard and irregular. An enlarged
left lobe may be felt in the epigastrium or even the left hypochondrium. In right heart failure,
the liver is usually soft and may be tender. A pulsatile liver indicates tricuspid
incompetence.

Causes of hepatomegaly (Kundu, 2005):

Chronic Malignancy Right heart Haematological Rarities

parenchymal failure disorders
liver disease
Alcoholic liver Primary Lymphoma Amyloidosis
disease hepatocellular
cancer Leukaemia Budd-Chiari
Autoimmune syndrome
hepatitis Secondary Myelofibrosis
metastatic Glycogen
Viral hepatitis cancer Polycythaemia storage
disorders
Primary biliary
cirrhosis

70
How to examine:

Main method
- Sit on the couch beside the patient.
- Place both hands side-by-side on the abdomen in the right sub- costal region
lateral to the rectus with the fingers pointing toward ribs.
- if resistance is encountered, move the hands further down until this resistance
disappears.
- ask the patient to breathe in deeply and, at the height of inspiration, press the fingers
firmly inward and upward.

Alternate method

- Start palpating in the right iliac fossa. If you start in the right hypochondrium, you
may already be above the lower border of a massively enlarged liver.
- Use either the radial border of your right hand, i.e. the outside edge of the forefinger,
or the finger pads; in both cases keep your hand flat on the abdomen. Do not dig in
with your finger tips as you may get a false impression of the liver edge.
- Keep your hand stationary and ask the patient to take a deep breath in. Try to feel
the edge of the enlarged liver as, it moves downwards on inspiration.
- Move your hand progressively further up the abdomen a centimeter or so at a time
repeating the request to breathe in until you reach the costal margin or detect the
edge.
- If you feel the liver edge, work out if it is enlarged or displaced downwards as occurs
in patients with hyper inflated lungs from emphysema. The liver is dull to percussion
whereas the lung is resonant, so locate the upper border of the liver by percussion
over the right lateral chest wall. The lower three to four ribs are normally dull to
percussion.
- reduced area of dullness suggests emphysema, a shrunken liver (as occurs in end-
stage cirrhosis) (Swash, 2002; Macgilchrist and Park, 2007).
• Measure the distance below the costal margin in centimeters in the midclavicular line.

71
The aim is to feel if the lower border of the liver is palpable. If you detect the liver edge,
describe:
- size, e.g. in cm below the costal margin
- surface, - smooth or irregular
- edge - smooth or irregular
- consistency - soft or hard
- if it is tender
- if it is pulsatile
- whether there is an audible bruit.

GALLBLADDER

The normal gallbladder is not palpable, when distended; it may be palpable in the right
hypochondrium. It has a characteristic firm, smooth, globular feel with distinct borders and,
unlike the liver, one can palpate above it. It is felt just lateral to edge of rectus abdominis
near the tip of 9th costal cartilage. It moves with respiration. It becomes swollen due to
obstruction either of the cystic duct (resulting in a mucocele of the gall bladder) or of the
common bile duct if the cystic duct is patent, as in pancreatic cancer. A gall bladder with
gallstone disease is not palpable because it becomes thickened and contracted. If the gall
bladder is palpable in a jaundiced patient the obstruction is not due to gallstones but is
likely to be pancreatic cancer or distal cholangiocarcinoma (Courvoisier's law). A painless
gallbladder is palpable in

- Carcinoma of head of pancreas

- Mucocele of the gallbladder
- Carcinoma of gallbladder

Murphy’s sign: In acute inflammation of GB severe pain is present. Ask the patient to
breathe in deeply, and palpate for GB in the normal way; at the height of inspiration the
breathing stops with a gasp as the mass is felt. This is murphy’s sign; it is not found in
chronic cholecystitis or uncomplicated cases of gallstone (Swash, 2002; Macgilchrist and
Park, 2007).

72
SPLEEN
Splenomegaly refers to enlargement of the spleen. The spleen has to increase in size
threefold to be palpable, so a palpable splenic edge always indicates splenomegaly. The
spleen enlarges from under the left costal margin down and medially towards the right iliac
fossa. If the spleen is significantly enlarged, a characteristic notch may be palpable midway
along its leading edge.

SPLENOMEGALY (Cox and Roper, 2006):

Just palpable spleen Moderate palpable Massive
spleen splenomegaly

-acute malaria - chronic malaria - chronic malaria

- acute kala-azar - chronic kala-azar - storage disorders
- enteric fever - portal hypertension - portal hypertension
- acute viral hepatitis
- subacute bacterial - lymphoma - polycythemia vera
endocarditis - chronic lymphatic - chronic myeloid
- acute leukemia leukemia leukemia
- thalassaemia - thalassaemia major

How to examine:
- With your right hand start in the right iliac fossa and ask the patient to breathe in
deeply as you press posteriorly and caudally for 1-2 centimetres. Try to detect the
spleen as it moves down against your fingers.
- Move your hand diagonally upwards and across the abdomen 1-2 centimetres at a
time into the left hypochondrium repeating this manoeuvre.
- Feel the costal margin along its length as the position of the spleen tip is variable.
- If you cannot feel the splenic edge, ask the patient to roll towards you onto the right
side and repeat the above.
- Palpate with your right hand while using your left hand to press forward on the
patient's left lower ribs from behind.
- Feel along the left costal margin (Swash, 2002; Macgilchrist and Park, 2007).

KIDNEYS

73
 To examine the right kidney you must place your left hand under the patient in the
renal angle. This is below the twelfth rib, above the posterior iliac crest. Now place your
right hand flat on the abdomen on the right flank, lateral to rectus muscle. This hand should
be lying over the lower hand, with the patient's flank sandwiched between the two. Now
press down with your right hand while flexing upwards with the fingers of your left. If the,
kidney is large enough you can feel it bumping against the right hand. This is called
balloting.

- Place your left hand behind the patient's back below the lower ribs.
- Place your right hand over the upper quadrant anteriorly just lateral to the rectus muscle.
Firmly, but gently, push your two hands together as the patient breathes out. Then ask the
patient to breathe in deeply. You may feel the lower pole of the kidney moving down
between the hands.
- If this happens, gently push the kidney back and forwards between your two hands to
demonstrate its mobility. This is known as ballotting, and helps to confirm that the
structure is the kidney.
- It is usually easier to feel the right kidney as it is lower than the left.
- If the kidney is palpable; assess its size, surface and consistency.
- Tenderness of the kidney is most obvious posteriorly in the renal angle - the angle formed
between the 12th rib and the spine. Make the patient sit forward and palpate firmly but
gently with your fingers. If this does not cause the patient discomfort, firmly (but with
moderate force only!) strike the renal angle once with the ulnar aspect of your closed fist
after warning the patient what to expect (Swash, 2002; Macgilchrist and Park, 2007).

PERCUSSION OF THE ABDOMEN (Swash, 2002; Macgilchrist and Park, 2007):

Structures containing air or gas are resonant on percussion. Solid or fluid-filled structures
are dull. Normally the abdomen is resonant due to the gas content of the intestine.
• Use a lighter touch when percussing the abdomen than when you percuss the chest.
• Always percuss from the area of resonance to the area of dullness to identify the position
accurately.
• Percuss the centre of the abdomen. Now percuss in steps out toward the left flank.
• If the percssion note is dull in the flanks then it is likely that ascites is present.
• This requires confirmation by looking for Shifting dullness.

74
• Keep the percussed finger firmly on the flank then ask the patient to roll onto toward you.
When ascites is present, the note becomes resonant.

There are two methods:

1. Keep your finger on the site of dullness in the flank and ask the patient to turn onto the
opposite side. Pause for at least 10 seconds to allow any ascites to gravitate; then percuss
again and if that area is now resonant, you have demonstrated shifting dullness as the
ascitic fluid became dependent.
2. Mark the point at which the percussion note changes from resonant to dull with a pen on
a line parallel to the flank. Ask the patient to turn to the same side and repeat the
manoeuvre: if the line has moved 'up' the abdomen towards the midline, you have
demonstrated shifting dullness.
Always wait for few moments after the patient turns before repeating percussion, to allow
time for the fluid to shift and settle.

Another method is to elicit a Fluid thrill

This technique is particularly good in the presence of large amounts of ascitic fluid. Place
the palm of your left hand flat against the left side of the abdomen; flick a finger of your right
hand against the right side of the abdomen. If you feel a ripple against your left hand, ask
the patient (or an assistant) to place the edge of a hand on the midline of the abdomen.
This prevents transmission of the impulse via the skin. If you still feel a ripple against your
left hand this is a fluid thrill. This sign is only present when ascites is obvious.
Another classical but not recommended method is 'puddle sign'. This is performed with the
patient kneeling on all fours. The centre of the abdomen should sound dull to percussion.

AUSCULTATION OF THE ABDOMEN

With the patient lying on the back place the diaphragm of the stethoscope to the right
of the umbilicus and do not move it. Bowel sounds are gurgling sounds caused by normal
peristaltic activity of the gut. They occur every 5-10 seconds, but the frequency varies
75
widely. You must listen for upto 2minutes·before concluding that they are absent. Absence
of bowel sounds indicates paralytic ileus or peritonitis. In intestinal obstruction, bowel
sounds occur at increased frequency and have a high-pitched tinkling quality. Listen above
the umbilicus over the aorta for bruits which indicate turbulent flow from atheroma or an
aneurysm. Now place the stethoscope 2-3 cm above and lateral to the umbilicus to listen
for renal artery bruits as in renal artery stenosis. Listen over the liver for bruits which occur
in hepatoma or acute alcoholic hepatitis. You may hear a friction rub in perihepatitis. Very
occasionally you may hear a venous hum in the upper abdomen over a caput medusa.
A succussion splash sounds like shaking a half filled water bottle. Shake the
abdomen with both hands under the pelvis. Explain first what you are going to do. An
audible splash more than 4 hours after the patient has eaten of drunk anything, indicates
delayed gastric emptying, e.g. pyloric stenosis (Swash, 2002; Macgilchrist and Park, 2007).

HERNIAS
An external abdominal hernia is an abnormal protrusion of an organ or tissue,
usually bowel and/or omentum, from the abdominal cavity. Hernias occur at sites of natural
openings of the abdominal wall, e.g. the inguinal, femoral and obturator canals, the
umbilicus and the oesophageal hiatus. They may occur at sites of weakness, related to
previous surgical incisions or stretching of the abdominal wall.
Internal hernias occur through defects of the mesentery or into the retroperitoneal
space and are not visible. External hernias are more prominent in the erect position, when
the pressure within the abdomen rises, and during coughing when an impulse can often be
felt in the hernia. This is the cough impulse.
A reducible hernia is one whose contents can be returned to the abdominal cavity,
spontaneously or by manipulation. If not, the hernia is irreducible. An abdominal hernia has
a covering sac of peritoneum, and the neck of the hernia is a common site of compression
of the contents. If bowel is involved in the hernia, bowel obstruction may occur. If the
process leads to compression and compromise of the blood supply to the contents (bowel
or omentum) the hernia is strangulated. Hernias most commonly occur· in the groins and
you should examine these sites as part of your routine examination of the abdomen. The
inguinal canal extends from the pubic tubercle to the anterior superior iliac spine. It has an
internal ring at the mid-inguinal point and an external ring at the pubic tubercle. Note that
the mid-inguinal point is midway between the pubic symphysis and the anterior superior

76
iliac spine not at the midpoint of the inguinal ligament. In males the inguinal canal contains
the spermatic cord and its blood vessels.
• Inguinal hernias are palpable above and medial to the pubic tubercle.
• Femoral hernias are palpable below the inguinal ligament and lateral to the pubic tubercle
(Cox and Roper, 2006).

How to examine:
- Hernias may reduce spontaneously when a patient lies supine so, if possible, examine the
patient standing.
- Ask the patient to stand, carefully inspect the inguinal and femoral canals and the
scrotum for any lumps or bulges.
- Ask the patient to cough and look for any impulse over the femoral or inguinal canals and/
or scrotum.
- Identify the anatomical relationships between the bulge, the pubic tubercle and the
inguinal ligament to distinguish a femoral from an inguinal hernia.
- Palpate the external inguinal ring and posterior wall of the inguinal canal for possible
muscle defects. Ask the patient to cough and feel for any impulse.
- Ask the patient to lie down and see if the hernia reduces spontaneously. If so, press with
two fingers over the internal inguinal ring at the mid-inguinal point and ask the patient to
cough or stand up while you continue to press over the internal inguinal ring and see if the
hernia reappears. If you can prevent it from reappearing it is an indirect inguinal hernia.
- Always examine the opposite side as well to detect an asymptomatic hernia (Cox and
Roper, 2006).

GENITAL EXAMINATION (Swash, 2002; Macgilchrist and Park, 2007):

- Put on gloves and ask the patient to lie down on his back on the examination couch
with his genital area and upper thighs fully exposed.
- Look at the whole area for redness, swelling or ulcers. Note the hair distribution, in
particular alopecia or infestation. Patients who shave their pubic hair may develop
dermatitis (inflammation of the dermis) or folliculitis (infection around the base of the
hairs causing an irritating red rash).
- Check the groin, perineum and scrotal skin for these rashes and intertrigo (infected
eczema) in the skin creases and eczema (another name for dermatitis).

77
Penis
Inspection
The penile skin has more sebaceous follicles than most other areas. Numerous uniform
pearly penile papules around the corona of the glans are a common normal fmding. Look at
the shaft of the penis and check the position of the urethral opening.
Palpation
Retract the prepuce to check for phimosis or adhesions. Note any rashes, abnormal
curvature, pigmentation, nodules, ulces or discharge.

Scrotum
Inspection: Look at the scrotum for redness, swelling or ulcers; sebaceous cysts are
relatively common. Remember to inspect the posterior surface.
Palpation: If either you or the patient is cold, the cremaster muscle will contract and you
will not be able to palpate the testes properly. Testicular sensitivity varies, so ask the man
whether palpation is painful.
• Palpate the scrotum gently-using both hands. Check that-both testes are present in the
scrotum.
• Place the fingers of both your hands behind the left testis to immobilize it and use your
index finger and thumb to methodically palpate the body of the testis. Feel the anterior
surface and medial border with your thumb and the lateral border with your index finger.
• Check the size and consistency of the testis and note any nodules or irregularities. Very
gently squeeze the fingers of your left hand to push the testis inferiorly and allow you to
assess the upper pole of the organ. Reverse this procedure to feel the lower pole. Repeat
the procedure for the right testicle. The testes are normally soft and smooth, and may be
slightly different sizes.
• Palpate the spermatic cord with your right hand. Gently pull the right testicle downward
and place your fingers behind the neck of the scrotum. Bring those forwards to your
thumb which is anterior. You will be able to feel the spermatic cord.
• Ask the patient to stand to look for a varicocele.
• If there is a bulky soft mass in the scrotum transilluminate it. In a darkened room hold a
pen-torch against the swelling and see if light is transmitted as a bright red glow to the
skin of the scrotum. This confirms it is fluid-filled, whereas no transmission of light occurs
with a solid mass.
78
• Decide whether a swelling arises from within the scrotum or from an indirect inguinal
hernia. Use your finger to see whether you can feel above the swelling. If so it is a true
scrotal swelling, and if not it has come through the inguinal canal.

ANOGENITAL REGION

The anal margin, rectum and prostate gland should all be examined as part of the male
genital assessment. Perianal warts are common, often in association with genital warts
(condylomata acuminata). Their presence is not always caused by sexual transmission. A
rectal discharge may be due to sexually transmitted infections such as N. gonorrhoeae or
C. trachomatis, and secondary syphilis may present as flat warty lesions (condylomata
lata). Sexually transmitted infections are a cause of proctitis so take swabs at proctoscopy if
the history suggests there is a history of anal penetration (Swash, 2002).

RECTAL EXAMINATION (Cox and Roper, 2006):

• Ask the patient to lie in the left lateral position with the buttocks at the edge of the couch,
the knees drawn up to the chest and the heels clear of the perineum.
• Put on gloves and have a good movable light source.
• Separate the buttocks and inspect the perianal skin looking for dermatological conditions,
infestations, external haemorrhoids, fistulae or fissures, and signs of trauma.
• Lubricate your finger with water-based gel. Place the pulp of your forefinger on the anal
margin with your palm facing posteriorly. Use steady pressure on the sphincter to pass
your finger gently through the anal canal into the rectum. If there is anal spasms ask the
patient to breathe out and relax. Pain and spasm are usually caused by an anal fissure. In
this case try again after applying local anaesthetic gel to the anal margin for a few
minutes.
• Palpate round the rectum systematically. Sweep the mucosa through 3600 checking for
masses, stricture or points of tenderness.
• Identify the uterine cervix in women and the prostate in men. Assess the size, shape and
consistency and note any tenderness.

79
• Withdraw your finger gently to avoid sudden spasm, look at the glove for blood, mucus
and stool colour.

THE ACUTE ABDOMEN

The 'acute abdomen' includes a spectrum of underlying causes ranging from minor self-
limiting conditions to severe life threatening diseases that present with a history of < 1
week's duration. The diagnosis and management of a patient with an acute abdomen
depends on information from the history and examination. The commonest presenting
feature is acute abdominal pain. The site of abdominal pain may indicate the likely origin of
the underlying pathology. Pain experienced predominantly in the upper abdomen arises
from foregut structures, e.g. duodenal ulcer, gall bladder pathology or pancreatitis. Central
abdominal pain arises from midgut structures, such as conditions affecting the small bowel
and appendix. Lower abdominal pain may result from the large bowel. Gynaecological
pathology may also cause lower abdominal pain. Inflammation and obstruction are the two
main pathological processes accounting for acute abdominal pain. Inflammation produces a
more constant pain exacerbated by movement or coughing. Patients therefore typically lie
very still in order not to exacerbate the pain. Obstruction of a muscular viscus produces a
colicky pain. Characteristically patients with colic move around or draw their knees up
towards the chest during painful spasms (Swash, 2002).

Inspection
Assess the general state and demeanour of the patient. Does the patient look unwell with
pallor, sweating and reluctance to move? Critically ill patients may be confused and may
have a depressed level of consciousness.

Palpation, percussion and auscultation

Gentle percussion is useful in determining the presence of fluid within the peritoneal cavity.
One may find diminished or absent liver dullness to percussion in patients with perforation
of a hollow viscus and air under the diaphragm. Absent audible peristalsis, i.e. a completely

80
silent abdomen on auscultation may indicate diffuse peritonitis. Increased peristalsis
produces high pitched 'tinkling' bowel sounds characteristic of intestinal obstruction,
gastroenteritis or fulminant inflammatory bowel disease (Swash, 2002; Macgilchrist and
Park, 2007).

References

Cox, L.T. and Roper, T.A. Abdominal System. In Cox, L.T. and Roper, T.A. Clinical skills
(15th edition). Oxford: Oxford University Press, 2006:125-184.

Kundu, A.K. Gastrointestinal System. In: Bedside Clinics in Medicine (5th edition). Academic
Publishers. 2005: 106-134

Macgilchrist, A. and Parks, R.W. The Gastrointestinal System .In: Douglas, G., NICOL, F.,
ROBERTSON, C. eds. Mecleod's. Clinical examination (llth edition). London:
Elsivier, Churchil1 Livingstone, 2007:153-180.

Swash, M. The Gastrointestinal Tract and Abdomen. In: Swash, M. Hutchinson's Clinical
Method (21 edition). London: W.B. Saunders, 2002:125-163.11.

81
CHAPTER-V
 DISORDERS OF HIGHER MENTAL FUNCTIONS

The topic will be presented under following headings:

 Introduction
 Consciousness
 Attention and concentration
 Orientation
 Language
 Memory
 Higher cognitive functions : Abstract ability General information Calculation Intelligence
 Lesions in different parts of cerebrum and cognitive functioning
 Conclusions

Introduction
The human brain is the basis of what a person senses, does, feels, and thinks; or put in more formal
terms, our sensory, behavioral, affective, and cognitive experiences and attributes. The higher mental
functions make exclusive ability that distinguishes human beings clearly from other creatures. However,
the strict localization of many of these functions is still far from clear. Some of these functions are not
strictly localized to one single lateralized brain region. Instead, these are distributed across various parts
of the çortex. These functions are attention and concentration, memory, higher order intellectual
functions, social behaviour and personaIity. On the other hand, certain functions are localized, i.e.
lateralized to one hemisphere, and often one part of a hemisphere. Out of these language, calculation
and praxis are associated with dominant hemisphere; while, complex visuo-perceptual skills,
constructional abilities and prosodic components of language are associated with non-dominant
hemisphere. Assessment of all these functions is part of routine mental status examination (Hodges,
1996)

Consciousness
Consciousness is a state of normal cerebral activity in which the patient is aware of both self and
environment and is able to respond to internal changes, for example hunger, and to changes in external
environment.

Anatomical consideration
Experimental work in animals and clinical observations in humans suggest that the following structures
play key roles in the maintenance and modulation of wakefulness: cholinergic nuclei in the upper
brainstem and basal forebrain; noradrenergic nuclei, in particular the locus ceruleus in the upper
brainstem; histaminergic and hypocretinergic projections from the hypothalamus; and probably
dopaminergic and serotonergic projections arising from the brainstem (Robbins & Everitt, 1995). Part of
the influence exerted by these pathways is mediated by the thalamus, especiallv its intralaminar nuclei,
which makes a major contribution to the maintenance of cerebral arousal as well as providing a critical
synaptic relay in sensory, motor and corticocortical pathways (Zeman, 2008).

Assessment (Strub & Black, 2000)

Amongst many general terms used to describe the basic level of consciousness, representing points on a
continuum from full alertness to deep coma, most clinicians distinguish five principal levels:
Alertness implies that the patient is awake and fully aware of normal external and internal stimuli.
Lethargy or Somnolence is a state in which the patient is not fully alert and tends to drift off to sleep when
not actively stimulated.

82
Coma is traditionally applied to those patients who are completely unarousable and remain with their
eyes closed.
Stupor, obtundation, and other descriptions such as ‘semiconscious’ are non-qualitative descriptions of
an altered mental state that is difficult to define precisely. (Coats, 2007)
Akinetic mutism is a state of silent, alert-appearing immobility. The patient’s eyes are open and may
follow environmental events; there are regular sleep-wake cycles. The patient may lie completely inert or
may have occasional brief movements to adjust posture spontaneously or in response to vigorous
stimulation. The disorder occurs with large frontal lobe injuries, bilateral cingulate gyrus damage, and
midbrain pathology.
Locked-in syndrome occurs with bilateral pontine lesions that render the patient mute and paralyzed.
lntellectual function, however, is not impaired and the patients can communicate by eye movements or
eye blinks (Chow & Cummings, 2000).
One of the most commonly used methods to assess the level of consciousness is through Glasgow
Coma Scale (Jennett & Teasdale, 1981).

ATTENTION/CONCENTRATION (Strub & Black, 2000)

Attention is the patient’s ability to attend to a specific stimulus without being distracted by extraneous
internal stimuli. This capacity for focusing on a single stimulus contrasts with the concept of alertness or
vigilance. Vigilance refers to a more basic arousal process in which the awake patient can respond to any
stimulus appearing in the environment. The vigilant but inattentive patient will be attracted to any novel
sound, movement or event occurring in the vicinity; the attentive patient can screen out irrelevant stimuli.
Alert patients may show deficits in sustained attention to external stimuli (vigilance) or internal stimuli
(concentration). Attention presupposes alertness but alertness does not necessarily imply attention.
Sustained attention is the ability to maintain attention to a specific stimulus over an extended period. A
wide variety of factors have been shown to interfere with attention; the intensity and frequency of the
stimulus: environmental stressors (e.g., noise, temperature, complexity of the environment), emotional
factors (e.g., anxiety or depression), and to some extent lower IQ.

Anatomical Considerations
Maintenance of attention depends upon integrated activity of the neocortex (especially prefrontal areas),
thalamus and brainstem. These structures are functionally linked by reticular activating system. The
thalamus acts as a major relay station between the cortex reticular formation: the intralaminar nuclei
receive inputs from the brainstem nuclei and relay information widely to the cortex. A reciprocal feedback
loop from the cortex modulates these ascending pathways via thalamus. Thus the thalamus plays an
essential role in regulating and integrating attentional mechanisms. The areas of the cortex most involved
in these functions are the so called ‘higher-order multimodal association areas’, which receive inputs from
many primary sensory cortical and association areas and relay to the limbic system.

Tests of attention/concentration

Digit repetition: Attend to a verbal stimulus and to sustain attention for the period of time required to
repeat the digits.
Instructions: Tell the patient that you are going to say some simple numbers, to listen carefully and
when finished to carefully repeat them in the same order. Present the digits in a normal tone of voice at a
rate of one digit per second – without clustering. Numbers should be presented randomly without natural
sequences (e.g., 2-4-6-8). Begin with a two-number sequence; two trials are given at any level. If the
subjects pass on the first or on the second trial, then the next – length sequence is administered. Digit
span is the highest level at which the patient passes either trial.
Exactly the same technique is employed on reverse digit span; however the patient is required to repeat
the numbers in reverse order. It may be necessary to give some patients several demonstrations at two

83
digits. Normal range for digits forward is 5-7. Normal in the elderly, or those of low intellectual ability, 5
can be considered normal, but a span of 4 is definitely borderline or impaired; and a span of 3 is always
defective. Reverse span is one less than the forward one.
Digit span is generally vulnerable to focal left hemisphere and frontal lesions. Disorders of attention (for
example, delirium or acute confusional states) cause severe reduction, especially in reverse digit span. In
alzheimer’s disease, digit span is well maintained initially; but it is reduced in subjects with subcortical
dementias.

Tests for sustained attention

“A” Random letter test: Subject is presented with a series of random letters among which a target letter
appears with greater than normal frequency. He is required to indicate whenever the target letter is
spoken by the examiner.
Instructions: Tell the patient: “I am going to read you a long series of letters. Whenever you hear the
letter ‘A,’ indicate by tapping the desk.
The average person should complete the task without error. Examples of common errors are: (1)
omission error – failure to indicate when the target letter has been presented; (2) commission error –
indication made when a non target letter has been presented; and (3) perseveration error – failure to stop
tapping with the presentation of subsequent non target letters.
Other tests being serial seven’s subtraction test (e.g., counting backward form 100by 7s: 100, 93,
86,…), recitation of the months of the year or the days of the week backwards, spelling of familiar words
backwards (e.g., WORLD – DLROW) and orientation of time and place (also dependent upon memory)
(Hughes, 1996).

Orientation
The patient’s orientation to time, place and person are actually measures of recent memory, as they test
the patient’s ability to learn these continually changing facts. If a patient is not fully oriented, this alone
suggests a significant recent memory deficit.
Indian adaptation: In Hindi five questions are asked, each correct answer scored 1 and the answers are
to be verified from informant. Examples: what did you eat in dinner last night? What did you had in
breakfast this morning? What month is this? etc. (Pershad & wig, 1988).

Language (Strub & Black,2000)

The Network for Language: Language allows the communication and elaboration of thoughts and
experiences by linking them to arbitrary symbols known as words. The neural substrate of language is
composed of a distributed network centered in the perisylvian region of the left hemisphere. The posterior
pole of this network is located at the temporoparietal junction and includes a region known as Wernicke's
area. An essential function of Wernicke's area is to transform sensory inputs into their lexical
representations so that these can establish the distributed associations that give the word its meaning.
The anterior pole of the language network is located in the inferior frontal gyrus and includes a region
known as Broca's area. An essential function of this area is to transform lexical representations into their
articulatory sequences so that the words can be uttered in the form of spoken language. The sequencing
function of Broca's area also appears to involve the ordering of words into sentences that contain a
meaning-appropriate syntax (grammar).

Tests for language (Strub & Black, 2000)

Determination of handedness
Because of the close alliance between handedness and cerebral dominance for language, handedness
should be determined first.
 Ask the patient whether he is right or left handed
84
 Demonstrate which hand is used to throw a ball, hold a knife or flip a coin.
 Ask the patient about any tendency to use the opposite hand for any skilled movement
 Family history of left-handedness or ambidexterity

Spontaneous speech
Instructions: Listen carefully to the patient’s spontaneous speech? If patient offers none, open ended
questions should be asked in order to elicit speech production.
 Is speech output present?
 Is speech dysarthric or dysprosodic?
 Is there any evidence of specific aphasic errors?

Verbal fluency
It refers to the ability to produce spontaneous speech fluently without undue word finding pauses
or failure in word searching.
Animal naming
Instructions: Tell the patient to recall and name as many animals as possible within 60 seconds and is
scored for the correctly produced names in that time.
Scores: Normal individual names 18-22 animals, < 13 raises the question of impaired verbal fluency.
Controlled oral word association test(FAS test).
Instructions: Tell the patient to name as many words as possible (not proper nouns) that begin with the
stipulated letter (“F”,”A”,”S”) during each 60 second trial.
Scoring: Normal individuals name from 36-60 words, while inability to name more than 12 words per
letter is indicative of reduced verbal fluency.
Indian adaptation: In Hindi the test is done by using the words क, प, म.
Comprehension: This could be tested by two methods: pointing commands and questions with ‘yes’ or
‘no’ response.
Pointing commands: Starts with asking the patient to point out single objects in the room, body parts
etc to an increasing number of objects in sequence (point to the wall, to the window and your nose) until
the patient fails consistently. The patient with average intelligence without aphasia should succeed in
pointing to four objects or more.
Questions: A series of simple and complex questions that require only ‘yes’ or ‘no’ answers should be
asked. Correct answers should alternate between ‘yes’ to ‘no’ randomly because of the tendency of brain
damage patients to perseverate. Atleast seven questions should be asked because correct responses
can occur by chance alone 50% of the time with yes’ and ‘no’ questions.

Repetition: Testing should present material in ascending order of difficulty, beginning with single
monosyllabic words and proceeding to complex sentences. The patient is asked to repeat the word or
sentence verbatim after the examiner. The examiner should listen for paraphasias, grammatic errors,
omissions and additions.

Naming and word finding: Naming ability is almost invariably disturbed in all types of aphasia. Impaired
naming ability is called anomia. Word finding difficulty, which is closely related to anomia, is a reduced
ability to retrieve the nouns and verbs used in spontaneous speech. Specific word finding problems can
be detected by listening to the spontaneous speech of the patient with aphasia. Asking the patient to
describe a picture that contains objects and actions usually brings out any word finding defect.

85
Instructions: Tested with a confrontation naming test where the examiner points to a variety of objects
or pictures of objects(colours, body parts, room objects, articles of clothing) and asks the patient to name
them.

Reading: It is important to determine the patient’s educational background before testing reading as this
ability is directly related to educational experience. Both reading comprehension and reading aloud ability
should be tested. Both are usually defective in the same patient, but either can be disturbed in isolation.
Instructions: Patients are asked to read aloud short single words, then phrases, sentences, and finally
paragraphs. Finally, they are asked to read questions that have answered ‘yes’ or ‘no’ or are asked
questions about what was written. Any syllable or word substitutions, omitted words, and defects in
comprehension are noted.

Writing: Initially the patient is asked to write letters and numbers to dictation, progressing to names of
common objects or body parts, and finally to write a short sentence describing the weather, their job or a
picture from a magazine.
Agraphia is diagnosed when a patient demonstrate basic language errors, gross spelling errors, or use
paragraphias. A patient with aphasia usually invariably shows evidence of agraphia.

Spelling: Spelling is a complex, little studied, higher language function that is strongly associated with
educational experience. Spelling can be evaluated by asking the patient to spell dictated words. Gross
errors in spelling can be detected in bedside testing, though in order to establish actual level of
competence standardized achievement tests should be used.

CLINICAL IMPLICATIONS (Strub & Black, 2000)

Wernicke's Aphasia: Language output is fluent but is highly paraphasic and circumlocutious. The
tendency for paraphasic errors may be so pronounced that it leads to strings of neologisms, which form
the basis of what is known as "jargon aphasia". The lesion site most commonly associated with
Wernicke's aphasia is the posterior portion of the language network and tends to involve at least parts of
Wernicke's area.

Broca's Aphasia: Speech is nonfluent, labored, interrupted by many word-finding pauses, and usually
dysarthric. Abnormal word order and the inappropriate deployment of bound morphemes (word endings
used to denote tenses, possessives, or plurals) lead to a characteristic agrammatism. Speech is
telegraphic and pithy but quite informative. The cause is most often infarction of Broca's area and
surrounding anterior perisylvian and insular cortex, due to occlusion of the superior division of the middle
cerebral artery.

Global Aphasia: This syndrome represents the combined dysfunction of Broca's and Wernicke's areas.
Most patients are initially mute or say a few words, such as "hi" or "yes."

Conduction Aphasia: The lesion sites spare Broca's and Wernicke's areas but may induce a functional
disconnection between the two so that lexical representations formed in Wernicke's area and adjacent
regions cannot be conveyed to Broca's area for assembly into corresponding articulatory patterns.

Transcortical Aphasias: In nonfluent type (motor) the lesion site disconnects the intact language
network from prefrontal areas of the brain. In fluent type (sensory) the lesion site usually involves the
temporoparietal cortex posterior to Wernicke's area and disconnects the intact core of the language
network from other temporoparietal association areas.

86
Anomic Aphasia: The lesion sites can be anywhere within the left hemisphere language network,
including the middle and inferior temporal gyri. Anomic aphasia is the single most common language
disturbance seen in head trauma, metabolic encephalopathy, and Alzheimer's disease.

Subcortical Aphasia: Damage to subcortical components of the language network (e.g., the striatum
and thalamus of the left hemisphere) can also lead to aphasia. The resulting syndromes contain
combinations of deficits in the various aspects of language but rarely fit the specific patterns described
above.

Memory (Strub & Black, 2000)

Memory allows us to store, retain, and retrieve information. These three processes influence and are
modified by the type of information that is to be remembered, the duration of time over which it must be
retained, and the way in which the brain will use the information in the future. The neural circuits
underlying these processes are dynamic, reflecting the flexibility of memory itself.
From a physiologic point of view, memory is divided into explicit and implicit forms.
Explicit memory, which is also called declarative or recognition memory, is associated with
consciousness—or at least awareness—and is dependent on the hippocampus and other parts of the
medial temporal lobes of the brain for its retention. It is divided into the memory for events (episodic
memory) and the memory for words, rules and language etc (semantic memory).
Implicit memory does not involve awareness and is also called nondeclarative or reflexive memory. Its
retention does not involve processing in the hippocampus, at least in most instances, and it includes,
among other things, skills, habits, and conditioned reflexes. However, explicit memories initially required
for activities such as riding a bicycle can become implicit once the task is thoroughly learned.
Explicit memory and many forms of implicit memory involve (1) short-term memory, which lasts
seconds to hours, during which processing in the hippocampus and elsewhere lays down long-term
changes in synaptic strength; and (2) long-term memory, which stores memories for years and
sometimes for life. During short-term memory, the memory traces are subject to disruption by trauma and
various drugs, whereas long-term memory traces are remarkably resistant to disruption. Working
memory is a form of short-term memory that keeps information available, usually for very short periods,
while the individual plans action based on it.

Tests for memory (Strub & Black, 2000)

Valid memory testing presumes that the patient is reasonably attentive, can relate to and cooperate with
the examiner, and has no defect that impairs language comprehension or expression.

Immediate recall (short term memory)

Immediate memory usually tested by digit repetition.

Recent memory: already tested in orientation

Remote memory
These evaluate the patient’s ability to recall personal and historic events. Personal events must be
verified from a reliable source other than the patient, and performance on the recall of historic information
must be interpreted in light of the patient’s premorbid intelligence, education, and social experience.
Indian adaptation: The following items to be enquired- each correct answer to be scored one thus a
maximum score of 6 (Pershad & Wig, 1988).
Four unrelated words
Instructions: Tell the patient, “I am going to tell you four words that I would like you to remember. In a few
minutes, I will ask you to recall these words”. To ensure that the patient has heard, understood, and

87
initially retained the four words, have him or her to repeat the words immediately and to correct any
errors. Older patients may require several trials to learn the words.
Then he is asked to recall the words at 5, 10 and 30 minutes. To eliminate possible mental rehearsal,
interference should be used between presentation and recall of words.
Scoring: Normal persons accurately recall 3-4 words after a 10-minute delay. In some, after being
reminded of the correct words i.e., by verbal cues, whether he/she recognizes the appropriate word from
the series of words and improve their performance after 10 and 30 minutes may be seen, but patients
with dementia cannot improve even on subsequent trials.
Indian adaptation: 1st set: 2nd set: (Pershad & Wig, 1988)
Verbal story for immediate recall
Instructions: tell the patient, “I am going to read you a short paragraph. Listen carefully, because when I
finish reading, I want you to tell me everything that I told you.” A short paragraph is read out to the patient
which he is required to reproduce immediately. As the patient retells the story the number of items
recalled is indicated. The normal individual is expected to produce at least 10 of these items, though this
number decreases with age. If recall is good then he may be asked for another recall after 30 minutes.
Indian adaptation: There are three sentences of increasing length. First sentence is read slowly, distinctly
and at a uniform rate and note down the recalled sentence verbatim or each of the correctly recalled
clauses. One mark for each clause correctly reproduced. (Pershad & Wig, 1988)
Visual memory (hidden objects)
Five small, commonly used, easily recognizable objects are hidden in the patient’s vicinity while he is
watching. Each item is named while being hidden. Then interfering stimuli is provided for 5 minutes. After
this period he is asked to name and indicate the location of each hidden object. Finding out fewer than
three objects indicates impaired visual memory.
Paired associate learning
Instructions: Tell the patient, “I am going to read you a list of words, two at a time. Listen carefully
because I will expect you to remember the words that go together. When the patient understands the
directions, continue as follows: “Now listen carefully to the words as I read them.” The patient is read out
a list of paired words at the rate of one pair every 2 seconds. Then he is given the first words from the
pairs, one after another and given 5 seconds for each response. After completion of the first recall list the
second presentation list is provided after a 10 second interval and proceeded in the same way.
A normal person under 70 years is expected to recall the two easy paired associates and at least one of
the hard associates of the first recall trial and to recall all paired associates on second trial. Some
patients can learn the paired words with strong natural associations but cannot learn the pairs without
such associations which indicate an inability to learn new material that cannot be associated with
memories already in storage.
Indian adaptation: Retention for similar pairs: For dissimilar pairs: (Pershad & Wig, 1988)

Higher Cognitive Functions

Overview: Attention, language and memory are the basic processes that serve as building blocks for the
development of the higher mental abilities. These basic functions are necessary, but not sufficient in and
of themselves, to execute more complex cognitive functions. The higher cognitive functions, including the
manipulation of well learned material, abstract thinking, problem solving, judgment, arithmetic
computations, and so forth, represent the highest level of human intellectual functioning readily
assessable by formal testing methods. These complex neuropsychologic functions are predicted on the
integrity and interaction of more basic processes.
Because they represent the most advanced stages of intellectual development, the higher cognitive
functions are often highly susceptible to the effects of neurologic disease. The evaluation of these
functions may demonstrate the early effects of cortical damage before the more basic processes of
attention, language and memory are impaired. The ability to perform effectively within the environment is

88
determined in large part by an individual’s adequacy in performing such higher order functions (Strub &
Black, 2000).

Anatomical considerations and clinical implications

Higher cognitive functions rely primarily on an intact cerebral cortex, although subcortical lesions can also
affect performance. Except for calculating ability, however, these functions have not been well localized.
Abstract ability, the ability to manipulate old knowledge, and similar functions are probably well
represented in the cortex, though, subcortical structures are also important.
Many of these higher cognitive functions are probably localized in posterior frontal areas of brain. Loss of
abstraction has been considered a sign of extensive frontal lobe dysfunction. Intelligence and other
higher cognitive functions are more commonly impaired with posterior lesions. Dominant hemisphere
lesions frequently interfere with verbal reasoning and abstraction. Impaired performance on calculations
may be seen with brain lesions that are bilateral or unilateral on either side. Left hemisphere lesions in
the right handed typically result in more severe impairment in calculations than do corresponding lesions
of the non dominant hemisphere. (Strub & Black, 2000)

Tests for Higher Cognitive Functions:

Abstract thinking
Proverb interpretation: Interpreting proverbs accurately requires an intact fund of general information, the
ability to apply this knowledge to unfamiliar situations, and the ability to think in the abstract.
Instructions: Tell the patient, “I am going to read you a saying that you may or may not have heard
before. Explain in your own words what the saying means.” A total of five proverbs arranged in increasing
order of difficulty is presented. This is continued only until the patient fails on two successive proverbs. If
the patients response to the first proverb is concrete or if he is unable to interpret it, he is supplied with
the correct answer and is explained it is the expected type of response. Often, uneducated patients will
initially give a concrete response but can give abstract interpretations when specifically asked if there is
another way of explaining the proverb. Such cued responses should be scored as semi-abstract.
The interpretation is scored as abstract (2 points), semiabstract (1 point) and concrete (0 points) based
on the degree of abstraction demonstrated in explaining the meaning of the proverb. The possible total
for this section is 10 points. Concrete responses are pathologic in all but for the retarded or illiterate
patient. The average patient should provide abstract interpretations to at least the first three easy
proverbs and minimally semiabstract response to the remaining proverbs. (Strub & Black, 2000).
Indian adaptation: In our population some commonly known proverbs are asked, e.g., “ulta chor kotowal
ko dante”, “naach na jaane angan teda” etc (Kulsresth, 2000).
Similarities: Here the patient has to explain the basic similarity between two overtly different objects or
situations. This test requires analysis of relationships, formation of verbal concepts, and logical thinking.
The patient is given some pairs of objects in ascending order of difficulty and asked to explain how they
are similar. If he fails on the first item he is provided with the answer and shifted to the next item.
However, no assistance is provided in the following items.
Scoring: Two points should be given for any abstract similarity or general classification that is highly
pertinent for both items in the pair. One point is given for responses that indicate specific properties of
both items in the pair and that constitute a relevant similarity. A score of 0 is given when the response
reflects properties of only one member of the pair, differences or generalizations that are not pertinent to
the item pair, and failure to respond. Total for this section is 10 points. (Strub & Black, 2000)
Indian adaptation: In our population similarities between some common objects are asked: coal and
wood, mango and guava, train and car etc. In the same manner, differences are asked between some
common items (e.g. wood and glass, bird and dog) (Kulsresth, 2000).

89
The fund for acquired information or the store of knowledge
Questions (10 in number) of increasing difficulty are asked to the patient until the test is completed or the
patient fails on three successive questions. If the patient’s answer is not clear he is asked to explain more
fully. Some of the questions are: how many weeks are in a year, why do people have lungs, name of the
capital of the country etc.
The patient’s answer must either be exact or very closely approximate to the acceptable response. The
average patient with an adequate educational background should answer a minimum of six questions
appropriately. Less adequate performance indicates an impaired fund of general information and
suggests reduced intelligence, limited social and educational exposure or significant dementia.
Indian adaptation: In Hindi adaptation this test consists of 33 questions which are read clearly to the
patient. If the response to a question is incomplete or not clear then he is asked to explain it further. The
test is discontinued after 7 successive failures. Examples: what is the shape of a ball? How many months
are there in a year? Name any three persons who had been prime ministers of India etc (Pershad &
Verma, 1990).

The manipulation of old knowledge (e.g., calculation or problem solving)

Calculations are complex neurologic functions that involve the somewhat distinct components of number
sense and manipulation. Components of calculations include the following: Rote tables (e.g., addition,
subtraction and multiplication), Basic arithmetic concept of carrying and borrowing, Recognition of the
signs, Correct spatial alignment for written calculations.
Verbal rote examples: 4+6, 8-5, 2x8, 9/3 etc
Verbal complex examples: 14+ 17, 43-38 etc. 20 seconds is given for a response, a failure to respond
within that time, even if a correct response is given ultimately, is scored as failure.
Written complex examples: 108+ 79, 605-86 etc. failure to respond within 30 seconds is noted as failure.
Each response should be scored as correct or incorrect. By comparing performance on each subtest, the
patient’s overall level of calculation ability and area of adequacy and deficit can be determined. Errors
specific to a particular aspect of computation or to a modality of presentation should be noted.
Calculation ability is stable across all age groups, although variable performance is seen within each
group. Performance in early dementia is not significantly impaired; it deteriorates dramatically in the
second and third stage of the disease.

Lesions in different parts of cerebrum and cognitive functioning

The cerebral hemispheres have been anatomically compartmentalized into four lobes, and within these
lobes special regions have been identified. These anatomic units rarely, if ever, function completely
independently. Most higher functions require the coordinated activity of more than one brain region.
Study of deficits after single lesions is further complicated by the poorly understood process of recovery
of function, even though the anatomy of the lesion remains unchanged.

Frontal Lobe

Frontal Lobe function tests (Strub & Black, 2000)

Alternating motor patterns test
This test consists of a series of changes in hand position (adapted from Luria) which are first
demonstrated to the patient and then he is asked to perform.
Fist-Palm- Side test: The patient is asked to hit the top of the table repeatedly, first with a fist, then with
an open palm, and then with the side of the hand. The patient is asked to perform it until asked to stop.
Performance for 15-20 seconds should suffice to assess the adequacy of these alternating movements.

90
Fist- Ring test: The patient is instructed to extend his arm several times, first with the hand in a fist, and
then with the thumb and forefinger opposed to form a ring. With successive extension of the arm, the
patient alternates between these two positions.
Reciprocal Coordination test: Here the patient places both hands on the table, one in a fist and one
with fingers extended palm down. The patient is asked to alternate the position of the two hands rapidly
(simultaneously extending the fingers of one hand while making a fist with the other.
Normal individuals should have no difficulty in easily mastering these alternating sequences after one or
two attempts. Any appreciable disruption of the smooth performance of these tasks indicates dysfunction
of the premotor areas of the cerebral cortex. Patients with lesions involving the dominant dorsolateral
prefrontal cortex, have difficulty abandoning the initial pattern of responses, and tend to perseverate. In
copying tasks involving drawing simple figures with multiple loops, patients with perseveration may insert
extra loops.
Another test is a motor go/no-go task in which the subject is instructed to tap the table twice in response
to a single tap by the examiner (out of the subject’s view) and not to tap the table at all in response to two
taps by the examiner. Ten trials are administered, and performance is scored as either correct or
incorrect for each trial (Rothlind & Brand, 1993).
Alternating sequences –Visual Pattern Completion Test: The patient is given visual patterns to
reproduce. Patients with intact motor and sensory systems should be able to complete these sequences
without error. A loss of sequence or perseveration in the reproduction of sequences suggests a loss of
the ability to move from one motor movement to another and an ability to shift sets efficiently.

Frontal lobe dysfunctions

Frontal lobe dysfunction may be subtle. The usual methods of bedside testing, including formal
neuropsychological assessment, may fail to detect even significant frontal lobe dysfunction. Comparison
with the patient's premorbid personality and behavior are often more telling than assessment based on
population-derived reference information. In addition to the standard tests of abstract thinking and
proverb interpretation, special techniques designed to evaluate frontal lobe function may be useful. Tests
helpful for evaluating frontal lobe function include verbal fluency by word list generation, assessment of
the ability to alternate tasks or switch between tests, abstraction ability, and tests for perseveration,
apathy, and impulsivity.

Three behavioral complexes are currently recognized with frontal systems dysfunction: an orbitofrontal
disinhibition syndrome, a medial frontal apathetic-akinetic syndrome, and a frontal convexity
neuropsychological deficit and motor programming disorder. Combinations of symptoms are common in
most patients with frontal lobe disorders. (Strub & Black, 2000)

The orbitofrontal syndrome is the most well known and flamboyant of the frontal lobe behavioral
disorders. The patients are disinhibited, making tactless remarks and acting on impulse. They are
coarsened, lack empathy, and show little concern for the feelings of others. They fail to plan ahead and
exhibit little concern about their illness or future. Mood is typically irritable and labile with a fatuous
euphoria. Inappropriate jocularity with an insensitive humor (witzelsucht) may be observed. There is a
lack of social restraint and an undue familiarity with strangers. Despite the marked behavioral alterations,
these patients may have few or no neuropsychological deficits and exhibit intact language, memory, and
visuospatial skills. Deficits in olfaction commonly accompany the syndrome because of the proximity of
the olfactory nerves, bulbs, and tracts to the orbital surface. This syndrome has been observed with
inferior caudate lesions as well as disturbances of the orbitofrontal cortex (Chow & Cummings, 2000).

The medial frontal lobe syndrome is also a striking behavioral disorder. The severity of the syndrome
extends from akinetic mutism at the most severe end of the spectrum to a mild lack of motivation on the
other. An attenuated form of this syndrome occurs with unilateral medial frontal lobe lesions. Loss of

91
initiative, poor motivation, limited gesturing, and apathy characterizes the spontaneous behavior of
patients with medial frontal lesions. Patients with left-sided lesions manifest transcortical motor aphasia
with little speech initiation, nonfluent output, intact comprehension, and preserved repetition. With lesions
of either hemisphere, a callosal apraxia with inability to perform learned motor acts on command with the
left hand may also be present.

Frontal convexity lesions produce abnormalities of sequential behavior including perseveration

(abnormal continuation of behavior), impersistence (abnormal early termination of behavior), deficits in
set shifting, and disturbances of programming sequential motor acts such as alternating programs,
reciprocal programs, multiple loops, and serial hand sequences. Patients also have difficulty developing
strategies that will facilitate copying complex figures, exhibit poor judgment, and are concrete on tests of
abstraction. There may be no elementary neurological abnormalities. The condition has been observed
with dorsal caudate lesions as well as frontal convexity lesions.

Parietal Lobe: Dominant side – Calculation, Language, Planned movement, Appreciation of size,
shape, weight and texture. Non-dominant side: spatial orientation, constructional skills

Tests for Parietal lobe

They intend to test tactile sensation (cortical), visuospatial functioning, reading and calculation. Relevant
tests already discussed.

1. Cortical sensory loss:

Astereognosis (stereoanesthesia) (Strub & Black, 2000)
It is the loss of the ability to recognize and identify an object by touch despite intact primary sensory
modalities. There is no loss of perceptual ability. The patient can feel the object, sensing its
dimensions, texture, and other relevant information. However, he is unable to synthesize this
information and correlate it with past experience and stored information about similar objects in order
to recognize and identify it.
Instructions: Stereognosis is tested by asking the patient to identify, with eyes closed, common
objects placed into his hand (e.g., coin, key, button etc.). Astereognosis usually indicates a lesion
involving the contralateral parietal lobe. It has also been reported to occur with lesions involving the
anterior corpus callosum and the thalamic radiations.
Graphesthesia is a similar function. Instructions: It is tested by writing numbers on the patient's palm
or fingertips. The inability to recognize the numbers is referred to as agraphesthesia; in the presence
of intact primary sensory modalities, it usually indicates a lesion involving the contralateral parietal
lobe.
Two point discrimination: Two-point or spatial discrimination is the ability to differentiate between
stimulation by one and stimulation by two points. A Weber's compass or a calibrated two-point
esthesiometer is used, and the patient is stimulated by either a single point or the simultaneous
application of two points. The minimum distance between the two points when they are felt separately
is noted. The distance varies considerably in different parts of the body. Two points can be
differentiated from one at a distance of 1 mm on the tip of the tongue, at 2 to 4 mm on the fingertips,
at 4 to 6 mm on the dorsum of the fingers, at 8 to 12 mm on the palm, and at 20 to 30 mm on the
dorsum of the hand. Greater distances are necessary for differentiation on the forearm, upper arm,
torso, thigh, and leg. The findings on the two sides of the body must always be compared. Two-point
discrimination is sometimes considered a variety of critical tactile sensibility that is carried through the
dorsal funiculi. Clinically, however, it has been found that loss of two-point discrimination with
preservation of tactile sensation results from lesions of the parietal lobe (DeJong & Haerer, 1996).

92
 Test of sensory inattention (bilateral sensory stimulation):
Instructions: It is tested by using double (bilateral) simultaneous stimulation in all major sensory
modalities after excluding deficit in any modality on either side.
In tactile testing, corresponding areas on both sides of the body are touched simultaneously with
equal intensity. Visual testing is done by having the patient face the examiner and fix his or her gaze
at a point on the examiner’s face. The examiner then wiggles a finger in right and left peripheral fields.
Auditory testing is carried out by having the examiner stand behind the patient and provide a stimulus
of equal intensity to each ear.
Extinction is present when the patient suppresses stimulus from one side of the body. Extinction may
occur in all modalities (polymodal neglect) or may be restricted to a single modality. When extinction
is elicited, the degree of inattention can be assessed by increasing the magnitude of the stimulus on
the inattentive side. When the double simultaneous stimulation includes one proximal and one distal
stimulus, the distal stimulus tends to be neglected or extinguished. This test (Face – Hand Test) is a
very useful simple test for organic disease. Patients with organic brain syndromes rarely recognize
the hand stimulus even after as many as 10 trials. Some normal elderly individuals will also extinguish
the hand stimulus; therefore, the test must be interpreted with caution in patients over 65.

2. Constructional ability
Constructional ability is the ability to construct or draw two or three dimensional figures or shapes. A
high level nonverbal cognitive function, constructional ability is a very complex perceptual motor ability
involving the integration of the occipital, parietal and frontal lobe functions. Because of the extensive
cortical area necessary to perform constructional tasks, early or subtle brain damage frequently
disrupts performance.
The parietal lobes are the principle cortical areas involved in visual motor integration. The visual
receptive areas of the occipital lobes and the motor areas of the frontal lobes are necessary for the
completion of all of the tests, but it is the association areas of the parietal lobes that is responsible for
most of the complex integration (Strub & Black, 2000).
It is believed that the right (non dominant) parietal lobe is actually dominant for constructional ability.
Generally, right lesions produce a higher incidence and greater severity of defect than do left
hemisphere lesions. The most dramatic example of construction impairment occurs in patients with
bilateral cortical disease, particularly cerebral atrophy.

Tests for constructional ability (Strub & Black, 2000)

Patients with brain lesions show differences in the incidence, severity, and quality of constructional
impairment, depending on the type of test used and the nature, size, and location of their lesions. The
use of these tests presumes that the patient has adequate visual acuity and sufficient motor ability to
use pencil, paper, and blocks effectively.
Reproduction drawings: The patient is given a list of drawings organised in order of increasing
difficulty (e.g., vertical diamond, two-dimensional triangle within a triangle etc.) and asked to draw
the designs exactly as they look. A different pen may be used, to reduce the possibility of
confusion between the drawings of the patient and those drawn by a hurried examiner. Separate
sheets of paper may be needed for patients who are highly distractible or perseverative.
Instruction: introduce each item by saying, “please draw this design exactly as it looks to you.”
The adequacy of patient’s performance is judged using an objective scoring system.
0- Poor: non recognizable or gross distortions of the basic design
1. Fair: moderately distorted or rotated two dimensional drawings or a loss of all three
dimensionality with moderate distortions or rotations on three dimensional designs
2. Good: minimal distortions or rotations with adequate integration on two dimensional designs
and some evidence of three dimensionality but less than perfect
3. Excellent: perfect or nearly perfect reproductions

93
 Drawings to command: The patient is required to draw three pictures (a clock with numbers and
hands on it, a flower in flower pot, and a house in perspective, so that two sides and the roof is
seen), according to verbal commands. A simple scoring system similar to that used in reproduction
drawings may be used to quantify the performance on this test.
Normal individuals obtain almost perfect scores on simple reproduction and command drawings
though a modest deterioration occurs with increasing age. Several specific type of errors on
constructional tests are usually accepted as almost pathognomonic of brain damage when made
by a non retarded patient over age 10 years, some of which are:
1. Rotation by > 45 degrees or the disorientation of the whole figure or a component of it on the
background.
2. Preservation or the repetition of the entire figure or part of it.
3. Fragmentation of the design or omission of the parts of the figure
4. Significant difficulty in either integration or placement of individual parts at the correct angles or
location.
5. Substitution or addition of ‘dog-ears’ for angles on the draw figure.
Other test- block designs: the patient is given stimulus designs and multicoloured cubes and
asked to accurately draw the designs. This test requires four multicoloured cubes and four
stimulus designs.
Finger agnosia: refers to the loss or impairment of the ability to recognize, name, or select individual
fingers of the patient's own hands or the hands of the examiner. The patient loses the ability to name
individual fingers, point to fingers named by the examiner, or move named fingers on request, in the
absence of any other naming deficit.
Right-left orientation test: may be tested by asking the patient to raise a specific hand, to touch a
body part on one side (e.g., the right ear) with a specific digit of the other side (e.g., the left thumb),
etc

Finger agnosia and right-left confusion, along with agraphia and acalculia make up Gerstmann's
syndrome. Finger agnosia alone is not highly localizing, but when all components of the syndrome
are present the lesion is likely to lie in the region of the dominant angular gyrus.

3. Apraxia: It is a failure of the ability to carry out well-organised voluntary movement correctly despite
the fact that motor, sensory and co-ordinative functions are not significantly impaired.

Tests for Apraxia (Strub & Black, 2000)

1. Ideomotor apraxia: This is the most common type of apraxia. There is a hierarchy of difficulty in
performing these ideomotor tasks. The most difficult level requires the patient to perform the action to
verbal command. These movements must be mimed without the actual object and in the absence of
any non verbal cues from the examiner. If the patient fails at this level the examiner performs the
action and the patient is asked to imitate it. Most patient with apraxia finds imitation easier than
miming the movement on command. If the patient again fails, he is provided the actual object and
asked to follow the command (Heilman et al, 1982).
 Buccofacial commands: “blow out a match’, protrude your tongue”, “drink through a straw”.
Patients may try to cue themselves by pretending to have the object in their hands, which has to be
discouraged. Buccofacial apraxia involves apraxic deficits in movements of the face and mouth.
 Limb commands: The patient is asked how to- salute, use a toothbrush, flip a coin etc. Although
ideomotor apraxia is usually a bilateral phenomenon, occasionally it may be unilateral. Accordingly,
commands should be alternated between left and right limbs. The patient is not allowed to perform
the same command sequentially with both hands, because visual self cueing will improve
performance on second trial. Limb apraxia encompasses apraxic deficits in movements of the arms
and legs.

94
  Whole body commands: The patient is asked to show how to- stand like a boxer, swing a bat
etc.
Ideomotor apraxia is almost always caused by lesions in the left hemisphere and is commonly
associated with aphasic syndromes, especially Broca's aphasia and conduction aphasia. Its presence
cannot be ascertained in patients with language comprehension deficits. Traditionally, it has been
thought that, just as one hemisphere is dominant for language, the other is dominant for the
performance of movement formulas and object-free motor acts. In right-handed individuals, the left
hemisphere would be dominant for praxis and speech.
2. Ideational apraxia: It is a disturbance of complex motor planning of a higher order than is seen in
ideomotor apraxia. It refers to a breakdown in performance of a task that involves a series of related,
but separate steps. The patient can perform each individual step of the task in isolation but cannot
integrate the parts accurately to complete the sequence.
Instructions: The patient may be asked to show how to fold a letter, place it in an envelope, seal it,
address it and place a stamp on the envelope.
Ideational apraxia refers to a deficit in the execution of a goal-directed sequence of movements in
patients who have no difficulty executing the individual components of the sequence. These motor
sequencing problems are usually seen in the context of confusional states and dementias rather than
focal lesions associated with aphasic conditions.
3. Constructional apraxia the patient fails to make designs with matches, either spontaneously or
by copying. The side of figure opposite the lesion may be omitted altogether. Often in writing he
cramps everything into one small corner of the paper. It occurs in lesions of angular gyrus of either
hemisphere, but when isolated is usually from non-dominant parietal lesions (Spillane, 2005). It can
be tested with Koh’s blocks.
4. Dressing apraxia the patient becomes muddled in trying to dress and undress, puts cloths in the
wrong way round, or may be unable to start the necessary motions. This defect usually results from
non-dominant posterior parietal lobe lesions (Spillane, 2005).
Patients with left posterior lesions shows lower verbal than performance IQ scores, while right posterior
lesions affect only the performance IQ. Working memory may be affected by parietal lesions, leaving
long-term memory relatively spared. Receptive aphasia and conduction aphasia are believed to be
secondary to lesions in the left supramarginal gyrus or subcortical arcuate fasciculus. Damage to the left
angular gyrus is believed to be responsible for reading disorders (alexia). Lesions of the right parietal
lobe results in deficit of visual perception of faces, overlapping or incomplete figures, and the
identification of objects from unusual views has been documented. Visual-spatial disorientation is
associated with biparietal disease characterized by errors in absolute localization of individual objects,
errors in relative localization, inability to compare the dimensions of two objects, difficulty in counting
objects, defective visual attention, and fixity of gaze with impaired voluntary ocular movements. Patients
with parietal lobe lesions may get confused about the spatial arrangement of their own body parts, may
show impaired appreciation of two- and three-dimensional extrapersonal space, might be unable to
disengage attention from a current focus when a target occurs on the side opposite the lesioned
hemisphere. Visuospatial skills that have a motor (manipulative) component are often impaired after
parietal lesions. Such impairments are more severe after right than left hemisphere damage.

95
Temporal Lobe: Functions- Dominant lobe - Auditory perception, Speech, Language, verbal
memory, & smell. Non-dominant lobe – Auditory perception, Music, tone sequences, Non-verbal
memory (faces, shapes, music) & Smell.

Tests for Temporal lobe. (Strub & Black, 2000)

They intend to test Audition, Language comprehension, Sensory prosody, Memory and Emotion.
Relevant tests already discussed.
Memory loss is one of the most characteristic features of temporal lobe lesions. General fund of
knowledge has been shown to be poorer in unilateral temporal lesions. Bilateral damage to the mesial
temporal lobe results in global amnesia for events that occur after the lesions. Left temporal lesions
cause verbal memory deficits. Right temporal lobe lesions impair learning and retention of material that is
difficult to verbalize, such as faces, nonsense designs, spatial location, and odors.
Temporal lobe lesions are sometimes associated with a syndrome of humorless sobriety, dependence,
and obsessionalism characterized by overemphasis on trivia, pedantic speech, egocentricity, paranoia,
preoccupation with religion, and aggressive outbursts. Acute bilateral temporal lobe lesions may produce
Kluver-Bucy syndrome (hypersexuality, excessive oral behavior and visual agnosia) (Brazis et al, 2007).

Occipital Lobe: Functions – Analysis of vision

Tests for Occipital lobe. (Strub & Black, 2000)

Agnosia
Gnosia (Gr. gnosis “knowledge”) refers to the higher synthesis of sensory impulses, with the resulting
perception, appreciation, and recognition of stimuli. Agnosia refers to the loss or impairment of the ability
to know or recognize the meaning or import of a sensory stimulus, even though it has been perceived.
Agnosia occurs in the absence of any impairment of cognition, attention, or alertness. The patients are
not aphasic and do not have word-finding or a generalized naming impairment (Campbell & William,
1994).

1. Visual Agnosia: Visual agnosia is an impairment of the ability to recognize objects visually in the
absence of a loss in visual acuity or general intellectual functions that would account for it. Two
factors are at work in object recognition: (a) the act of conscious perception of a sensory impression
(apperception) and (b) the act of linking the content of the perception with previously encoded
percepts, thereby acquiring meaning (association). Therefore, there may be two types of visual
agnosia: apperceptive visual agnosia and associative visual agnosia (Brazis et al, 2007).
Apperceptive visual agnosia. The defect lies in an impairment of visual pattern recognition. They
cannot name items presented to them, draw them, or match them to samples. They cannot point to
objects named by the examiner. Yet they can distinguish small changes in the intensity or hue of a
minute source of light, and visual acuity and visual fields are normal. Bilateral lesions of the calcarine
cortex or occipitotemporal regions cause this disturbance.
Associative visual agnosia. This term refers to the deficit of patients who cannot recognize objects
visually but can draw them or point to them when they are presented in an array of objects. In the
process of recovery, this deficit tends to progress into a milder deficit, optic aphasia, which is
characterized by the inability to name objects that are recognized. This usually occurs following lesions
affecting the mesial aspect of the left occipital lobe and the splenium of the corpus callosum.

2. Color Agnosia: Patients with color agnosia can read Ishihara plates or sort colors according to hue
but cannot name colors or point to a color named by the examiner; however, they perform well in
verbal tasks. Dominant hemispheric lesions that involve the inferomedial aspect of the occipital and
temporal lobes are most probably responsible for color agnosia. Patients with color agnosia usually

96
 have lesion responsible for this condition affecting the left mesial subsplenial area, which is
transitional between the occipital and temporal lobes.

3. Prosopagnosia : Inability to identify faces visually or objects that are visually similar (such as a
specific car in a parking lot), caused by bilateral inferior occipitotemporal lesions. However, these
patients are still able to perceive faces and identify separate facial features. Lesions of fusiform gyri
have been implicated to cause this condition (Cohn et al, 1977) (De Haan et al, 1991).

Metamorphopsia has been described with occipital lesions, some special forms of which include
palinopsia (perseveration of the visual image), optic allesthesia (false orientation of objects in space),
monocular diplopia or triplopia, and polyopia (one object appearing as two or more objects). Other
features of extensive occipital lesions include defective memory for visual images, defective topographic
memory, problems in visuospatial judgments etc.

Object agnosia has been associated with lesions in areas 18 and 19 of the dominant hemisphere and in
the splenium of the corpus callosum or with bilateral occipital lesions.

Simultanagnosia is the inability to appreciate more than one aspect of a visual stimulus at a time
caused by lesions in bilateral parietal-occipital regions. Prosopagnosia may be caused by bilateral
occipital-temporal lesions. Color achromatopsia, in which the patient cannot match colors, has been
associated with posterior lesions, especially of the right hemisphere bilateral lesions. Pure word
blindness (pure alexia) refers to alexia in the absence of dysgraphia or aphasia, which is thought to be
secondary to damage in the left occipital region and in the splenium of the corpus callosum (Brazis et al,
2007).
In general, intellectual, memory, speech, motor, and somatosensory functions are unaffected by
restricted occipital lobe lesions. When cortical blindness is accompanied by anosognosia for the
blindness, the condition is called Anton's syndrome. Such patients deny that they are blind, and often
behave as if they have their sight. Their behavior may be one of apathy or euphoria. Memory for visual
impressions is lost. A full explanation for this altered behavior and for the features is unknown, but the
extent of the lesions in Anton's syndrome extends beyond area 17.

Conclusion
A systematic mental status examination usually allows the clinician to differentiate patients with organic
brain disease from both normal persons and those with functional disorders. Although it is not always
necessary to evaluate exhaustively every aspect of mental functioning, the current discussion is more
focused on bedside tests for certain critical functions to be assessed in every patient.

97
References:
*Brazis, P.W., Masdeu, J.C. and Biller, J. (2007). The Localization of Lesions Affecting the Cerebral
Hemispheres. In: Localization in Clinical Neurology, 5th ed, Lippincott Williams & Wilkins. pp.
457-521.
*Campbell. and William, W. (1994). Agnosia, Apraxia, and Related Disorders of Higher Cortical Function.
In: DeJong's The Neurologic Examination, 6th ed, DeJong, R. N. Philadelphia: Lippincott
Williams & Wilkins. pp. 57-65.
*Chow, T. W. and Cummings, J. L. (2000). Neuropsychiatry: Clinical Assessment and Approach to
Diagnosis. In: Sadock, B.J. and Sadock, V.A. (Eds.). Comprehensive Textbook of Psychiatry,
7th ed. Philadelphia: Lippincott Williams & Wilkins, pp. 310-338.
Coats, T. (2007). Unconscious patients. In: Hutchison’s Clinical Methods. (Eds.). Swash, M Glynn. M,
Philadelphia, pp- 415.
De Haan, E.H., Young, A.W. and Newcombe, F. (1991). Covert and overt recognition in prosopagnosia.
Brain, 114, 2575-2591.
*DeJong, R. N. and Haerer, A. F. (1996). Case Taking and the Neurologic Examination. In: Clinical
Neurology (CD-ROM). Griggs, R.C. and Joynt, R.J. (Eds.). Philadelphia: Lippincott-Raven
Publishers.
*Hodges, J.R. (1996). Cognitive Assessment for Clinicians, Oxford: Oxford University Press. Pp. 2-5.
Jennet, B. and Teasdale, G. (1981). Assessment of Impaired Consciousness. In: The Mental Status
Examination in Neurology, 4th ed, Strub, R.L. & Black, F.W. (Eds.). New Delhi: Jaypee
Brothers Medical Publishers. pp. 13-145.
Kulsresth, S.K. (2000). Stanford-Binet Intelligence Scale Hindi Adaptation of Third Revision-Form L-M.
Part IV. Varanasi: Prasad Psycho Corporation. pp. 95-159.
*Pershad, D. and Verma, S.K. (1990). PGI Battery of Brain Dysfunction. Agra: National Psychological
Corporation
Pershad, D and Wig, N.N. (1988). Revised Manual for PGI Memory Scale(PGIMS). National
Psychological Corporation, Agra.
Robbins, T.W. and Everitt, B.J. (1995). Arousal systems and attention. In: Gazzaniga, M.S. (Ed.), The
Cognitive Neurosciences. MIT Press, Cambridge, MA, pp. 703–720.
Rothlind, J.C. and Brand, J. (1993). A Brief Assessment of Frontal and Subcortical Functions in
Dementia. The Journal of Neuropsychiatry and Clinical Neurosciences, 5, 73-77.
Strub, R. L . and Black, F. W. (2000). The mental status examination in neurology. Philadelphia: F. A.
Davis.
Zeman, A. (2008). Consciousness: Concepts, neurobiology, terminology of impairments, theoretical
models and philosophical background. In: Handbook of Clinical Neurology, Vol. 90 (3rd
series), Young, G.B. & Wijdicks, E.F.M. (Eds.). Exeter: Elsevier B.V. pp. 3-31.

98
Higher mental function assessment proforma:
1. Consciousness: Alert, Drowsy/Lethargy, Coma
2. Attention:
Digit repetition: digit forward & digit backward
“A” Random letter test: The examiner reads a series of letters and the patient is asked to tap the desk
each time the letter “A” is heard. Possible errors include errors of omission, errors of commission and
errors of perseveration.
Serial subtraction test (100-7 or 20-3), recitation of months of the year/ days of the week backwards
3. Orientation:
To time: year, month, day of the week, date, time of the day.
To place: country, state, city, hospital and native place.
To person: should be able to identify the doctor, a relative and self.
4. Language
Handedness
Spontaneous speech: Open ended questions
Verbal fluency: Animal naming test, FAS test
Comprehension: Pointing commands:- Ask the patient to point to various objects in the room. Ask
question which can be answered in “yes” or “no.” Ability to understand two or three step commands.
Repetition: Start with monosyllabilic words and proceed to complex sentences.
Naming and word finding: Colors, body parts, parts of clothing, and objects.
Writing, reading and spelling.
5. Memory
Immediate memory: Tested by digit repetition
Recent memory: Tested in orientation
Remote memory:
Personal information: Names of schools and colleges where the patient studied, year of passing pre-
university/graduation, names of children, spouse & family members, birthdays and anniversary days.
New learning ability: Ability to recall four unrelated words after 5,10 and 30 minutes. Pencil, Garden,
Clever & Hungry.
Verbal story for immediate recall
Visual memory (hidden objects): Ability to recall after 5 minutes 4-5 objects shown and hidden. Pen,
Comb, Coin, Keys, Spoon.
Paired associated learning:
6. Abstract thinking
Proverb interpretation: The grass is always greener on the other side. Don’t cry over spilled milk. Rome
wasn’t built in a day.
Similarities (coal and wood, mango and guava, train and car) and dissimilarities (wood and (wo.od and
glass, bird and dog).
7. Fund of information/ store of knowledge. What is the shape of a ball?, How many months are there in
a year?, Name any three persons who had been prime ministers of India? etc
8. Manipulation of old knowledge (calculation or problem solving)
Verbal rote: 4+5, 8-5, 2×8, 9/3
Verbal complex: 14+17, 43-38, 96×6, 76/4
Written complex: 108+79, 605-86, 112×8, 772/8
9. Lobe functions:
Frontal lobe tests: Alternating motor patterns:- Fist-ring test, Fist-palm-side test, Reciprocal co-ordination
test. Alternative visual patterns.
Parietal lobe tests:

99
Cortical sensory loss: Stereognosis – To identify the objects placed in hand with eyes closed.
Graphaesthesia – To identify the numbers written on the patient’s palm/hand. Two – point discrimination
– Ability to differentiate two stimulated points. Tests of bilateral sensory stimulation.
Constructional ability: Reproduction drawings – geometric shapes, two-dimensional block designs, three
dimensional block constructions. Errors made by the patient include rotation, perseveration and “closing
in.” drawings to a command- picture of a clock, a house with two sides and a roof, picture of a man.
Finger agnosia: Ask the patient to show various fingers on self and the examiner’s hand.
Left-right disorientation – check on the patient and also “crossed on examiner’s.”
Apraxia: Ideomotor apraxia. 1. buccofacial commands- blow out a match, protrude your tongue, drink
through a straw. 2. Limb commands – salute, use a toothbrush, hammer a nail, comb your hair, kick a
ball, crush out a cigarette. 3. Whole body commands: Stand like a boxer, swing a cricket bat.
Ideational apraxia: 1. Folding a letter, placing it in an envelope, sealing it, addressing it and putting a
stamp on it. 2. Placing candle in candleholder, taking match-out of box, lighting candle and blowing out
the match. 3. Opening toothpaste, taking out paste, putting it on the toothbrush and brushing the teeth.
Temporal lobe tests: Tests for auditory perception, speech, language, verbal and non-verbal memory and
smell already been tested.
Occipital lobe tests: Visual agnosia – Inability to recognize object visually as shown by the examiner in
the absence of loss in visual acquity or general intellectual function. Color agnosia – Inability to identify
color or point to color instructed by examiner. Prosopagnosia - Inability to identify faces visually or objects
that are visually similar.

100
CHAPTER –VI
 EXAMINATION OF CRANIAL NERVES

Introduction:
Cranial Nerve examination remains a very important part of neurological examination as it
gives an easy and practical method of localizing a lesion by simple bed-side examination
techniques. In a human body there are 12 pairs of cranial nerves namely – Olfactory, Optic,
Oculomotor, Trochlear, Abducens, Facial, Vestibulo-Cochlear (Auditory),
Glossopharyngeal, Vagus, Accessory and Hypoglossal nerves. Some of these nerves have
many functions while a few functions are overlapping for a number of cranial nerves. In
spite of these overlaps there are precise methods of examining each and every function of
individual cranial nerve.

Examination
Cranial nerve examination involves a good amount of cooperation from the subject; hence a
good rapport with the subject is essential to start with. After mutual introduction and
greeting, the nature and purpose of examination to follow should be explained, consent
taken and cooperation on the part of the subject asked for. Examination is conducted while
examiner and subject sit on chair at equal heights at arms distance from each other.

Props and Instruments Required:

1. A comfortable sitting arrangement
2. Some recognizable, non-irritant common substances for smelling – soap, tooth
paste, coffee, asafetida, ginger etc.
3. A well illuminating Torch.
4. Snellen's chart, a Reading material, Ishihara's chart
5. Ophthalmoscope
6. Red hat pin
7. Neurological pins
8. Wisp of cotton
9. Test tubes containing warm and cold water
10. Tendon hammer
11. Some non-irritant edibles-salt, sugar, lime, quinine solution in drinking water with
separate swabs. Drinking water to wash mouth each time
12. Cards with name of 'tastes' written on them
13. Tuning fork (512 or 256 Hz)
14. Tongue depressor and swab stick, laryngeal mirror

Brief History before starting

 Chief complaints
 H/O weakness in any part of the body, head injury, unconsciousness, fits.
 H/O Hypertension, Diabetes Mellitus, other medical diseases
 H/O any rash
 H/O asymmetry of face, eyes, pupil
 Decreased eyesight, any difficulty of hearing, taste and smell; double vision,
hoarseness, nasal regurgitation of food/drink, nasality of speech, difficulty in
deglutition
 Loss of sensation on a part of face
 Dryness of eye, mouth.
Gross General Survey
101
  Any facial asymetry
 Eyelid or pupilary abnormality
 Any rash
 Hoarseness or nasal speech
 Wearing spectacles, contact lens, using hearing aids

INDIVIDUAL CRANIAL NERVES

OLFACTORY NERVE
Neuroanatomy
Bipolar sensory cells with ciliated process in distal end located on lateral and septal
surfaces of nasal mucosa in medial wall or superior nasal choncha form the olfactory
epithelium. The olfactory nerves, consist of a collection of many sensory nerve fibers that
extend from the olfactory epithelium to the olfactory bulb, passing through the many
openings of the Cribriform plate of the Ethmoid bone; a sieve-like structure. Olfactory
receptor neurons continue to be born throughout life and extend new axons to the olfactory
bulb. Olfactory ensheathing glia wraps bundles of these axons and facilitates their passage
into the central nervous system.

The sense of smell (olfaction) arises from the stimulation of olfactory (or odorant) receptors
by small molecules of different spatial, chemical, and electrical properties that pass over the
nasal epithelium in the nasal cavity during inhalation. These interactions are transduced
into electrical activity in the olfactory bulb which then transmits the electrical activity to other
parts of the olfactory system and the rest of the central nervous system via the olfactory
tract.The olfactory nerve is the shortest of the twelve cranial nerves and only one of two
cranial nerves (the other being the optic nerve) that do not join with the brainstem.

Function
To carry sensations of smell from the nasal mucosa to the olfactory bulb.

Methods of Testing:
 Ask patient if there is any difficulty with smelling, if there has been a recent upper
respiratory tract infection or any head trauma in past
 Check that the nasal passages are clear. For this the pt. must compress each nostril
in turn and by sniffing through the other.
 Ask the patient to close his eyes and shut one nostril with one finger.
 Commonly available test odours are placed under one nostril while other is closed.
Patient is told to take 2 good, but not over exuberant sniffs, He is then asked
 If he can smell anything and.
 If he can recognise the odour.
 The test is then repeated using the other nostril and he is asked
 If the odour is the same in each nostril. After an interval to allow the odour to
disperse, the test is then repeated with 2 further odours and he is asked
 If he can distinguish the different odours.

Interpretation of Results
CATEGORY CRITERIA

Normal Those who recognize and name the odours quickly (usually women)
102
Normal Those who recognize, but can't name them (usually men)
Normal Those who can detect smell, and easily distinguish differences, but can neither
recognize nor name.
True Anosmia Those who can smell nothing in one or both nostrils or whose sense is much
reduced on one side compared to the other

Common causes of Anosmia

 TEMPORARY  PERMANANT
URTI (Acute) Colds or Influenza. Head Injury- usually thought due to tearing of olfactory
filaments. The trauma may be surprisingly slight and often
occipital
Allergic Rhinitis, for e.g. hay fever. Chronic inflammatory nasal diseases: Heavy smoking
Nasal Polyps Cranial surgery.
Drug or Chemicals Intracranial Tumors of the anterior fossa eg. Inferior frontal
Glioma.

Long Term application of Nasal sprays.

Atrophy of olfactory bulbs: Atrophic rhinitis
Chronic Meningeal inflammation (Syphilis) or Infiltration
(Sarcoidosis).

Other Disorders of Olfaction

CONDITION CRITERIA FOUND IN
Hyperosmia Increase in olfactory Hysteria, psychic states, migraine, hyperemesis
acuity gravidarum, Strychnine poisoning, cystic fibrosis
Parosmia Perversion of smell Recovery from head trauma, aura of CPS,
TLE,psychosis( olfactory hallucination)
Cacosmia Presence of do
disagreeable odours
Foster Kennedy Unilateral anosmia Frontal lobe tumour
Syndrome with optic atrophy

OPTIC NERVE
It is the most important cranial nerve since it reflects conditions existing inside the cranial
cavity. Because it is a forward extension of a part of the brain and not a peripheral nerve.
Satisfactory examination is a must in trying to detect lesions in the visual pathway.

Functions
 To carry visual impulses from the retina to the optic chiasma and in the optic tract to the
lateral geniculate body.
 To act as the afferent pathway for the pupillary light reflex along the fibers travelling to
the superior colliculus of the midbrain.

Purpose of the Tests

1. To measure the acuity of vision and to determine if any defect is due to local ocular
disease.
2. To chart the visual fields
3. Color vision testing
103
4. Directly Inspecting a part of the Nerve itself (i.e. Fundoscopy)

Methods of Testing
History
Ask for any problem with eyesight. Do you wear glasses or contact lenses?
Are you short or long sighted?
If patient is wearing any glasses ask them politely: Could you take off your glasses?

Inspection
Look at the eyebrows, eyelids, sclera and pupils, is there any difference between the eyes?
Specially look for dropping eyelids (ptosis), any deviation of the eyes (Strabismus or
squint), unequal pupils or prosthetic eye.

Visual Acuity
The standard Snellen's Type charts are used for testing distant vision and the Jaegar’s type
charts for near vision.
 Ask the pt. to use their appropriate glasses.
 Use good ambient lighting and place Snellen's or Log mar chart at 6m from the pt
who covers one eye & is asked to read smallest line.
 Snellen’s visual acuity of 6/60 indicates that at 6 meters the pt. can only see letter
they should be able to read 60 meters away normal vision is 6/5-6/6. If 6/6 vision not
obtained; then a pinhole is placed directly in front of the patient's glasses which
allows any central rays of light to enter the eye correcting for about 4 Diopters of
refractive error.
 If patients can't see the top line of the chart at 6 meters bring them forward till they
can & record that vision.
 If patients still cannot see the top letter at 1 meter then check whether they can count
fingers (CF), see hand movements (HM) or just see perception of light (PL).
 For children use different sized objects instead of letters; for illiterates 'E' with. Its
open end pointed in different directions.
The Jaegar type card must be held at 30 cm from pt's eye & a similar test is carried out.
Different types labeled as J.4 etc. according to their size. Avg. acuity lies between J.1 and
J.4.

Loss of visual acuity

Commonest causes include Refractive errors; cataracts; vitreous opacities.
In all cases and especially if routine inspection of the eye reveals no such lesion the next
stages are the examination of the visual fields , the optic nerve head and Retina.

Visual Fields
Normal visual field extends 1600 horizontally and 1300 vertically.
The blind spot located 150 to the temporal side of the point of visual fixation & represents
the optic nerve head. Bedside examination is by confrontation method and more accurate
assessments by perimetry.

The usual method of examining visual field is-

Confrontation: Patient and the examiner face each other about 1 meter away
 Examiner covers the right eye & the patient covers left taking care to avoid obscuring
the nasal field of the other eye.
104
 Patient must fix carefully on the examiner's pupil while the examiner moves test objects
of varying size (whole hand, moving finger, white or red pin) inwards in each of the 4
quadrants from just outside limits of his own field: & and then the patient is asked to say
‘one’ or rise his another hand the moment pt. sees the
object. Also ask whether the clarity is equal in each
quadrant. Remember to move from blind area to areas of
vision because it is easier to detect appearance than
disappearance of objects
 Central area of vision can be tested to map out the
Blind spot scotomata by using disc of white paper about
5mm diameter attached to rod or long pin or a white or red
hat pin.
 For visual Inattention: Uncover both eyes, examiner
holds both hands in the outer parts of the fields & moving
one or other hand or both together asks the patient to point
to the hand moved. In parietal disorders though the fields
tested in each eye separately are normal, only one object
is appreciated when both are moved simultaneously

Also it can detect if a homonymous hemianopia is present.

In all cases of unexplained visual failure, suspected
intracranial tumor, demyelinating disease or doubts on
confrontation fields should be charted on a good perimeter
& on the Bjerrum screen. The latter enlarges the central
area (out to 300) & makes it easier to detect scotomata & to
measure the Blind spot.

Major Visual field defects & their Significance:

CONDITION SITE OF LESION COMMON CAUSES
Total unilateral loss of vision ( Ipsilateral optic nerve Optic nerve injury, Optic
with contralateral upper temporal lesion neuritis
field defect)
Altitudinous hemianopia Partial lesion to blood Trauma, Vascular accident
supply of Optic Nerve
**Homonymous hemianopia From optic tract toVascular accident, cerebral
occipital cortex tumor,
Vascular anomalies, injury
Upper Quadrantic homonymous Lesion of optic Vascular accident, cerebral
defect radiation in temporal tumor,
lobe near temporal Injury, cerebral abscess.
horn of lateral
ventricles
Lower Quadrantic homonymous Lesions of upper Vascular accident, cerebral
defect radiations or calcarine tumor,
area Injury
Bitemporal hemianopia Lesion at optic chisma Pituitary ,Hypothalamic
tumors, midline aneurysm,
gross IIIrd ventricular
dilatation
105
Bitemporal Upper Quadrantic Early stages of Pituitary tumors
defect chiasmal compression
from below
Bitemporal Lower Quadrantic Early stages of Hypothalamic tumors,
defect chiasmal compression suprasellar cyst or tumors
from above

**Varying presentation of Homonymous Hemianopia-

Site of Lesion Completeness Congruity Macular
Sparing
Optic tract Complete Incongruous Absent
Optic radiation Incomplete Congruous Present
Calcarine cortex Complete Congruous Variable

Color Vision
Red desaturation, the impaired ability to identify red objects is an early indicator of
pathology affecting the optic nerve.

Examination Sequence
 Red green color vision assessed with Ishihara test plates. These consist of colored
spots forming number which the pt is asked to pick out.
 The first plate is a test plate and if the number is not seen, it indicates poor visual
acuity or functional visual loss.

Common Abnormalities
 Optic Nerve damage anywhere from the photoreceptors to the lateral Geniculate
nucleus of the thalamus cause impaired red-green color vision that precedes loss of
visual acuity.
 Congenital Red-Green Blindness is an X-inked recessive condition affecting 7% of
the male population.

Fundoscopy
Eye should be examined first undilated to see the pupils & iris and then dilated using a
mydriatic such as Tropicamide to visualize the lens, vitreous and retina. If patients have
particularly thick lenses examine their eyes with their glasses in place. After dilating
patient's eyes advice not to drive or use machinery until the effect has completely worn off.

 To obtain clear view of the fundus there are certain requisites. (i) Good ophthalmoscope
(ii) Large pupil and (iii) a still field.
 To overcome the light Reflex darken the room, to overcome accommodation for near
vision instruct the patient to look at a distant point clearly defined keeping the eye still.
 Use the Right eye to examine the right eye and then walk around the bed to examine
the left eye with the left eye.
 Catch the lowered upper eyelid and gently retract it against the orbital rim . It enables
you to approach the patient's head as closely as possible without fear of bumping into it
& secondly to present the upper eyelid from obscuring the view.
 Now come close to the patients head such that you are touching your hand resting on
the patient's forehead.

106
Features to be examined
 Find the Optic Disc noting its color, clarity of its edges, & the side of the depression in its
centre - the optic cup.
 Look the vessels as they leave & enter the disc, veins being wider & darker; noting the
degree of curvature as they pass over the edge of the disc; if their curves are gradual or
acute & continuously visible or if they appear & disappear. Also look at the points of
crossing of the arteries & veins if one vessel obliterates the other.
 Look for hemorrhage their size, shape & relationship to the vessels & for exudates, their
size color & texture.
 Finally Inspect the Retina itself noting any deviations from the uniformity of color; when
the patient directly looks at the light the vessel free macula area can be inspected.

In the Disc look for pallor, swelling: The temporal side of the disc is usually paler than
the nasal side.
The myopic disc normally looks very pale; greatly enlarged & often has also crescent of
pallor immediately around it Examine it through the pt's own spectacles to get most
accurate view.

Swelling: The area covered by the disc enlarges; margins cannot be defined & irregular
radial streaks appear giving the disc an angry appearance. Veins become swollen &
engorged & the hump of the vessels entering & leaving the disc becomes very pronounced.
The vessels appear & disappear as they course near the disc. Finally small haemorrhages
or large irregular ecchymoses appear usually near a vein. In addition white streaks &
patches of exudate appear near the disc margins & spreads outwards towards the macula
to produce a macular fan.

This is papilloedema due to increased intracranial pressure from any cause; vision may be
well preserved, the visual fields showing only enlargement of the Blind spot.
Foster-Kennedy syndrome: A tumor in the post inferior frontal region can cause optic
atrophy on one side by compressing the optic nerve & papilloedema on the other by
obstructing venous return or causing raised intracranial pressure.

Pseudopapilloedema is a disc appearance very similar to mild swelling but without vessel
engorgement, & symptomless throughout the patient’s life.
It should not be confused with ‘pseudo tumor’ or benign intracranial hypertension.

THE OCULOMOTOR, TROCHLEAR & A BDUCENS NERVES

The action of these nerves is so closely related that they are considered together.

Functions
Control of all the extraocular muscles and the elevators of the lids. Autonomic fibres running
in relation to these nerves and the Vth Nr. control the pupillary muscles.

Purpose of tests
1. To inspect pupils and determine if any abnormalities discovered are due to local
diseases or peripheral autonomic lesions or nuclear involvement in Brain stem.

107
 2. To examine eye movements and to determine if any defect is of local muscular origin
or due to lesions of the oculomotor nerves peripherally, their nuclei in the brain stem,
or the pathways of supranuclear control.
3. To detect and analyze nystagmus.

METHODS OF EXAMINATION
Preliminary inspection
Not the presence or absence of ptosis and squint, whether it is unilateral or bilateral,
constant, or variable. Compare the size of the palpebral fissures and note if the eyeballs are
protruded (exophthalmos), or recessed (enophthalmos).

A. Exophthalmos
Assess protrusion by looking down on the eyes from above and behind the patient's head.
Most common cause is thyrotoxicosis. True exophthalmos, with lid retraction, occurs in
thyrotoxicosis, and becomes severe, with injection and chemosis of the conjunctiva,
oedema of the lids and oculmotor paralysis in dysthyroid eye disease (Exophthalmic
ophthalmoplegia).
Other causes: Craniosynostosis, hydrocephalus.

Unilateral exophthalmos, still occurs most commonly due to thyroid dysfunction, may also
be caused by orbital or retro-orbital neoplasms and granulomata,

B. Enophthalmos
Most commonly part of Horner's syndrome, may be due to mal-developed eye. Don’t be
fooled by recessed prosthesis, or by the true abnormality being prominence of eye or orbit
on the other side.

C. Hypertelorism
Not uncommon normally but should alert to the possibility of intracranial congenital
abnormalities.

Look next at the conjunctiva, cornea and iris while the patient moves the eyeball in all
directions.

THE CONJUNCTIVA
Look for Subconjunctival haemorrhage, Telangiectases,
 Retro-orbital tumours may grow forwards as a red or grey felting visible on extreme
deviation of the eyeball. A yellow tint may be the only sign of liver disease.
 An intense inflammatory reaction occurs in leptospira causing acute meningitis. And
also during the migration of filarial (Loa loa) which also may cause encephalitis.
Conjunctival ulcers form part of the triad of Behcet's syndrome.

THE CORNEA AND IRIS

Look for different colouring of the two eyes; pale atrophied iris of the tabetic; and the
Kayser-Fleischer ring, Arcus senilis in elderly
The K-F ring is golden-brown ring, lying inside the limbus of the cornea, may be complete
or at times only crescent at the upper and lower margins. It is seen most easily in light
coloured eyes, and is diagnostic of hepatolenticular degeneration e.g. Wilson’s disease. If
suspected should be confirmed by slit-lamp examination.

108
The Eyelids
Look for the position of the lids in relation to the iris & the width of the palpebral fissure. Ask
the patients to open the eyes widely and notice both the lid movement and the degree of
movement of the frontalis muscle.
Ask the patient to follow an object upwards and maintain forward gaze for at least 30-45
seconds without blinking.

Ptosis
If the pupil is partly covered by the upper lid there is a slight degree of ptosis, which may be
due to paralysis of the Levator palpebrae superoris as a result of IIIrd nerve lesion, or to
weakness of the tarsal muscles due to a sympathetic lesion. In the former, the frontalis
muscle contract to overcome the drooping and there may be a permanent wrinkling of the
forehead.
In myasthenia gravis, the degree of drooping of the lid varies from moment to moment, and
may change sides, Lids will droop progressively on prolonged upward fixation, but a blink
restores its position.
In ocular myopathy the ptosis is fixed and the head extended in an attempt to see.

Lid Retraction
Lid is buried under the brow and the sclera is clearly visible above the iris in
hyperthyroidism.

The Pupils
Look at the size, shape, equality and regularity of the pupils taking account of ambient
lighting.
 Ask the patient to fix the eyes on a distant point straight ahead. Bring a bright
torchlight from the side to shine on the pupil. Look for constriction of the pupil shone
on (direct light reflex) and for constriction of the opposite pupil (consensual light
reflex).
 With the patient's vision fixed on a distant point, present an object about 6 inches in
front of the eyes and ask the patient to focus on it (convergence). Look for pupil
constriction (accommodation reflex).
Common abnormalities
1. Essential Anisocoria: It's common abnormality where one pupil bigger then the
other.
2. Miosis: It indicates a lesion at some point in the very circuitous pathway taken by
the sympathetic supply to the papillary dilator muscle
Common causes: Pontine tumours or haemorrhages, primary or secondary
tumours invoving the cervical sympathetic chain, and vascular lesions of the carotid
artery or its sheath.
3. Mydriasis: It results from paralysis of the parasympathetic fibres, either at their
origin from the pre-tectal nuclei and the Edinger-Westphal nucleus in the midbrain,
during their course with the IIIrd nerve, or at the ciliary ganglion in the orbit. Most
common cause is use of a mydriatic, other common lesions are due to vascular
accidents in the midbrain, tentorial herniation due to SOL or anerysms of the carotid
artery.
 Argyll Robertson Pupil: They are pin point irregular pupils that constrict only on
convergence. Seen in syphilis
 Also in Diabetes Mellitus: Autonomic neuropathy may lead to the presence of small
pupils responding poorly to mydriatic mimicking the Argyll Robertson pupil.
109
 An Adie pupil: It is usually mid dilated and only poorly responding to convergence it's a
result of ciliary ganglion malfunction within the orbit, with time it may shrink in size and
be confused with Argyll Robertson pupil. It's frequently bilateral & when associated with
absent neurological reflexes termed the Holmes Adie syndrome.
Damage to the optic nerve results in a relative afferent pupillary defect (Marcus Gunn
pupil). Both pupils dually innervated at the midbrain level. The undamaged optic nerve
becomes dominant and whatever lighting the dominant optic nerve is exposed to will then
determines the size of both pupils.

Examining ocular movement

The patient must look at a clear and definite point, such as the point of a pen or a fine point
o flight.
The examiner then moves this point precisely and deliberately to right and left horizontally,
upwards and downwards in the midline, and vertically when the eyes are deviated to one
side.
Do not attempt to make the eyes deviate beyond the point of comfort, and hold each
deviation for at least 5seconds.
The aim is:
1. To observe lagging of one or other eye.
2. To analyse any diplopia the patient may describe.
3. To detect nystagmus.

Action of the ocular muscles

A. The external rectus (VIth nerve) – Moves the eye
horizontally outwards.
B. The internal rectus (IIIrd nerve) – Moves the eye
horizontally inwards.
C. The superior rectus (IIIrd) – elevates the eye when it is
turned outwards.
D. The inferior oblique (IIIrd) - elevates the eye when it is
turned inwards.
E. The inferior rectus (IIIrd) – depresses the eye when it is
turned outwards.
F. The superior oblique (IVth nerve) – depresses the eye
when it is turned inwards.
Muscles paired together above act together.

Ocular muscle paralysis

The following general rules can be deduced.
1. If an eye fails to move outwards, there is either a VIth nerve lesion, or a local lesion
of the external rectus muscles (see A above).
2. If the eye, when deviated inwards, will not then move downwards, there is either a
IVth nerve lesion, or a local lesion of the superior oblique muscle (see F above).
3. All other defects in movement are due to IIIrd nerve lesions, a local lesion of the
muscles, myasthenia gravis or an internuclear ophthalmopelgia.

Analysis of Diplopia
Diplopia can indicate ocular muscle weakness before it is evident.

110
Mechanism: The light rays fail to fall on exactly corresponding parts of the two retinas, and
a false image is formed which is usually paler and less distinct.

Rules
1. Displacement of the false image may be horizontal, vertical or both.
2. Separation of the images is greatest in the direction in which the weak muscle has its
purest action.
3. The false image is displaced furthest in the direction in which the weak muscle should
move the eye.

Method of Examination
Cover one of the patient's eye with a transparent red shield and, using a point of light, move
the object as described for ocular movement. In each position ask the patient;
1. Whether he sees one object or two.
2. If double, do the two images lie side by side, or one above the other.
3. In which position are they furthest apart.
4. Which is the red image?

Analysis of result
If the images are exactly side by side, it will be only the external or internal recti that are
involved. And if they are one above the other, either of the obliques, or the superior and
inferior recti may be defective.

The muscle pair involved

It is the position in which there is maximum displacement that indicates which pair of
muscles is involved e.g. If maximal displacement occurs when the eyes are deviated to the
right and upwards, this is the movement carried out by the right superior rectus and the left
inferior oblique.

The individual muscle responsible

Various charts exist for representing diplopia diagrammatically, of which the Hess chart and
those used in orthoptic analysis are the most useful.

Common Causes of Oculomotor Paralyses

 VIth nerve can be involved in many conditions at or near the base of the skull. As in
pontine lesions, neoplasms, vascular accidents, demyelinating lesions, meningits (acute
or chronic). False localizing sign is seen in generalized increase of intracranial pressure.
 IVth nerve isolated lesions very rare but may occur in lesions of cerebral peduncles,
Head injury is the commonest Cause.
 IIIrd nerve isolated lesions are seen in upper midbrain vascular accidents and
demyelinating lesions, and peripherally due to compression by carotid and posterior
communicating artery aneurysms, parasellar neoplasms, sphenoidal wing neoplasms
and also neoplasms at base of the skull.
 Total paralysis of all three nerves usually indicates a lesion in the cavernous sinus, most
commonly a carotid aneurysm.

111
Conjugate Ocular Movement
The centre for control of conjugate movement to say, the right, is situated in the posterior
part of the left frontal lobe and there is probably a further centre in the occipital region. The
final common pathway for controlling this movement lies, however, in the brain stem and
depends upon connections, running through the median
longitudinal bundle, between the innervation of the left
internal rectus and the right external rectus.
 Lesion of the frontal lobe causes contralateral
paralysis of conjugate gaze.
 Lesion of the brain stem causes ipsilateral
paralysis of conjugate gaze.
Paralysis of the normal control of conjugate deviation to
one side usually results in deviation of the eyes to the
opposite side, which may be slight and transient, or
marked and permanent.
In the supranuclear destructive lesions, the face and
limbs are paralysed on the side opposite to the ocular
deviation; in brain stem lesions, on the same side; but in
the latter, if the face is paralysed it will be a lower motor
neuron lesion on the side opposite to the hemiplegia.
The situation is reversed for irritative lesions, but the
deviation is spasmodic.

Inter-nuclear paralysis
Lesion of brain stem involving median longitudinal
bundle there is disorganization of the conjugate
movement of the two eyes when looking laterally.
Internal deviation of the adducting eye is defective and
out of step with the external deviation of the other eye.
Marked nystagmus may develop called 'Ataxic Nystagmus’.

Detecting and Analysing Nystagmus

Nystagmus is an involuntary rhythmic oscillation of the eyes. It may be Horizontal, Vertical
or Rotatory and either Pendular or Jerk in type. When acquired usually caused by
abnormalities of the vestibular system and its connections.

Purpose of the tests

1. To detect nystagmus.
2. To determine its direction, rate and amplitude.
3. To deduce from its character whether it is due to peripheral labyrinthine or central
vestibular disease, to muscle weakness or to visual defects.

Methods of testing
Note for any nystagmus on forward gaze; whether it is constant or occurring in bursts.
 Ask the patient to look at definite point such as tip of pencil.
 Hold this object first in midline, and then move it clearly and deliberately to left, to
right, upwards and downwards, during this last movement, hold the eyelids by the
other hand.

112
  Lateral deviation should be maintained for at least 5 seconds and it should never be
to the extreme of lateral movements.

Recording nystagmus
The information required is:-
1. The position of the eyes when nystagmus occurs.
2. The deviation produces its greatest amplitude, usually to the side towards which the
quick phase beats.
3. The direction, in each oscillation, of the fast movement not which deviation produces
the quickest oscillation.
It is customary to describe the direction of the nystagmus acc. to its fast movement e.g. On
deviation to the right, fine horizontal nystagmus, fast component to the right.
Alternatively it can be described by 'Degree’:
1. First Degree: When present only on deviation of the eyes.
2. Second Degree: When present looking straight forward.
3. Third Degree: When visible even in the direction opposite to the fast beat.

Types of nystagmus

Pendular nystagmus is characterised by oscillations about a central point that are equal in
rate and amplitude and may occur in any plane. In children it is usually congenital and may
be associated with impaired vision. In adults it usually reflects brainstem or cerebellar
disease and is usually associated with a head tremor.

Jerk nystagmus is characterised by oscillations which have a slow initiating phase and a
fast corrective phase. The direction of the fast phase defines the direction of nystagmus.
Thus 'nystagmus to the right' refers to the direction of the rapid component not the direction
of gaze in which nystagmus occurs.

Jerk nystagmus may be peripheral or central in origin.

 Peripheral lesions affecting the vestibular apparatus or VIII nerve produce a
unidirectional nystagmus away from the affected side irrespective of the direction of
gaze and dampened by visual fixation. It is often aggravated by head movement and
accompanied by vertigo, deafness and tinnitus.
 Central lesions in the brain stem or cerebellum produce bidirectional nystagmus (the
direction of nystagmus changes with the direction of gaze) which is unaffected by
visual fixation. Other causes include toxicity from alcohol or drugs, especially
anticonvulsants and benzodiazepines.
 Lesions of the medial longitudinal fasciculus in the pons produce nystagmus in the
contralateral abducting eye along with impaired adduction of the ipsilateral eye.
When bilateral (dysconjugate or ataxic nystagmus) it is characteristic of
demyelination due to multiple sclerosis.
o Vertical nystagmus- oscillation is in vertical (up-down) direction and can occur at any
position of eye, and quick phase is mostly upwards (upbeat nystagmus).Commonest
cause is drug induced-Benzodiazepines, Phenytoin and Barbiturates. Found in- intrinsic
disturbance of brainstem due to vascular accident, encephalitis, syringobulbia, multiple
sclerosis, Arnold-chiari syndrome.
o Rotatory nystagmus- also has fast and slow components but oscillations are rotatory.
Found in- labyrinthine and brainstem pathology.

113
TRIGEMINAL NERVE

Anatomy: It is the largest Cranial Nerve and has 3 long branches through which it provides
sensations to the face, front half of the scalp, sensation to the mucous membranes and
sinuses and the motor supply to the muscles of mastication.

"The Cell bodies of the sensory fibers are located in the Trigeminal (Gasserion) ganglion
which lies in cavity (Meckel’s cave) in the petrous temporal dura. The peripheral processes
of these cells give rise to the 3 major branches of the nerve.

1) Ophthalmic (V1), 2) Maxillary (V2) 3) Mandibular (V3)

Motor, Sensory and Autonomic Innervation of the 3 divisions of the Trigeminal Nerve.
Division Innervation Course
Ophthalmic (V1) Upper face, nose, cornea & eyelid. Via superior orbital fissure to
Scalp to vertex. Lacrimal gland via cavernous sinus, to Meckel’s cave.
vidian nerve.
Maxillary (V2) Middle face, Nasal mucosa, upper Via inferior orbital fissure to
teeth, pharynx, tonsils, and inner sphenopalatine fossa and foramen
quadrant of cornea. rotundum into cavernous sinus to
Meckel’s cave.
Autonomic fibres (nervus
intermedius) form greater petrosal
nerve, fusing with deep petrosal
nerve to form Vidian nerve.
Mandibular(V3) Lower face (not angle of jaw), lip Via infratemporal fossa through
(Sensory) and teeth, tongue. Part of external skull base and foramen ovale to
ear. Parasympathetic fibres Meckel's cave.
innervate parotid gland.

Mandibular(V3) Muscles of mastication: Via. V3

(Motor) masseter, digastric, pterygoids and
temporalis

Examination
The functions of the V nerve: 1) Sensory, 2) Motor & 3) Two Reflexes.

Purpose of the Tests

(1) To determine which, if any of the modalities of sensation impaired.
(2) To decide from this whether the lesion is one of the peripheral branches in the
Gasserion ganglion or sensory root, or in the brain stem.
(3) To determine whether motor weakness is unilateral or bilateral & of lower or upper
motor neuron origin.
Examination sequence
(A) Sensory:
- Test light touch & superficial pain in the territories of V1, V2, & V3.
- Use an orange stick to test touch sensation on the anterior 2/3rd of tongue. Six areas on
each side are tested: near but not at the midline.
(i) The forehead & upper part of side of Nose (Ophthalmic Division)

114
 (ii) The malar region & upper lip (Maxillary Division)
(iii) The chin and anterior part of the tongue (Mandibular Division)

Method
For touch take wisp of cotton wool and ask your patient- “Close year eyes please & say
'yes” if you can feel me touching you. Next ask- Does it feel like you would expect cotton
wool to?"
For pain use the neuropins and say to your patient- “Close your eyes & tell me if this feels
sharp or blunt?
Also you can check temperature by cold tongs of Tuning fork, esp. if not sure whether pain
sensation impaired or not; if it’s impaired the cold Tuning fork is often perceived as warm.

Abnormalities of Sensation
(1) Total loss of sensations over the whole distribution of the nerve- Indicates lesion of the
ganglion or sensory root or an extensive lesion anterior to ganglion, when motor root is
usually involved as well. E.g. Tumors eroding the Base of the skull, large Neurofibromata of
the Vth & VIIIth Nerves, Epidermoids, Chronic meningeal lesions such as Sarcoidosis or
Syphilis. Also Idiopathic form of Trigeminal sensory neuropathy with pathological changes
like lupus or granulomatous syndrome in Gasserion ganglion.
If sensory loss accompanied by total loss down the whole of that side of the body, the
lesion is in the neighborhood of the opposite thalamus.

(2) Total sensory loss over one or more of the main divisions. Found in partial lesions of the
ganglion (e.g. Herpes Zoster), or of the Root (Acoustic Neuroma).
Ophthalmic Division:-
 In Cavernous sinus, compression by carotid aneurysm.
 And in orbital fissure by Tumors,
Maxillary Division (rare):-
 Local Trauma,
 Also in cavernous sinus
Mandibular Division:-
 Basal Tumors also affecting the motor root.

(3) Touch only is lost: This is due to pontine lesion affecting Principal Sensory Nucleus &
usually due to:- (1) Vascular diseases, (2) Pontine tumors or (3) Brain stem displacement
by large Tumors.

(4) Pain & Temperature are lost but touch preserved: Dissociated anaesthesia from lesions
of the Descending root & occurs in Syringobulbia, Foramen magnum Tumors or anomalies
& Bulbar vascular accidents, e.g. Thrombosis of posterior inferior cerebellar artery causes
ipsilateral loss of pain & temperature sensation on the face & contralateral loss on the rest
of the body.

(5) Hyperesthesia over all or part of the distribution of the nerve: Irritative rather than
destructive lesion & it is of little localizing value. Most common in Vascular lesions & Herpes
& least common in Syringomyelia.

115
The Corneal Reflex: It’s useful protective mechanism for the eyes. When either cornea is
touched, it results in the reflex blinking of both eyes. The sensory inputs are by the
Trigeminal Nerve & motor response occurs via the Facial Nerve.

 Explain to the Patient: “I am going to dab this piece of cotton wool on to year eye, it
may feel a little uncomfortable”. Patient must look ahead as upward as possible,
then bring the wisp of cotton wool in from the side of the face touching the cornea
lateral to or below the pupil on either side. A little puff of breath on one cornea,
while shielding the other is a quick alternative method normally resulting in bilateral
blinking.
Loss of this reflex may be the first & only sign of the Vth Nr. lesion & is of great value in
early cerebellopontine angle tumors & in aneurysms & tumors in relation to the cavernous
sinus & orbital fissure.

Motor functions of the 5th Nerve

The Temporal muscles, Masseters & Pterygoids are tested.
- Inspect for wasting of the muscles of mastication. Note the symmetry of the temporal
fossa & the angle of Jaw.
- Palpate the masseters, estimating their bulk while the patient chinches his Jaws. The
muscles can be compared as they stand out as hard lumps.
- Ask the patient to open the Jaw against resistance, by putting hand under the Jaw,
noting any deviation.

Motor abnormalities
Wasting of muscles due to LMN or local muscular lesions produces hollowing of the
temples & flattening of the angle of the Jaw.

Causes
 Nuclear lesions as in Motor neuron disease B/L
 Peripheral nerve lesion as in compression of motor root unilaterally or muscular
dystrophy.
Pterygoid weakness causes the Jaw to deviate towards the paralysed side on opening as a
result of the action of the normal muscle.

Jaw Jerk
- Ask the patient to let his mouth hang loosely open.
- Place your forefinger or little finger in the midline between lower lip & chin.
- Percuss your finger with the tendon hammer,
- A slight palpable upward jerk immediately after the purely percussive effect is over,
but in many normal people no response is obtained.
Brisk or exaggerated Jaw Reflex even amounting to Jaw Clonus may be found in lesions of
the UMN above the level of the Pons. E.g. Pseudobulbar palsy, Motor neuron Disease,
Multiple Sclerosis.

Keypoints:
(1) The corneal reflex may be the earliest sign of Vth Nerve palsy.
(2) Always approach from the side when testing the corneal reflex & make sure you
touch the cornea & not the sclera, eyelids or conjunctiva.

116
 (3) Sensory dysfunction of the Nerve is more common than motor dysfunction.
(4) The Jaw Jerk is of limited value & is only abnormally brisk in the presence of B/L
UMN lesions.

FACIAL NERVE
Function
The Facial Nerve sends motor fibers to the muscles of facial expression & parasympathetic
secreto-motor fibres to the Lacrimal, Submandibular & Sublingual salivary glands(Via
Nervus Intermedius) & receives taste sensation from the anterior 2/3rd of the tongue(by its
Chorda Tympani branch). It also provides efferent supply to several reflexes.

Examination
It is usually confined to motor function & taste.

Inspection
Observe the patient when talking to him & look for symmetry.
(1) The face as a whole.
(2) The wrinkles of the forehead & the nasolabial folds.
(3) Blinking & whether the eyeballs can be seen to turn up with each blink.
(4) Movement of the mouth while talking, smiling, etc.
(5) Observe for spontaneous movements or any involuntary movements.
(6) Upper facial muscles are tested by asking the patient to wrinkle his forehead or look
up above his head.
(7) Telling the patient to close his eyes (noting whether he can do so), then to screw
them tightly shut & to resist attempts to open them. Later for LMN:
(8) Ask the patient to bare his teeth demonstrating yourself & then asking the patient to
mimic is often helpful, also at the sometime time, if asked to open mouth helps test
the platysma.
(9) Test Power by asking the patient: Blow out your cheeks with your mouth closed. And
this will distinguish proper weakness from mere asymmetry.

Examination of Taste: Four primary tastes viz: Sweet, Salt, Sour, Bitter & all others are
flavors, their appreciation depends upon intactness of sense of smell, Tests carried outwith
sugar, salt, vinegar & quinine in that order with the 4 possible tastes written on a card.
- Instruct the patient not to speak during the test.
- Ask the patient to put out his tongue the tip of which is held gently with a piece of gauze
& the side of the tongue moistened about 2cm from the tip with a little of the taste
substance using cotton buds.
- Ask the patient to indicate the taste by pointing to the card.
- Between tests of each taste ask the patient to rinse his mouth with water.

Secretory functions:
Schirmer's Test:- The flow of Tears on the two sides can be compared by giving the
patient ammonia to inhale. The actual amount of tear production is seen by hanging a strip
of filter or litmus paper from the lower eyelids & measuring the length of moistening on each
side. The flow of saliva is compared by placing a highly spiced substance on the tongue
and by asking the patient to raise the tip so that the submaxillary salivary flow is witnessed.
These tests are often not required as the patient is usually able to describe any defects
spontaneously.

117
Abnormal Findings: - It is worth considering the sites in the nervous system where the
facial nerve is vulnerable to Injury.

(1) Upper motor neuron lesions:

 Contralateral facial nerve palsy.
 Only lower face altered because of dual innervation of the upper face.
 Also possible contralateral hemiplagia be associated with hemianopia.
Causes:
1. Stroke
2. Tumors
3. Multiple Sclerosis

(2). Lower Motor Neuron lesion: The pattern of other cranial nerve involvement and other
clinical features may give further clue to location of the lesion.

(2) (a). The Pons:

 Ipsilateral facial nerve palsy
 Ipsilateral VIth Nerve palsy. (Since both VIth & VIIth Nerve are at the same level in
Pons)
 Contralateral Hemiplegia (The Corticospinal track don't cross the midline till lower down in
the medulla)

Causes:
1. Stroke
2. Tumor
3. Multiple Sclerosis

(2) (b). Cerebellopontine Angle:

 Ipsilateral facial nerve palsy
 Ipsilateral Vth, VIIIth nerve palsy.
 Ipsilateral cerebellar signs.
 Possibly IX, Xth, & XIth palsy also.
 In addition the facial nerve palsy at this level will lead to dysfunction of the three
major braches.
(i) The Greater superficial petrosal nerve-loss of lacrimation & salivation
(ii) The Nerve to stapedius – leads to Hyperacusis
(iii) The Chorda Tympani nerve – Leads to loss of taste over the ant. 2/3rd of the
tongue.
Causes:
1. Acoustic neuroma
2. Meningioma

(2) (c). Facial Canal

 No other cranial nerve is involved at this level.
 The other 3 branches discussed above in 2b come off in the order given & the
location of lesion within facial canal will dictate clinical symptoms. A location
after the Greater superficial petrosal nerve but before the nerve to stapedius
will spare lacrimation & salivation but will still lead to hyperacusis.
Causes:
118
  Bell's Palsy
 Ramsay-Hunt syndrome
 Fracture of the Skull Base.
 Spread from Otitis media

(2) (d). Distal to Stylomastoid foramen.

 Facial nerve has exited the skull and is traveling through the substance of the parotid
gland dividing into its final branches to supply the facial muscles. Some of the facial
muscles may be spared depending on which branches have been affected.
Causes:
1. Tumor in the parotid gland
2. Surgery to the parotid gland
3. Sarcoidosis

(3). Bilateral facial nerve palsies: Often causes difficulty in detection because symmetry
is maintained.
a. Bilateral emotional facial palsy - There is a mask like face, complete lack of the
normal play of expressions, and diminished blinking, yet when it occurs it is normal
and there is transformation when the patient smiles.

b. Bilateral UMN palsy – Masking is not so marked. Blinking is little affected, but the
mouth cannot be moved on command, yet often appears to move quite well during
ordinary conversation. Causes: (i) Bilateral Strokes (ii) Multiple sclerosis.

c. Bilateral LMN palsy – flattening of all normal folds. The corners of the mouth sag,
all attempts at voluntary movement fail and the white of the eyes are seen when the
patient attempts to close them or to blink. The patient talks as if protecting a very
sore mouth.

Also long after facial palsy, there may be aberrant reinnervation. If it is bilateral the whole
face wrinkles when any expression is attempted. Spontaneous twitching is also common
and often interpreted as potential recurrence.

Scales to measure Facial Nerve Palsy-

i) House-Brackman Facial Neuropathy Grading Scale
ii) Yanagihara Facial Neuropathy Grading Scale

THE AUDITORY/VESTIBULOCOCHLEAR NERVE

It has vestibular and cochlear branches largely concerned with equilibrium and hearing
respectively.

Examination:
 Ask for any hearing loss and a complaint of vertigo or an abnormality of posture or
gait.
 Examine the external auditory meatus before undertaking the test, excluding cervical
lesions before testing for positional nystagmus or the oculocephalic reflex.

Purpose of the test:

119
  To determine whether any deafness is bilateral or unilateral and whether due to
disease of the middle ear, or of the cochlear nerve.
 To determine whether disturbance of vestibular function originate in the labyrinth the
vestibular nerve, or the brain stem.

Examination sequence (cochlear):

Whisper test
 Position the patient's head so that he cannot lip-read what you say.
 Place your finger in the external auditory meatus of the patient's non-test ear and
move it constantly to produce a masking noise.
 Ask the patient to repeat words and numbers that you speak. Initially whisper but
increase in volume as necessary.
Tuning fork tests (Rinne's and Weber's)
 RINNE'S TEST: Strike tuning fork gently and hold it near one external auditory
meatus while masking the other. Then place its base over mastoid process and ask
if he still hears it and report immediately when he stops hearing. Quickly hold the
tuning fork near same meatus again and ask if he can still hear. Usually, air
conduction is better than bone conduction (Rinne positive)
 WEBER'S TEST: Place the vibrating tuning fork in the midline high on the forehead.
Ask whether he can hear the sound all over the head, in midline, in both ears equally
or predominantly by one ear.

TYPE OF DEAFNESS:
Conduction of sound through the air to the drum and bony ossicles is the normal method
of hearing and is about twice as efficient as conduction through bone. Rinne's positive is
the normal response, which occurs also with nerve deafness. Rinne's negative indicate
reduced air conduction and middle ear deafness.
Common causes of deafness
TYPE OF RINNE’S WEBER’S FOUND IN
DEAFNESS TEST TEST
Conduction -VE Louder on Wax in the external ear canal
deafness (AC<BC) affected Damage to tympanic membranes, Fluid in
side inner ear Ossicular chain disruption (head
injury) Otosclerosis (degenerative)
Sensorineural +VE Louder on Damage to cochlear nerve & Organ of
deafness (AC>BC) unaffected Corti
side Acoustic neuroma
Transverse fracture of petrous temporal
bone
Bilaterally in the elderly (degenerative)

Causes depending upon lesion:

1. At cochlear level: Meniere's disease, advanced otosclerosis, deafness due to drugs.
Internal auditory artery occlusions and prolonged exposure to loud noise.
2. In the nerve trunk: Old age, post inflammatory lesions, toxic lesions, meningitis,
Cerebello-pontine angle tumors and trauma.
3. In the brain stem: Severe pontine vascular lesions, severe demyelinating lesions and
occasionally tumors.

120
Other Tests of Audiometry function
 Pure tone audiometry
 Speech discrimination audiometry
 Loudness recruitment
 Tone decay
 Bekesy Audiometry

Tests of vestibular function

The disturbances of the vestibular function usually results in vertigo, nystagmus, past
pointing and falling. By stimulation of the vestibular system, usually the labyrinth features
can normally be produced at will and defects may be detected, helpful in localizing lesions.

Examination sequence (vestibular)

Induction of positional nystagmus (Dix-Hallpike's test)
 Position the patient seated on the couch so that when supine the head and neck will
overlap the end of the couch.
 Ask the patient to keep the eyes open throughout the test and explain what you are
going to do.
 Quickly lower the head of the couch so the patient is supine with the head tilted 30°
below the horizontal and turned 30-45° to one side.
 Maintain this position and look for nystagmus for 20-30 seconds.
Repeat the procedure turning the head to the other side.

Positional vertigo and nystagmus are peripheral when they result from lesions of the
labyrinth such as Benign paroxysmal positional vertigo or Central when they are due to
damage to the vestibular nerve or its connections. The latter being uncommon but may
occur after trauma or with brain stem demyelination.
In normal individuals the Hallpike manoeuvre does not induce nystagmus. In peripheral
lesions, vertigo and nystagmus may occur after a delay of 5-15 seconds. They decline as
the position is maintained, and fatigue if the test is repeated. With central lesions there is no
latency or fatigue, and vertigo is often less prominent or absent.

Oculocephalic (doll's eye) reflex

 With the patient supine, hold his head in both hands with your thumbs holding the
eyes open.
 Rock the head briskly from side to side, noting the movement of the eyes.
Normally the eye moves in the opposite direction to the head movement as occurs in a doll.
In cases of brain stem damage this eye movement may be lost.

Oculovestibular reflex:
 Examine the external auditory meatus to ensure it is free of wax and that the tympanic
membrane is intact. The test should not be performed if there is tympanic perforation.
 Place the patient supine on the couch.
 Flex the patient's head to 30°.
 With a bowl held at the side of the head to collect the water, slowly irrigate 50 ml of cold
(30 degree Celsius) and warm (44 degree Celsius) water into the external auditory
meatus in turn. Look for deviation of the eyes for about 30 seconds.
Normally, irrigating the right ear with warm water produces nystagmus to the right, & with
cold water, to the left. Similarly irrigating the left ear with warm water produces nystagmus
to the left, & with cold water to the right.
121
It is primarily used for assessing brain stem death. In a comatose patient with an intact
brain stem, tonic movements occur towards the irrigated ear without the quick phase
movement away. When there is severe brain damage no response occurs.

GLOSSOPHARAYNGEAL AND VAGUS NERVES

The IX and X nerves are intimately related anatomically. Both contain sensory, motor and
autonomic components.

Functions
 Common sensation from the pharynx, tonsils, soft palate, and posterior one third of
the tongue.
 Sense of taste from the posterior 1/3rd of the tongue (IXth nerve)
 Motor supply to the palatal and pharyngeal muscles.
 To give motor supply to the vocal cords (purely the Xth nerve)

Purpose of the tests

1. To determine the integrity of the reflex arc for the gag reflex.
2. If abnormal to differentiate between a breach on the sensory side by testing
sensation in the pharynx and palate and on the motor side by testing elevation of the
palate and contraction of the pharynx.
3. To examine the movements of the vocal cords
Testing pharyngeal sensation and the gag reflex are unpleasant for the patient and should
be restricted to patients with swallowing difficulties (dysphagia) or nasal regurgitation.

Preliminary observation
 Notice the pitch and quality of the patient’s voice, and of his cough, and whether
there is any difficulty in swallowing his saliva.
 Ask if there's been any nasal regurgitation of fluids.

A high pitched, hoarse voice may mean vocal cord paralysis, a nasal tone that increases if
the head is bent forward means palatal paralysis, when lying back this becomes almost
normal.
If the patient chokes on his saliva while talking, there may be both palatal and pharnygeal
weakness and if any of these features increases towards the end of each sentences, this
may be due to myaesthenia gravis.

Motor functions
 Ask the patient to open his mouth wide and wait for tongue to settle to see the palate
without the use of tongue depressor.
 Patient then asked to say 'Ah' while breathing out, followed by 'ugh' while breathing
in (The palate should move symmetrically upwards and backwards uvula remaining
in midline and the two sides of the pharynx should contract symmetrically).
 Ask the patient to puff out his cheeks (with the lips tightly closed),while examiner will
look and feel for air escaping from the nose
 Patient should then be asked to phonate several times in succession and the palate
is watched to see if any defect worsens with repeated use.

Sensory functions
 Test pharyngeal sensation using a throat swab.

122
  Elicit the gag reflex by touching the posterior pharyngeal wall or faucial pillars with a
tongue depressor.
 Apply the stimuli to both sides in turn.

The gag reflex varies in sensitivity from individual to individual.

Taste
Testing the taste sensation on posterior part of the tongue so difficult it’s hardly worth doing.
Method
Using a galvanic current of 2-4 mA and touching the tongue in this area with the anode
on either side will produce a metallic taste which the patient should be able to detect and
allows the two sides to be compared.

ABNORMALITIES
On inspection
FINDINGS CONDITION
Uvula lies to one side of Asymmetry at the palate wherein movement on phonation is
mid line normal
1. Swelling is the tonsillar region.
2. Unilateral muscle paralysis.
Constant rhythmic vertical Called palatal nystagmus, due to lesion in the central
oscillation of the palate, tegmental tract.
pharynx.
Palatal fasciculation Motor neuron diseases
On phonation
 The palate moves up and over to one side when there is paralysis of the opposite
side, owing to the pulling movement of the unopposed normal muscle.
 In pharyngeal paralysis, the muscle will also appear to move towards the normal
side, so resembling a flat sheet being drawn across that is called the curtain
movement. Caused by LMN lesion of the Vagus.
 If no movement of the palate & pharynx, there should also be dysphagia, nasal
regurgitation and nasal speech indicating either a bilateral medullary nuclear lesion
or a bilateral UMN lesion as seen in pseudobulbar palsy. Both may be combined in
motor neuron disease.

On testing sensation
Unilateral absence of the gag reflex may be due to loss of sensation or motor power or
both, phonation having already shown if one side is paralysed

CAUSE OF LOSS
OF GAG REFLEX FINDING CONDITION
Due to loss of Stimulation of normal side produce a IX nerve lesion
sensation normal symmetrical reflex (rare)
Due to combined Stimulation of the normal side causes IX and X both
motor and the palate to be pulled towards that side (common)
sensory loss

123
Examining vocal cords
This examination, while not carried out routinely should be included in any case where
hoarseness is present or where it is suspected that there is a neurological lesion
responsible for the palatopharnygeal abnormalities.

Method
 Patient should sit upright, and open the mouth wide.
 A laryngeal mirror is passed rapidly through a flame to minimize misting and is then
carefully introduced into the back of the throat without touching the palate or pharynx.
 On good view, the movements of the cords are first watched during inspiration and
expiration and then patient is then asked to say a long 'Ah'.
 Normally the cords abduct during inspiration and come together during phonation.

Most common lesions

NERVE LESION MUSCLE FINDING
PARALYSED
Recurrent laryngeal nerve Unilateral abductor Hoarseness
paralysis
Severe lesions of Vagus Total unilateral Hoarseness
paralysis
Bilateral lesions of Vagus. Bilateral Total Both cords immobile in mid
paralysis abduction and no phonation
possible
Bilateral recurrent laryngeal Bilateral abductor Both cords lie together,
nerve lesion or occasionally paralysis immobile on inspiration,
in nuclear lesion in brain severe respiratory obstruction,
stem.

THE ACCESSORY NERVE

It is the spinal root of the XIth nerve that is examined, the cranial root joining the vagus after
leaving the brain stem and being considered part of that nerve.

Anatomy
The spinal nuclei arise from the anterior horn cells of C1-5, and fibres emerge from the
spinal cord, ascend through the foramen magnum, and exit via the jugular foramen. They
pass posteriorly to supply the upper half of trapezius and the sternocleidomastoid.

Functions
To supply motor power to the upper part of the trapezii & sternomastoids and also to
influence the posture and movement of head and shoulder girdle.

Method of examinations
When the patient is first seen severe trapezius weakness may be suspected if the head
falls forwards and sternomastoid weakness if it falls backwards.

124
 Sternomastoid
 Face the patient and inspect the sternocleidomastoid muscles for wasting or
hypertrophy and palpate them to assess their bulk.
 To test power in the left sternocleidomastoid, ask the patient to turn the head to the
right while you provide resistance with your hand placed on the right side of the
patient's chin. Reverse the procedure to check the right sternocleidomastoid.
 Rest a hand on his forehead and ask him to bend his head forwards, both
sternomastoids will stand out together and are easily compared.
Trapezius
 Stand behind the patient to inspect the trapezius muscle for wasting or asymmetry.
 Ask the patient to shrug the shoulders as you apply downward pressure with your
hands.

Abnormalities
TYPE OF FINDINGS CONDITION
LESION
Bilateral When patient sits up the head seems to In myotonic & oculopharyngeal
sternomastoid be left behind and then raised with dystrophies, spinal muscular
weakness difficulty atrophies, poliomyelitis, MND.
Unilateral Fail to turn head against resistance to Trauma in the neck or base of
sternomastoid the opposite side. The muscle will not skull, polio, tumors at jugular
weakness stand out clearly either then or when the foramen, bony anomalies at
head is flexed forwards against base of skull, syringomelia.
resistance.

Bilateral Shoulder drop, unable to shrug motor neuron disease,

trapezius especially against resistance polyneurpathy, poliomyelitis.
weakness
Unilateral Trapezius weakness results in the Trauma in the neck or base of
trapezius shoulder drooping on one side and the skull, polio, tumors at jugular
weakness scapula being displaced downwards foramen, bony anomalies at
and laterally giving a steeper gradient to base of skull, syringomelia.
the contour of the neck.
-.
Movements: Fasciculation in these muscles mean a nuclear lesion as seen in motor
neuron disease. But coarse twitching is seen in irritative and compressive lesions of the
nerve trunk near its origin.

THE HYPOGLOSSAL NERVE

Examination sequence
 The patient is asked to open his mouth. Look at the tongue at rest for wasting,
fasciculation or involuntary movement.
 The patient is asked to protrude the tongue. Look for deviation or involuntary
movement.
 The patient is asked to move the tongue from side to side.
 Test power by asking the patient to press the tongue against the inside of each
cheek in turn while examiner presses from the outside with finger.
 Assess speech by asking the patient to say 'yellow lorry'.
Common abnormalities:

125
 On inspection and protrusion
Macroglossia Large tongue Down’s syndrome,
Cretinism
Microglossia Small tongue Atrophy, MND
Crossed tongue Caustic fluid ingestion
Glossitis Atrophy of papilla with Vitamin B complex
smooth glistening deficiency
redish tongue

On percussion
Normally the dent will disappear immediately. In myotonia it persists and may enlarge for a
few seconds in linear manner. Tapping the tongue on one side will produce a dent on both
sides.

FINDINGS IN XII th NERVE PALSY

Type of Tongue Longitudin Tip and Examination Condition
Lesion Appearanc al Folds Median Findings
e raphe
Unilateral Normal Surface little Deviate Slight Hemiplegia due
Supranuclea looking altered towards Speech to vascular
r lesion symmetrical opposite disturbance lesions or deep
(UMN) tongue side of seated
lesion neoplasms.
Bilateral Small tight, Surface little Remain Almost Bilateral
Supranuclea compact altered central incapable of vascular lesions
r lesion looking protrusion producing a
(UMN) tongue lying with gross pseudobulbar
in the floor disturbance palsy, ALS.
of the mouth of speech,
Jaw jerk will
be
exaggerated.
Unilateral Folds on Deviate Fasciculation Syringomyelia,
Unilateral muscle lesion side towards may be there polio, tumor at
Nuclear and wasting are greatly the but speech is or near the
Infra-nuclear exaggerated affected little affected. jugular
lesion (LMN) side on foramina,
protrusion angiomas of the
stem, trauma,
tumors or
glandular
enlargement
high in the neck
and early motor
neuron disease.

Bilatera Bilateral Folds Remain difficulty in Progressive

Nuclear and muscle exagerated central protrusion bulbar palsy,
Infra-nuclear wasting, and syringomelia,

126
lesion ( greatly speech.fascic foramen
LMN) reduced ulation magnum
size marked ( anomalies.
nuclear
lesion)

Tremor on protrusion may be seen in Neurosyphilis and some cases of Parkinsonism.

o An up and down flapping movement with alternate protrusion and retraction is
common in chorea.
o Dystonic movements of the tongue follow high and prolonged dosage of
antipsychotics.

MULTIPLE CRANIAL NEUROPATHIES AND BRAINSTEM SYNDROMES

The overview is given in table below.

SYNDROME STRUCTURES INVOLVED CLINICAL FINDINGS
WEBER’S Part of midbrain, Contralateral weakness of upper
SYNDROME CNN III and lower extremities(CSP),
(MIDBRAIN) Ipsilateral lateral gaze palsy(III CN)
RAYMOND Ventral pons, CNN VI Contralateral weakness of upper
SYNDROME and lower extremities(PT),
(VENTRAL Ipsilateral lateral gaze palsy(VI CN)
PONTINE)
MILLARD- GUBLER Basis pontis, CNN VI & CNN Contralateral weakness of upper
SYNDROME (BASAL VII and lower extremities(PT),
PONTINE) Ipsilateral lateral gaze palsy(VI CN)
& entire side facial weakness(VII
CN)
FOVILLE Unilateral dorsal tegmentum of Contralateral weakness of upper
SYNDROME caudal 1/3 of pons, CNN VI & and lower extremities(CSP),
(INFERO-MEDIAL CNN VII Ipsilateral lateral gaze palsy(VI CN)
PONTINE) & entire side facial weakness(VII
CN)
WALLENBERG Lateral medulla, Nucleus Contralateral hemisensory loss,
SYNDROME ambiguous and vestibular ataxia,
(LATERAL nucleus, sympathetic fibres, nystagmus,nausea,vomiting,vertigo
MEDULLARY) cerebellum , hoarseness, horner’s syndrome
DEJERINE Medial medulla, CNN XII Contralateral weakness of upper
SYNDROME and lower
(MEDIAL extremities(PT),Contralateral
MEDULLARY) hemisensory loss of vibration &
proprioception(ML),Ipsilateral
Tongue weakness and atrophy
CNN- Cranial nerve nucleus; CSP-Corticospinal tract; PT-Pyramidal tract; ML-Medial
lemniscus; CN- Cranial nerve.

127
DISORDERS OF CRANIAL NERVE GROUPS
SYNDROME NERVES FINDINGS CAUSES
INVOLVED
CAVERNOU III,IV,VI,V1 &V2 Ophthalmoplegia, Carotid aneurysm,
S SINUS Orbital congestion, Thrombosis from PNS
SYNDROME Periorbital oedema, infection,orbital cellulitis,
Ptosis, Facial Lymphoma,meningioma,
Sensory loss pituitary and PNS tumor
extension
HORNER’S lesions of the miosis, ptosis, carotid cathererization
SYNDROME superior cervical enophthalmos, and ,periodic migrainous
ganglion in the dryness and warmth of neuralagia ,cluster
neck, and fibres that half of the face headache
surrounding the
carotid artery

CEREBELLO VIII,VII,V Tinnitus, progressive C-P Angle tumors

-PONTINE S-N hearing loss, gait
ANGLE Disequilibrium, LMN
Facial paresis without
hyperacuosis, facial
sensory loss
Later nystagmus and
gaze palsies due to
pontine compression

JUGULAR IX,X,XI,XII Dysphagia,dysphonia, Glomus tumour,

FORAMEN dysarthria Schwannoma,Meningioma
SYNDROME ,
Retro-parotid abcess,

PERIPHERAL NERVOUS SYSTEMCONSIDERATION OF CRANIAL NERVE

INVOLVEMENT:

TYPE POLYNEUROPATHY NEUROMASCULAR MYOPATHY WITH

WITH Cranial Nerve JUNCTION BULBAR
INVOLVMENT DISORDER INVOLVEMENT
CAUSES Guillain-Barre Syndrome Myasthenia gravis Chronic progressive
Diabetes Botulism external
Diphtheria ophthalmoplegia
HIV AIDS (mitochondrial)
Lyme disease Oculopharyngeal
Sarcoidosis dystrophy
Chemotherapy related
neuropathy
(Vincristine,Cisplatin)

128
References:
Pentland, B., Statham, P., Olson, J. (2007). The Nervous system including the eye In:
Douglas, G., Nicol, F., Colin, R, eds. Macleod's clinical examination (11th
edition). London: Elsevier, Churchill Livingstone, 241-263.
Spillane, J. (1996). In Bickerstaff's Neurological Examination in clinical practice (6th
edition), 35-110.

McAuley, J., Swash, M. (2007). Nervous system, In: Swash M, Glynn M, Hutchison's
Clinical Methods (22nd edition), London: W.B. Saunders . 187-202.
Brazis, P.W., Masdeu, J.C., Biller, J. (1996). Localisation in clinical Neurology (3rd edition).
109-335.
Haerer, A.F. (1992). The Cranial Nerves. In DeJongs. The Neurologic Examination (5th
edition), London: J.B. Lippincott Company, 87-257.
Roos, L.K. (2009). Disorders of the Cranial Nerves, Seminars in Neurology,29(1).3-92.

Mnemonics –
NAME OF CRANIAL NERVES- One Of Our Telegu Teachers Asked For Very Good
Vadas and Halwas.( Olfactory, Optic, Oculomotor, Trochlear, Abducens, Facial, Vestibulo-
Cochlear (Auditory), Glossopharyngeal, Vagus, Accessory and Hypoglossal nerves)

FUNCTIONS OF CRANIAL NERVES- Some Say Money Matters But My Brother Says Big
Brain Matters More. (s=sensory, m=motor, b=both or mixed)

FORAMINA FOR EXIT OF CRANIAL NERVES (COSSSROSIIJJJH) – Come on soft sweet

scented roses of Sweden in inspiring Joy’s joyful journey home.
Cribriform plate(I), Optic canal(II), Superior orbital fissure(III), Superior orbital
fissure(IV) , Superior orbital fissure(V1), Foramen Rotendum(V2), Foramen Ovale(V3),
Superior orbital fissure(VI), Internal acoustic meatus(VII), Internal acoustic meatus(VIII),
Jugular formen(IX), Jugular formen(X), Jugular formen(XI), Hypoglossal canal(XII).

129
CRANIAL NERVES – AT A GLANCE
Clinical presentation
Nerve Name Nucleus Origin/Relay Nature Function
of lesion
CN I Olfactory Olfactory bulb Limbic Cortex Special Smell Anosmia, Parosmia
Sensory
CN II Optic Lateral Geniculate body Special  Vision Anopsia, Visual field,
Sensory  Sensory limb of light rifles sensory limb of light
CN III Oculomotor  Oculomotor Midbrain Motor  Supply all ext. ocular  Loss of parallel
Nucleus muscles except LR & SO. gaze; eye remain
 Edinger westphal  Upper eyelid elevator (LPS) adducted
nucleus  Accomodation reflex  Motorlimb of
 Motor Light Reflex Light reflex
 Ptosis
130
  Accomodation
CN IV Trochlear  Trochlear nucleus Midbrain Motor  Superior Oblique muscle-  Weakness looking
depress eyeball with down with
intorsion adducted eye
 Head tilt away from
side of lesion
CN V Trigeminal  Spinal and Main Pons Mixed  Sensory from face, tympanic  Loss of general
V1 – Ophthalmic Sensory membrane, deep sensation sensation (touch,
V2 – Maxllary  Mesencephalic of head and neck, dura pain, temp) of
V3 – Mandibular  Trigeminal motor  Muscle spindle, mechano V1 – forehead, scalp,
receptors of head neck. cornea
 Muscles of mastication , eg ( V2 – palate, nasal cavity,
lateral and medial pterigoid, maxillary face and teeth.
masseter, temporalis, V3 – anterior 2/3 of
anterior belly of digastrics), tongue, mandibular
myelohyoid, tensor palatine face, teeth
and tensor tympani. Weakness of muscles
of mastication , jaw
deviation occurs
towards lesion side.
CN VI Abducens Abducens nucleus Posterior Motor Lateral Rectus Abducts eye Diplopia, loss of parallal
margin of gaze,pseudoptosis,
pons internal strabismus
CN Facial  Facial motor Cerebello- Mixed  Muscles of facial expression  Weakness of
VII  Spinal Trigeminal pontine angle and stapedius. facial musdes
 Solitary above olive  Sensory from external ear  Loss of motor
 Superior and stapedius blink reflex
Salivatory  Taste from Ant 2/3 tongue  Loss of taste
 Secretomotor to lacrimal and  Hyperacusis
salivary glands (Sublingual   salivary output
and submandibular)  Xerophthalmia

CN Vestibulo  Cochlear nuclei Cerebello- Sensory  Hearing  Sensoryneural

VIII Cochlear  Vestibular nuclei pontine angle  Linear acceleration (gravity) hearing loss
131
 lateral to CN  Angular acceleration (head  Balance lost
VII turning)  Nystagmus
CN IX Glossopharyngeal  Nucleus Medulla Mixed  Motor of pharynx (stylo  Loss of sensory
ambiguous pharyngeus) limb of gag reflex
 Spinal trigeminal  Sensory from posterior 1/3  Loss of taste and
 Solitary nucleus tongue, oropharynx, carotid sensation
 Inferior salivatory body and carries taste from   salivation
posterior 1/3 tongue
 Parotid gland secretomotor
CN X Vagus  Nucleus Posterolateral Mixed  Muscles of palate except  Palate drop uvula
ambiguous sulcus of tensor palatine (v) Muscles away from lesion
 Spinal trigeminal medulla of pharynx exept.  Dysphagia,
nucleus stylopharyngeous (ix) hoarsensess
 Solitary nucleus Muscles of Larynx and dysphonia
 Dorsal motor palatoglossus  Loss of motor
nucleus  sensory of limb of gag reflex
 Descending larynx/Laryngopharynx and  Ptosis
hypothalamic smooth muscles in thorax,  Miosis
nucleus (motor) foregut,midgut.  Anhidrosis
 Upper eyelid elevator
superior tarsal
 Mydriasis
 Sweat gland of face/scalp

CN XI Accessory  Nucleus Cranial and Motor  Turn head to opposite side  Weakness to turn
ambiguous Spinal roots (Sternocleidomastoid). head to opposite
 Accessary  Elevates and rotates scapula side
nucleus (trapezeus)  Shoulder drop
CN Hypoglossal  Hypoglossal Medulla Motor  All tongue muscles except  Tongue deviates
XII nuclei palatoglossus to lesion side
 Dysarthia

132
CHAPTER –VII
 EXAMINATION OF MOTOR AND SENSORY SYSTEM
Introduction
. Purpose-to arrive at the conclusion whether the presenting problem lies within the
nervous system, and, if so, its location and pathological genesis.
. Examination begins right from the moment the patient walks into room. The facial
expression, manner of relating, dress, posture, speech, the individual’s mood, cognitive and
physical state should all be noted. Finally, a detailed relevant history and clinical
examination brings out the pathological condition.
History
To ask a few preliminary questions before examining the patient is very important to
have an gross idea about the deficits our patient might be having.
Motor:
 Have you observed wasting/skin change of any limb?
 Do you feel weakness of any limb? Any difficulty in performing any particular
task?
 Any difficulty in standing up from squatting? (proximal muscle)
 Difficulty in wearing slippers? (distal muscle)
 Difficulty in combing? (proximal muscle)
 Difficulty in buttoning/unbuttoning? (distal muscle/ coordination) etc.
Sensory:
 Burning sensation over any part of body?
 Any lack of intensity of sensation?
 Lack or excess of pain/heat sensation?

EXAMINATION OF THE MOTOR SYSTEM

The Assessment
The assessment of the motor system is considered under the following headings:
 Inspection and palpation of muscles
 Assessment of tone
 Examination of reflexes
 Testing movement and power
 Testing coordination
The first step in each of those tests is obtaining patient’s consent after explaining
him the procedure and proceed further only after ensuring that he has understood
what is going to be done and what he is supposed to do. Presence of female
attendant is required while examining female patient.

INSPECTION AND PALPATION

 Proper inspection of the muscles requires adequate exposure in keeping with

the patient's comfort and modesty. Examine the patient lying, sitting and
standing, placing the limbs in symmetrical positions.

133
  Inspect the asymmetry both proximally and distally. Note any deformities,
such as, clawing of the hands or pes cavus. Examine specifically for wasting
or hypertrophy, fasciculations and involuntary movements.

 For minor differences, measurement by a tape may be very useful.

Measurement should be made from fixed point or landmarks and the sites
such as distance 10 cm above and below the olecranon, 18 cm above patella
and 10 cm below tibial tuberosity. The extremeties should be in the same
position and in comparable states of relaxation. The length of the limbs may
also be measured in case of any suspected differences.

 While examining the abnormal movements, the following should be noted:

A. The part of the body involved.
B. The distribution of the movement across joints and whether simple or
complex.
C. The rhythmicity, uniformity and regularity of the recurrence.
D. The span, speed and frequency of each particular movement.
E. The amplitude of the movement.
F. The relationship to posture, rest, voluntary activity or exertion, fatigue and
time of the day.
G. The response to heat and cold.
H. The relationship to emotional tension and excitement.
I. The degree that movements are suppressible by attention and distraction.
J. The presence or absence of movements during sleep.

 The muscles should also be palpated to assess their bulk and tone.
Wasted muscles feel “flabby”. Inflammation of muscles ( myositis )
may be accompanied by tenderness and some forms of acute
muscle necrosis ( rhabdomyolysis ) produces a firm “woody” feel.

Common abnormalities

Muscle bulk: Wasting and Hypertrophy

Wasting is not seen in acute lesions. Lower motor neuron lesions may cause wasting
in specific muscles. Longstanding or developmental upper motor neuron damage can result
in disuse atrophy of muscle groups. Muscle disorders may result in muscle wasting, usually
proximal (the notable exception is dystrophia myotonica where it is distal); rheumatoid
arthritis is associated with wasting of the small muscles of the hands, and widespread
wasting occurs in cachexia.
Certain occupations and sports lead to muscle hypertrophy. This can also occur in
muscular dystrophy but differs on palpation from healthy hypertrophic muscles with a
'doughy' feeling.
Fasciculation
Fasciculations are fine, rapid, flickering or vermicular twitching movements due to
contraction of a bundle, or fasciculus, of muscle fibers. When assessing fasciculations, the
patient should be comfortable and completely relaxed. Fasciculations may be brought out
by mechanical stimulation of the muscle (e.g., light tapping, flicking the skin over wasted
muscle or simply exercising the muscle). Non-pathological fasciculation occasionally occurs
after vigorous exercise in healthy people.

134
Myoclonic jerks
These are sudden shock-like contractions of one or more muscles which may be
focal or diffuse. They may occur singly or repetitively. Healthy individuals may experience
these when falling asleep or surprised by a sudden noise. They may also occur in
association with epilepsy, diffuse brain damage and dementias.
Tremor
A tremor is a series of involuntary, relatively rhythmic, purposeless, oscillatory
movements. Tremors are described according to their speed (fast: 10-20 Hz or slow: 3-5
Hz), amplitude (fine or coarse) and whether they are maximal at rest, on maintaining a
posture or on carrying out an active movement.
Coarse tremor is well evident by naked eye. Fine tremor has to be observed keenly.
Tremor could be tested by asking the patient to stretch his hands with fingers wide apart.
Fine tremor could be elicited by placing a piece of paper on these fingers.
Physiological tremor seen with anxiety is a fine, fast postural tremor. It occurs in
hyperthyroidism and those who take alcohol or caffeine to excess.
The slow, coarse tremor of Parkinson's disease is worst at rest and reduced by
voluntary movement. It is more common in the upper limbs and usually asymmetrical. The
traditional description of a 'pill rolling' tremor (movement of the thumb across the finger tips)
is not particularly helpful.
Cerebellar damage is the most common cause of tremor which is absent at rest but
maximal on movement, so-called action or intention tremor.
Coarse, even violent, action tremors are associated with lesions of the red nucleus
(rubral tremor) and subthalamic nucleus. They are most often caused by damage from
vascular disease or multiple sclerosis.
Other involuntary movements
These include dystonias, chorea and athetosis, which are often caused by
disturbance to extrapyramidal pathways. Dystonia is the slow development of an abnormal
posture, often of the limb or the neck, which is maintained. Chorea and athetosis are both
writhing movements; the former tends to be irregular, jerky and brief, the latter is slower,
and more sustained.
Dyskinesia is a group term for these types of involuntary movements, particularly when
they arise as an adverse effect of neuroleptics and antiparkinsonian agents.
Tics or habit spasms are more stereotyped and essentially normal movements which
recur involuntarily.

Motor strength and power

Motor strength and power indicate the ability of muscles to exert force. Decreased strength
is called weakness or paresis, absence of ability to contract is called paralysis or plegia.
Weakness may cause loss of the speed, rapidity or agility of movement and a decrease in
the range or amplitude of movement before there is loss of power to formal strength testing.
Other manifestations of loss of strength include easy fatigability, variation in strength on
repeated tests, diminished range and rate of movement, loss of coordination, irregularities
and clumsiness of motion, tremulousness, loss of associated movements, and lack of ability
to carry out skilled acts.
Muscle power is graded as below
0. No muscle contraction visible.
1. Flicker of contraction but no movement.
2. Joint movement when effect of gravity eliminated.
3. Movement against gravity but not against examiner’s resistance.

135
 4. Movement against resistance but weaker than normal ( 4-, 4, 4+ ).
5. Normal power.

The following list of joint movements could be used to determine power.

Upper limbs
 Shoulder: abduction, adduction, flexion and extension
 Elbow: flexion and extension
 Wrist: flexion and extension
 Finger: abduction, adduction, flexion and extension
 Thumb: extension and opposition
Lower limbs
 Hip: abduction, adduction, flexion and extension
 Knee: flexion and extension
 Ankle: dorsiflexion, plantarflexion, inversion and eversion of foot
 Large toe: extension (i.e. dorsiflexion).
When performing a quick screening of muscle power as part of a routine assessment
when no weakness is volunteered by the patient, examiner should at least perform tests of
both proximal and distal muscle groups in each limb (e.g. shoulder and finger abduction in
the upper limb). For more specific complaints, and particularly in trauma, careful
assessment of individual muscles is necessary.
Examination sequence
 To test the power of individual muscle groups in both limbs alternately to compare.
 To ask the patient to contract a group of muscles to maintain a position and to
resist any attempt to displace the limb (isometric testing).
 To ask the patient to put the joint through a movement while examiner tries to
oppose the action (isotonic testing).
Muscles of shoulder girdle and scapula (Adapted from Campbell, 2005; Spillane, 1996)
Muscle Segmental Peripheral Nerve Test
Innervation
Rhomboids C 4-5 Dorsal scapular Hand on hip, the patient tries to
nerve force the elbow backwards
Deltoid C 5-6 Axillary nerve The patient holds his arm abducted
to 60 degree against the examiners
resistance
Supraspinatus C (4) 5-6 Suprascapular The patient tries to initiate
nerve abduction of the arm from the side
against resistance
Infraspinatus C (4) 5-6 Suprascapular Semiflexed elbow is held in side,
nerve then patient attempts to turn the
forearm backwards against
resisitance
Serratus C 5-7 Long thoracic Patient pushes the arm forwards
anterior nerve against firm resistance
Pectoralis C 5-T 1 Lateral and Placing hands on hip and press
major medial anterior inwards-sternocostal part; Raising
thoracic nerves the arm forwards above 90 degree
and attempt to adduct against
resistance-clavicular portion.
Latissimus C 6-8 Thoracodorsal Ask the patient to cough while
dorsi nerve palpating it; Resist the patient’s
attempt to adduct the arm when

136
 abducted to above 90 degree.

Muscles of elbow joint. (Adapted from Campbell, 2005; Spillane, 1996)

Biceps brachii C 5-6 Musculocutaneous The patient flexes his elbow
nerve against resistance, the forearm
being supinated.
Brachioradialis C 5-6 Radial nerve The patient pronates the
forearm and draws the thumb
towards nose against
resistance.
Triceps brachii C 6-8 Radial nerve The patient attempts to extend
the elbow against resistance.

Muscles of forearm and wrist joint. (Adapted from Campbell, 2005; Spillane,
1996)
Extensor C (5)6- Radial nerve The patient holds the fingers partially
carpi 7 extended and dorsiflexes the wrist
radialis towards the radial side against
longus resistance.
Extensor C 7(8) Radial nerve As above but dorsiflexion must be
carpi ulnaris towards the ulnar side.
Extensor C 7(8) Radial nerve The examiner attempts to flex the
digitorum patients extended fingers at the
communis metacarpophalangeal joints.
Flexor carpi C 6-7 Median nerve The examiner resists the patients

137
radialis attempts to flex the wrist towards the
radial side.
Flexor carpi C 7-T Ulnar nerve Fixes the point of origin of abductor
ulnaris 1 digiti minimi.

Muscles of the hip girdle. (Adapted from Campbell, 2005; Spillane, 1996)
Muscle Segmental Peripheral Test
Innervation Nerve
Iliopsoas L1,2,3 Femoral Patient lies on his back & attempts
nerve to flex his thigh against resistance
Adductor L5 S1 Obturator Attempts to adduct the leg against
femoris nerve resistance
Gluteus L (3)4-S 1 Superior Lying face down the patient flexes
medius Gluteal the knee & then forces the foot
nerve outward against resistance.
Gluteus L 5-S 1,2 Inferior Still lying on stomach, should
maximus gluteal nerve tighten the buttocks- palpated; try
to raise thigh against resistance.

Muscles of the thigh and knees. (Adapted from Campbell, 2005; Spillane,
1996)
Muscle Segmental Peripheral Test
Innervation Nerve
Biceps femoris L4,5 S1,2 Sciatic nerve The patient lying on

138
Semimembranosus stomach, attempts to flex
Semitendinosus knee against resistance.
Quadriceps L 2-4 Femoral Lying on back, attempts to
femoris nerve extend the knee against
resistance.

Muscles of lower leg and ankle. (Adapted from Campbell, 2005; Spillane,
1996)
Muscle Segmenta Peripheral Nerve Test
l
Innervatio
n
Tibialis L 4-L5 Deep peroneal Patient dorsiflexes the foot
anterior nerve(anterior against examiner’s hand on
tibial) the dorsum of foot.
Tibialis L 5-S 1 Tibial nerve Patient planter flexes the foot
posterior slightly & then tries to invert it
against resistance.
Peronei L5,S1 Musculocutaneous Patient everts the foot against
n. resistance.
Gastrocnemiu S1 Medial popliteal n. Patient planter flexes the foot
s against resistance.

Muscles of the foot and great toe. (Adapted from Campbell, 2005; Spillane,
1996)
Muscle Segmental Peripheral Nerve Test
Innervation
Extensor L 5-S 1 Deep peroneal Dorsi flexion of toes against
digitorum nerve(anterior resistance.
longus tibial)
Flexor L 5-S 1 Tibial nerve (medial Flexion of terminal phalanges
digitorum popliteal) against resistance
longus
Extensor L5 Deep peroneal Dorsi flexion of the great toe
hallucis nerve(anterior against resistance
longus tibial)
Extensor L 5-S 1 Deep peroneal Dorsi flexion of the great toe
digitorum nerve(anterior against resistance
139
 brevis tibial)

Common abnormalities
 Paresis: Partial paralysis
 Plegia: Complete paralysis
 Monoplegia: Involvement of a single limb
 Hemiplegia: Involvement of one-half of the body
 Paraplegia: Paralysis of the legs
 Quadriplegia:Paralysis of all four limbs
Causes of muscle weakness (Adapted from Douglas, 2005)

Aetiology Associated features Common causes

Lower motor Muscle atrophy Peripheral neuropathies
neurone Fasciculation Radiculopathies
Reflexes absent or Anterior horn cell damage (e.g.
diminished poliomyelitis)
Hyptonia Motor neurone disease
Upper motor 'Patterned' weakness
neurone Little or no muscle wasting Cerebrovascular disease (e.g.
hemiplegia)
Hyperreflexia
Spinal injury or disease (e.g. paraplegia)
Hypertonia Multiple sclerosis
Hypokinesia of movement
Myopathies Muscle wasting (usually
proximal) Hereditary conditions (e.g. muscular
dystrophy)
Hypotonia
Alcohol and other toxins
Tenderness (myositis)
Psychological Inconsistent weakness Stress
No associated features Anxiety
Compensation claims

Upper motor neuron lesions result in weakness of a relatively large group of muscles
(e.g. a limb or more than one limb). In contrast, lower motor neuron damage can cause
paresis of an individual and specific muscle.
Upper motor neuron lesion
• Muscle weakness
• Increased deep tendon reflexes
• Depressed abdominal responses
• An extensor plantar response
• Spasticity
Lower motor neuron lesion
• Muscle weakness
• Depressed deep tendon reflexes
• Fasciculation
• Wasting
• Flaccidity

TONE

140
 Tone is the degree of tension present in a muscle at rest. Clinically, tone is the
resistance felt by the examiner when moving a joint passively through its range of
movement.
Examination sequence
 The examination room should be comfortable.
 Patient is asked to lie supine on the examination couch.
 Is asked to relax and 'go floppy'.
 To check the tone of a particular muscle it is moved in just the opposite way of
its natural action, that is, it is stretched passively and the resistance is felt. For
example, the function of biceps is to flex elbow and hence, to test its tone elbow is
extended passively.
 Passive movements of the joints should be through as full a range as possible and
both slowly and quickly.
 In the upper limb patient's hand is held as if shaking hands, using examiner’s other
hand to support the patient's elbow, to rotate the forearm, flex and extend the wrist, elbow
and shoulder, varying the speed and direction of movement.
 In lower limb examination begins by rolling or rotating the leg from side to side, then
briskly lifting the knee into a flexed position
 It is better to keep the patient distracted by talking to him throughout these
procedures.
Common abnormalities
Muscle tone may be decreased (hypotonia) or increased (hypertonia).
Hypotonia or flaccidity may occur in lower motor neuron lesions and is usually
associated with muscle wasting, weakness and hyporeflexia. It may be a feature of
cerebellar disease and occur in the early phases of cerebral or spinal shock when the
plegic limbs are atonic prior to developing spasticity.
There are two principal types of hypertonia: spasticity and rigidity.
Spasticity is a velocity-dependent resistance to passive movement (i.e. it is detected
with quick movements) and is a feature of upper motor neuron pathology. It is usually
accompanied by weakness, hyperreflexia, an extensor plantar response and sometimes
clonus. In mild forms it is detected as a 'catch' at the beginning or end of passive movement
but in severe cases it limits the range of movement possible and may be associated with
contracture. In the upper limbs it may be more obvious on attempted extension; in the legs
it is more evident on flexion.
Rigidity is a sustained resistance throughout the range of movement and is most
easily detected when the limb is moved slowly. In Parkinson's disease this is classically
described as 'lead-pipe' or 'plastic' rigidity. In the presence of tremor there may be a regular
interruption to the movement giving it a jerky feel. This is 'cog-wheel' rigidity. Other
extrapyramidal conditions may also be associated with rigidity.

DEEP TENDON REFLEXES

Anatomy
A tendon reflex is the reflex contraction of a muscle in response to stretch. It is
mediated by a reflex consisting of an afferent (sensory) and an efferent (motor) neuron with
one synapse between (i.e. a monosynaptic reflex). Muscle stretch activates the muscle
spindles, which send a burst of afferent signals that in turn lead to direct efferent impulses,
causing contraction of muscles. These stretch reflex arcs are subserved by a particular
141
spinal cord segment which is modified by the influence of descending upper motor neurons
and other neurons.
Examination sequence
 The patient should be as relaxed and comfortable as possible as anxiety and pain
can cause an increased response. Patient is asked to lie supine on the examination couch
in a comfortable relaxed position with the limbs exposed.
 Any inflammation/ pain of the tendon/ joint and any restriction of mobility of
the concerned joint is excluded before testing reflex. The tendon (and not the
muscle) is struck by the hammer when testing the reflexes. The technique is to flex
the wrist and allow the weight of the hammer head to determine the strength of the
blow. Alternatively, with quick flexion of the wrist a sharp, crisp blow is delivered to
the tendon, fair enough, though not really hurting.
 Ensuring that both the limbs are positioned identically the symmetry of response is
checked by comparing each reflex with that of the other side.
 Reinforcement is used whenever a reflex appears to be absent. For knee and
ankle reflexes the patient is asked to interlock the fingers and pull one hand against the
other on examiner’s command immediately before he strikes the tendon (Jendrassik's
manoeuvre). To reinforce the upper limb reflexes patient can clench his teeth. While using
reinforcement, the patient must relax between repeated attempts.
Responses are documented as:
 Hyperactive (+++)
 Normal (++)
 Diminished (+)
 Absent (-)
When only present using reinforcement (±) (Douglas et al, 2005)
Alternatively, reflexes could be graded as:
 absent
 present (as a normal ankle jerk)
 brisk ( as a normal knee jerk)
 very brisk
 clonus (Swash & Glynn, 2007)
Abnormally brisk reflexes (hyperreflexia) are generally a sign of upper motor neuron
damage. Diminished or absent jerks are most commonly due to lower motor neuron lesions
but also occur in myopathies and myasthenia. The isolated loss of a reflex may suggest a
mononeuropathy or radiculopathy (e.g. loss of ankle jerk with lumbrosacral (S1) disc
prolapse). A normal reflex contraction with delayed relaxation (‘hung up’ reflex) may occur
in hypothyroidism.
In cases of cerebellar damage the reflexes may be pendular and muscle contraction
and relaxation tend to be slow.
Inverted reflexes are phenomena caused by combined spinal cord and root
pathology. For example, in an inverted biceps reflex, when the biceps tendon is tapped
there may be no biceps jerk but the triceps contracts (C5/6 segment lesion). In an inverted
supinator reflex, when the supinator jerk is tested there is no response but finger flexion
occurs (C5/6 lesion).
Commonly Elicited Deep Tendon (Muscle Stretch) Reflexes (Adapted from Campbell,
2005)
Reflex Segmental Level Peripheral Nerve

Biceps C5-C6 Musculocutaneous

142
 Triceps C7-C8 Radial

Brachioradialis C5-C6 Radial

Quadriceps L3-L4 Femoral

Achilles S1 Sciatic

Reflex reinforcement are the methods which help in bringing out the reflexes. In the
Jendrassik maneuver, the patient attempts to pull the hands apart with the fingers
flexed and hooked together as the strike is made for lower limb reflexes. The effect is
short lasting and only during the initial phase. Other techniques include firmly grasping
the arm of the chair, side of the bed, clenching one or both fists, grinding the teeth. It
may also be done by slightly increasing the tension of the muscle being tested.

Biceps Triceps Supinator Knee Ankle Plantar

Right ++ ++ ++ ++ ++
Left ++ ++ ++ ++ ++

THE UPPER-EXTREMITY REFLEXES

The biceps, triceps, brachioradialis, and finger flexor reflexes are the most important
upper-extremity reflexes.
The Biceps Reflex.
The arm is relaxed and the elbow is kept at about 90 degrees with the forearm
slightly pronated, the examiner slightly presses downwards on the patient's biceps tendon,

143
and then strikes his own thumb with the reflex hammer. The contraction of the biceps
muscle with flexion of the elbow is looked for. Sometimes a part of is supination included.

The Triceps Reflex.

The arm is placed in a relaxed and rested position midway between flexion and
extension. The triceps tendon is struck just above its insertion on the olecranon process of
the ulna. The contraction of the triceps muscle with extension of the elbow is the major
response.

The Supinator (Radial Periosteal or Brachioradialis) Reflex

The forearm is placed in a semiflexed and semipronated position, and the tap is
made just above the styloid process of the radius for contraction of brachioradialis. The
major response is flexion of the elbow, with some component of supination. The supination
component can be increased by a different placement-the forearm extended and pronated.

Finger jerk (Wartenberg reflex)

→ Examiner’s middle and index fingers are placed across the palmar surface of the
patient's proximal phalanges.
→ Examiner’s own fingers are tapped with the hammer.
→ To observe for flexion of the patient's fingers.

Hoffman's reflex

144
→ Placing right index finger under the distal interphalangeal joint of the patient's middle
finger.
→ To flick the patient's finger downwards using right thumb.
→ To look for any reflex flexion of the patient's thumb.
→The patient's hand is in supination, resting on a table or a solid surface, with the fingers
slightly flexed.
→The examiner places his fingers against the patient's fingers, and taps the backs of his
own fingers lightly with the reflex hammer.
→The response is flexion of the patient's fingers and the distal phalanx of the thumb. The
nerve supply is through the median and ulnar nerves (C8-T1).
Positive Hoffman's (excess thumb flexion) reflex and finger jerk indicate hypertonia.

THE LOWER EXTREMITY- REFLEXES

The Knee Jerk (Quadriceps Reflex, Patellar Reflex)
There are various ways to test for knee jerk. With the patient seated in a chair the
knees are kept in partial extension and the heels on the floor, or the legs may be dangling.
If the patient is supine in bed, the examiner partially flexes the knee by placing one hand
beneath it, resting on opposite knee. The tendon is then struck with the hammer. The
contraction of the quadriceps femoris muscle, with resulting extension of the knee is the
knee jerk. The patellar reflex is mediated by the femoral nerve (L2-L4). In hyperreflexia
extension of the knee may be accompanied by adduction of the hip; also response may be
obtained by tapping just above the patella (suprapatellar or epipatellar reflex). Marked
exaggeration of the patellar reflex may be accompanied by patellar clonus. Absence of the
patellar reflex is called Westphal's sign.

The Ankle Jerk (Triceps Surae Reflex, Achilles Reflex)

While the patient is lying in bed, the thigh is held in partial abduction and external
rotation and the knee is in flexion; or the legs are placed in frog-leg position with the knees
apart and the ankles close together; or the leg is placed over the other shin or ankle (“figure
four position,” as the legs form a ‘4’). The examiner slightly dorsiflexes the ankle to about a
right angle by placing his hand under the foot. The jerk is obtained by striking the Achilles
tendon just above its insertion on the calcaneus. The contraction of the the gastrocnemius,
soleus, and plantaris, causes plantar flexion of the foot at the ankle. This reflex is mediated
by the tibial nerve (S1).

Clonus:

145
 It is the state of sustained contraction of a muscle in response to sudden stretch,
seen in hypertonic state.
 Knee clonus: with the patient relaxed and the knee extended, a sharp push is
administered above the patella towards the foot, sustaining the pressure for a few seconds.
 Ankle clonus: support the patient's leg with both the knee and ankle resting in 90°
flexion. Briskly dorsiflex and partially evert the foot and sustain the pressure

SUPERFICIAL REFLEXES
This group of reflexes are polysynaptic and elicited by cutaneous stimulation.
Examination sequence
Plantar response (L4-S2)
Patient lies supine with lower limbs slightly flexed at knee joint, a little apart
and externally rotated. Limb is exposed upto thigh. Any restriction of movement of
toes to be excluded. A blunt object (key) is run along the lateral border of the sole of
the foot right from the heel towards the little toe and then medially towards the
middle metatarsophalangealjoint.. A normal response is flexion of the large toe and
adduction of the other toes.

Abdominal reflexes (T7-T10)

→ The patient should be supine and relaxed with abdomen exposed.
→ To stroke briskly but lightly in a medial direction across the upper and lower
quadrants of the abdomen using a key.
→ The normal response is contraction of the underlying muscle with the umbilicus
moving laterally and up or down depending upon the quadrant tested.

Cremasteric reflex (L1-2)

→ To abduct and externally rotate the patient's thigh.
→ Using the key to stroke the upper medial aspect of the thigh.
→ Normally the testicle on the side stimulated will rise briskly.
Common abnormalities
An abnormal plantar response is dorsiflexion (extension) of the large toe (extensor
plantar response) often accompanied by abduction (‘fanning’) of the other toes (Babinsky
sign). This is an unequivocal sign of upper motor neurone damage. It will usually be
associated with spasticity, clonus and hyperreflexia. Babinski sign may sometimes be found
in deep anesthesia and narcosis; drug and alcohol intoxication; metabolic coma such as
hypoglycemia; deep sleep; postictally; and in other conditions of altered consciousness.
The superficial abdominal reflexes are lost in upper motor lesions but will also be
affected by lower motor neurone damage affecting T8-12. They may be difficult to elicit in
the obese, the elderly or those who have had abdominal surgery. The cremasteric reflex is
used to assist identifying the level of spinal cord lesions, particularly after injury.
146
PRIMITIVE REFLEXES
The primitive reflexes (snout, grasp, palmomental and glabellar tap) have little
localizing value and when present singly are of limited significance, but found in numbers
they suggest diffuse or frontal cerebral damage. These reflexes are present in normal
neonates and young infants, indeed their absence in the 4 months after birth may indicate
pathology, but they disappear as the nervous system matures. People with congenital or
hereditary cerebral lesions and a few healthy individuals retain these reflexes but their
return after early childhood is usually associated with brain damage or degeneration.
Common abnormalities
In adults these reflexes are often present in severe acquired brain damage from
trauma, anoxia, diffuse vascular or malignant disease, encephalopathy and in dementia.
Unilateral grasp and palmomental reflexes are strongly suggestive of contralateral frontal
lobe pathology. The glabellar tap is positive in Parkinson's disease.

Primitive reflexes (Adapted from Douglas, 2005)

Snout Lightly
reflex t Tap the lips. An abnormal response is protrusion of the mouth

Grasp reflex Firmly stroke the palm from the radial side. In an abnormal
response, your finger is gripped by the patient's hand
Palmomental Apply firm pressure to the palm next to the thenar eminence
reflex with a tongue depressor. An abnormal response is puckering of the chin.
Glabellar Stand behind the patient and tap repeatedly between the eyebrows with the
tap tip of your index finger. Normally the blink response stops after 3 to 4 times.

COORDINATION
The ability to perform complex movements smoothly and efficiently depends upon
intact sensory as well as motor function. Tests for coordination clinically intends to assess
cerebellar function.
Anatomy
The cerebellum consists of two hemispheres with a central vermis and lies in the
posterior fossa. It is attached to the brain stem by three pairs of cerebellar peduncles.
Afferent and efferent pathways convey information to and from the cerebral motor cortex,
basal ganglia, thalamus, vestibular and other brain stem nuclei and the spinal cord. In
general, midline structures, e.g. vermis, are key to body equilibrium while each hemisphere
controls coordination on the same (ipsilateral) side.
Examination sequence
Rebound phenomenon
→ The patient is asked to stretch his arms out in front and maintain this position.
→ To push the patient's wrist quickly downward and observe the returning movement.
Finger-nose test
→ The patient is asked to held out his hand straight sideway, make a light fist with
the index finer sticking out. Now he is asked to look straight, close his eyes and

147
touch his nose with the tip of the forefinger. Next he is asked to open his eyes,
perform the same with an additional task to reach out and touch examiner’s finger tip
held just within the patient's arm's reach. The process is repeated a number of times
as quickly as possible.
→ To make the test more sensitive the position of target finger could be changed.
Heel-shin test
→ The patient is asked to lie supine on the examination couch.
→ Patient is to raise one leg and place the heel on the opposite knee and then slide the
heel tip up and down the shin between knee and ankle.
Rapid alternating movements(Dysdiadokokinesis)
→ To demonstrate the act of repeatedly patting the palm of one hand with the palm and
back of examiner’s opposite hand as quickly and regularly as possible.
→ Patient is asked to copy these actions.
→ To repeat with the opposite hand.
Common abnormalities
In cerebellar disorders the displaced outstretched arm may fly up past the original
position (the rebound phenomenon); the normal response is to return to the original
position.
The finger-nose test may reveal a tendency to fall short or overshoot the examiner's
finger (past-pointing). This is dysmetria. In more severe cases there may be a tremor of the
finger as it approaches the target finger and the patient's own nose (intention tremor). The
movement may be slow and generally disjointed and clumsy (dyssynergia).
The heel-shin test is the equivalent test for the lower limbs. An abnormal finding is if
the heel wavers away from the line of the shin.
Impairment of rapid alternating movements is dysdiadochokinesis which is evident
as slowness, disorganization and irregularity of movement. Dysdiadochokinesis is typical of
cerebellar disorders and is also seen in Parkinson's disease.
In disorders which predominantly affect midline cerebellar structures, e.g. tumours of
the vermis and alcoholic cerebellar damage, the finger-nose, heel-shin and tests of
dysdiadochokinesis may be normal. Difficulty in stance and gait, as truncal ataxia may be
the only abnormal finding.
Cerebellar dysfunction occurs in many conditions, and differential diagnosis varies
with age. The most common causes of acute signs are drugs, e.g. phenytoin and alcohol,
vascular lesions, trauma and demyelination (multiple sclerosis). Alcohol also causes a
chronic cerebellar syndrome.

APRAXIA

Dyspraxia or apraxia is difficulty or inablility to perform a motor action despite the

patient’s understanding the task and in the absence of motor weakness, cerebellar,
extrapyramidal or sensory impairment. If, after formal motor and sensory examinations are
normal, you suspect that the patient has difficulty formulating and executing skilled
movements, perform the following tests:
Examination sequence
 Ask the patient to perform an imaginary act. Eg. Drinking a cup of tea,
combing the hair, folding a letter and placing it in an envelope.
 Ask the patient to draw a geometrical figure and to write a sentence.
 Ask the patient to put on a pyjama top or dressing gown, one sleeve of which
has been pulled out.

148
 Common Abnormalities

 Ideational apraxia: The patient may explain the nature of the task but can’t
initiate it. Associated with frontal or parietal lesions.
 Ideomotor apraxia: The patient may perform it in an odd or bizarre fashion.
Also associated with frontal or parietal lesions.
 Constructional apraxia: Difficulty in drawing a figure. Associated with
parietal lesion.
 Dressing apraxia: Associated with spatial disorientation and neglect due to
non dominant hemisphere parietal lesions.

STANCE AND GAIT

Stance and gait depend upon vision, proprioceptive, corticospinal, extrapyramidal
and cerebellar pathways together with lower motor neurones and spinal reflexes. Station is
the way a patient stands, gait the way he walks. Standing may be considered a postural
reflex that is dependent on reflexes mediated through the brainstem and influenced to a
major degree by tonic neck and labyrinthine reflexes.
Examination sequence
Stance
• Ask the patient to stand up straight with feet close together and eyes open
(preferably with bare feet).
• Swaying or lurching with the eyes open suggests a cerebellar defect (cerebellar
ataxia).
• Ask the patient to close his eyes. Make sure he does not fall. Swaying, lurching or
loss of balance indicates sensory ataxia (proprioceptive deficit).
Gait
• Ask the patient to walk a measured 10 metres, with walking aid if needed, then turn
through 180° and return.
• Record the time taken to complete the first 10 metres and note the length and width
of steps and any tendency to veer, sway or stumble to one side.
• Ask the patient to walk heel to toe in a straight line (tandem gait). This emphasizes
any gait instability (gait ataxia).

ABNORMALITIES OF STATION
The healthy individual stands erect with head up, chest out, and abdomen in. Any
skeletal changes should be noted. If the patient is unable to stand alone, or unable to stand
at all, document how much support and assistance is required and describe the posture
(e.g., stands with a walker, chair bound, bed bound). The patient with a hemiparesis may
stand with the upper extremity flexed and pronated and the lower extremity extended.
Patients with Parkinson's disease stand in a flexed posture, stooped over with head and
shoulders bent forward and arms and knees flexed. Pelvic girdle weakness may cause
pronounced lordosis, especially in muscular dystrophy. Patients with depression may
appear stooped; in manic states an erect, domineering, aggressive posture may be present.

149
Hyperkinesias, such as athetoid and choreic movements may become evident during the
evaluation of station.
The Romberg sign is a difference between standing balance with eyes open and
closed. In order to test this function, the patient must have a stable stance eyes open and
then demonstrate a decrease in balance with eyes closed, when visual input is eliminated
and the patient must rely on proprioception to maintain balance. A patient with an acute
unilateral vestibulopathy may fall toward the side of the lesion when standing with eyes
closed.
ABNORMALITIES OF GAIT
Under normal circumstances the medial malleoli pass within about 2 in of each other
during walk. This width is decompensated first in problems with balance. Asymmetry of toe
lift may be the earliest evidence of foot drop. A shortened stride length may be early
evidence of bifrontal or extrapyramidal disease. Excessive movement of the hips may occur
with any process causing proximal muscle weakness. A decreased swing on one side is
sometimes an early indicator of hemiparesis or hemiparkinsonism. Tandem walking
stresses the gait and balance mechanisms even further. While walking briskly ask the
patient to stop abruptly on command, or make quick turns, first in one direction and then in
the other. Making the patient walk on heels and toes may bring out weakness of
dorsiflexion or plantar flexion. A useful screening test is to have the patient hop on either
foot. Individuals who can hop on either foot are unlikely to have significant neurological
disease. Note whether the patient has any obvious orthopedic limitations.
Common abnormalities
• Instability which only occurs, or is markedly worse, on eye closure is indicative of
proprioceptive sensory loss, referred to as sensory ataxia (or Rombergism).
• Steppage (Equine) Gait: Patients with foot drop may do this in order to help the foot
clear the floor and avoid tripping. Patients with sensory ataxia, classically tabes dorsalis,
may also lift the feet up high and then slap them down smartly to improve proprioceptive
feedback.
• A hemiplegic gait, due to a unilateral upper motor neuron lesion, is characterized by
the leg being extended at the knee and ankle and circumduction at the hip.
• Bilateral upper motor neuron damage leads to adduction at both hips and a scissors-
like stance and gait.
• Cerebellar dysfunction leads to a broad-based, unsteady (ataxic) gait which usually
makes tandem walking impossible. In disease localized to one cerebellar hemisphere or in
unilateral vestibular disease, there is persistent swaying or deviation toward the abnormal
side. As the patient attempts to walk a straight line or to walk tandem he deviates toward
the side of the lesion. When attempting to walk a fixed circle around a chair, clockwise then
counterclockwise, the patient will tend to fall toward the chair if it is on the side of the lesion,
or to spiral out away from the chair if on the opposite side.
• In Parkinson's disease initiation of walking may be delayed, the steps short and
shuffling and there is loss of arm swing. The turning is slow and ‘en block’. The stooped
posture and impairment of postural reflexes can result in a rapid short-stepped hurrying
(festinant) gait.
• Proximal weakness associated with muscle diseases may lead to a waddling
(myopathic) gait. Trendelenburg's sign is an abnormal drop of the pelvis on the side of the
swing leg due to hip abductor weakness. When the weakness is bilateral, there is an
exaggerated pelvic swing that results in a waddling gait.
• The marche à petits pas (walk of little steps) gait resembles that of parkinsonism, but
lacks the rigidity and bradykinesia. Locomotion is slow, and the patient walks with very
short, shuffling, and somewhat irregular footsteps. The length of the step may be less than

150
the length of the foot. Seen in normal elderly persons, also in patients who have diffuse
cerebral hemispheric dysfunction, particularly involving the frontal lobes.
• Bizarre gaits with no other neurological signs may be psychogenic. Care should be
taken, however, as conditions such as Huntington's disease can be associated with a
strange walking pattern. The gait abnormality in dissociative disorders (astasia-abasia) is
nonconformist and bizarre, and may take any number of forms that do not conform to a
specific organic disease pattern. The gait is irregular and variable, with a great deal of
superfluous movement and often marked swaying from side to side. The patient may
appear to be in great danger of falling, but rarely does so, often demonstrating superb
balance during the contortions. If patient does fall, it is in an exaggerated manner without
injury.
• A cautious gait is seen in older patients who have no neurological disease but are
uncertain of their balance and postural reflexes. The gait takes on the characteristics seen
when a healthy person walks on an icy surface: velocity slows, steps shorten, and the base
widens.

EXAMINATION OF SENSORY SYSTEM

Sensory symptoms include pain, spontaneous abnormal sensations usually of

'tingling' or 'pins and needles' (paraesthesia), and loss of sensation or numbness.
Anatomy
Conscious proprioception (joint position sense) and vibration are conveyed
in large, fast-conducting fibres in the posterior (dorsal) columns. Pain and temperature
sensation are carried by small, slow-conducting fibres of the spinothalamic tract. The
posterior column remains ipsilateral from the point of entry up to the medulla but most pain
and temperature fibres cross within one or two segments of entry to the contralateral
spinothalamic tract. All sensory fibres relay in the thalamus before sending information to
the sensory cortex in the parietal lobe.
Sensory Modalities

151
 In addition to the modalities conveyed in the principal ascending pathways (touch,
pain, temperature, vibration and joint position sense) sensory examination includes tests of
discriminative aspects of sensation which may be impaired by lesions of the sensory cortex.
Clear explanation of precisely what is required is vital and avoid repetition of testing. In
general it is better to ask patients to avert their gaze or close their eyes. When mapping out
an area of altered sensation it is best to move from reduced to higher sensibility (i.e. from
hypoaesthesia to normal or normal to hyperaesthesia).
Examination sequence
Light touch
→ To touch using a wisp of cotton wool and ask the patient to respond to each touch.
→ To time the stimuli irregularly and make a dabbing rather than a stroking or tickling
stimulus.
→ To examine different dermatomes and then compare each side for symmetry.
Superficial pain
→ Use a fresh neurological pin.
→ To explain and demonstrate that the ability to feel a sharp pinprick is being tested.
→ To follow the testing points in different regions, comparing for symmetry.
→ To map out the boundaries of any area of reduced, absent or increased sensation.
Deep pain
→ To explain the test and ask the patient to report as soon as he feels discomfort.
→ To squeeze the muscle bellies, e.g. calf, biceps, or apply pressure to finger or toe nail
beds. Not to apply pressure with an instrument, e.g. pen.
Temperature
→ To touch the patient with a cold metallic object, e.g. tuning fork, and ask if it feels cold.
More sensitive assessment requires tubes of hot and cold water at controlled temperatures
but this is seldom performed.
Vibration
→ To place a vibrating 128 Hz tuning fork over the sternum/clavicle. Ask the patient
'Do you feel it buzzing?' Once being sure that he feels it he is explained that
examiner is going to place it over different parts of his body and that he is supposed
to close the eyes recognize the sensation, as well as, to report when examiner stops
the fork vibrating with his fingers.
→ Now the vibrating fork is placed on the tip of the big toe. If sensation is impaired, to place
it on the interphalangeal joint and progress proximally - the medial malleolus, tibial
tuberosity and anterior iliac spine depending upon the response.
→ To repeat the process in the upper limb. Starting at the distal interphalangeal joint of the
forefinger and if sensation is impaired to proceed proximally - radial styloid, olecranon,
acromion.
Joint position sense
→ With the patient's eyes open to demonstrate the procedure. The distal phalanx of the
patient's large toe is held at the sides to avoid giving information from pressure (or middle
finger) and moved up and down.
→ The patient is asked to respond with 'up' or 'down' as the examiner makes these
movements without the patient assisting or resisting. Then the patient is asked to close the
eyes and identify the directions in a random sequence of small movements (e.g. up, down,
down, up).
→ To test both large toes (or middle fingers). If impaired, to move to more proximal joints in
each limb.
Two-point discrimination
→ An instrument like a pair of blunt-tipped school compass is used for the purpose.

152
→ The patient is asked to look away or close the eyes.
→ To apply either one or two points to the pulp of the patient's forefinger and ask whether
one or two stimuli were felt.
→ Then the distance between the two points is adjusted to determine the minimum
separation at which they are felt separately.
Test both fingers and thumbs.
Point localization
→ With the patient's eyes closed, lightly touch various body parts, e.g. hand, finger,
shoulder, and to ask which part has been touched and whether on the right or left side.
→ To repeat touching individual fingers asking the patient to identify which is touched.
Inability to do so is finger agnosia.
Stereognosis and graphaesthesia
→The patient is asked to close his eyes.
→ To place familiar small objects (e.g. coin, key, matchstick) in the patient's hand and ask
the patient to identify what they are after feeling them (stereognosis).
→ To use the blunt end of a pencil or orange stick and trace letters or digits on the patient's
palm. Ask the patient to identify the figure (graphaesthesia).
Sensory inattention
→ The patient is asked to close eyes. To touch the back of each of the patient's hands in
turn and ask which has been touched.
→ Then to touch both hands simultaneously and ask whether the left, right or both sides
were touched.
Common abnormalities
Abnormalities on sensory testing are best considered according to whether the
lesion(s) is in the peripheral nerve(s), dorsal root(s), spinal cord or intracranial
Peripheral nerve and dorsal root.
A large number of pathological processes affect peripheral nerves, generally
resulting in peripheral neuropathies or polyneuropathies. Peripheral neuropathies tend to
affect the lower limbs first and more prominently. In many case touch and pinprick
sensation are lost in a 'stocking and glove' distribution.
In some large fibre peripheral neuropathies, vibration and joint position sense are
disproportionately affected. When such patients are asked to close their eyes and hold their
hands outstretched, their fingers will make involuntary slow wandering movements
(pseudoathetosis).
Injuries and other damage to individual nerves lead to loss of all modalities in that
nerve's territory. Sensory root damage leads to dermatomal sensory loss.
Spinal cord
Traumatic and compressive lesions of the spinal cord cause loss or impairment of
sensation in a dermatomal distribution below the level of the lesion. A zone of
hyperaesthesia may be found immediately above the level of sensory loss.
Anterior spinal artery syndrome usually results in loss of spinothalamic sensation
and motor function, with sparing of dorsal column sensation. A similar pattern of pain and
temperature loss and sparing of dorsal column sensation (dissociated loss) occurs in
syringomyelia.
When one half of the spinal cord is damaged the Brown-Séquard syndrome may
occur. This is characterized by ipsilateral motor weakness and loss of vibration and joint
position sense with contralateral loss of pain and temperature.
Intracranial
Brain stem lesions are often vascular in origin and determining the site of the lesion
relies on understanding the relevant anatomy. Alternating analgesia is a term for the loss of

153
 pain and temperature sensation on one side of the face (V nerve nucleus damage) and the
opposite side of the body (spinothalamic tract damage) and occurs in lower brain stem
lesions.
Thalamic lesions may cause a patchy sensory impairment on the opposite side with
a very unpleasant, poorly localized pain often of a burning quality.
Cortical lesions in the parietal lobe lead to impairment of some of the principal
presenting pathway sensations, particularly joint position sense, but are more likely to result
in the abnormalities described above.

REFERENCES

Campbell, W. (2005) DeJong’s The Neurological Examination, 6th Ed. Philadelphia, Lippincott
Williams & Wilkins.
Douglas, G., Nicol, F. &Robertson, C. (2005) Macleod's Clinical Examination, 11th Ed.
Edinburgh, Elsevier Churchill Livingstone.
Siddiqui, M.A. & Nizamie, S.H. (2009) Exaxmination Of Motor System, Sensory System And
Motor-Sensory Links. Seminar: Central Institute of Psychiatry.
Spillane, J.A. (1996) Bickerstaff's Neurological Examination in Clinical Practice, 6th Ed. Oxford,
Blackwell Sciences Ltd.
Swash, M. & Glynn, M. (2007) Hutchison's Clinical Methods- An Integrated Approach to
Clinical Practice, 22nd Ed. Edinburgh, Saunders Elsevier.

APPENDIX

Tests to differentiate with functional disorder

Nonorganic Motor Loss (Hoover sign)
It is a useful test for evaluating suspected nonorganic leg weakness. When a patient
lying supine flexes the hip to lift one leg, there is a downward movement of the other leg.
The extension counter-movement of the opposite leg is a normal associated movement.
The same thing also occurs in walking. As the person tries to lift the paretic limb, the
normal limb presses downward and can be felt if the examiner if hands are placed beneath
the heels. In nonorganic leg weakness, there is no downward pressure of the heel of
normal power side. Similarly in normal persons and those with organic hemiparesis, if the
patient presses down on the bed with the good leg the opposite leg may flex slightly; this
movement does not occur in nonorganic weakness. Hoover's sign is absence of the
expected associated movements in the good limb on trying to move the paretic limb.
Nonorganic Sensory Loss
Nonorganic sensory abnormalities do not follow any sort of anatomical distribution.
They are usually areas of decreased sensibility. Also areas of hypesthesia, anesthesia,
hypalgesia, and analgesia are commonly encountered that may be complete or partial,
affect all modalities or be dissociated. The demarcation between normal and abnormal
often occurs at some visible body structure/point that has no neurologic significance, such
as a joint or skin crease, causing a finding such as numbness circumferentially below the
elbow, wrist, shoulder, ankle, or knee. The deficits are not consistent on repeated testing,
use of alternate methods. In spite of complete loss of cutaneous sensibility, the patient may
have intact stereognosis and graphesthesia, or in spite of complete loss of position sense
may be able to perform skilled movements and fine acts without difficulty, and have no
Romberg's sign. It is often possible to confuse the patient and confirm the absence of

154
organic changes by checking sensation while the hands are in some bewildering position
where it is difficult to tell which side is which, such as crossed behind the back or with
fingers entwined with one another. The patient responds as digits are stimulated randomly.
The patient with nonorganic hemianalgesia may make errors, while the one with organic
loss will not.
Signs of Meningeal Irritation
Meningeal signs are elicited most frequently when the meninges are inflamed—from
infection (e.g., bacterial meningitis) or from the presence of a foreign material (e.g., blood in
the subarachnoid space). Meningismus refers to the presence of nuchal rigidity and other
clinical signs of meningeal inflammation. It may be accompanied by headache, pain and
stiffness of the neck; irritability; photophobia; nausea and vomiting; and other
manifestations of infection, such as fever and chills.
Nuchal (cervical) Rigidity
Nuchal rigidity is characterized by varying degrees of stiffness and spasm of the
neck muscles, with pain on attempted voluntary movement as well as resistance to passive
movement ranging from slight resistance to marked spasm. Nuchal rigidity primarily affects
the extensor muscles, and the most prominent early finding in meningeal irritation is
resistance to passive neck flexion. It is not possible to place the patient's chin on his chest,
but the neck can be hyperextended without difficulty; and rotatory and lateral movements
may also be preserved. Opisthotonos may also result. In terminal disease, coma and in
infants neck rigidity mat be absent.
Kernig's Sign
Kernig is the involuntary flexion at the knee when the hip is flexed passively with the
knee extended. Another method is to flex the hip and knee to right angles, and then attempt
to passively extend the knee which is not possible beyond 135 degrees as it movement
produces pain and resistance. This is present bilaterally.
Brudzinski's Neck Sign
Placing one hand under the patient's head and flexing the neck while holding down
the chest with the other hand causes flexion of the hips and knees bilaterally. The leg may
fail to flex on one side when meningeal irritation and hemiplegia coexist.
Other Signs
Chvostek's Sign
Tapping over the facial nerve causes spasm or a tetanic, cramplike contraction of
some or all of the facial muscles.
Trousseau's Sign
Ischemia of the peripheral nerve trunks increases nerve excitability and causes
spontaneous discharges. Compression of the arm by manual pressure, a tourniquet, or a
sphygmomanometer cuff is followed first by distal paresthesias that progress centripetally,
then twitching of the fingers, and finally by cramping and contraction of the muscles of the
fingers and hand with the thumb strongly adducted and the fingers stiffened, slightly flexed
at the metacarpophalangeal joints, and forming a cone clustered about the thumb
(obstetrician's hand).
Alternate Methods for Eliciting the Toe Dorsiflexion in Lesions of the Corticospinal
Tract. (Adapted from Campbell, 2005)
Chaddock sign Stimulating the lateral aspect of the foot, not the sole,
beginning about under the lateral malleolus near the junction
of the dorsal and plantar skin, drawing the stimulus from the
heel forward to the small toe.
“Reverse The stimulus moves from the small toe toward the heel
Chaddock”

155
 Oppenheim Dragging the knuckles heavily down the anteromedial
sign surface of the tibia from the infrapatellar region to the ankle
Gordon's sign Squeezing of calf muscles
Schaefer sign Deep pressure on Achilles tendon
Bing sign Pricking dorsum of foot with a pin
Moniz sign Forceful passive plantar flexion at ankle
Throckmorton's Percussing over dorsal aspect of metatarsophalangeal joint
sign of great toe just medial to EHL tendon
Strumpell Forceful pressure over anterior tibial region
phenomenon
Cornell Scratching dorsum of foot along inner side of EHL tendon
response
Gonda (Allen) Forceful downward stretching or snapping of either second,
third, or fourth toe; if response is difficult to obtain, flex toe
slowly, press on nail, twist the toe and hold it for a few
seconds
Stransky Small toe forcibly abducted, then released
Allen and Sharp upward flick of second toe or pressure applied to ball
Cleckley of toe
Szapiro Pressure against dorsum of second through fifth toes,
causing firm passive plantar flexion, while stimulating plantar
surface of foot

Detection of Subtle lesions

Drift of Outstreched Hand
The patient is asked to hold the arms outstretched in front, with wrists supine and
eyes closed. The deviation can be induced by having the patient raise and lower the arms
several times, or by tapping the patient's outstretched wrists. In pronator drift (Barré's sign)
due to a pyramidal lesion, the arm sinks downward along with pronation of the forearm. In
parietal drift, the arm usually rises and strays outward (updrift). With cerebellar drift the arm
drifts outward movement is more prominent, either at the same level, rising or less often
sinking toward the side of the lesion.

156
CHAPTER-VIII
Examination of Autonomic Nervous System

INTRODUCTION
The human internal environment is regulated in large part by integrated activity of the
Autonomic Nervous System (ANS) and endocrine glands. The ANS is organized on basis of
reflex arc. There are numerous medical diseases that implicate this system in some ways
like Hypertension, Asthma, and Ventricular Tachycardia etc. Many neurological diseases
involve the ANS to varying intent, giving rise to symptoms such as Syncope, Sphincteric
Dysfunction, Papillary Abnormalities, Diaphoresis and Disorders of Thermoregulation.

ANATOMIC ORGANIZATION OF AUTONOMIC OUTFLOW

ANS is divided into three parts - 1. Sympathetic Nervous System

2. Parasympathetic Nervous System
3. Enteric System
The peripheral motor portions of ANS are made up of preganglionic and postganglionic
neurons. The cell bodies of preganglionic neurons are located in the visceral efferent
intermediolateral grey column of Spinal cord or the homologous motor nuclei of the cranial
nerves and their axons synapse on the cell bodies of postganglionic neurons that are
located outside the CNS. The axons of the postganglionic neurons end on the visceral
effector sites.

SYMPATHETIC NERVOUS SYSTEM

The preganglionic neurons of sympathetic division originate in the intermediolateral cell
column of Spinal cord grey matter from 8th cervical to 2nd lumbar segment. Axons of nerve
fibers originating in intermediolateral column are myelinated and form white communicating
rami. Then preganglionic fibers synapse with the cell bodies of postganglionic neurons
which are collected into 2 large ganglionated chains, one on each side of the vertebral
column. There are 3 Cervical (Superior, Middle & Inferior), 11 Thoracic and 4-6 Lumbar
Sympathetic ganglia. Axons of sympathetic ganglion cells are unmyelinated. Most of the
postganglionic fibers pass via grey communicating rami to spinal nerves T5 to L2.

PARASYMPATHETIC NERVOUS SYSTEM

There are two division of Parasympathetic Nervous System- Cranial and Sacral.

The cranial division originates in the visceral nuclei of midbrain, pons and medulla which
lie in close proximity to the somatic afferent nuclei and which include Edinger Westphal
(EW) nucleus, superior and inferior salivatory nucleus, and dorsal motor nucleus of vagus.
Axons of visceral nuclei course through the occulomotor, facial, glossopharyngeal and
vagus nerves.
Preganglionic fibers from EW nucleus runs in occulomotor nerve and synapse in ciliary
ganglion. Preganglionic fibers from superior salivatory nucleus enters facial nerve and form
greater petrosal nerve near geniculate ganglion. Preganglionic fibers from inferior salivatory
nucleus enters glossopharyngeal nerve reach the otic ganglion. Preganglionic fibres from
dorsal motor nucleus of vagus enters vagus nerve and terminate in ganglia situated in walls
of many thoracic and abdominal viscera.

157
Sacral division-originate in lateral lancets of 2nd, 3rd, & 4th sacral segment. Axons of these
sacral neurons which constitute the preganglionic fibers traverse the sacral nerve and
synapse in ganglia that lie within the walls of distal colon, bladder and other pelvic organs.

CLINICAL ASSESSMENT OF THE AUTONOMIC NERVOUS SYSTEM

The History taking regarding ANS

Questions to be asked to patients about Autonomic dysfunction:

 Cardiovascular - Light headedness, dizziness, palpitations
 Pupils - Blurred vision or drooping of eyelids
 Sweating - Skin temperature regulation, Excessive or diminished
 Sexual dysfunction - Difficulty initiating or maintaining an erection,
ejaculation difficulties
 Gastrointestinal - Dysphasia, abdominal pain, diarrhea, constipation,
Fecal incontinence
 Urinary function - Frequency, urgency, incontinence, recurrent urinary
tract infection

158
  In addition to general medical history and neurological histories, an evaluation of
orthostatic symptoms and vasomotor, sudomotor, pupillomotor function should be
done.
 Symptoms of orthostatic hypotension may be manifested as syncopal or near-
syncopal episodes, palpitations, tremulousness, weakness, confusion or slurred
speech which worsen on standing.
 Vasomotor symptoms may initially be manifested as a feeling of coldness. Later
there are color and trophic changes of the skin.
 Sudomotor function is tested by asking patient if they sweat on hot humid summer
weather. The presence of heat intolerance is assessed.
 Secretomotor function should also be determined by asking patients about dry eyes
and dry mouth.
 Symptoms of pupillomotor disturbance should be determined by asking patients
about blurring of vision or a glare in bright sunlight. These symptoms are usually
related to difficulties with accommodation.

INSPECTION

 The Skin and Mucous Membranes. Evidence of autonomic dysfunction may be

seen in the skin and mucous membranes. If a change in color, such as pallor,
erythema, flushing, or cyanosis, is present, the examiner should determine whether it
is localized, limited to the extremities, or generalized. Variations in the texture,
consistency, and appearance of the skin include glossiness, hardness, thickening,
wasting, scaling, seborrhea, looseness or tightness, oiliness and moistness or
dryness. Urticaria, generalized or localized edema, myxedema, dermatographia,
vesicles, bullae, and perforating ulcers should be noted.
 Perspiration. Excessive perspiration or decreased perspiration, anhidrosis, and
localized change in sweating may be seen.
 The Hair and Nails. Hypertrichosis, hypotrichosis, abnormal distribution of hair,
localized alopecia, abnormal brittleness, color change, and either localized or
premature graying of the hair may be noted. Important abnormalities of the nails
include brittleness, striations, fissuring, and cyanosis.
 The Extremities. The color and temperature of the extremities as a whole, the
character and pulsation of the arteries, and the effect of changes in position should
be evaluated. By these criteria conditions such as erythromelalgia, acrocyanosis,
Raynauds syndrome, and Buerger's disease may be diagnosed.
 Salivation and Lacrimation. The secretory responses of the salivary and lacrimal
glands to physical and sensory stimulation may provide information about autonomic
nervous system dysfunction.
 Endocrine system. Evidence of endocrine imbalance may be related to diseases of
autonomic nervous system such as dwarfism, gigantism, acromegaly, and cretinism
and other dysfunctions of pituitary, adrenal, thyroid and sex glands.
 Regulation of vital processes. The blood pressure should be noted in each arm
with patient recumbent, seated and standing. The rate and regularity of pulse and
respiratory rate and rhythm should be noted.
 Fat Metabolism. Obesity, wasting, lipodystrophy, and adiposis dolorosa are seen in
autonomic dysfunction. The localization of wasting and the bodily distribution of the
adipose tissue should be noted.

159
AUTONOMIC NERVOUS SYSTEM REFLEXES

CARDIO VASCULAR REFLEXES

The simpler physiological tests are based upon the responses of the heart rate and blood
pressure to various stimuli. Sympathetic and parasympathetic function is involved.

Postural hypotension
Assessment of orthostatic changes in blood pressure (BP) and heart rate (HR) are
basic tests of cardio vascular autonomic function.

 At the bedside, BP and pulse are taken with the patient supine and after
standing for periods of 1, 3, and 5 minutes.
 Normally, systolic blood pressure (SBP) on standing does not decrease by more
than 20 mm Hg, and the diastolic blood pressure (DBP) by not more than 10 mm
Hg.
 When BP measurement is done with a standard sphygmomanometer, the cuff
should be kept at heart level to minimize hydrostatic influence on the measurement.
 When routine measurements are unrevealing, orthostatic blood pressure declines
can sometimes be detected by having the patient perform 5 to 10 squats and then
repeating the measurement.

Blood pressure response to pressure stimuli

Mental arithmetic, sustained handgrip or exposure to cold cause a rise in BP. Less than 10
mm Hg rise in diastolic pressure is abnormal. Both central and peripheral (sympathetic)
lesions affect these tests.

Heart rate responses

 The HR should not increase by more than 30 beats per minute above baseline on
standing. This can be quantified by using continuous ECG recording:
 Note the pulse rate from the R-R interval at the 15th and 30th beats after standing.
The 30th: 15th pulse ratio is > 1.03 in normal subjects, and ≤1.0 when there is
autonomic disturbance.
 In hypovolemia, the most common cause of orthostasis, a reflex tachycardia
develops in response to the fall in standing blood pressure. When autonomic
cardiovascular reflexes are impaired, the reflex tachycardia may not occur.
 Patients with the postural tachycardia syndrome will develop a brisk tachycardia
without orthostatic hypotension (increased pulse rate more than 30 beats per minute
above baseline or more than 120 beats per minute)
 Massage of the carotid sinus stimulates the baroreceptors and vagal
parasympathetic activity then slows the heart rate. Afferent or efferent lesions
abolish this response. Care should be taken in this test; severe bradycardia and
hypotension can result in hypersensitive persons.

Deep breath test

Lay the patient flat. When the pulse has steadied, record the pulse rate during six slow
maximal deep breaths. In normal subjects the pulse rate should fall by >15 beats/min; with
autonomic disturbances the pulse rate slows <10 beats/min.

The Valsalva manoeuvre

160
Here there is a change in both blood pressure and heart rate. In the first exhalation
(against a closed glottis), the blood pressure drops and the heart rate increases. On
releasing (by 'opening the glottis), the blood pressure 'overshoots' the resting value and
the heart slows. The test can be performed by the patient exhaling into a mouthpiece
connected to a manometer or sphygmomanometer to hold the pressure at 40 mmHg for 15
seconds. An ECG records the heart rate response. The ratio of the highest pulse rate in the
preliminary rest period to the lowest pulse rate during the test is >1.5 in normal subjects
and <1.1 in patients with autonomic disturbances. The test may be repeated up to three
times if the initial result is equivocal. Afferent or efferent parasympathetic lesions impair the
response. (Patients with lesions at the foramen magnum such as Cerebellar ectopia
develop a characteristic headache).

SKIN RESPONSES
Erythema
Scratching the skin will produce a line surrounded by a spreading flare and followed by a
wheal with central pallor. This is often exaggerated below the level of a transverse cord
lesion, and, according to the lesion, may be unilateral or bilateral, often becoming
apparent after testing cutaneous sensation to pin prick. At the level of the lesion, even
the normal response may be absent. Exaggerated responses unfortunately can occur in
normal or psychoneurotic individuals. This 'dermatographia' is, however, not simply
limited to the skin below a segmental level.

Temperature
The measurement of skin temperature by means of accurate skin thermometers can
show:

1) Increased temperature below a recently denervated level;

2) Decreased temperature following chronic neurological lesions which have caused
prolonged immobility;
3) Increased response to warming of the part or of distant parts over the denervated
area in sympathetic lesions; but .
4) Decreased response to warming in areas where the deficit is circulatory rather than
neurogenic.

When lesions of the sympathetic division develop there is temporary vasodilation and
a rise in skin temperature, followed by vasoconstriction and a fan in temperature in
those areas supplied by the nerves of fibers involved. With vascular disease of the
extremities whether the result of vasospasm or of organic obstruction the skin
temperature is lower than in the corresponding normal extremities.

The Pilomotor Response ,

Piloerection may be provoked by gentle stroking of the skin, tickling, scratching with a
sharp object, or the application of cold. Ice, cotton soaked in alcohol or ether, or a
methyl chloride spray may be used. Piloerection is elicited best at the nape of the
neck, in the axillas, on the abdominal wall, and at the upper border of the trapezius.
The patient should be in a warm room, since cold influences the response. It may be
helpful to warm the body before the application of a cold stimulus. Emotional stimuli
may also provoke piloerection.

The reaction appears slowly, after a latent period of 4 - 5 see; it is complete or at its

161
maximum in 7-10 sec and lasts 15-20 sec. It first occurs at the site of stimulation and
then spreads slowly and widely. If one side of the body is stimulated, the response is
ipsilateral, but if the midline is stimulated, it is bilateral. Piloerection is absent in
lesions that involve the descending autonomic pathways in the brain stem and spinal
cord, sympathetic trunk, preganglionic and postganglionic fibers, and peripheral
nerves. It is abolished below transverse spinal lesions.

Sweating test

Various methods of color determination of sweating include the following:

A. The areas to be tested are first thoroughly dried, and then liberally dusted with
Quinizarin powder. The patient is placed under a heat cradle, and given a hot
drink combined with 0.5 g acetyl salycilic acid. Areas of sweat production are
clearly outlined as the powder turns black when exposed to moisture.
B. The skin is painted with a solution of ferric chloride and then dusted with tannic
acid powder, which turns black in the presence of iron and moisture.
C. A saturated alcoholic solution of cobalt chloride, which turns pink when moist, is
painted on the skin, or cobalt blue papers are applied to it. .
D. Absorbent paper impregnated with silver nitrate and potassium chromate is
applied to the skin; the chloride in the sweat reacts with the silver nitrate to
form silver chloride.
E. Iodine in oil is painted on the skin and the painted areas are dusted with starch
powder, which turns bluish black in the presence of iodine and moisture.
In sympathetic lesions there will be a segmental loss of sweating corresponding to the
distribution of the affected sympathetic fibers. Below a transverse cord lesion,
sweating may be absent in the early stages, but may later become abnormally
profuse. At the segmental level of a recent transverse lesion the response is often
exaggerated.

This is a good test for the results of sympathectomy, of section or injury to peripheral
nerves, and for demonstrating and photographing denervated areas. It can show,
objectively, areas of sympathetic denervation in syringomyelia.

Tests for sudomotor and thermoregulatory functions include the QSART (Quantitative
Sudomotor Axon Reflex Test), thermoregulatory sweat test (TST) and sympathetic
skin response (SSR) test. QSART is a more quantitative and reproducible
examination, developed by Low and assess the postganglionic sudomotor fibers by
measuring the sweat output in response to iontophoresis into the skin of 10% solution
of acetylcholine using 2mA for 5 minutes. The TST assesses both the central and
peripheral sympathetic components by analyzing the sweating response to a rise in
body temperature. The SSR measures the resistance of skin to the passage of a
weak current through skin and assesses peripheral sympathetic function.

Thermography

Infrared photography of part or whole body surfaces will give detailed areas of
temperature difference undetectable clinically, and again objectively is useful for
localization and comparison. Again, great experience in interpretation is required and
artefacts may abound.
PUPILLARY RESPONSE
Loss of function of the sympathetic innervations of the pupil leads to a Horner syndrome,
which consists of anhidrosis on the ipsilateral side of the face, ptosis, a small pupil, and

162
enophthalmos. Patients usually do not notice anhidrosis and generally cannot provide
information about it. The degree of ptosis present usually is not sufficient to obstruct the
pupil, and so patients notice it only as a cosmetic problem. Ask patients with asymmetric
pupils about their use of eyedrops, as people often omit mentioning these medications in
the history. Patients with congenital Horner syndrome may have an iris that has never
become pigmented because of lack of sympathetic innervation.

The finding of a Horner syndrome indicates a lesion of the sympathetic nervous system
that can occur within or outside the central nervous system. Sympathetic involvement in
the cavernous sinus or a retro-orbital location can be detected by means of the
accompanying cranial nerve symptoms and signs. Homer syndrome frequently
accompanies retro-orbital headache, particularly cluster headache.
The parasympathetic fibers innervating the pupil arise in the Edinger Westphal nucleus in
the midbrain and project ipsilaterally to the orbit via the third nerve.

Patients with parasympathetic dysfunction to the eye have a dilated pupil and may
complain of blurred vision, especially in bright light or during accommodation. If the motor
fibers of the third nerve are also involved, strabismus usually results and the patient
complains of visual blurring or double vision.

LACRIMAL FUNCTION
Tearing can be estimated by Schirmer test. The tears wet the strip of filter paper,
producing a moisture front. After 5 minutes, the moistened area extends for a length of
approximately 15 mm in normal persons. An extent of less than 10 mm is suggestive of
hypolacrimia. Mainly this test is used to detect the dry eyes of sjogren syndrome.

GENITO URINARY FUNCTIONS

Sexual Function
Diffuse autonomic failure, local spinal or root lesions may interfere with sexual function.
The history alone may be of considerable diagnostic value. Sexual dysfunction may be the
earliest manifestation of autonomic insufficiency. There are occasions when potency is
disturbed before bladder function in a male with a developing spinal cord disorder.
Relevant questions include enquiring whether erection is absent or occurs normally or
whether just reflexly (nocturnal tumescence)? If ejaculation is present, is it of normal force
or not? Is orgasmic sensation normal?

Proper psychically induced erection is a function of the parasympathetic hypogastric

nerves. Reflex erection is mediated by the pelvic nerves from sacral roots.
Spinal lesions may cause initial priapism (reflex painful erection).
Subsequently, spinal disorders above T12 may cause impotence with retained reflex
erection but without ejaculation.
A complaint of impotence with retained reflex erection and ejaculation is characteristic of a
psychological disorder.
Use may be made of both the cremasteric and scrotal reflexes in the assessment of
impotence. Rarely performed, but also valuable, is the bulbo cavernosus reflex. Cauda
equina lesions will usually result in failure of both erection and ejaculation with impaired
sensation.
In autonomic neuropathy, especially from diabetes, retrograde ejaculation may precede the
development of impotence. Because the internal vesical sphincter does not close, semen
goes into the bladder rather than externally through the urethra. The patient with retrograde
ejaculation may notice milky appearing urine.

EXAMINATION OF BLADDER FUNCTION

Bladder function involves both the autonomic and the voluntary nervous systems, and
disorders of bladder function may follow lesions of the paracentral lobule, hypothalamus,

163
descending pathways in the spinal cord, pre- or postganglionic parasympathetic nerves, or
pudendal nerve. The detrusor muscle of the bladder is innervated by parasympathetic
neurons located in the S2-S4 intermediolateral column .The internal uretheral sphincter at
the neck of the bladder receives its innervations from the intermediolateral column at the
T12-L1 level, via the sympathetic prevertebral plexus and the hypogastric nerve.
Micturition is a spino-bulbo-spinal reflex. Normal micturition requires intact autonomic and
spinal pathways, and cerebral inhibition and control of the external sphincter must be
normal. Lesions of the superior frontal and anterior cingulated gyri reduce awareness of
bladder function and cause incontinence. More posterior lesions of the frontal lobe may
cause spasticity of the striated muscles sphincters and therefore produce retention.
Incomplete lesions of the upper motor neuron pathways above the sacral spinal cord
interfere with the storage and voiding of urine. A complete transaction of the spinal cord in
the first place causes retention with ‘overflow incontinence’ and then later a ‘reflex bladder’.
In Tabes dorsalis damage to the sympathetic and parasympathetic sensory side of the
reflex arc results in painless bladder enlargement.

The examination should always include testing the sacral segments. Bladder swelling may
be palpable. The superficial anal reflex should be tested. The condition of the motor and
sensory pathway to the lower limbs will testify to any spinal cord, conus medullaris, or
cauda equina lesion.

A useful assessment of detrusor function can be made by asking the patient while passing
urine to breathe deeply, thus interrupting abdominal muscle straining. If the detrusor is not
functioning the flow will cease.

Residual urine can be assessed by a post-micturition X-ray of the bladder as part of an

intravenous pyelogram, without catheterization.

URODYNAMIC STUDIES
'Urodynamics' refers to the investigation and assessment of the bladder and lower urinary
tract. The essential requirement, however, is to measure intravesical pressure during
bladder filling (the 'filling cystometrogram'), and the relationship between intravesical
pressure and urinary flow rate during voiding (the 'micturition cystometrogram').
Sophisticated urological departments will now use a four-channel recording of abdominal
pressure (via rectal catheter), total bladder pressure (via bladder catheter), subtracted true
intravesical (detrusor) pressure and flow rate. The filling volume and voiding volume will be
recorded. A note is made of the patient's awareness of bladder sensation, the capacity
before a strong desire to void is appreciated, the compliance of the bladder (the volume
change for a given pressure), and the contractility of the detrusor (eg. spontaneous
contractions before complete filling). If the bladder is filled with contrast medium, then
video-radiological screening is possible, detecting abnormalities of structure and visualizing
the bladder contraction and sphincter mechanisms. These can then be interpreted
alongside the pressure-flow measurements. The pressure in normal and empty bladder is
about 1 cm of water and if quantities of about 50 ml are introduced at a time the pressure
rises steadily. Vesical sensation is felt at about 100-150 ml when a pressure of about 6 cm
of water is registered. The bladder can usually be distended to 400-600 ml. The rhythmical
contractions which are accompanied by a slight sense of urgency will build up until reflex
micturition occurs accompanied by a sharp rise in pressure.
Neurogenic bladder refers to bladder dysfunction caused by disease of the nervous
system. Symptoms
of bladder dysfunction are often among the earliest manifestations of nervous system
disease. Frequency, urgency, precipitate micturition massive or dribbling incontinence,
difficulty in initiating urination, urinary retention, and loss of bladder sensation may occur.
Classification of neurogenic bladder dysfunction is based on urodynamic criteria and
includes the following types: uninhibited, reflex, autonomous, sensory paralytic, and motor

164
paralytic bladder.

In Uninhibited neurogenic bladder, there is a loss of the cortical inhibition of reflex

voiding, while bladder tone remains normal. Bladder distention causes contraction in
response to the stretch reflex. There is frequency, urgency, and incontinence that are not
associated with dysuria. Hesitancy may precede urgency. Bladder sensation is usually
normal. There is no residual urine.

The reflex neurogenic bladder occurs with severe myelopathy or extensive brain lesions
causing interruption of both the descending autonomic tracts to the bladder and the
ascending sensory pathways above the sacral segments of the cord. The bladder capacity
is small, and micturition is reflex and involuntary. The residual urine volume is variable.

An autonomous neurogenic bladder is one without external innervation. It is caused by

neoplastic, traumatic, inflammatory, and other lesions of the sacral spinal cord, conus
medullaris or cauda equina, S2-S4 motor or sensory roots, or the peripheral nerves, and
with congenital anomalies such as spina bifida. There is destruction of the parasympathetic
supply. Sensation is absent and there is no reflex or voluntary control of the bladder;
contractions occur as the result of stimulation of the intrinsic neural plexuses within the
bladder wall. The amount of residual urine is large, but the bladder capacity is not greatly
increased.

A sensory paralytic bladder is found with lesions that involve the posterior roots or
posterior root ganglia of the sacral nerves, or the posterior columns of the spinal cord.
Sensation is absent, and there is no desire to void. There may be distention, dribbling, and
difficulty both in initiating micturition and in emptying the bladder. There is a large amount of
residual urine.

A motor paralytic bladder develops when the motor nerve supply to the bladder is
interrupted. The bladder distends and decompensate, but sensation is normal. The residual
urine and bladder capacity vary.

USE OF DRUGS

There are a few specific responses which are of occasional value.

 In suspected sympathetic lesions an injection of adrenaline causes excessive
vasoconstriction in the affected zone. Intracutaneous injection of 0.1 ml of 1/1000
histamine will not produce the normal wheal and flare in a totally denervated zone,
but will in an area of hysterical anesthesia.
 The ganglion blocking agents can distinguish between vasoconstriction due to
autonomic overaction and structural disease of the vessels. In the latter,
administration of the drug makes no difference to the blood flow and temperature of
extremities. . ' .
 Peperoxane, or phentolamine, given intravenously will produce a fall in blood
pressure in cases of hypertension due to phaeochromocytoma, but not in
hypertension of other causes, and can be used as a diagnostic test.
 Neostigmine and Tensilon are used in the diagnosis of myasthenia gravis and have
autonomic side-effects which are undesirable. In the case of neostigmine, the
concurrent injection of atropine will reduce these effects considerably.

LOCAL NERVE AND SYMPATHETIC BLOCK

Blocking of the middle or inferior sympathetic ganglia can be used to assess the possible

165
results of sympathectomy in Raynaud's disease, and in Sudeck's atrophy, where there are
painful wrist and finger joints, trophic changes in the hand, weakness, limitation of
movement, increased reflexes, X-ray changes showing osteoporosis and apparent
coalescence of the carpal bones. Local block of peripheral nerves or ganglia can also be
used to gauge the likely response to surgery in causalgia and other pain disorders.

EFFECTS OF SYMPATHETIC AND PARASYMPATHETIC SYSTEMS ON VARIOUS

ORGANS

Circulatory system

Sympathetic Parasympathetic
(adrenergic) (muscarinic)
Cardiac output β1, (β2): increases M2: decreases
SA node: Heart rate β1, (β2): increases M2: decreases
(chronotropic)
Atrial cardiac muscle: β1, (β2): increases M2: decreases
contractility (inotropic)
Ventricular cardiac muscle β1, (β2): ---
increases contractility
(inotropic)
increases cardiac muscle
automaticity
At AV node β1: M2:
increases conduction decreases conduction
increases cardiac muscle Atrioventricular block
automaticity

Blood vessels

Sympathetic (adrenergic) Parasympathetic (muscarinic)

Vascular smooth muscle α1: contracts; β2: relaxes M3: relaxes
Renal artery α1: constricts ---
Larger coronary arteries α1 and α2: constricts ---
Smaller coronary arteries β2:dilates ---
Arteries to viscera α: constricts ---
Arteries to skin α: constricts ---
Arteries to brain α1: constricts ---
Arteries to erectile tissue α1: constricts M3: dilates
Arteries to salivary glands α: constricts M3: dilates
Hepatic artery β2: dilates ---
Arteries to skeletal muscle β2: dilates ---
Veins α1 and α2 : constricts ---
β2: dilates

166
Other

Sympathetic (adrenergic) Parasympathetic (muscarinic)

Platelets α2: aggregates ---
Mast cells - histamine β2: inhibits ---

Respiratory system

Sympathetic (adrenergic) Parasympathetic

(muscarinic)
Smooth muscles of β2: relaxes (major M3: contracts
bronchioles contribution)
α1: contracts (minor
contribution)

The bronchioles have no sympathetic innervation, but are instead affected by circulating adrenaline

Nervous system

Sympathetic (adrenergic) Parasympathetic (muscarinic)

Pupil dilator muscle α1: contracts M3: relaxes
(causes mydriasis) (causes miosis)
Ciliary muscle β2: relaxes M3: contracts
(causes long-range focus) (causes short-range focus)

Digestive system

Sympathetic (adrenergic) Parasympathetic

(muscarinic)
Salivary glands: secretions β: stimulates viscous, amylase M3: stimulates watery
secretions secretions
α1: stimulates potassium cation
Lacrimal glands (tears) β: stimulates protein secretion ---
Kidney (renin) β1: secretes ---
Parietal cells --- M1: Gastric acid secretion
Liver α1, β2: glycogenolysis, ---
gluconeogenesis
Adipose cells β1, β3: stimulates lipolysis ---
GI tract (smooth muscle) α1, α2, β2: decreases M3, (M1): increases
motility
Sphincters of GI tract α1, α2, β2: contracts M3: relaxes
glands of GI tract no effect M3: secretes

167
Endocrine system

Sympathetic (adrenergic) Parasympathetic (muscarinic)

Pancreas α2: decreases secretion from beta cells, M3 increases stimulation from alpha
(islets) increases secretion from alpha cells cells and beta cells
Adrenal N (nicotinic ACh receptor): secretes ---
medulla epinephrine and norepinephrine

Urinary system

Sympathetic Parasympathetic
(adrenergic) (muscarinic)
Detrusor urinae muscle of β2: relaxes M3: contracts
bladder wall
Urethral sphincter (internal) α1: contracts Relaxes
sphincter α1: contracts; β2 relaxes M3: relaxes

Reproductive system

Sympathetic (adrenergic) Parasympathetic (muscarinic)

Uterus α1: contracts (pregnant) ---
β2: relaxes (non-pregnant)
Genitalia α1: contracts (ejaculation) M3: erection

Integumentary system

Sympathetic (Muscarinic and Parasympathetic

Adrenergic) (muscarinic)
Sweat gland M: stimulates (major contribution); α1: ---
secretions stimulates (minor contribution)
Arrector pili α1: stimulates ---

CLINICAL TESTS OF AUTONOMIC FUNCTION

Test Normal Response Part of Reflex arc tested

NON INVASIVE BEDSIDE TESTS
Blood-pressure response to Fall in BP<= 30/15 mm Hg Afferent & sympathetic
standing or vertical tilt efferent limbs
Heart rate response to Increase 11-90 beats/ min vagal afferent & efferent limbs
Standing
Isometric Exercise Increase in Diastolic BP, 15 Sympathetic efferent limb
mm Hg
Heart rate variation with Maximum-minimum HR > 15 Vagal afferent & efferent limbs
respiration beats/min, E:I Ratio 1.2
Valsalva ratio >1.4 Afferent and efferent limbs
Sweat test Sweating over all body & Afferent & efferent limbs
limbs
Axon reflex Local piloerection, sweating Postganglionic sympathetic
efferent fibres
Plasma NA level to vertical Rises on tilting from horizontal Sympathetic efferent limb

168
posture to vertical
Plasma vasopressin level Rise with induced Afferent limbs
Hypotension

INVASIVE TESTS
Valsalva maneuver Phase 1: rise in BP Afferent and sympathetic
Phase 2: gradual reduction of efferent limbs
BP to plateau
Phase 3: fall in BP
Phase 4: overshoot of BP;
bradycardia.
Baroreflex sensitivity 1) slowing of HR with induced 1) parasympathetic afferent
rise of BP. and efferent limbs
2) steady state responses to 2) afferent and efferent limbs
induced rise & fall of BP
Infusion of pressor drugs 1) rise un BP 1) adrenergic receptors
2) slowing of HR 2) afferent and efferent
parasympathetic limbs
OTHER TESTS OF VASOMOTOR CONTROL
Immersion of hand in hot Increased blood flow of Sympathetic efferent limb
water opposite hand
Cold pressor test Reduced blood flow Sympathetic efferent limb
Emotional stress Increased BP Sympathetic efferent limb
TESTS OF PUPILLARY INNERVATION
4% Cocaine Pupil dilates Sympathetic innervation
0.1% Adrenaline No response Postganglionic sympathetic
innervation
1% Hydroxyamphetamine Pupil dilates Postganglionic sympathetic
hydrobromide innervation
2.5% Methacholine No response Parasympathetic innervation
0.125% Pilocarpine

DISORDERS OF THE AUTONOMIC NERVOUS SYSTEM

This is progressive, degenerative

Pure autonomic failure disorder of the ANS in which
dysautonomia occurs in isolation, without
other evidence of neurologic disease.

Involvement of preganglionic neurons in

the brainstem and spinal cord, prominent
Multiple system atrophy (MSA) dysautonomia c/b orthostatic
hypotension, impotence, constipation,
and urinary incontinence; may be
associated with respiratory symptoms
such as laryngeal stridor and sleep
apnea.

169
REFERENCES
Ropper, A.H. & Brown, R.H. Disorders of autonomic nervous system, respiration &
swallowing. In Adam
and Victor's Principles of neurology (8th edition). New York, McGraw -Hill, 2005: 452- 479

Victor, M & Ropper A.H. Disorders of autonomic nervous system, respiration & swallowing.
In Adam
and Victor's Principles of Neurology(7th edition).New York, McGraw-Hill, 2001: 550-585

Spillane, J.A. The Autonomic Nervous System. In Bickerstaff's Neurological Examination in

Clinical Practice (6th, edition). Oxford, Blackwell Sciences Ltd., 1996: 275- 283

McAuley J. & Swash M. Nervous system: In Swash M, Glynn M.eds. Hutchison's Clinical
Methods (22nd edition). London: W.B.Saunders,2007: 229-230

Low, P.A. & Engstrom, J.W. Disorders of the Autonomic Nervous System, In Fauci, A.S,
Braunwald, E, Kasper, D.L, Hauser, S.L, Longo, D.L, Jameson, J.L, & Loscalzo, J (eds)
Harrison's Internal Medicine(l7th edition) New York, McGraw -Hill,2008: 2576-2582

Ganong, W.F. The Autonomic Nervous System. In Review of Medical Physiology (21st
edition) New York McGraw-Hill, 2003: 226-234

Paul, I. The Examination of Autonomic Nervous System 2009:1-9

170
CHAPTER –IX
 PHENOMENOLOGY AND PSYCHOPATHOLOGY

Psychopathology
Psychopathology is the systematic study of abnormal experience, cognition and
behavior. It is the study of the products of a disordered mind. It includes the explanatory
psychopathologies where there are assumed explanations according to theoretical
constructs (for example, on a cognitive, behavioral, psychodynamic or existential basis, and
so on), and descriptive psychopathology which is the precise description and categorization
of abnormal experiences as recounted by the patient and observed in his behavior.

There are two distinct parts of descriptive psychopathology: the observation of behavior
and the empathic assessment of subjective experience. Accurate observation is extremely
important to look out for the objective expression of the subjective experiences.
The other part of descriptive psychopathology assesses subjective experience through
empathy, which means literally ‘feeling oneself into’. In descriptive psychopathology the
concept of empathy is a clinical instrument that needs to be used with skill to measure
another person’s internal subjective state using the observer’s own capacity for emotional
and cognitive experience as a yardstick.

Phenomenology

Phenomenology is the study of events, either psychological or physical, without

embellishing those events with explanation of cause or function. As used in psychiatry,

171
phenomenology involves the observation and categorization of abnormal psychological
events, the internal experiences of the patient and his consequent behavior. An attempt is
made to observe and understand the psychological event or phenomenon, so that the
observer can, as far as possible, know for himself what the patient’s experience must feel
like.
Phenomenology, the empathic method for the eliciting of symptoms, is best learnt
from patients, though it is necessary to know what one is looking for the practical, clinical
aspects in which the patient describes himself, his feelings and his world, the doctor tries to
unravel the nature of the sufferer’s experience to understand it well enough and to feel it so
that the account of his findings evokes recognition from the patient. The method of
phenomenology in psychiatry is to render the patient’s experience understandable so that
classification and rational therapy may proceed.
Understanding the Patient’s Symptoms
Understanding, in both an everyday and a phenomenological sense, cannot be
complete unless the doctor has a detailed knowledge of the patient’s background culture
and specific information about his family and immediate environment. The method of
phenomenology facilitates communication; its use makes it easier for the doctor to
understand his patient. The patient is also helped to have confidence in the doctor, because
he realizes his symptoms are understood and therefore accepted as ‘real’. The precise
description and evaluation of symptoms also helps communication between doctors.
Symptom/ Sign
As clinical medicine makes a clear distinction between signs and symptoms, this
distinction is not usually made with the phenomena of the mental state. Patient’s description
of an abnormal mental phenomenon, about something that distresses him, or simply
accounts of his experiences are therefore considered as symptoms. When these symptoms
are aggregated they may be regarded as the signs of whatever diagnosis is indicated.
Symptom then, which is taken to include sign, may be either an item of complaint or an item
of phenomenological description. For a symptom to be used diagnostically, its occurrence
must be typical of that condition and it must occur relatively frequently in this condition.
The method of empathy
The use of phenomenology in psychiatry is an extension of the history in that it
amplifies the description of the present illness revealing the mental state. It is neither
possible for the interviewer to observe somebody’s hallucination nor in any direct way to
measure it. However, one can still comprehend him by using those human characteristics
172
one holds in common with him, his ability to perceive and to use language they share. The
method of empathy implies using the ability to feel oneself into the situation of the other
person by proceeding through an organized series of questions; rephrasing and reiterating
where necessary until one is quite sure of what is being described by the patient.
Thus the purpose of phenomenological method is to (i) describe inner experiences;
(ii) order and classify them; and (iii) create a reliable terminology. Empathy is also
invaluable therapeutically in establishing a relationship with the patient. Knowing that the
doctor understands and is even to some extent able to share his feelings, gives the patient
confidence and a sense of relief. This empathy is also useful as a way of extending
knowledge more generally in the field of psychiatry as it allows a diagnostic terminology to
be developed.

Primary/ Secondary
Jaspers discusses the different meaning which can be given to the terms primary
and secondary when applied to symptoms. The distinction may be in terms of
understanding: what is primary can not be further reduced by understanding, for example
hallucinations. What is secondary is what emerges from the primary in a way that can be
understood, for example delusional elaboration arising from the healthy part of the psyche
in response to hallucinations arising from the unhealthy part of the psyche.

The Analysis of Experience

What the patient considers important while describing his distress may not
necessarily be identical with what is clinically regarded as significant. While in order to
arrive at a diagnosis the interviewer tries to ascertain the psychopathological entities that
are present, perhaps, the patient remains concerned to communicate the distress
experienced, its intensity and the way it is perceived as a threat.
Prediction/ Quantification
Quantification of object is an essential tool in scientific process, though it is
secondary, more important aspect being its quality to be predictive. It is possible to quantify
subjective psychology using phenomenology at the stage of forming hypotheses, though it
may not be as objective in conventional sense.
Form/ content
The form of a psychic experience is the description of its structure in
phenomenological terms, whereas, content is the colouring of the experience. The form is
173
dependent upon, and is therefore a diagnostic key to, the particular mental illness from
which the patient suffers. The content can be understood in terms of the patient’s life
situation with regard to culture, peer group, status, sophistication, age, sex, life events and
geographical location. While patient is usually concerned with the content of his experience,
the phenomenologist tries to single out the form, and both are taken into account to
understand the problem as a whole when psychiatrist looks for a suitable diagnosis. The
patient often finds the doctor’s interest in form unintelligible and a distraction from what he
regards as important, and hence, irritating.
Subjective/ Objective
Objectivity in science has come to be revered as the ideal, so that only what is
external to the mind is considered to be real, measurable and valuable. But objective
assessments are also subjectively value laden in what the observer chooses to measure.
Thus both subjective and objective assessments are associated with value judgements, or
to think it other way, there is no such thing as an unprejudiced observation (Popper, 1974).
The method of phenomenology tries to increase our knowledge of subjective events so that
they can be classified and ultimately quantified. For instance on seeing an irritated person
one can objective label him as ‘irritable’, can even apply some kind of scale to quantify that
irritation objectively. But it is when through an empathic subjective analysis the interviewer
associates this expression with his own on feeling irritated and acknowledges the other
person’s subjective experience, the event is assessed precisely. In order for it to happen,
the doctor has to be receptive to this communication, has to be able to establish rapport
himself, and has to have a capacity for human understanding.
Process/ Development
Development implies that an experience is understandable in terms of the person’s
constitution and history; while, process is seen as the imposition of an event from outside.
In the same way that understanding or explaining depend upon the perspective of the
interviewer – empathically from inside or observing from the outside – so process or
development depends upon whether the person experiences an event as within their usual
pattern of life or outside it.
Theoretical Stances of Psychopathology
Descriptive/ Dynamic Psychopathology
Psychopathology is the study of abnormal psychic processes. Descriptive
psychopathology is concerned with describing the subjective experiences and also the
resultant behaviour during mental illness without venturing explanations accounting for
174
these experiences or commenting upon the etiology or the process of its development.
This contrasts quite sharply with other theoretical frameworks of psychopathology, like
psychoanalytic where at least one of several basic mechanisms are assumed to be taking
place and the mental state becomes understandable within this framework. Explanations of
what occurs in thought or behaviour are based on these underlying theoretical processes,
such as transference or ego defence mechanisms.

Psychopathology – descriptive versus psychoanalytic

Descriptive Psychoanalytic
Summary Empathic evaluation of patient’s Study of the roots of current
subjective experience behavior and conscious
experience through
unconconsious conflicts.

Terminology Description of phenomena Theoretical process

demonstrated

Methods Understanding the patient’s Free association, dreams,

subjective state through transference
empathic interview

Differences in 1. Makes distinction between Understanding in terms of

practical understanding and notional theoretical
application explanation: understanding processes
through observation and
empathy
2. Form and content clearly No distinction made;
separated: form of concerned with content
importance for diagnosis
3. process and development No distinction made;
distinguished: process symptoms seen as having
interferes with development unconscious psychological
basis basis

MAIN CHARACTERISTICS OF PHENOMENOLOGICAL PSYCHOPATHOLOGY

1. Empirical (as opposed to speculative )
2. Detailed (emphasis on the idiosyncratic features of the subject)
3. Individualistic (as opposed to statistical)
4. Subjective
5. Anti inferential
6. A-theoretical with respect to etiology
7. Anti-reductionistic

175
USE OF PHENOMENOLOGY
Every psychiatrist uses phenomenology to some extent but it is much more valuable tool if
used rigorously. The four practical applications of phenomenology are as follows:
1. Communication – it enables clinician to speak and write to each other about the
problem of their patient in a mutually comprehensible way, which is of value both
clinically and for research purpose.
2. Diagnosis- psychiatry diagnosis is mainly a psychopathological one and will remain
so until there is more evidence for etiology and underlying pathology for the different
conditions
3. Therapy- the use of empathy is a rational way of establishing a therapeutic
relationship. It enables the therapist to understand what the patient is going through
and which in turn gives the patient confidence to further entrust the secrets of his
internal environment to the therapist
4. The law-this is the only reasonable way of determining what is mental illness and
what are the difference between the different mental illness, from a forensic point of
view.
CONCLUSION
The ultimate aim of psychiatry is to help people function and feel better. With a more
precise understanding of patient’s psychopathology, the clinician would possess a more
exact basis for the selection and use of treatment methods leading to greater benefits to
the patient.

176
CHAPTER-X
 DISORDERS OF PERCEPTION
 Perception
Perception is the awareness of objects, qualities or events stimulating the sense organs, a
person’s immediate experience of the world. Any sensation which has meaning in itself is a
perception. Perception is the process that gives coherence and unity to sensory input. It is a
synthesis or fusion of the elements of sensation (Morgan & King, 1993).
Sensation is only the first stage in receiving information from outside the self. It involves all
the sense organs. Hearing, vision taste, smell and touch are the main five senses.
For visual stimuli to be perceived they must be made meaningful and this is a process of
eliminating the irrelevant and associating what is seen with other important data to form a
percept.

 IMAGERY
When a percept has been created within the mind- imagery is formed. Imagery is the internal
mental representation of the world and it is actively drawn from memory. It can be created,
recreated and can be terminated by will. Imagery lacks the sense of reality. Imagery includes
visualizing and imagining places previously visited, recollection of spoken speech and also
mental arithmetic and map reading etc.
Another interesting concept is eidetic imagery that is persistent and vivid. The prominent
features of this kind are
A) One continues to see a representation of a visual stimulus, sometimes after it has been
removed;
B) One is “seeing” a true visual image and not merely the memory of the stimulus. This is
more common in children than in adults

Obsessive imagery is another kind of imagery which is recurrent, intrusive, repetitive and
thus distressing to the individual.

Difference between perception and imagery

Perception Images
Concrete reality Figurative
Character of objectivity Character of subjectivity
Sensory elements are full and fresh Mostly sensory elements relatively insufficient
Clearly delineated Not clearly delineated and incomplete
Occur in external objective space Occur in inner subjective space
Easily retained, unaltered, constant Always have to be recreated
Independent of will Dependent on our will

177
 Abnormal Perceptions

Sensory distortions
Sensory deception

Hallucinations
Changes in Quality Changes in Changes in Illusions
Intensity Spatial Form
(Dysmegalopsia)

Xanthopsia Macropsia Auditory Visual

Hallucination Autoscopy
Hyperesthesia Hypoesthesia Complete Affect Periodic Tactile
Chloropsia Illusion
Illusion Illusion
Smell Cenesthetic
Micropsia
Erythropsia
Gustatory
Extracampine

Functional
Reflex

178
Disorder of perception can be divided into sensory distortion and sensory deception.

 Sensory distortion
In sensory distortion, there is a constant real perceptual object which is perceived in a
distorted way (Hamilton, 1968). Disturbance of the mental state, with or without organic
brain pathology may cause sensory distortion. This distortion may involve:
a. Changes in intensity
b. Changes in quality
c. Changes in spatial form

 Changes in Intensity
Hyperaesthesia- Increased intensity of sensation or hyperaesthesia is resultant of the
following
 Intense emotion.
 Lowering of the physiological threshold.
It may occur in
-Organic syndrome caused by LSD administration.
-Functional psychosis, especially mania,
-Epileptic aura.
In visual hyperaesthesia different aspects of colour perception is affected, which include the
intensity of the colour, the actual hue and the quality of the colour is also sometimes
affected .For e.g., colour can be seen brighter, more vivid, etc.
In achromatopsia complete absence of colour is experienced. It occurs in unilateral and by
lateral occipital lesions. In dyschromomatopsia perseveration of colour perception occurs.
It is common in unilateral posterior lesions.

Hyperacusis – Heightening in the auditory modality is called hyperacusis. In which the

patient complaints at everything are sounding abnormally loud. Here ordinary conversation
may sound intolerably noisy and even whispering at a distance may be found
uncomfortable. The symptoms occur in depression, migraine, delirium, and in toxic states
.For example – Hear the noise of a door closing like the sound of a clap of thunder. In
palinacousis uniqueness of perceptual experience is disturbed and there is persistence of
sound that is heard. For e.g., subject returned to answer the door several times during a 30
minute period after the door bell actually rang.
Hypoesthesia – Intensity of perception is lowered here. It may occur in depressive illness.
Every thing looks black to them.
Gustatory Hypoesthesia – It may present in the form of a complaint that all foods taste the
same (Sims, 2009)
Hypoacusis – In this there is a decreased sensitivity of noise. A true hypoacusis occurs in
delirium where the threshold for all sensations is raised. The delirious patient has a defect
of attention which accentuates his perceptual difficulties.

 Changes in Quality – These are visual distortions brought about by toxic substances
which colours all perceptions. For example: the drug santonin used in the treatment of
Helminthiasis can produce violet or yellow vision. Another drug Sildenafil can cause
blue vision. Colouring of yellow named as 'Xanthopsia', green as 'chloropsia' and red as
'erythropsia'. So basically these are the qualitative changes of perception and not
hallucinations.

179
 Changes in Spatial Form
A change in the perceived shape is called dysmegalopsia. It can result from retinal disease,
disorders of accommodation and convergence and from temporal lobe lesions and delirium.
 Micropsia – In micropsia, objects seem smaller than their real size. Micropsia refers to
the experience of the retreat of objects into the distance without any change in size, is
called ‘Porropsia’ (Hamilton, 1968).
 Hemimicropsia- An apparent reduction in one hemi field of vision is called
hemimicropsia. It is commonly seen in temporal lobe epilepsy.
 Macropsia – Opposite kind of visual distortion known as macropsia or megalopsia. In
this case objects appear larger or closer.
 Metamorphosia- One type of macropsia is known as metamorphopsia. Scarring of the
retina with retraction naturally produces macropsia. But as the distortion produced by
scarring is usually irregular, metamorphopsia is more likely to result. Here alteration in
the shape of the perceived objects occurs. It is basically the appearance of the things
taking on a different aspect. For e.g, one woman saw people upside down, on their
heads. For this it is also known as inversion.
 Palinopsia- In visual perception, the recurrence or prolongation of a visual
phenomenon beyond the customary limits of the appearance of the real event in the
world is known as palinopsia. For e.g. after observing an individual in a gathering, often
the image of his/her appears keeps on appearing in various times and situation over few
days or months.
 Paraprosopia- Metamorphosia sometime affects faces then it is called as paraprosopia.
For eg, ward mates change their faces the very moment that one looks at them (Bleuler,
1950).
 Teleopsia- Here object appears far away than they actually are.
 Pelopsia- Here objects appear nearer than they really are.
 Alloaesthesia- Here one perceives the object in a different position from what is
expected. Here trans- position of objects occur.
 Akinetopsia- In this interesting kind individual’s visual perception of motion is impaired.
For this he or she is unable to perceive the motion of objects. This variety is quite rare
and occurring by lateral posterior cortical damage. For e.g., an individual had difficulty in
pouring tea into a cup because the tea appear to be frozen, like a glacier , for this she
could not stop pouring at the right time.

 Sensory Deception
It includes mainly illusions and hallucinations (Hamilton, 1968).

 Illusion – In illusion stimuli from perceived object are combined with mental image to
produce false perception. It can occur as a result of set, lack of perceptual clarity,
intense emotions. Illusions are not morbid in origin as they can occur in any body when
they can, usually be corrected. Illusion occurs in the severe depressive illness, delirium
and even in schizophrenia (Hamilton, 1968).

 Types of Illusion
There are three types of illusion-
 Completion Illusion- This depends on inattention for their occurrence. For e.g. we
commonly miss the misprints in a news paper because we read the word as if they are
written correctly. As soon as our attention is drawn to the mistakes, our perception

180
 alters. It demonstrates the principle of closure in Gestalt psychology: which says there is
a human tendency to complete a familiar but not quite finished pattern.
In incomplete perception, which is meaningless of itself is filled in by a process of
extrapolation from previous experience to produce significance.
 Affect Illusion – When illusion arises through affect, perception of everyday object is
changed. The illusion can only be understood in the context of the prevailing mood
state. For e.g. a child who is frightened of the balloons, wakes up from sleep ,or sees
anything big or round in shape, mistakes it as a balloon and becomes scared of it .The
experience only lasts a short time, and disappears when the intense fear goes, the
illusion is expelled by attention.
 Pareidolia – It can occur in a significant proportion of normal people and also can be
provoked by psycho mimetic drugs. Images are seen from shapes in pareidolic illusions.
In Pareidolia, vivid illusions occur without the patient making any effort. These are the
result of excessive fantasy thinking and a vivid impressive visual imagery. It also occurs
when the subject sees vivid pictures in the fire or in the clouds, without any conscious
effort on his part and sometimes even against his will. It cannot occur as a result of
affect or set, in this way they differ from the ordinary illusion. It occurs in children more
than in adults (Hamilton, 1968).

Illusion should be distinguished from the following conditions-

 Fantastic Illusion – In this, patient sees extraordinary modifications of his or her
environment. One of the classic example is a patient who looked in the mirror and
instead of seeing his own head he saw that of a pig.
 Intellectual Misinterpretations – These are basically wrong deductions and do not
imply alteration in the actual sense perception. Here the object is perceived in exactly a
same way, but a wrong interpretation has been put on it (Jaspers, 1962). For e.g. when
some one says that the doctor is not really a doctor but the public prosecutor.
 Perceptual Misinterpretations: It involves making a mistake as to the nature of
perception without that perception being particularly influenced by emotion mixed with
fantasy (Sims, 2009).

 Trailing Phenomena
This is another variety of perceptual abnormality associated with hallucinogenic drugs in
which moving objects are seen as a series of discrete and discontinuous images.
 Functional Hallucination – It occurs as a response to an environmental stimulus; both
the provoking stimulus and the hallucination are perceived by the patient.
 Fantastic Interpretation – Also known as elaborate daydreaming that is almost
similar to pariedolic illusions, where, there is a large mixture of fantasy with illusions
(Sims, 2009).

 Hallucinations
 Accordingly to Esquirol, it is a perception without an object.
 Jaspers (1962) suggested that hallucination is a false perception which is not a sensory
distortion or misinterpretation, but which occurs at the same time as real perception.
 Three criteria are essential for an operational definition of hallucination: (a) percept like
experience in the absence of an external stimulus (b) percept like experience which has
the full force and impact of a real perception, and (c) percept like experience which is
unwilled, occurs spontaneously and can not be readily controlled by the person
receiving the perception.

181
  A hallucination is a perception without an object (within a realistic philosophical
framework) or the appearance of an individual thing in the world without any
corresponding material event.
Subjectively, a hallucination is indistinguishable from a normal percept. The only clue is
that there is no corroborative evidence for the percept in other modalities. That is
hallucinatination should be tangible .Hallucination should also be substantial that is it
should have real and independent existence. Hallucination should have veridicality also
that means it should have life like quality.
Hallucinations vary according to sensory modalities, levels of conviction, content, Location,
degree of complexity of the hallucinated experience, degree to which it influences the
persons behaviour and degree of volitional control over them.

Aggernes pointed out the similarities between normal sensation & hallucination.
Normal sensation Hallucination
1. With normal sensation we are able to distinguish 1. Hallucinations also experienced
perceiving with our sense organs from imagining. as sensation and not thought or
fantasy.
2. When subject experiences something, he realizes 2. Hallucination also have this quality of
its possible relevance for his own emotions, need behavioural relevance.
or actions.
3. Normal sensation has a quality of objectivity in 3. The same also experience of the
that the experiencer feels that under favourable hallucination.
circumstances, he would be able to experience
the same something with another modality of
sensation.
4. An object is considered to exits if the observer 4. Hallucination also share this quality with
feels certain that it still exits even though nobody perceived object.
else is experiencing it at that time,
5. Experience of object perception is involuntary in 5. Hallucination also is involuntary.
that the experiencer feels that it is impossible or
extremely difficult to alter or dismiss the
experience simply by wishing to do so.
6. The quality of independence is present in normal 6. The quality of independence is also present
perception, that is the experiences is aware or in hallucination also.
through simple questioning becomes aware, that
his experience is not simply the result of being in
an unusual mental state.

 Pseudo hallucinations
The concept of pseudohallucinations was described by Griesinger under the name pale
hallucinations, by Kahlbaum who called them as apperceptive hallucinations and by Hagen
who gave them the name now currently used as pseudohallcinations. Jaspers did most of
his work on pseudohallucinations; according to him pseudohallucinations are vivid images
with far more sensory content than normal images and ideas. Pseudohallucinations can
occur in visual, auditory and tactile modalities.
Pseudo hallucination is a perceptual experience which is figurative not concretely real &
occurs in inner subjective space not in external objective space. It may have definite outline
& vivid detail. It may be retained for some time & it can not be deliberately evoked. It is
sometimes described ‘as if’ experience.

182
 These are not pathagnomonic to any particular mental illness. Jaspers stresses that there is
a gradation from the more fully formed pseudo hallucination to vivid imagery.

The nature of pseudohallucinations (partly derived from Jaspers and from

Aggernaes).
Perception = Hallucination Pseudo- Fantasy = Imagery
hallucination
1. Experience is concrete, tangible, 'inner eye' → pictorial subjective
objective, real
2. Location in outer objective space → inner subjective space
3. Definition definite outlines, complete  indefinite, incomplete only
sound individual details
4. Vividness full, fresh, bright  most elements are dim or
neutral
5. Constancy retained  Evanescent
6. Independence cannot be dismissed,  requires voluntary creation
from volition recalled or changed at will
7. Insight has quality of perception-no → fantasy has quality of idea
distinction made between
perception and
hallucinations
8. Behavioural relevant to emotions,  not relevant
relevance needs, actions
9. Sensory modality could experience object in → could not experience this
another modality object in another modality
10. Existence object exists independent → depends on observer for
of observer existence
11. Known to be independent  Dependent
dependent on 'my
abnormal state'

 Hallucination Involving Different Senses

Hallucinations can occur in any of the areas of the five special senses and also with
somatic sensation.

 Hearing
Hallucinatory voices were called phonemes by Wernicke. These voices vary in quality, can
be located in space and ascribed to specific individuals, these are extremely vague and
which the patient cannot describe in any way (Hamilton, 1968). Verbal hallucinations may
consists of voices speaking the individuals thoughts aloud, a voice carrying out running
commentary on the person’s behaviour, a collection of voices speaking about the
individuals in the third person, or voices issuing commands or instructions, and even both
male and female patients hear voices of either sex. In terms of localization, subjects may
attribute auditory hallucinations as coming from inside or outside their head or body parts,
report them as occurring both internally and also externally or often be unable to localize.
Hearing of voices can be grouped into following types : -
 Elementary Hallucination – It occurs in the form of voices, partly organized as music.
Basically these are unformed. Often the noise gives unpleasant and frightening
experience. This can occur in organic states and in schizophrenia (Hamilton, 1968).

183
 Musical Hallucination – It is common in older women with deafness or brain disease
but no history of psychiatric illness. These are experienced as tunes, lyrics and
instruments.
 Complex Hallucination – It occurs in the form of voices and characterized by sustained
voices clearly heard, originated in the objective space.
Often in organic states phonemes appear in simple words or short sentence and used to
speak to the patient in the second person. These phonemes mainly occur in schizophrenia.
The voices may be single or multiple, male or female, or both, and people known by the
patient on not known. The voices are clear, objective, definite and normal percept which at
the same time may be incomprehensible (Sims, 2009).
 Imperative or command Hallucinations:- These are a subtype of auditory
hallucinations in which the voice is experienced as commanding rather commenting.
Voices give instruction to some patients who may or may not feel obliged to carry them
out (Hamilton, 1968).
 Running Commentary - Here the voices talk about the person in the third person and
may even give a running commentary on his actions which is very trouble some.
 Thought Echo – In this, patient hears of his own thoughts being spoken aloud. This
special type is characteristic of schizophrenia. There is no accepted English term for this
symptom, so it is known as Gedankenlautwerden in German and Echo de Pensees in
French. Probably the best English term would be ‘thought echo’ .An alternative of this
which is rather cumbersome is thought sonorization. In acute schizophrenia patients
hear their thoughts being spoken as they think and the voice which speaks their
thoughts may come from inside or outside the head. In chronic schizophrenia the patient
complains that as he thinks, other people in his environment are talking about his
thoughts, so that his thoughts are being made known to other people, (Hamilton, 1968).
These voices can come before patient thinks or immediately after he thinks or
sometimes as the same time with his thinking .Some auditory hallucinations are
considered to be First Rank Symptoms of schizophrenia. These are
- Audible thoughts
- Voices heard arguing with each other or discussing
- Voices commenting on the patients behaviour
These three perceptual disturbances, each represent a massive interference with the
boundaries of self image, the discrimination of what is 'I' from what is not 'I' (Sims, 2009).
 Talky-Talky Tongue – In this special kind, patients hallucinate speech movement and
hear speech which comes from their own throat but has no connection with their
thinking (Hamilton, 1968).

 Vision
Hallucination occurs in visual modality also. All varieties of visual hallucinations are
frequently observed in organic states. Visual hallucinations are les prominent in
schizophrenia compared with auditory hallucinations.
 Elementary Visual Hallucination
This occurs in the form of flashes of light, partly organized as patterns or completely
organized as visions of people, animals or objects. It is often seen in clear consciousness
and known as unformed visual hallucination. All varieties of visual hallucination are found in
– Acute organic states rather than functional psychosis often this type of hallucinations are
isolated and do not have any accompanying noises or voices. Sometimes however visual
and auditory hallucinations form a coherent whole.

184
Visual hallucination occurs with occipital lobe tumours involving visual cortex cortical
blindness dyslexia, and alexia in a dominant hemisphere lesion. It is also associated with
Alzheimer's disease, Senile dementia, Pick's disease and Huntington's chorea.
 Formed Visual Hallucination
Here the subject use to see particular objects or people superimposed on real visual field. It
occurs in clear consciousness and in temporal lobe ictus.
 Hallucinations associated with bereavement
In bereavement often affected person experience this kind of hallucinations. An experiencer
may see the lost or loved person in his or her characteristic situation which includes his
sitting in a couch or working in a garden etc.
 Charles Bonnet Syndrome –
This is a condition in which individual experiences complex visual hallucinations in
association with impaired vision without demonstrable psychopathology or disturbance or
normal consciousness. It is more common in elderly but can occur at any age, it is usually
associated with central or peripheral reduction in vision.
 Scenic Hallucination –
The most interesting part of this kind of hallucination is the whole scenes are hallucinated
like a cinema. It is more common in psychiatric disorders associated with epilepsy. The
experiences may also have vision of fire and religions scenes. Some patients experience
scenic hallucination in the form of mass hallucinations, in which they see and hear people
being murdered, mutilated and tortured (Hamilton, 1968).
 Lilliputian Hallucination –
In this patient sees tiny people. Micropsia affect visual hallucinations as Lilliputian
hallucinations. This phenomena is associated with delirium or particularly with delirium
tremens.
 Experiential Hallucination –
It was first described by Penfield. These are hallucinations which appear to be vivid
memories and may have combined visual and auditory hallucinations which form a
coherent whole.

 Smell
Hallucinations of odour can occur in schizophrenia, temporal lobe epilepsy,(often known as
uncinate fits) and delirium. Olfactory sensation or memory is often associated with powerful
emotional resonances. (Hamilton, 1968)
It may or may not be unpleasant and usually has a special and personal significance. (Sims
2009).
 Taste
Hallucinations of taste are the rarest of the modalities. Gustatory hallucination occurs in
- Schizophrenia
- Acute organic states.
In schizophrenia, it sometimes occurs with delusion of being poisoned. Changes in
gustatory perception may occur in temporal lobe epilepsy (Sims, 2009).
 Touch or Bodily sensation –
It can be grouped into following types (Sims, 2009):-
- Superficial
- Kinaesthetic
- Visceral
Superficial Hallucinations affect the skin and are further classified into the following types -
- Haptic

185
 - Thermic
- Hygric
 Haptic Hallucination –
It is associated with sensation of touch .For eg, patient says knife stabbing my neck or
feeling of hand brushing against the skin.
 Thermic Hallucination:
Superficial hallucination affecting skin sensation is called thermic. It is associated with
abnormal perception of heat and cold. For eg, Cold wind blowing across the face.
 Hygric Hallucination: It is associated with perception of fluid.
 Kinesthetic Hallucination: This is associated with muscle or joint sense. The patient
feels that his limbs are being twisted. Kinesthetic hallucinations are perceptions of
movements of limbs or muscles being squeezed or sense of vibrations in the absence of
the said stimulus or the patients feels that the patients limbs have been pulled or moved.
 Paraesthesia:
It is associated with sensation of tingling or pins or needles (Sims, 2009).
 Visceral Hallucination:
These are the false perception of the inner organs. For eg; pain, heaviness, stretching,
palpitation etc (Sims, 2009).
 Vestibular Hallucination:
These are sensations of flying through the air or sinking through the bed. These are more
likely to be occurring in acute organic state and most commonly in delirium tremens.
 Formification:
It is basically a form of feeling that animals are crawling over the body and is sometimes
found in acute organic states. It also occurs in cocaine poisoning or cocaine abuse and is
popularly known as ‘cocaine bugs’.

Delusional Zoopathy:
Another interesting and unusual variety of somatic hallucinosis is delusional zoopathy. This
can be of two types –
 External delusional zoopathy-
In which patient experiences that there is an animal crawling about on his body. Though he
does not see the animal but can usually describe in detail (Hamilton, 1968).
 Internal delusional zoopathy-
In this, patient believes that there is an animal inside the body. For eg, A patient had
somatic sensation which she knew were the result of the wasp wandering around inside her
body (Hamilton, 1968).
 Phantom Limb-
It is another form of somatic hallucination. Here the experiencer feels that he has a limb but
he does not receive any sensation from it. Either because of limb has been amputed or
because sensory pathways from it have been destroyed.
 The Sense of Presence-
It is difficult to classify an abnormal sense of presence, because although it is not strictly a
sense deception, it can not be regard as a delusion. Most normal people have from time to
time the sense that someone is present in that place when they are alone. For example
many people when in dark street experience that there is someone behind them. This
experience is probably the result of lack of sleep and hunger and of religious enthusiasm
.The hallucination of presence can occur in organic states, schizophrenia, and hysteria
(Hamilton, 1968).

186
 Hypnagogic and Hypnopompic Hallucination –
These hallucinations can be regarded as special varieties of organic hallucinations. Though
very often found in normal individual also. Hypnagogic hallucinations are vivid perceptual
experiences occurring at sleep onset while hypnopompic hallucinations are similar
experiences that occur on awakening. Hypnogogic hallucinations occur during drowsiness.
These are discontinuous, appear to force themselves on the subject and the subject does
not participate as he does in a dream. This may be geometrical designs, abstract shapes,
faces, figures, or scenes from nature. Auditory hallucinations of this kind may be animal
noises, music or voices calling his or her names, ring tone of telephone etc. This occurs
due to sleep deprivation.

Multimodal hallucinations-
This is frequently reported form of hallucinations but referred by different authors in different
names. The commonly used named as dissociative hallucinations, fantastic hallucinations,
and multiple hallucinations. It occurs in a number of conditions: schizophrenia, organic
mental disorders, post traumatic stress disorder, grief reaction, dissociative states and
sleep disorders. In this, hallucinations occur simultaneously in more than one sense
modalities that are experienced as emanating from a single source.
 Sexual Hallucinations-
It is a rare kind of hallucinations in which experiencer may feel that ghosts make love to
them as they lie in the bed, often they experience sexual arousal as a result of alien
influence or induced by telepathy.

 Special Kinds of Hallucinations

 Functional Hallucination-
An external stimulus is necessary to provoke hallucination, but the normal perception of the
stimulus and the stimulus and the hallucination in the same modality are experienced
simultaneously (Sims, 2009). Fish (1968) viewed that a stimulus causes the hallucination,
but it is experienced as well as the hallucination
Reflex Hallucination-
Here a stimulus in one sensory modality producing a hallucination in another (Sims, 2009).
This is a morbid variety of synaesthesia. It is an image based on one sense modality is
associated with an image based on other (Fish 1968). The feeling of discomfort caused by
seeing and hearing somebody scratch a blackboard with his/her finger nails. In another
example a woman experienced pain whenever certain words were mentioned.
 Extracampine Hallucination-
Here hallucinations are experienced outside the limits of the sensory field, outside the
visual field or beyond the range of audibility.
Cenesthesia:
Change in the normal quality of feeling tone in a part of the body.

AUTOSCOPY
In autoscopy or phantom mirror image patient sees own image and knows that it is he. It is
rare and not just a visual hallucination as kinesthetic and somatic sensations are also
presents. It is one of the abnormalities of the unity of the self .This can also be experienced
by normal subject .Autoscopy occasionally a hysterical symptom too.
 Patients with schizophrenia may experiences this
 It also occurs in organic states such as temporal lobe epilepsy and parietal lobe
lesions.

187
  Also found in chronic alcoholism.
Another variation of this kind is negative autoscopy in which patient look in to the mirror and
sees no image. It is commonly found in organic states. An even new variety of autoscopy is
internal autos copy in which subject sees his own internal organs.

Difference between Autoscopy Dopelganger and Delusion of Doubles :-

Autoscopy Dopel Ganger Delusion of Doubles
Kinesthetic and somatic Sees his/her double Patient gives a false identity to
hallucination are involved with every stranger they meet or
the visual hallucinations denies the identity of people
whom he knows
Can occur in normal people, Occur in parietal lobe Occurs with home patient is
also occur in depressed disorder, cerebrovascular linked to emotionally, mainly in
subject, sub acute or acute disorder, and severe schizophrenia.
delirious state. infectious disease.
In this patient sees own image Myth that experiencer It is false unshakable belief of
and knows that it is he. Will die the patient not the perception

 Cinaesthetic Hallucinations: -
These are peculiar visual sensations usually occur in patients with schizophrenia.These
sensations are not experienced in appropriate physiological conditions. Feelings like
something burning in the brain, urine passing through the uterus or blood coursing through
ones own blood vessels are typical examples.
All the hallucinations mentioned above are considered as hallucination though stimulus is
involved in this kind of hallucination. In functional hallucinations-both the provoking stimulus
and the perception are occur simultaneously on the other hand perception based on one
sensory modality gives perception on another. In extra campaine hallucination patients
perceived something beyond the limits of his sensory field. In all the instances the
perception of specific modality is real but when it produces perception of other modality it is
the false perception that is called hallucination.

 Key Features of hallucinations in Schizophrenia: (Hamilton, 1984)

Hallucinatory voices in schizophrenia vary considerably in terms of content, intensity,
clarity, mode, attitude and attribution of the patient and continuity.
 The effect of content of voices may vary from patient to patient. For some patients since
the voices talk about the inner most secrets or private thoughts that the patient may feel
that his thoughts has been invaded, but for some patients content of voices are not that
much troublesome but are troubled by the phenomenon itself.
 Intensity of voices usually varies, but in many patients sudden increase intensity which
occurs from time to time for no apparent reasons may lead to outburst of shouting,
swearing, scolding and general excitement.
 Clarity is one factor which also varies from patient to patient and it determines the
patient’s ability to reproduce the content of voices.
 The mode of address also has its importance in schizophrenia. So that the voices may
talk about the patient, may talk to him, or may actually instruct him. Hallucinatory
conversation about the patient is diagnosis of schizophrenia.
 Attitude of patient towards voices is very variable. Many chronic paranoid
schizophrenics treat these voices as old friends, some complain about hallucinations as
such or their content and some realize the abnormality and refuse to talk about them.

188
 Quality of voices or their affect-laden nature determines patient’s inference of these
voices. At times these patients attribute all these voices to real people around him and
deny hearing voices but when they describe it in detail it becomes obvious that they are
hearing voices.
 Apart from it if the patient hears well organized voices, continuous in nature, in a state
of clear consciousness consisting of more than one sentence; he can be diagnosed with
schizophrenia unless it can be proved otherwise.

 Mood disorder
In mania hallucinations have been less commonly documented. Hallucinations,
predominantly auditory, have been reported in 14 to 40% of manic patients. It has been
seen that in manic patients, hallucinations are usually due to delusion of grandiosity. In the
state of ecstasy, manic patient hallucinates as if he is communicating with god. In
depression second person command type is found more. In case of depressive patient he
hears somebody telling him that he had committed sin and he deserves “punishment”. In
extreme cases they are commanded to commit suicide.

 Psychoactive Substance
Hallucinations caused by drugs are commonly visual hallucinations like those experienced
during alcohol withdrawal in 25% of people. People will classically "see" insects or worms
crawling on walls or over their skin (tactile hallucinations). This phenomenon is called
formication. Auditory hallucinations can also occur during withdrawal, although less
commonly. Patients with alcoholic hallucinosis experience visual, auditory, or tactile
hallucinations but otherwise have a clear sensorium.
Another important features of alcohol withdrawal is delirium tremens where patient is having
visual hallucination of insects, small animals etc, which make them fearful ,confused and
perplexed, level of consciousness is altered and the awareness of environmental stimuli is
decreased. Another associated feature is sundowning phenomenon where condition is
deteriorated after sunset (Kaplan & Sadock, 1998).
The acute behavioral effects of cannabinoids include transient hallucinated experiences
especially visual sensory modality; they also have altered spatial perception and time
perception.
Hallucinogens are mind altering natural or synthetic agents which can produce state of
intoxication with changes in mood, thoughts and perception. This recurrence has been
mostly described as visual disturbance in the form of geometric figures, flashes of colors,
and a trail of images of moving objects, positive afterimages, and halos around objects,
micropsia, or macropsia.
Hallucinogen-persisting perceptual disorder is characterized by the transient recurrence of
perceptual symptoms experienced while intoxicated with the hallucinogen, often called
“flashbacks”e.g. LSD-induced flashbacks.

 HALLUCINATORY SYNDROMES:-
It is defined as a recurrent and persistent occurrence of hallucinations. It usually occurs in a
clear intellectual field, without any intellectual disturbances or confusion or in a state of
confusion .It is commonly seen in alcohol or other substance intoxication or following any
kind of trauma. This state occurs with other signs. Schroder pointed out that hallucinations
could occur in four main syndromes, which he called confusional, self- reference, verbal
and fantastic.

189
 Confusional Hallucinosis:- In this kind consciousness is clouded and visual
hallucinations are prominent .Here auditory hallucinations are mainly music, noises or
odd words ,while connected sentences are occasionally heard.
 Self-reference Hallucinosis:- Here the patients hears the voices talking about him .He
can usually give only a rough idea of what the voices are saying and is unable to
reproduce them thoroughly. But patient is convinced that the voices come from people
in his environment.
 Verbal Hallucinosis:-Patient used to hear clear voices in this kind of hallucinatory
syndrome, which talks about him, and he also can reproduce their content accurately.
The voices may be attributing to real or imaginary people or machines.
 Fantastic Hallucinosis:-The most interesting point is here hallucinations of all kinds
seems to occur .The patient describes fantastic experiences which are based on
auditory , bodily or visual hallucinations. These patients usually have mass
hallucinations in which they see and hear large number of people being murdered or
tortured (Hamilton, 1968).

 Assessment of hallucination:
Hallucination is one of the core features of psychoses. Its presence, nature and severity
must be understood not for making the diagnosis or explaining psychosis but also for
further management and rehabilitation of the patients. There are many tools available for
assessment, which are follows.

 Mental Status Examination (MSE)

MSE is an important part of the clinical assessment process in psychiatry. It is a structured
way of observing and describing a patient’s current state of mind, under the domains of
appearance, attitude, motor behavior, speech, higher cognitive functioning, mood and
affect, stream of thought, thought content, perceptual disorder, insight and judgement.
In MSE, perceptual disorders are covered under following:
 Continuous/discontinuous
 Dimensionality
 Control
 Clarity
 Veridicality
 Diurnal pattern
 Objective /Subjective space
 Modality
 Content
 Insight into phenomenon
 Schneiderian hallucination
 Distinction between true hallucination, pseudo-hallucination, imagery, illusion and
autoscopic hallucination.
 Present Status Examination
Present State Examination (PSE) A test developed by psychiatrist John Wing and
colleagues at the Maudsley Hospital in Britain in the 1960s. It is a structured interview
schedule for conducting the mental status examination and scoring the findings (Wing et
al, 1974).

190
 Schedules for Clinical Assessment in Neuropsychiatry (SCAN)
The Schedules for Clinical Assessment in Neuropsychiatry (SCAN) is a semi-structured
clinical interview used by trained clinicians to assess and diagnose psychiatric disorders
among adults. The SCAN core is the Present State Examination (PSE) which has been
developed and tested globally during the past four decades with good validity and reliability.
The SCAN was developed within the framework of the World Health Organization (WHO)
and the National Institute of Mental Health (NIMH).

Present State Examination-9

Following questions should be asked for eliciting perceptual disturbances. The examiner
should use his/her own judgment while interpreting the answers given by the patients.

 Auditory hallucination
1. Ab mai aapse ek aisa sawal puchunga jo aksar ham sab se puchte hai-Kya aisa hota
hai jab aap akele hote hai, aura aas-paas koi nahi hota tab kaano mei shor ya
aawajein sunaayi padati hai? Kabhi-2 aaisa lagta hai ki koi aap ka naam pukar raha
hai?
2. Kya isi tarah se kuch cheeje ya shakle bhi dikhayi deti hai? Jab aas-paas koi nahi ho
to bhi? Is tarah ki koi aur ajeeb baat hui ho to bataayein.
3. Kya tak-tak ya gaane ki aawaz si sunayi deti hai.
4. Yeh awaaz kaisi hoti hai-khusur-fusur ki tarah ya jaise koi dheere-dheere muh mein
bol raha ho.
5. Kya shabd saaf-saaf sunaayi dete hai?
6. Awaaz kya kahti hai.
7. Kya aapka naam bhi pukara jaata hai.
8. Kya aisa lagta hai ki kai aawazein aap ke bare mein baatein karti hai?
9. Kya ye awaazein ‘vah’ kah kar bulaati hai, jaise ‘vah aise hai’, vah yeh kah raha hai?
10. Kya ye awaazein seedhe aapse baatcheet karti hai?
11. Kya ye awaazein aapko hukm (aadesh) bhi deti hai? Kya aap waisa karte hai.
12. Kya aap bhi unse baatcheet kar sakte hai?
13. Kya ye awaazein aapke man se uthti hai ya baahar se aati hai aur kaano me sunaayi
deti hai?
14. Ye awwazein kaha se aati hai, kyu aati ahi, kya iske bare me kuch bata sakte hai?

 Visual Hallucination
1. Kya aapko aisi cheezein dikhayi deti hai jinhe dusre log nahi dekh sakte kewal aap hi
dekh sakte hai?
2. Kya ye cheezein aap ke man mein hoti hai ya aankho se saaf-saaf dikhaayi deti hai?
3. Aap ne kya dekha tha, Kya us samay aap thodi neend mein the?
4. Jab aap pure jag rahe ho, kya aisa kabhi hua?
5. Us samay pata tha ki yeh upari ya baahri chhez dikh rahi hai?
6. Kya aise laga ki jo aap dekh rahe hai woh kisi parchaayi ya tasveer se nikal raha hai?
7. Yeh sab kaise hota hai bata sakte hai?

 Other Hallucination
1. Kya cheezo ki shakal, swaad aur gandh mein koi ajeeb si baat lagti hai, koi farak lagta
hai?

191
2. Kya aapka shareer thik-thak kaam karta hai ya isme koi farak lagta hai?
3. Kya aapko azeeb sib bu mahsoos hoti hai, jo auro ko nahi hoti?
4. Kya aisa lagta hai ki aap se badboo aati hai jiska doosro ko bhi pata chal jata hai?
5. Kya kabhi aisa lagta hai jaise kisi ne aapko chuaa ho, lekin aas-paas dekhne par koi
nahi hota?

 Other Perceptual Disorders (Not Hallucinations)

1 Kya aapko aisa lagta hai jaise koi cheez ajeeb si ho rahi hai jise aap theek se samajh
nahi paa rahe hai?
2 Kya aap ki kalpana aap ko dhokha bhi de jaati hai?
3 Kya aisa lagta hai ki cheezo ki shakal, awaaz, gandh ya swaad ajeeb hai, waise nahi
jaise ki hona chahiye?
4 Kya awaazein kuch jyada hi saaf aur unchi mahsoos hone lagi hai, Har cheez badi
rangeen aur saaf-saaf dikhaayi dene lagi hai?
5 Kya cheezein kaali si, dhundhali si ya berangi si mahsoos hone lagi hai?
6 Kya log ya cheezein kuch ajeeb dhang se badli – badly nazar aati hai-jaise unki
shakal badal gayi ho ya choti-badi lagti ho ya rang mein farak lagta ho?
7 Kya aisa lagta hai ki in dino aap ki shakal-surat mein koi farak aa gaya hai?
8 Kya aap ko aisa lagta hai ki samay bahut tegi se ya bahut dheere-dheere beet raha
hai?
9 Kya aisa lagta hai ki khushi-gami wagairah kuch bhi mahsoos nahi hoti?

192
CHAPTER-XI
 DISORDERS OF THOUGHT
Thinking consists of the cognitive rearrangement or manipulation of both information from
the environment and the symbols stored in long term memory. A symbol represents or
stands for some event or item in the world; as we will see, images and language symbols
are used in much of our thinking.

Types of thinking: divided by Fish (1967) in to three types:

Fantasy thinking (also called dereistic or autistic thinking) is usually understood to be

creation of images or ideas that have no external reality. This process can be completely
non-goal directed, even if the subject is to some extent aware of the mood, affect, or drive
which motivates it. In other cases fantasy thinking serves to exclude reality because it
requires actions that the subject does not want to accomplish. This second kind of fantasy
thinking is not undirected. Its goal is not to solve a problem but to avoid it via neglect,
denial, or distortion of reality. Normal subjects use fantasy thinking deliberately and
sporadically. However, if its content becomes subjectively accepted as a real fact, it
becomes abnormal. This pathological exclusion of reality can remain limited in extent (e.g.
in hysterical conversion and dissociation, pseudologia phantastica, and some delusions) or
it may be manifested as complete autistic withdrawal from the real world.

Rational (conceptual) thinking attempts to resolve a problem through the use of logic,
excluding fantasy. The accuracy of this depends on the person's intelligence, which can be
affected by various disturbances of the different components involved in understanding and
reasoning. Problem solving and reasoning are two key aspects of rational thinking

Imaginative thinking can be located between the fantasy thinking and rational thinking.
This is a process of forming a representation of an object or a situation using fantasy but
without going beyond the rational and possible. This thinking is goal directed but frequently
leads to more general plans than the solution of immediate problems. The essential
difference between imaginative and rational thinking is that the former neglects the notion
that each theoretical assumption should be accompanied by an attempt to falsify or refute it.
Imaginative thinking becomes pathological if the person attaches more weight to his
representation of events than to other objectively equally possible interpretations. In
overvalued ideas, the imagined interpretation surpasses other interpretations in strength; in
delusions, all other possibilities are excluded (Sims et al, 2003).

Freud considered division of thought into primary and secondary process-

Primary process thinking-The more primitive type, includes thinking that is dereistic,
illogical, magical; normally found in dreams, abnormally in psychosis. This type of thinking
disregards logic, permits contradictions to exist simultaneously, disregards the linear notion
of time, and is dominated by wish and fantasy. It uses symbol, metaphor, imagery,
condensation, displacement, and concretism in its organization, creating the jumbled and
incoherent style of thinking characteristic of dreams and has been associated with visual
images and creative thought.

Secondary process thinking is characterized by logic. In contrast to primary process

thinking, the secondary process uses linear notions of time, clearly delineated abstract
categories, and deductive rules of logic. The abilities to think abstractly and to think in detail

193
about future plans are characteristic of secondary process thinking. Normal secondary
process thinking is also characterized by predictability, coherence, and redundancy. Words,
vocal inflections, and gestures provide important contextual cues and create a sense of
overall coherence to the communication. Ideas follow one another in a sequence that is
understandable to the listener (Yager & Gitlin, 2005).

Schneider suggested three features of healthy thinking

1. Constancy: this is characteristic of completed thought that does not change in content
unless and until it is superseded by another consciously derived thought.
2. Organisation: the content of thoughts is related to each other in consciousness and do
not blend with each other, but are separated in an organised way.
3. Continuity: there is continuity of the sense continuum, so that even the most
heterogeneous subsidiary thought, sudden ideas or observations that emerge are arranged
in order in the whole content of consciousness.

Some important definations :

A belief (or an inference) is something thought to be true because of observation or

evidence. It can often be subjected to empirical testing or logic to derive facts, which tend to
be objective and universally agreed.

A value is something thought to be good or important to an individual. Hence strongly held

values are the principles on which one will not yield and are not subject to empirical testing.
Normal values may be divided between those that are terminal (e.g. the importance of
happiness) and those that are instrumental (e.g. the importance of being honest).

Evaluations (or attitudes) are associated with values. They are a rating of an event or
person on a scale of good and bad. In comparison to beliefs, values or evaluations are not
subject to empirical testing. They are more difficult to measure or challenge because they
are subjective and personal. The division between beliefs and values is often blurred. They
are like two sides of a coin (Veale, 2002).

Belief systems are the scaffolding of thought, chains of impressions, and expectations
around which plans and behaviours are organized. Belief systems may be attitudinal,
setting general expectations and biases about the world that inform how incoming
information is processed; examples are optimism, pessimism, and paranoia. Some beliefs
are effervescent and fleeting, whereas others are pervasive, tenacious, enduring, and
influential. The enduring belief systems are associated with behaviours consistent with the
belief, at times dominating interpersonal relationships and lifestyles. Some beliefs are
unique and private, whereas many are shared by others (Yager & Gitlin, 2005).

Abstract thinking
The ability to assume a mental set, to keep simultaneously in mind all of the aspects of a
complex situation, to move from feature to feature as indicated by the situation, and to
abstract common properties. Complex thinking also concerns the ability to simultaneously
consider many different, vague, and subtle aspects of situations; to appreciate differing and
contradictory points of view; and to integrate these multiple dimensions to form opinions
that are marked by differentiatedness and nuance (Yager & Gitlin, 2005).

194
Concrete thinking
This is a disturbance in the ability to form abstract concepts, generally illustrated by literal
mindedness and the inability to abstract the commonality of members of a group, for
example, the fact that a flea and a tree are similar in that they are both living things.
Concrete thinkers seem unable to free themselves from the literal or superficial meanings of
words. Concrete thinkers may be more prone to prejudice and stereotypical thinking and
more likely to manifest uni-dimensional or “all-or-none” reactions to complex situations.
Concrete thinking can be seen in individuals with lower intelligence, organic mental
disorders, and schizophrenia (Yager & Gitlin, 2005).

CLASSIFICATION OF DISORDERS OF THINKING

Classification of disorders of thinking is bound to be arbitrary, at least to a certain extent.
The term “thought disorder” is often used somewhat loosely. However for the purpose of
description and discussion, it can be divided into following four groups:
 Disorders of stream of thought, or to put it into more familiar language, disorders of
belief and disorders of reasoning. It is obvious that this division is somewhat artificial
because belief and reasoning cannot be sharply separated.
 Disorders of Possession of thought, there are disorders of the control of thinking, in
which the subject is not in control of their thoughts, which may even be foreign to
them. This might be considered as a disorder of volition or ego-consciousness
 Disorders of content of thought
 Disorders of form of thought

DISORDERS OF THE STREAM OF THOUGHT

FLIGHT OF IDEAS: a continuous stream of talk in which the patient switches rapidly from
one topic to another and each subject is incoherent and unrelated to the preceding one or is
stimulated by some environmental circumstance. Acceleration of flow of thinking occurs in
flight of ideas, thoughts follow each other rapidly & there is no general direction of thinking.
Patient’s speech is easily diverted to external stimuli and by internal superficial
associations. Goal of thinking not maintained for long and there is logical connection
between each of two sequential idea expressed, association of train of thought to be
determined by chance relationship, verbal association, clang association proverbs maxims
and clichés. Flight of idea is typical of mania and in hypomania ordered flight of ideas
occurs in which despite of many irrelevances patient is able to return to task in hand. Clang
and verbal association are not so marked and speed of emergence of thought is not so fast.
Marginal variety of flight of ideas has been called prolixity. Flight of ideas occasionally
occurs in individual with schizophrenia when they are excited. Pressure of speech is an
increase in amount of spontaneous speech as compared to what considered ordinary or
socially customary. The patient talks rapidly and is difficult to interrupt. The quantitative
measure is the rate of speech production greater than 150 words/min (Anderson & Grove,
1986)

RETARDATION or INHIBITION or SLOWING of THINKING: In terms of model of flow of

thinking ,there is in retardation in the formation of associations. In this thinking is although
goal directed proceeds so slowly with such a morbid preoccupation with gloomy thoughts.
The train of thought slowed down and the no. of images and ideas that present themselves
is decreased. This is experienced by patient as decision making difficulty, lack of
concentration and loss of clarity of thought. The attention is also reduced that’s why the
events which occurred during that period are poorly registered. This may lead to an

195
overvalued idea that he is losing his memory (pseudo-dementia) or things are going out of
their mind (Casey & Kelly, 2007).

CIRCUMSTANTIALITY: a thought pattern in which a patient has difficulty in separating

relevant from irrelevant information while describing an event. The patient often includes all
details and presents them in a sequential order, with the result that the main thread of
thought becomes lost as one association leads to another. Frequently the person may need
to have questions repeated because the main point of answers has become lost in the
confusion of unnecessary detail the stream of thought is not impeded by affect but by defect
of intellectual grasp, a failure of the figure ground. The goal of thinking is never completely
lost and thinking proceeds towards it by an intricate and convoluted path. His whole
conversation becomes mass of parentheses and subsidiary clause. Determining tendency
remains, and eventually he does answer the question.

TANGENTIALITY: A disturbance in the associative thought process in which one tends to

digress readily from one topic under discussion to other topics that arise through
association.Characterized by replying to an question in an oblique, tangential, or even
irrelevant manner the reply may be related to the question in some distant way. Or reply
may be unrelated and even irrelevant manner. Previously tangentiality has been used as
roughly equivalent to loose association or derailment. The concept of tangentiality has been
partially redefined so that it refers only to replies to question and not to transition in
spontaneous speech (Casey & Kelly, 2007).

DISOREDER OF CONTINUITY OF THINKING

PERSEVERATION: This term refers to uncontrollable repetition of a particular response,
such as a word, phrase, or gesture, despite the absence or cessation of the original
stimulus. Usually it is seen in organic disorders of brain, head injury, delirium or dementia,
however can be seen in schizophrenia as well. Occurs when mental operations persist
beyond the point at which they are relevant and thus prevent progress of thinking and it’s
mainly verbal and ideational. (Casey & Kelly,2007).

THOUGHT BLOCKING: thought blocking occurs when there is sudden arrest of train of
thought, leaving a ‘blank’. An entirely new thought may then begin. In patient who retain
some insight . occurs when a person's thought is suddenly interrupted by silences that may
last a few seconds to a minute or longer[1]. Blocking is often brought on by questioning or
discussing something of particularly large personal significance. When the person begins
speaking again, after the block, they will often speak about a subject unrelated to what was
being discussed when blocking occurred. It is experienced as an unanticipated, quick and
total emptying of the mind When thought blocking is clearly present it is highly suggestive of
schizophrenia. However, patients who are exhausted and anxious may also lose the thread
of the conversation and may appear to have thought blocking. (Casey & Kelly, 2007).

OBSESSIONS, COMPULSIONS AND DISORDERS OF THE POSSESSION OF

THOUGHT
Normally one experiences one’s thinking as being one’s own, although this sense of
personal possession is never in the foreground of one’s consciousness. One also has the
feeling that one is in control of one’s thinking. In some psychiatric illnesses there is a loss of
control or sense of possession of thinking.

196
Obsessions and compulsions :
An obsession (also termed rumination) is a thought that persists and dominates an
individual’s thinking despite the individual’s awareness that the thought is either entirely
without purpose or else has persisted and dominated their thinking beyond the point of
relevance or usefulness. Obsessions are persistent ideas, thoughts, impulses, or images
that are experienced as intrusive and inappropriate and that cause marked anxiety or
distress...the content of the obsession is alien, not within his or her own control, and not the
kind of thought that he or she would expect to have"
One of the most important features of obsessions is that their content is often of a nature as
to cause the sufferer great anxiety and even guilt. The thoughts are particularly repugnant
to the individual. Compulsions are, in fact, merely obsessional motor acts. They may result
from an obsessional impulse that leads directly to the action, or they may be mediated by
an obsessional mental image or thought (E.g. when the obsessional fear of contamination
leads to compulsive washing when the obsessional fear of contamination leads to
compulsive washing).
Obsessional images are vivid images that occupy the patient’s mind. At times they may be
so vivid that they can be mistaken for pseudohallucinations. Thus one patient was
obsessed by an image of his own gravestone that clearly had his name engraved on it.
Sometimes obsessional thinking takes the form of contrast thinking in which the patient is
compelled to think the opposite of what is said. This can be compulsive blasphemy
(Casey& Kelly, 2007).

Obsessions occur in obsessional states, depression, schizophrenia, and

occasionally in organic states; compulsive features appear to be particularly common in
post-encephalitic Parkinsonism (Lishman, 1998).

Depressive Ruminations

Rumination is a train of thoughts, usually unproductive and prolonged, on a particular

topic, repeatedly experienced and are felt to be less intrusive. Ruminations are linked to
abnormal emotion, the valence typically reflected in the content of the thoughts. Persistent
ruminations are typical of melancholia. When obsessions involve overwhelming concerns
about health or contamination, they can be confused with depressive ruminations.
Depressive individuals ruminate about every day, real-life events whereas obsessive-
compulsive individuals will tend to have obsessions about unusual and clearly defined
topics (e.g. contamination concerns, aggressive thoughts, sexual thoughts). Obsessive
thoughts tend to centre around a current or future event, whereas depressive rumination
typically involves a past incident. Second, obsessive compulsive individuals often describe
their thoughts as intrusive, senseless and unwanted, and often report an attempt to resist
them. In direct contrast, depressive ruminators maintain that their thoughts are non-
intrusive and are rarely resisted. Another distinction between ruminations and obsessions,
prima facie, is the behavioural outcome: obsessions lead to compulsions. Thus, despite
some overlapping features, there are several reasons to identify OCD and depressive
rumination as separate entities (Taylor & Vaidya, 2009).

Thought alienation
In thought alienation the patient has the experience that their thoughts are under the control
of an outside agency or that others are participating in their thinking. In pure thought
insertion the patient knows that thoughts are being inserted into their mind and they
recognise them as being foreign and coming from without; this symptom, although

197
commonly associated with schizophrenia, is not unique to schizophrenia, and a range of
related phenomena have also been described (Casey& Kelly, 2007).
In thought deprivation, the patient finds that as they are thinking, their thoughts
suddenly disappear and are withdrawn from their mind by a foreign influence. It has been
suggested that this is the subjective experience of thought blocking and ‘omission’.
In thought broadcasting, the patient knows that as they are thinking, everyone else is
thinking in unison with them. While this is the definition of thought broadcasting provided by
Fish (Hamilton, 1984), there are also a number of other different definitions. For example,
the term has been used to describe the belief that one’s thoughts are quietly escaping from
one’s mind and that other people might be able to access them, and the experience of
hearing one’s thoughts spoken aloud and believing that, as a result, other people can hear
them; these various definitions are reviewed by Pawar and Spence (2003).

DISORDERS OF THE CONTENT OF THINKING :

Anxiety
Anxiety is the response to a threat that is unknown, internal, vague or conflictual. It is
characterized by intense negative affect, associated with an undefined threat to one's
physical or psychological self, Cognitively, anxiety is characterized by hyper vigilance, poor
concentration, subjective confusion, and fears of losing control or of going crazy and
catastrophic thinking.
Behavioral symptoms include fearful expressions, withdrawal, irritability, immobility, and
hyperventilation. Perceptual disturbances, including depersonalization, derealisation, and
hyperesthesia (especially hyperacusis). Anxiety is additionally characterized by somatic,
cognitive, behavioural, and perceptual symptoms. The somatic symptoms of anxiety
includes twitching, tremors, hot and cold flashes, sweating, palpitations, chest tightness,
difficulty swallowing, nausea, diarrhoea, dry mouth, and decreased libido.

Anxious foreboding is defined as a fear that something terrible will happen although the
person cannot identify what they are frightened of. It is accompanied by physical symptoms
of anxiety and must be distinguished from understandable foreboding such as experienced
by a person with cancer awaiting a scan result. Anxious foreboding is present in several
disorders such as generalised anxiety, depressive illness and panic disorder (Yager &
Gitlin, 2005).

Fear is a response to a known, external, definite, or nonconflictual threat. Most fears are
learned responses, such as the person who develops a fear of dogs after being bitten.
Some phobias are secondary to morbid states, most commonly depressive illness, and
others, such as fear of contamination, are regarded as obsessional symptoms.

Phobias are irrational fears. In an effort to reduce the intense anxiety attached to phobic
objects and situations, patients do their best to avoid the feared stimuli. Thus, phobias
consist both of the fears and the avoidance components. The fear itself may include all the
symptoms of extreme anxiety, up to and including panic (Yager & Gitlin, 2005).

Preoccupation
In body dysmorphic disorder the preoccupation revolves around imagined or slight defects
in self-appearance, whereas OCD concerns generally involve the overestimation of threat
or harm. Hypochondriasis refers to a persistent preoccupation with exaggerated concerns
about one’s health. The patient is intensely preoccupied with bodily sensations, is fearful for

198
disease, and is almost convinced of having physical disease OCD, in contrast, does not
typically involve aberrant bodily sensations. Second, the interpersonal dimension of these
disorders differs substantially. Individuals with OCD are generally secretive about their
disorder and tend to conceal it from public knowledge. Hypochondriacal patients will often
vocalise their distress in an attempt to justify the seriousness of their perceived illness
(Menzies & Silva, 2003) .Common descriptors (anankastic) obsessive–compulsive
personalities are: preoccupation with details (rules, lists, order, and schedules), excessive
conscientiousness, rigidity and stubbornness, and being overly controlling. Morbid
preoccupation with worthlessness and wanting to die is common in depression
.
Worry
It has three central components-a round of painful and unpleasant thought, not controlled
by attending to usually absorbing subjects, often out of proportion to the context. The
content of worry is not relevant to recognition of its form (SCAN Glossary, 1994). Worries
typically focus on daily concerns; obsessions may be more intrusive than worries; and
obsessions lead to compulsions. Like worry, rumination is a repetitive, iterative and
somewhat uncontrollable thought process and is similarly associated with anxiety and
depression. However, ruminations and worries can be distinguished in terms of their
frequency, duration, ratio of verbal to visual image content, interference, ego-dystonic
nature and elicited emotions; worry is typically expressed verbally, is more distracting, more
realistic, more voluntary and is associated with a stronger urge to act, whereas obsessive
ruminations are typically ego-dystonic, can occur through images and impulses as well as
verbal thought, and are more intrusive. Worry also appears to focus on future events,
whereas depressive rumination typically focuses on past events and experiences (Taylor, &
Vaidya, 2009).

Worthlessness
Respondent feels inferior to others, even worthless, exaggerated false picture of self not
counter balanced by a recognition that most human beings have similar faults (SCAN
Glossary, 1994).

Loss of hope for future

View of future is bleak without comfort and pessimistic irrespective of true circumstances.
There may be some islands of hope or attempts to cope, neglect of personal and social
affairs (SCAN Glossary, 1994).

Magical thinking
The person believes that apparently irrelevant actions can make a difference to reality, and
patients with OCD engage in compulsive behaviours that are often unrealistically connected
to the dreaded event that they are trying to prevent. At times magical thinking may reach
near-delusional proportions (SCAN Glossary, 1994).

Ideas of reference

Ideas of reference involve people having a belief or perception that irrelevant, unrelated or
innocuous phenomena in the world refer to them directly or have special personal
significance.Those afflicted cannot help feeling that people take notice of them, and that
aspects of them that they would prefer not to be noticed are somehow publicly observable.
There is insight into the symptom but reassurance is rarely helpful. The accompanying guilt
and shame are out of proportion compared to any possible cause. It should be

199
differentiated from guilty ideas of reference in which context of depressive mood and
content of guilt are primary (SCAN Glossary, 1994).

Non delusional jealousy

The person is preoccupied that his or her sexual partner might be unfaithful inspite of lack
of evidence and assurances of fidelity. It manifests as doubts with fluctuating certainty. It
can lead to searching of evidence. Importance to infidelity varies in between culture and
between sexes (SCAN Glossary, 1994).

Self-harm
Self-harm (SH) or deliberate self-harm (DSH) includes self-injury (SI) and self-
poisoning and is defined as the intentional, direct injuring of body tissue without suicidal
intent. Although suicide is not the intention of self-harm, the relationship between self-harm
and suicide is complex, as self-harming behaviour may be potentially life-threatening. There
is also an increased risk of suicide in individuals who self-harm (SCAN Glossary, 1994).

Overvalued idea
this is a thought which, because of the associated feeling tone, takes precedence over all
other ideas and maintains this precedence permanently or for a long period of time.
An over-valued idea may be generally conceptualised as follows (Veale, 2002):
a. Is held strongly, with less than delusional intensity.
b. Usually preoccupies the individual’s mental life, compared to many delusions.
c. Is ego-syntonic, compared to most obsessions.
d. Often develops in an abnormal personality.
e. Is usually comprehensible with knowledge of the individual’s past experience and
personality.
f. The content is usually regarded as abnormal compared to the general population (but not
bizarre as some delusions).
g. Causes disturbed functioning or distress to the patient and others.
h. Is associated with a high degree of affect (e.g. anxiety or anger when there is a threat to
the loss of their goal or object of the belief).
i. Compared to many delusions, is more likely to lead to repeated action which is
considered as justified.
j. Could progress to a delusion.
k. Patients may not seek help from mental health services but may be brought to the
attention of the services by a concerned relative or another agency.
l. Have some similarities to passionate religious or political convictions where the individual
usually remains functional.

Delusions
It is a false unshakable belief that is out of keeping with patient’s educational, cultural, and
social background; it is held with extraordinary conviction and objective certainty.
Karl Jaspers considered the lack of understandability of how the patient reached the false
conclusion to be the defining factor of a delusional idea. (Jaspers, 1962; Taylor & Vaidya,
2009)
For Jaspers, characteristics of delusion are
a. They are false judgement.
b. They held with extraordinary conviction and in comparable subjective certainty.
c. They are impervious to other experiences and to compelling counter argument.

200
d. Their content is impossible.

Kendler et al, (1983) have proposed several poorly correlated dimension or vectors of
delusional severity
a. Conviction: The degree to which the patient is convinced of the reality of delusional
beliefs.
b. Extension: The degree to which the delusional belief involves areas of patient’s life .
c. Bizarreness: The degree to which the delusional belief departs culturally determined
consensual reality.
d. Disorganization: The degree to which the delusional belief are internally consistent,
logical and systematization.
e. Pressure: The degree to which the patient is preoccupied and concerned with expressed
delusional beliefs.
f. Affective response: The degree to which the patient’s emotions involved with such beliefs.
g. Deviant behaviour resulting from delusion: Patients sometimes, but not always, act on
their delusions.

There is a distinction between true delusions and delusion-like ideas. True delusions are
the result of a primary delusional experience that cannot be deduced from any other morbid
phenomenon, while the delusion like idea is secondary and can be understandably derived
from some other morbid psychological phenomenon – these are also described as
secondary delusions (Sims, 2003).

Primary delusions

The essence of the primary delusional experience (also termed apophany) is that a new
meaning arises in connection with some other psychological event. Schneider (1959)
suggested that these experiences can be reduced to these forms of primary delusional
experience:

In the delusional mood (or atmosphere) the patient has the knowledge that there is
something going on around him that concerns him, but he does not know what it is. Usually
the meaning of the delusional mood becomes obvious when a sudden delusional idea or a
delusional perception occurs.
In the sudden delusional idea (delusional intuition) a delusion appears fully formed in
the patient’s mind. This is sometimes known as an autochthonous delusion. The form of
this symptom is not in itself diagnostic of schizophrenia because sudden ideas ‘out of blue’
or ‘brain-waves’ occur in individuals both with and without mental illness. In patients with
depressive disorders or severe personality disorders sudden ideas of the nature of
delusion-like ideas or overvalued ideas can occur. If a patient has a very grandiose or
bizarre sudden idea, a diagnosis of schizophrenia should be actively considered.

The delusional perception is the attribution of a new meaning, usually in the sense
of self-reference, to a normally perceived object. The new meaning cannot be understood
as arising from the patient’s affective state or previous attitudes. This last provision is
important because the delusional perception must not be confused with delusional
misinterpretation. Schneider emphasised the importance of this symptom’s ‘two
memberedness’, as there is a link from the perceived object to the subject’s perception of
this object, and a second link to the new significance of this perception (sometimes also
called delusional significance). Using this criterion,
201
 Schneider (1959) divided delusional memories into delusional perceptions and
sudden delusional ideas. For example, if the patient says that they are of royal descent
because they remember that the spoon they used as a child had a crown on it, this is really
a delusional perception because there is the memory and also the delusional significance,
i.e. the ‘two memberedness’. On the other hand, if the patient says that they are of royal
descent because when they were taken to a military parade as a small child the king
saluted them, then this is a sudden delusional idea because the delusion is contained within
the memory and there is no ‘two memberedness’. Primary delusional experiences tend to
be reported in acute schizophrenia but are less common in chronic schizophrenia, where
they may be buried under a mass of secondary delusions arising from primary delusional
experiences, hallucinations, formal thought disorder and mood disorders (Casey& Kelly,
2007).
Delusional memories can be distorted or false memories coming spontaneously into the
mind like delusional intuitions. In other cases they occur, like delusional percepts, in two
stages which mean that normal memories are interpreted with delusional meaning.
Delusional awareness is an experience which is not sensory in nature, in which ideas or
events take on an extreme vividness as if they had additional reality (Sims, 2003).

Secondary delusions and systematisation

Secondary delusions can be understood as arising from some other morbid experience.
There is now considerable acceptance that delusions can be secondary to depressive
moods and hallucinations, and that psychogenic or stress reactions can give rise to
psychotic states with delusions.Delusions are divided into systematised and non-
systematised. In the completely systematised delusions there is one basic delusion and the
remainder of the system is logically built on this error. There may, however, be differing
degrees of systematisation in different patients, and the level of systematisation may vary
over time, with systematisation being generally more common in older patients or in
patients whose delusions prove persistent.

Delusional evidence is the basis of delusion, the reason the patient gives for holding his
belief; which like the belief itself is false, unacceptable and in corrigible.

Partial delusion
Ideas not held with complete conviction but the content is so bizarre that entertaining them
at all seems abnormal (Mckenna, 1994). Wing et al (1974) have also called it partially held
delusion. Such doubts may be seen during the slow development of a delusion, as the
delusion is gradually given up, or intermittently throughout its course.

Pathoplastic delusion
Normal social beliefs or overvalued ideas that may be expressed with individuals own
pathoplastic colouring, so that other members of the same parent group recognise it as
abnormal. E.g. culture specific disorders (SCAN Glossary, 1994).

The content of delusions

The content of delusions in schizophrenia is dependent, to a greater or lesser extent, on the
social and cultural background of the patient. Common general themes include persecution,
jealousy, love, grandiosity, ill health, guilt, nihilism and poverty.

202
Delusion of persecution
a delusion that one is being attacked, harassed, persecuted, cheated, or conspired against.
Delusions of persecution can take many forms. In delusions of reference the patient knows
that people are talking about him, slandering him or spying on him. Ideas and delusions of
reference are not confined to schizophrenia and can occur in depressive illness and other
psychotic illnesses. Some patients with severe depression may believe that they are
extremely wicked and that other people know this and are therefore quite justifiably spying
on them.The supposed persecutors of the deluded patient may be people in the
environment (such as members of the family, neighbours or former friends) or may be
political or religious groups, of varying degrees of relevance to the patient. Some patients
believe that they or their loved ones are about to be killed, or are being tortured. In the latter
case the delusions may be based on somatic hallucinations. The belief that the family is
being harmed may be deduced from the content of the hallucinatory voices or the patient
may claim that their relatives appear to be strange in some way and are obviously suffering
from some interference. These symptoms may also be related to a perceptual or mood
change in the patient. Some patients with delusions of persecution claim that they are being
robbed or deprived of their just inheritance, while others claim they have special knowledge
that their prosecutors wish to take from them.
(Casey& Kelly, 2007).

Bizarre delusions
Bizarre delusions are defined as " . . . clearly implausible and not understandable and not
derived from ordinary life experiences". In ICD-10(World Health Organization, 1992) a
patient can be diagnosed with schizophrenia if she/he has any one of Schneider's FRS that
are specifically named or if she/he has "persistent delusions of other kinds that are
culturally inappropriate and completely impossible, such as religious or political identity,
superhuman powers and ability . . . ". Examples of delusions rated as both Schneiderian
and bizarre are, "Even people in Venezuela can hear my thoughts" and "There is a camera
in my tooth which is taking photographs of the contents of my mind." (Tanenberg-Karant, M.
et al, 1995).

Delusions of infidelity (Othello syndrome/ Morbid or pathological jealousy)

The commonly used term ‘delusion of jealousy’ is generally a misnomer as patients tend to
have morbid jealousy with delusions of infidelity, rather than delusions of jealousy (Munro,
1999). Delusions of infidelity may occur in both organic and functional disorders. Often the
patient has been suspicious, sensitive and mildly jealous before the onset of the illness.
Delusions of infidelity are also seen in the affective psychosis, where they may again
represent a morbid exaggeration of a premorbid mildly jealous attitude. Delusions of
infidelity may develop gradually, as a suspicious or insecure person becomes more and
more convinced of their spouse’s infidelity and finally the idea reaches delusional intensity.
The severity of the condition may also fluctuate over the course of time, and during
episodes of marked disturbance, the spouse may be interrogated unceasingly and may be
kept awake for hours at night. behaviour may progress to violence against the spouse and
even to murder. Apart from delusions of infidelity, these patients tend not to show any other
symptoms that would suggest schizophrenia (Casey& Kelly, 2007).

Delusions of love (de Cleramboult syndrome)

This condition has also been described as ‘the fantasy lover syndrome’ and
‘erotomania’. The patient is convinced that some person is in love with them although the

203
alleged lover may never have spoken to them (Kelly, 2005). They may pester the victim
with letters and unwanted attention of all kinds. If there is no response to their letters, they
may claim that their letters are being intercepted, that others are maligning them to their
lover, and so on. Occasionally, isolated delusions of this kind are found in abnormal
personality states. Sometimes, schizophrenia may begin with a circumscribed delusion of a
fantasy lover and subsequently delusions may become more diffuse and hallucinations may
develop (Casey& Kelly, 2007).

Grandiose delusions (identity, ability and mission)

There is considerable variability in the extent of grandiosity associated with grandiose
delusions in different patients. Some patients may believe they are God, the Prime Minister,
a famous film star and so on. Others are less expansive and believe that they are skilled
sportspersons or great inventors The expansive delusions may be supported by auditory
hallucinations, which tell the patient that they are important, or confabulations, when, for
example, the patient gives a detailed account of their coronation or marriage to the king.
Grandiose and expansive delusions may also be part of fantastic hallucinosis in which all
forms of hallucination occur. (Casey& Kelly, 2007).

Delusions of ill health :

Delusions of ill health are a characteristic feature of depressive illnesses, but are also seen
in other disorders, such as schizophrenia. Delusions of ill health may develop on a
background of concerns about health; many people worry about their health and when they
become depressed they naturally may develop delusions or overvalued ideas of ill health.
This paradigm is similar to that advanced in the case of persecutory delusions, which may
occur on a background of worry about one’s relationships with others or suspiciousness
about the intentions of other people. Such individuals, when depressed, may develop
overvalued ideas or delusions of persecution. Individuals with delusions of ill health in the
context of depression may believe that they have a serious disease, such as cancer,
tuberculosis, acquired immune-deficiency syndrome (AIDS), a brain tumour, and so on.
Depressive delusions of ill health may involve the patient’s spouse and children.Delusions
of ill health may take the form of primary or secondary delusions of incurable insanity.

Hypochondriacal delusions in schizophrenia can be the result of a depressed mood,

somatic hallucinations or a sense of subjective change. In the early stages, these delusions
are usually the result of depression and may develop as mistaken explanations of
psychological or physical symptoms. In individuals with chronic schizophrenia, they are
usually the result of somatic hallucinations. In Hypochondriacal delusions in context of
depression respondents feel that their body is unhealthy, rotten or diseased. They can only
be reassured for a brief while that this is not the case. In more intense forms of the
symptom, there is a delusional conviction of the presence of incurable cancer, or that the
bowels are stopped up or rotting away. This symptom is in many ways similar to delusions
of depersonalization and both can be coded together Somewhat similar to these delusions
are the delusional preoccupations with facial or bodily appearances, when the subject is
convinced that their nose is too big, their face is twisted, or disfigured with acne, and so on.(
World Health Organization, 1992).

Olfactory delusions that one emanates a foul odour are common in social anxiety
syndromes, in which individuals are particularly concerned about potentially embarrassing
themselves and others (Casey & Kelly, 2007).

204
Nihilistic delusions (Cotard Syndrome)
Nihilistic delusions or delusions of negation occur when the patient denies the existence of
their body, their mind, their loved ones and the world around them. They may assert that
they have no mind, no intelligence, or that their body or parts of their body do not exist; they
may deny their existence as a person, or believe that they are dead, the world has stopped,
or everyone else is dead. These delusions tend to occur in the context of severe, agitated
depression (Cotard’s syndrome) and also in schizophrenia and states of delirium.
Sometimes nihilistic delusions are associated with delusions of enormity, when the patient
believes that they can produce a catastrophe by some action e.g. they may refuse to
urinate because they believe they will flood the world (Casey & Kelly, 2007).

Delusions of guilt in context of depression

This symptom is grounded in a depressed mood. Those affected think they have brought
ruin to their family by belling in their present condition or that their symptoms are a
punishment for their wicked incompetence. In a more severe form of the symptom, there is
a delusional conviction that they have sinned greatly, or committed some terrible crime, or
brought ruin upon the world; i.e. there may be a grandiose quality to the delusion. They may
feel that they deserve punishment, even death or hell-fire, because of it. They may say that
their offense and the punishment it has merited are unnamable (SCAN Glossary, 1994) .

Delusional ideas of reference based on guilt

People suffering from severe depression may believe that others are blaming them for, or
accusing them of, actions of feelings about which they themselves feel guilty. One woman
thought the local council were leaving 'skips' (containers for the disposal of waste) in her
neighborhood, as a hidden message that they knew she had not been keeping up her usual
high standards of cleanliness and housework. Another thought that nursing staff were
disguised police officers, keeping her under surveillance because of her delusional belief
that she had allowed a cannabis plant to grow in her garden (SCAN Glossary, 1994).

Delusions of catastrophe in context of depression

Respondents believe that terrible things are going to happen to their families and others
with whom they are connected. Their family, friends and colleagues may be dragged down
to financial ruin, and may end up starving of in prison as a result of R's failings. Delusions of
poverty should be rated under this rubric. Affect is depressed the symptom may be more
intense, as when the subject has a delusional conviction that the world is about to end, that
some enormous catastrophe has occurred or is going to occur, that the world is decayed,
dirty and rotten (SCAN Glossary, 1994).
Delusions of poverty
The patient with delusions of poverty is convinced that they are impoverished and believe
that destitution is facing them and their family. These delusions are typical of depression
but appear to have become steadily less common over the past decades (Casey & Kelly,
2007).

Delusions of reference :
Delusions of reference consist of a further elaboration of the ideas of this experience in so
far as other people are involved. Thus what is said may have double meaning, or someone
makes a gesture which subjects construe as a deliberate message, e.g., someone
crossing his legs may be taken to mean that respondent is homosexual. The whole
neighborhood may seem to be gossiping about respondents far beyond the bounds of

205
possibility, or they may see references to themselves on the television or in newspapers
(SCAN Glossary, 1994).

Delusional misinterpretation
This item is a further extension of the delusion of reference in that not only do people seem
to refer to respondent directly but whole situations are interpreted in a self-referential way.
The arrangement of objects may seem to have special significance. Things seem to be
arranged to test respondents, street signs or advertisements on buses, or patterns of color
seem to have been put there in order to give messages. This may go so far that whole
armies of people may seem to be preoccupied with respondent (SCAN Glossary, 1994).

Delusional ideas of reference based on expansive mood

Respondents who are elated may have such an expansive notion of their talents, beauty,
attention for the neighborhood (SCAN Glossary, 1994).

Delusional paranormal explanations

This includes any delusional explanation or elaboration of other abnormal experience, such
as thought insertion or broadcast of delusions of reference of persecution, in terms of
paranormal phenomena. Include explanations in terms of hypnotism, telepathy, magic,
witchcraft', etc. Note that using the word telepathy merely to describe a process of thought
transfer is not a delusional explanation. If telepathy is used in the sense of explaining a
mechanism it may be rated here (SCAN Glossary, 1994) .

Delusional memories and fantastic delusions

Delusional memories are experiences of past events which clearly did not occur but which
the subject equally clearly remembers. Classically, these memories come suddenly into the
mind and have the characteristic of something forgotten once more recollected. Fantastic
delusions, unlike, for example, delusions of reference or persecution, are physical
impossibilities, rather than social improbabilities. it should be differentiated from
confabulation in compensation for short term memory loss (SCAN Glossary, 1994).

Delusional misidentification
In this item, although there is no change in perception, respondents misidentify those
around them in a way that fits their own self-reference and their overall delusional system.
They may claim that bystanders are people from their past brought in, in order to convey
impostors. This is otherwise known as the Fregoli Syndrome (SCAN Glossary, 1994).

Familiar people impersonated

Respondents believe that people well known to them, often friends or members of the
family, are not who they purport to be, but are being deliberately impersonated by
strangers. The clinical context can be very varied and the symptom should be rated
independently of possible diagnosis (Capgras Syndrome) (SCAN Glossary, 1994).

Delusions of pregnancy (Pseudocyasis/Couvade)

Respondents think they are pregnant although the circumstances make it clear that they
cannot possibly be. They may be male, or clearly menopausal, or virgin, or abstinent. One
subject was a widow, had not had intercourse for several years, and was well past the
menopause, but was convinced that she had been pregnant for two years, after a
momentary encounter with a strangest in a lift. Why she thought this incident which, from
her description was completely innocent, could have made her pregnant, never came close

206
to consciousness. The symptom has many of the characteristics of a hypochondriacal
delusion (SCAN Glossary, 1994).

Delusion that others accuse Respondent of homosexuality

Respondents who apparently have no particular leaning towards their own sex nevertheless
believe that they are being accused of belling homosexual. They may think they overhear
remarks about some peculiarly of gait or manner of physique, or base their conviction on
the interpretation of meaningful' looks and signs (SCAN Glossary, 1994).

Influence playing on the body, somatic passivity.

The patient is a passive and invariably a reluctant recipient of bodily sensations imposed
upon him by some external agency. According to Jaspers the perception is simultaneously
experienced as being both a bodily change and externally controlled. It is a single
experience and not simply the delusional interpretation of an abnormal bodily sensation.
These somatic perceptions may be due to haptic, thermic or kinaesthetic hallucinations.
Sometimes there may be an admixture of different hallucinations. Jaspers states that the
physical sensation may occasionally be genuine and not a hallucination (Sims, 2003).

Made impulses (drives)

A powerful impulse overcomes the patient to which he almost invariably gives way. The
impulse to carry out this action is not felt to be his own, but the actual performance of the
act is. The impulse is made by an external agency and imposed upon the helpless victim
from without. There is usually a secondary delusion to explain the mechanism by which the
impulse is imposed (Sims, 2003).

Made volitional acts

The patient experiences his actions as being completely under the control of an external
influence. The movements are initiated and directed throughout by the controlling influence,
and the patient feels he is an automaton, the passive observer of his own actions (Sims,
2003).

Made feelings (emotions)

The patient experiences feelings which do not seem to be his own. The feelings are
attributed to some external source and are imposed upon him (Sims, 2003).

The reality of delusions

Not all individuals with delusions act on their delusional beliefs. Usually, when a delusional
illness becomes chronic there is a discrepancy between the delusions and the patient’s
behavior. Depressive delusions of guilt and hypochondriasis may lead to action if the
patient does not exhibit psychomotor retardation. Hypochondriacal delusions may lead to
suicide or, if they involve the patient’s family, homicide. Individuals with depression with
severe delusions of guilt may try to give themselves up to the police. Delusions of infidelity
are particularly
dangerous and may be associated with violence or homicide (Munro, 1999). It is also
possible that similar actions may be taken on the basis of delusion like ideas or overvalued
ideas, which may occur in individuals who do not have a major mental illness. (Casey &
Kelly, 2007)

207
DISORDERS OF THE FORM OF THINKING
The term ‘formal thought disorder’ is a synonym for disorders of conceptual or abstract
thinking that are most commonly seen in schizophrenia and organic brain disorders. Most
other descriptions of formal thought disorder in schizophrenia describe the same
phenomena in terms of different psychological concepts.
Bleuler (1911) considered the ability to communicate in speech was thought to depend on
the strength and universality of associations, so that a word spoken will evolve similar
associations in the audience to those that it does in the speaker. Loosening of associations
was the basic disorder on the premise of which Bleuler (1911) described schizophrenic
thought disorder. The absence of central determining tendency led thought to be
determined by incidental thoughts (coexisting with the original one), clang associations
(when ideas are associated by sound), condensation (when two or more ideas are fused
into one), displacement (an associated idea is used in place of the correct one), indirect
association (when one association step is omitted), perseveration (when certain ideas,
words or phrases come to dominate the train of thought), and symbolism (use of symbols in
a concrete way). Bleuler borrowed these concepts from Freud, who had pointed out that
these mechanisms were characteristic of thinking in dreams (Casey & Kelly, 2007).
Cameron (1938, 1944); was an American psychiatrist who was one of the earliest to carry
out an empirical study of thought disorder with the help of logical problems and concept
formation test. He mentioned four types of thought disorders:

Asyndetic thinking: This involves use of loose cluster of more or less related thoughts for
well integrated concepts. Resulting in the lack of adequate connections between
successive thoughts.

Metonymy: Substitution of a related term in place of a more appropriate term and may
include excessive personal idiom and fantasy material in their speech.

Interpenetration of themes: Two concurrent streams of thought- one dealing with current
situation and other dealing with personal matters or fantasy -keep interfering with one
another resulting in confused speech.

Overinclusion: The schizophrenic is unable to maintain the boundaries of the problem,
which is an inability to narrow down the operations of thinking and bring into action the
organised attitudes and specific responses relevant to the task at hand.

Goldstein (1944) emphasised the loss of abstract attitude in patients with schizophrenia,
which leads to a ‘concrete’ style of thinking, despite the fact that the patient has not lost
their vocabulary (unlike patients with organic brain disorders). (Hamilton, 1984)
Karl Kleist: Kleist (1960) mentioned three kinds of thought disorder-incoherence (no
understandable connection between one thought and the next), paralogia or sensory
thought disorder (concepts emerge in an incomplete way resulting in derailment and
displacement) and alogia or motor thought disorder (no new thoughts emerge) (Hamilton,
1984).
Schneider claimed that individuals with schizophrenia had three different disorders of
thinking that correspond to these three features of normal or non-disordered thinking, as
follows:

Transitory thinking
Transitory thinking is characterised by derailments, substitutions and omissions. Omission
is distinguished from desultory thinking because in desultoriness the continuity is loosened
but in omission the intention itself is interrupted and there is a gap. The grammatical and
syntactical structures are both disturbed in transitory thinking.

208
Drivelling thinking
With drivelling thinking, the patient has a preliminary outline of a complicated thought with
all its necessary particulars, but loses preliminary organisation of the thought, so that all the
constituent parts get muddled together. The patients with drivelling have a critical attitude
towards their thoughts, but these are not organised and the inner material relationships
between them become obscured and change in significance.
Desultory thinking
In desultory thinking speech is grammatically correct but sudden ideas force their way in
from time to time. Each one of these ideas is a simple thought that, if used at the right time
would be quite appropriate.

Schneider claimed that five features of formal thought disorder could be identified:
derailment, substitution, omission, fusion and drivelling. In derailment the thought
slides on to a subsidiary thought, while in substitution a major thought is substituted by a
subsidiary one. Omission consists of the senseless omission of a thought or part of it. In
fusion, heterogeneous elements of thought are interwoven with each other, while in
drivelling there is disordered intermixture of constituent parts of one complex thought.
These disorders may be difficult to distinguish from each other in the clinical setting.

Loosening of associations (Derailment)

A pattern of spontaneous speech in which the ideas slip off the track onto another one
which is clearly but obliquely related, or onto one which is completely unrelated. Things
may be said in juxtaposition which lack a meaningful relationship, or the patient may shift
idiosyncratically from one frame of reference to another. At times there may be a vague
connection between the ideas, and at others none will be apparent. This pattern of speech
is often characterized as sounding "disjointed.’ Perhaps the commonest manifestation of
this disorder is a slow, steady slippage, with no single derailment being particularly severe,
so that the speaker gets farther and farther off the track with each derailment without
showing any awareness that his reply no longer has any connection with the question which
was asked This abnormality is often characterized by lack of cohesion between clauses and
sentences and by unclear pronoun referents. Tangentiality has been defined herein as a
different phenomenon in that it occurs as the immediate response to a question
.(Andreason & Grove, 1986)

Incoherence (Word Salad, Jargon Aphasia, Schizophasia, Paragrammatlsm)

A pattern of speech which is essentially incomprehensible at times. The incoherence is due
to several different mechanisms, which may sometimes all occur simultaneously.
Sometimes portions of coherent sentences may be observed in the midst of a sentence
which is incoherent as a whole. Sometimes the disturbance appears to be at a semantic
level, so that words are substituted in a phrase or sentence so that the meaning seems to
be distorted or destroyed; the word choice may seem totally random or may appear to have
some oblique connection with the context. Sometimes "cementing words" (coordinating and
subordinating conjunctions such as "and," "although"; adjectival pronouns such as "the,"
"a," and "an") are deleted.
Incoherence is often accompanied by derailment. It differs from derailment in that the
abnormality in incoherence occurs within the level of the sentence or clause, which contains
words or phrases that are joined incoherently. The abnormality in derailment involves
unclear or confusing connections between larger units, such as sentences or clauses
(Andreason & Grove, 1986).

209
Neologisms
New word formations. A neologism is defined here as a completely new word or phrase
whose derivation cannot be understood; it may be a distortion of another word. Sometimes
the term "neologism" has also been used to mean a word which has been incorrectly built
up but with origins which are understandable as due to a misuse of the accepted methods
of word formation. Holophrastic is defined as using a single word to express a combination
of ideas and seen in schizophrenia.

Word Approximations (Paraphasia, Metonyms)

Old words which are used in a new and unconventional way or new words which are
developed by conventional rules of word formation. Often the meaning will be evident even
though the usage seems peculiar or bizarre (i.e., a ballpoint pen referred to as
"paperskate," etc.). Sometimes the word approximations may be based on the use of stock
words, so that the patient uses one or several words repeatedly in ways that give them a
new meaning (i.e., a watch may be called a "time vessel," the stomach a "food vessel," a
television set a "news vessel," etc.).

Conclusion
The disorders of thinking are as vivid as the process of normal thinking itself, but despite
the vividness it can be lucidly understood after demarcating the domains. Normal thinking
has a proper flow, is goal directed, reality oriented, consists of symbols and ideas from
environment and memory, and results in transfer of meaningful information from stimulus to
a response to it.
Disorders of thought are assessed in four major domains
a) Stream: Tempo[Fast or Slow, Goal Directedness], Continuity[Perseveration, Blocking]
b) Possession: Obsessions, Thought Alienation
c) Content: Ideas, Delusions, Overvalued Ideas; Worry, Preoccupations, Anxiety
d) Form: Loosening of Associations, Incoherence

REFERENCE :-

 Abu-Akel,A.(1999)Impaired theory of mind in schizophrenia .Pragmatics and Cognition,7,247-282.

 Adams,A.(1959)’Psychopathologie des Gedachtnisses’ (psychopathology of the memory). Fartschr.
Neurol. Psychiat. 27,243.
 Adler,A.(1927).U ber den nervosen Charakter:Grundzuge einer vergleicheden Individual psychologie
and psychotherapie. In K.H.Witte (Ed),Kommentierte text Kritische. Ausgabe.Gettingen:Vandenhoeck
and Ruprech
 American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th
edn) (DSM–IV). Washington DC, APA.
 American Psychiatric Association, 1980. Diagnostic and StatisticalManual of Mental Disorders, (DSM-
III), 3rd ed. American Psychiatric Association Press, Washington, DC.
 Andreasen, N.C, (1979) Thought language and communication disorder. Clinical assessment,
definition of terms and evaluation of their reliability, Archive of General Psychiatry, 36, 1315-1321.
 Andreasen, N.C., & Grove, W.M. (1986) Thought, language, and communication in schizophrenia:
Diagnosis and prognosis. Schizophrenia Bulletin, 12, 348-359.
 Andreasen,N.C(1984). Scale for the assessment of positive symptoms. Iowa city, Iowa: University of
Iowa, Department of psychiatry, Iowa city, Iowa.
 Baron –Cohen,S.,Leslie,A.M., and Frith,U.(1995)Does the autistic child have a ‘theory of mind’?
Cognition,21:37-46.
 Baron-Cohen ,S.,1995.Mind blindness: An Essay on Autism and Theory of Mind.Cambridge,
MA.Bradford/MIT Press.

210
 Berriors GE (1985)The History of Mental Symptoms: Descriptive Psychopathology Since the
Nineteenth cenury.Cambridge:Cambridge University Press.
 Blackwood,N.J.,Howard,R.J.,Bentall,R.P.,&Murray,R.M.(2001).Cognitive Neuropsychiatric models of
persecutory delusions. American journal of Psychiatry,158,527-539.
 Bleular E (1911).Dementia Precox or the Group of Schizophrenics(transl .Zinkin J.1950).New
York:International Universities Press.
 Bleuler, E. (1911) Dementia Praecox or the Group of Schizophrenias. Reprinted 1950 Zinkin, J.,
(Trans. & Ed.). New York: International University Press as cited in Casey. P.R. & Kelly, B. (2007)
Fish's Clinical Psychopathology: Signs and Symptoms in Psychiatry, 3rd ed. London, RCPsych
Publications,32-54
 Cameron, N. (1938) Reasoning, regression and communication in schizophrenics. Psychological
Monographs,50,1-34.
 Cameron, N. (1944) Experimental analysis of schizophrenic thinking. In: Kasanin, J. (Ed) Language
and Thought in Schizophrenia. Berkeley, CA: University of California Press as cited in Casey. P.R. &
Kelly, B. (2007) Fish's Clinical Psychopathology: Signs and Symptoms in Psychiatry, 3rd ed., London,
RCPsych Publications. 32-54
 Caplan, R., Guthrie, D., Tang, B., Komo, S., Asarnow, R.F., 2000.Thought disorder in childhood
schizophrenia: replication andupdate of concept. Journal of the American Academy of Child and
Adolescent Psychiatry 39, 771–778.
 Casey, P.R. & Kelly, B. (2007) Fish's Clinical Psychopathology: Signs and Symptoms in Psychiatry,
3rd ed. London, RCPsych Publications pp. 32-54.
 Chadwick,P.D.J.,&Lowe ,C.F,(1994) A cognitive approach to measuring and modifying delusions.
Behaviour Research and Therapy,25,35-49.
 Colby KM(1975)Appraisal of four psychological theories of paranoid phenomena.Journal of Abnormal
Psychology 86,54-59.
 Cummings,J.L(1985) Organic delusions: Phenomenology, anatomical correlations, and review.British
Journal Of Psychiatry,146,184-197.
 Epstein, S (1953) Overinclusive thinking in a Schizophrenic and a control group. Journal of
Counselling Psychology,17,384-388.
 Exner,J.E.(1993) The Rorschach : A Comprehensive System .Volume 1:Basic foundations (3rd
Ed).New York:Wiley.
 Exner,J.E.(2000). A Primer for Rorschach Interpretation . Ashville,NC,:Rorschach Workshops.
 Faught, W.S.,Colby,K.M.,Parkinson,R.C.(1977). Inferences, affects, and intentions in a model of
paranoia. Cognitive Psychology,9, 153-187.
 Ford, J M., Pfefferbaun, A., Roth, W., (1992). P3 and Schizophrenia., Ann. NY Acad, Science, 658,
146-162.
 Freud,S (1953) The interpretation of dreams. In: The complete works of Sigmund Freud, Vol 4,
London, Hogarth press.
 Freud,S. (1978). Psychoanalytische Bmerkungen “uber einen autobiographisch beschreivenen.” Fall
von Paranoia (Dementia Paranoides). Gesammelte Werke, Vol.8.Frankfurt, Germany: Fischer Verlag.
(Originally published in 1911)
 Frith, C.D.,& Frith, U(1992). Interacting minds- a biological basis-Science ,286,1692-1695.
 Fukuchi – Shimogori, T., & Grove, E. A. (2001) Neocortex pattering by the secreted signaling
molecule FGF8, Science, 294, 1071–1074.
 Hamilton, M. (1984), Fish’s Schizophrenia, 3rd ed., Bristol, John Wright & Sons, 38-77.
 Goldstein,K.& Scheerer,M.(1944) Abstract and Concrete behaviour : An experimental study with
special tests .Psychological Monographs,53,1-239.
 Hagen, F.W. (1870) Studien auf dem gebiet der seelenheilkunde. Erlangen, Germany: Besold.
 Hamilton M (1978) Fish’s outline of Psychiatry,3rd edn.Bristol:John Wright.
 Harrow,M.& Quinlan ,D.(1985) Disordered Thinking and Schizophrenic Psychopathology, New York:
Gardener Press.
 Harrow,M.& Quinlan ,D.(1985) Disordered Thinking and Schizophrenic Psychopathology, New York:
Gardener Press.
 Hawton ,K.,Salkovskis ,P.,Kirk, J.and Clark, D. (1989) Cognitive Behavior Therapy for Psychiatric
Problems: A Practical Guide. New York: Oxford University Press.
 Jaspers, K.(1962) General Psychopathology (Trans. Hamilton,M.W. and Hoeing,J.) Manchester:
Manchester University Press.

211
 Jaspers,K.(1911)’Zui Analyseder Trugwahrnehmungen (Leibhaftigkeit and Realitat Surteil)’ Analysis
of sense deception-Substantiality and reality judgement, Z.Ges.
M.Neurol.Psychiatry.,Originalien,6,460.
 Johnston,M.H.& Holzman ,P.S.(1979)Assessing Schizophrenic Thinking. A Clinical and Research
Instrument for Measuring Thought Disorder. San Francisco: Jossey –Bass.
 Kaplan,H.I., Sadock’s Synopsis of Psychiatry(9th ed).Philadelphia: Lippincott William &Wilkins.
 Kay,S.R.,Opler,L.A.,Lindermayer,J.P.(1989)The Positive and Negative syndrome
Scale(PANSS):Rationale and standardisation .British Journal of Psychiatry,155,59-65.
 Kelley,H.L. (1967) Attribution theory in social psychology In .D.Levine( Ed.)Nebraska Symposium on
Motivation, 15. Lincoln: University of Nebraska Press.
 Kelly, B. D. (2005) Erotomania – epidemiology and management. CNS Drugs, 19,657–669 as cited in
Casey. P.R. & Kelly, B. (2007) Fish's Clinical Psychopathology: Signs and Symptoms in Psychiatry,
3rd ed., pp., London, RCPsych Publications, 32-54
 Kleist, K. &Schwab, H.(1960) Die Verworrenen Schizophrenien auf Grund Katamnestischer Unters
uchungen.Teil II.Die denkverwirrten Schizophrenien ‘(The confused Schizophrenias as seen in a
follow –up study.PartII. The thought-confused schizophrenias).Archieves.Psychiatry
NervKrankh.184,28.
 Kleist, K. (1914) Aphasia and Geisteskrankheit. Munchener Medizinische Wochenschrift, 61, 8-12.
 Kleist, K.(1960) Schizophrenic symptoms and mental pathology. Journal of Mental Sciences, 106,
246-255. Goldstein, K. (1944) Methodological approach to the study of schizophrenic thought
disorder. In: Kasanin, J. (Ed) Language and Thought in Schizophrenia. Berkeley, CA, University of
California Press, as cited in Hamilton, M. (1984), Fish’s Schizophrenia, 3rd ed., , Bristol, John Wright
& Sons, 38-77
 Liddle,P.F.,Ngan,E.T.C. & Caissie ,S.L.,(2002) Thought and Language Index : an instrument for
assessing thought and language in Schizophrenia, British Journal of Psychiatry,181,326-330.
 Lishman, W.A. (1998) Organic Psychiatry, 3rd edn. Oxford: Blackwell Science.
 Maher, B. A., & Ross, J. S. (1984) Delusions. In H. E. Adams & P. B. Sutker (Eds.), Comprehensive
handbook of psychopathology(1st ed.). New York: Plenum.
 Maher, B. A., & Ross, J. S. (1984). Delusions. In H. E. Adams & P. B. Sutker (Eds.), Comprehensive
handbook of psychopathology(1st ed.). New York: Plenum.
 Mandal,M.K.,Nizamie,S.H.(2004) Current development in Schizophrenia.Allied Publishers Pvt Ltd.
 McGrath P(1990) Spider.London:Penguin.
 McKenna PJ(1991)Disorders with overvalued ideas.British Journal of Psychiatry 145,579-585.
 McKenna, P. J. (1984)Disorders with overvalued ideas. British Journal of Psychiatry, 145, 579–585.
 McKenna, P.J. (1994) Schizophrenia and related syndromes, 1st ed., pp.1-30, New York, Oxford
University PressAmerican Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental
Disorders (4th edn) (DSM–IV). Washington DC, APA.
 Menzies, R.G. & Silva, P. (2003) Obsessive-Compulsive Disorder: Theory, Research and Treatment.
pp.3-20, West Sussex, John Wiley & Sons Ltd. Veale, D. (2002). Over-valued ideas: a conceptual
analysis, Behaviour Research and Therapy, 40, 383–400.
 Munro, A. (1999) Delusional Disorder: Paranoia and Related Illnesses. Cambridge, Cambridge
University Press.
 Murray,H.A.(1943) The Thematic Apperception Test Manual .Cambridge ,M.A.: Harvard University
Press.
 Overall, J.E& Gorham,D.R., Shawver,J.R.(1962) Basic dimensions of change in the symptomatology
of chronic schizophrenics. Journal of abnormal and Social Psychology, 63,597-602.
 Overall,J.E., Gorham ,D.R.(1962)The Brief Psychiatric Rating Scale .Psychological Report,10,799-
812.
 Pavlov,I.P. (1934) An attempt at a physiological interpretation of obsessional neurosis and paranoia.
Journal of Mental Science, 80, 187-197.
 Pawar, A. V. & Spence, S. A. (2003) Defining thought broadcast: semi-structured literature review.
British Journal of Psychiatry, 183, 287−291.
 Payne ,R.(1966) ‘The measurement and significance of over inclusive thinking and retardation in
schizophrenic patients ; in psychopathology of Schizophrenia (ed. Hoch P.H. and Zubin , J.).New
York, Grune & Station.
 Pritchard, W. S., (1986) Cognitive event – related potencial correlates of schizophrenia, Psychological
Bulletin, 100, 43-66.
 Rachman,S. (1997)A cognitive theory of obsessions. Behavioral Research and Therapy,35,793-802.

212
 Rachman,S.(1998)A cognitive theory of obsessions: Elaborations. Behavioral Research and Therapy,
36,385-401.
 Roberts G (1992)The origins of delusions.British Journal of Psychiatry 161,298-308.
 Salisbury, D.F., Shenton, M.E., Sherwood, A.R., (1998) First episode Schizophrenic psychosis differ
from first episode of affective psychosis and controls in P300 amplitude over left temporal lobe,
Archives of General Psychiatry 55,173-180.
 SCAN Glossary (1994) World Health Organization, American Psychiatric, Washington, DC.
 Schneider, C. (1930) [Psychologie der Schizopheren] (Psychology of Schizophrenics). Leipzig:
Thieme as cited in Casey. P.R. & Kelly, B. (2007) Fish's Clinical Psychopathology: Signs and
Symptoms in Psychiatry, 3rd ed.pp.32-54, London, RCPsych Publications.
 Schneider, K. (1958) Klinische Psychopathologie. Stuttgart, Thime; New York, Grune and Stratton,
1959.
 Schneider,K. (1959)Clinical Psychopathology ,5th edn (transl.Hamilton,M.W.).New York and London:
Grune & Stratton.
 Silverman, L. H., & Candall, P. (1970) On the relationship between aggressive activation, symbolic
merging, intactness of body boundaries, and manifest pathology in schizophrenia.Journal of Nervous
and Mental Diseases, 5, 387–399
 Sims, A. (2003) Symptoms in the Mind: An Introduction to Descriptive Psychopathology, 3rd
ed.pp.117-171. Philadelphia, Saunders.
 Sims, A., Mundt, C., Berner, P. et al (2003) Descriptive phenomenology. In: Gelder, M.G., Lopez-Ibor
J.J., Andreasen, N. (Eds) New Oxford Textbook of Psychiatry, 1st ed. New York; Oxford University
Press, pp. 55-69.
 Spitzer, M.(1994) The basis of psychiatric diagnosis.In: Sadler, J.Z.Wiggins, O.P. and Schwartz,
M.A.(eds)Philosophical Perspectives on Psychiatric Diagnostic Classification. Baltimore:Johns
Hopkins University Press
 Stoddarts, W.H.B.(1908)Mind and its Disorders.London:Lewis.
 Strauss, J.S.& Carpenter,W.T.(2001) Characteristic symptoms and outcome in schizophrenia’.
Archives of.General Psychiatry,30,429-434.
 Swanson,D.W.,Bohnert,P.J.,and Smith, P.J.(1970) The Paranoid. Boston: Little, Brown.
 Tanenberg-Karant, M. et al (1995) Bizarre Delusions and First-Rank Symptoms in a First-Admission
Sample: A Preliminary Analysis of Prevalence and Correlates, Comprehensive Psychiatry, 36, 6, 428-
434.
 Taylor, M.A. & Vaidya, N.A. (2009) Descriptive Psychopathology : The Signs and Symptoms of
Behavioral Disorders, pp. 293-309. New York, Cambridge University PressJaspers, K. (1959).
General psychopathology (J. Koenig, & M. W. Hamilton, Trans). Manchester: Manchester University
Press.
 Tolle, R. (1987) Wahnentwicklung bei k¨orperlich behinderten.Nervenartz, 759–763
 Veale, D. (2002). Over-valued ideas: a conceptual analysis, Behaviour Research and Therapy, 40,
383–400.
 Wilkinson (1993) Talking about psychiatry. London: Gaskell.
 Wing,J.K.,Cooper,J.E.Startorius,N.(1974) The measurement and classification of psychiatric
symptoms. Newyork: Cambridge University Press.
 Wing.J.(1960) Present State Examination. Britain. Maudsley Hospital
 World Health Organization (1992) The ICD–10 Classification of Mental and Behavioural Disorders:
Clinical descriptions and diagnostic guidelines (10th ed). Geneva: WHO.
 Yager, J. & Gitlin, M.J. (2005) Clinical Manifestations of Psychiatric Disorders In Sadock, B.J. &
Sadock, V.A. (Eds) Kaplan and Sadock’s Comprehensive Textbook of Psychiatry, 8th ed. Baltimore,
Lippincott Williams & Wilkins pp. 964-1002.

213
CHAPTER –XII
 SPEECH AND LANGUAGE DISORDERS

Introduction:
Speech difficulties refer to problems with the perception or articulation of speech sounds,
while language difficulties refer to a range of problems that can interfere with
communication and the cognition.

Speech and language problems fall into two categories: receptive and expressive. Any child
who has difficulty understanding language will also have problems with expression, but
some children have good receptive skills while being unable to formulate their thoughts and
feelings into spoken language. For this reason, the Diagnostic and Statistical Manual of
Mental Disorders - 4th Edition (DSM-IV, 1994) gives criteria for Receptive and Mixed
Expressive/Receptive Language Disorder.

Problems can occur with both categories (receptive and expressive) at several levels:
phonology, syntax, semantics and pragmatics:

Receptive Expressive

problems distinguishing between sounds as articulatory problems e.g.

Phonology
in 'van' and 'than' 'fink' for 'think'

problems extracting meaning from

grammatical construct
grammatically complex sentences e.g.
Syntax interferes with meaning e.g.
thinking that 'the cat was bitten by the dog'
'the cat that dog bit'
means 'the cat bit the dog'

Semantics understanding meaning communicating meaning

understanding the communicative purpose of using language in a socially

language, including non-literal meaning as in appropriate way e.g. tone of
Pragmatics sarcasm, irony and metaphor e.g. an autistic voice, eye-contact, turn-
child may see a sign saying 'Please knock taking, maintaining a shared
the door' and knock each time he passes topic

It is important to remember, when looking at the above table, that a child's speech and
language are only delayed if inappropriate for his/her age. Deviant language difficulties are
those that are considered 'odd' for a child of any age.

Some children will be generally delayed, i.e. their development in all cognitive areas will be
slower than is usual. When development occurs at a generally normal pace with the
exception of one or more areas of speech and language, the term specific language
impairment or difficulty, is used.

214
The above linguistic categories help us to describe, understand and assess speech and
language difficulties. The reasons, or aetiology, of the problems fall into medical categories:
structural defects of the speech apparatus; hearing loss; brain loss; brain damage;
emotional/behavioural disorders (e.g. elective mutism); environmental deprivation. The
difficulties can be primary, or the secondary effect of another disorder - as in the case of
hearing loss.

“People do not think in English or Chinese, Hindi or Bengali, they think in the language of
thought”. This language of thought looks similar in all languages probably has symbol of
concepts and arrangement of symbols in activities ideas and concepts. This view
contradicts the point to point relationship between language and thought by Maher and
Sapir-Whorf Hypothesis (Oyebode, 2008).

Propositional, or symbolic, language differs from emotional language in several ways.

Instead of communicating feelings, it is the means of transferring ideas from one person to
another, and it requires the substitution of a series of sounds or marks for objects, persons,
and concepts (Oyebode, 2008).

Normal development of speech and language:

Age of
Typical Language Development
Child
Vocalization with intonation, responds to his name, responds to human
6
voices without visual cues by turning his head and eyes, and responds
Months
appropriately to friendly and angry tones.
Uses one or more words with meaning (this may be a fragment of a
12
word), understands simple instructions, especially if vocal or physical
Months
cues are given, practices inflection, is aware of the social value of speech.
18 Vocabulary of approximately 5-20 words (chiefly nouns), some echolalia,
Months much jargon with emotional content, follow simple commands.
Name a number of objects common to his surroundings, use at least two
prepositions, usually : in, on, under, uses short sentence-largely noun-
24 verb combinations (mean length 1.2 words), approximately 2/3 of what
Months child says should be intelligible, vocabulary - 150-300 words, rhythm and
fluency are often poor, volume & pitch of voice not yet well-controlled, can
use two pronouns : I, me, you, responds to "show me your eyes "
Starts using some plurals and past tenses, at least three prepositions,
knows chief parts of body, uses three word in sentences, vocabulary is
36
around 900-1000 words (90% intelligible), verbs begin to predominate,
Months
able to reason "what must you do when you are sleepy, hungry, cool, or
thirsty?", give his sex, name, age.
Uses names of familiar animals, at least four prepositions, names
common objects in picture books or magazines, one or more colours,
48 repeat 4 digits, words of four syllables, most vowels & consonants p, b, m,
Months w, n, indulges in make-believe, verbalization as he carries out activities,
understands such concepts when a contrast is presented, follows simple
commands even thought the stimulus objects are not in sight.
Child descriptive words spontaneously-both adjectives and adverbs, uses
60
common opposites: big-little, hard-soft, can count to ten, completely
Months
intelligible, in spite of articulation problems, can use all vowels and the

215
 consonants, repeats sentences as long as nine words, define common
objects in terms of use (hat, shoe, chair), follows three commands given
without interruptions, simple time concepts: morning, afternoon, tomorrow,
yesterday, speech is grammatically correct.
6 Years Intelligible and socially useful, connected story about a picture.
Masters the consonants s-z, r, voiceless th, ch, wh, and the soft g as in
7 Years George, opposite analogies easily: girl-boy, man-woman, time to quarter
hour, simple reading and to write or print many words.
Can relate events that occurred at some time in the past, complex and
compound sentences, reading with considerable ease and writing simple
8 Years compositions, control of rate, pitch, and volume are generally well, carry
on conversation at rather adult level, follows fairly complex directions with
little repetition.

Developmental speech and language disorder

Developmental language disorder which is also called Specific Language Impairment is a
disorder characterized by slow, abnormal language development. It belongs to the category
of specific disorders: where the language level observed is substantially below the
nonverbal intellectual capacity. This limitation cannot be explained by any cognitive or
neurological deficits such as hearing impairment, low verbal intelligence, neurological
damage or psychological problem (Gandotra, 2009).

Warning signs of Developmental language disorder: (Gandotra, 2009)

1. Limitations in expressive language-
a. feeding problem like sucking, swallowing and chewing.
b. fails to verbalize to social stimuli and 2 syllables at 8 months.
c. fail to utter 3 words by the age of 3 years.
2. Limitations in vocabulary-
a. small repertoire of words understood or used.
b. acquired new words slow or with difficulty.
c. rarely volunteers an answer, or becomes terribly nervous when asked to
speak verbally.
d. speaks in incomplete sentences, or spoken language has little meaning.
3. Limitations in comprehending language-
a. have difficulty understanding word meanings.
b. relies too much on contextual cues to understand language.
4. Limitations on social interaction – except to have needs met.
5. Limitations in play–
a. not developed symbolic, imaginative play by age 3 years.
b. does not play interactively with peers.
6. Limitations in learning language-
a. numerous articulation errors.
b. unintelligible to unfamiliar listener.
7. Limitations in using strategies for learning language–
a. overuse imitation (echolalia).
b. does not imitate verbalization of others (dyspraxia).
c. does not use questions like why
8. Limitations in attention for learning activity–
a. little interest in reading, talking or communicating with peers.
b. has sequencing and problem solving difficulties.

216
Criteria according to ICD-10 (WHO 1992):
1. An onset that is invariably during infancy or childhood.
2. An impairment or delay in the development of functions that are strongly related to
biological maturation of the central nervous system and
3. Steady course that does not involve the remissions and relapses that tend to be
characteristic of many mental disorders.
In most cases, the functions affected include language, visuo-spatial skills and/or motor
coordination. It is characteristic for the impairments to lessen progressively as children grow
older (although milder deficits often remain in adult life). Usually, the history is of a delay or
impairment that has been present from as early as it could be reliably detected, with no
prior period of normal development. Most of these conditions are several times more
common in boys than in girls.

These are disorders in which normal patterns of language acquisition are disturbed from the
early stages of development. The conditions are not directly attributable to neurological or
speech mechanism abnormalities, sensory impairments, mental retardation, or
environmental factors. The child may be better able to communicate or understand in
certain very familiar situations than in others, but language ability in every setting is
impaired. Language delay that is sufficiently severe to fall outside the limits of 2 standard
deviations may be regarded as abnormal.

When a language delay is simply part of a more pervasive mental retardation or global
developmental delay, a mental retardation coding (F70-F79) should be used.

Specific speech articulation disorder (F80.0):

It is defined as a specific developmental disorder in which the child's use of speech
sounds is below the appropriate level for his or her mental age, but in which there is
a normal level of language skills.

Diagnostic guidelines: The age of acquisition of speech sounds, and the order in
which these sounds develop, show considerable individual variation. It includes
developmental articulation disorder, developmental phonological disorder, dyslalia
(An articulation disorder resulting from impaired hearing or structural abnormalities of
the articulatory organs), functional articulation disorder and lalling.

Expressive language disorder (F80.1):

A specific developmental disorder in which the child's ability to use expressive
spoken language is markedly below the appropriate level for his or her mental age,
but in which language comprehension is within normal limits. There may or may not
be abnormalities in articulation.

Diagnostic guidelines: Absence of single words (or word approximations) by the age
of 2 years, and the failure to generate simple two-word phrases by 3 years, should
be taken as significant signs of delay. The diagnosis should be made only when the
severity of the delay in the development of expressive language is outside the limits
of normal variation for the child's mental age, but receptive language skills are within
normal limits (although may often be somewhat below average). The use of
nonverbal cues (such as smiles and gesture) and "internal" language as reflected in
imaginative or make-believe play should be relatively intact, and the ability to

217
 communicate socially without words should be relatively unimpaired. The child will
seek to communicate in spite of the language impairment and will tend to
compensate for lack of speech by use of demonstration, gesture, mime, or non-
speech vocalizations.

Receptive language disorder (F80.2):

A specific developmental disorder in which the child’s understanding of language is
below the appropriate level for his or her mental age. In almost all cases, expressive
language is markedly disturbed and abnormalities in word-sound production are
common.

Diagnostic guidelines: Failure to respond to familiar names (in the absence of

nonverbal clues) by the first birthday, inability to identify at least a few common
objects by 18 months, or failure to follow simple, routine instructions by the age of 2
years should be taken as significant signs of delay. Later difficulties include inability
to understand grammatical structures (negatives, questions, comparatives, etc.), and
lack of understanding of more subtle aspects of language (tone of voice, gesture,
etc.).

Acquired aphasia with epilepsy [Landau-Kleffner syndrome] (F80.3):

A disorder in which the child, having previously made normal progress in language
development, loses both receptive and expressive language skills but retains general
intelligence. Onset of the disorder is accompanied by paroxysmal abnormalities on
the EEG (almost always from the temporal lobes, usually bilateral, but often with
more widespread disturbance), and in the majority of cases also by epileptic
seizures. Typically the onset is between the ages of 3 and 7 years but the disorder
can arise earlier or later in childhood. In a quarter of cases the loss of language
occurs gradually over a period of some months, but more often the loss is abrupt,
with skills being lost over days or weeks. The temporal association between onset of
seizures and loss of language is rather variable, with either one preceding the other
by a few months to 2 years. It is highly characteristic that the impairment of receptive
language is profound, with difficulties in auditory comprehension often being the first
manifestation of the condition. Some children become mute, some are restricted to
jargon-like sounds, and some show milder deficits in word fluency and output often
accompanied by misarticulations. In a few cases voice quality is affected, with a loss
of normal inflexions. Sometimes language functions appear fluctuating in the early
phases of the disorder. Behavioural and emotional disturbances are quite common in
the months after the initial language loss, but they tend to improve as the child
acquires some means of communication.

Other developmental disorders of speech and language (F80.0) includes lisping

Developmental disorder of speech and language, unspecified (F80.9):

This category should be avoided as far as possible and should be used only for
unspecified disorders in which there is significant impairment in the development of
speech or language that cannot be accounted for by mental retardation, or by
neurological, sensory or physical impairments that directly affect speech or
language.

218
Behavioural and Emotional Disorders with onset usually occurring in childhood and
Adolesence (WHO 1992):

Elective mutism (F94.0): The condition is characterized by a marked, emotionally

determined selectivity in speaking, such that the child demonstrates his or her language
competence in some situations but fails to speak in other (definable) situations. Most
frequently, the disorder is first manifested in early childhood. It occurs with approximately
the same frequency in the two sexes, and it is usual for the mutism to be associated with
marked personality features involving social anxiety, withdrawal, sensitivity, or resistance.
Typically, the child speaks at home or with close friends and is mute at school or with
strangers, but other patterns (including the converse) can occur.

Diagnostic guidelines:
1. A normal, or near-normal, level of language comprehension.
2. A level of competence in language expression that is sufficient for social
communication.
3. Demonstrable evidence that the individual can and does speak normally or almost
normally in some situations.

Stuttering [stammering] (F98.5): Speech that is characterized by frequent repetition or

prolongation of sounds or syllables or words, or by frequent hesitations or pauses that
disrupt the rhythmic flow of speech. Minor dysrhythmias of this type are quite common as a
transient phase in early childhood, or as a minor but persistent speech feature in later
childhood and adult life. They should be classified as a disorder only if their severity is such
as markedly to disturb the fluency of speech. There may be associated movements of the
face and/or other parts of the body that coincide in time with the repetitions, prolongations,
or pauses in speech flow. Stuttering should be differentiated from cluttering (see below) and
from tics. In some cases there may be an associated developmental disorder of speech or
language, in which case this should be separately coded under F80.

Cluttering (F98.6): A rapid rate of speech with breakdown in fluency, but no repetitions or
hesitations of a severity to give rise to reduced speech intelligibility. Speech is erratic and
dysrhythmic with rapid, jerky spurts that usually involve faulty phrasing patterns (e.g.
alternating pauses and bursts of speech, producing groups of words unrelated to the
grammatical structure of the sentence).

According to DSM IV-TR (American Psychiatric Association):

1. Speech Disorder
a. Phonological disorder
b. Stuttering
2. Language disorder
a. Expressive
b. Mixed expressive-receptive
3. Communication disorder NOS

219
Speech disorder which are mainly functional (Hamilton, 1984):

1. Stammering and stuttering: As describe earlier, it generally improves with time and
noticeable only when person is anxious. Rarely does it persist as severely handicapping
condition. Severe adolescent crisis or acute schizophrenia may present as stammering.

2. Mutism: This is complete loss of speech. It may occur in disturbed children, hysteria,
depression, schizophrenia and coarse brain disease. Elective mutism occurs in children
in which they refuse to speak to a certain person. Hysterical mutism is rare although the
commonest speech disorder of hysteria is aphonia. Mutism is almost always present in
catatonia and is associated with depressive stupor. In pure word dumbness, patient in
mute but can read and write but in akinetic mutism, which occurs in course brain
disease patient is aware of his surroundings.

3. Talking Past the Point (Vorbeireden): In this disorder, the content of patient replies
shows that he understands what has been asked and deliberately talks on associated
topics. It occurs in hysterical pseudodementia, when mental symptoms are being
unconsciously being presented for some known advantage. Often it is real malingering.
This condition was described by Ganser in imprisoned criminals waiting for trial. These
symptoms may accompany lack of insight, disorientation, and fluctuating level of
consciousness of short duration, hysterical analgesia and hyperaesthesia. Conrad
called this syndrome as pseudo-pseudo-dementia. When painful personal questions are
asked chronic schizophrenics talk past the point. They seem to say whatever comes to
their mind and will reply no matter how weird a question is.

4. Neologism: In neologism new words are constructed by patient or old word is used in a
special way by patients with schizophrenia. The derivation of the new words is not
understood, may be a distortion of another word or new word constructed from faulty
use of accept use of word formation. Some aphasic person may distort the phonetic
structure of word, use wrong word or invent new words which may appear as neologism,
but known as paraphasia. Catatonics having mannerism or stereotype may appear as
neologism after distorted pronunciation of the word. Technical neologism is making a
technical word to explain personal psychotic experience. Hallucinatory voices may use
technical word which can be reflected in patient’s speech. Malapropism which is
ludicrously misused words should be differentiated from neologism as they carry no
psychiatric significance.

5. Speech Confusion and Schizophasia: It may superficially appear as aphasia, but it is

a varity of thought disorder occurring in chronic schizophrenics where patient utter
nonsense, may be able to carry out responsible work which doesn’t require speech.
Bleurer called this prominent disorder as Schizophasia which is also known as speech
confusion and word salad.

Motor Speech Disorder in Psychoses (Hamilton, 1984):

1. Attitude to conversation: Patient with negative symptoms turn away from all the
attempt to speak to them. Other patients with schizophrenia may not be able to maintain
conversation because of the hallucinating voices. Many patient would continue
muttering during examination, some may turn faces towards examiner with an

220
 expressionless face and reply to all the questions whether the question make sense or
not. Patient with confusional psychoses may be mute or have poverty of speech and
may speak in bewildered way.

2. Flow of speech: Some patients may be mute or some may have pressure of speech,
usually associated with flight of ideas as in mania and sometimes in schizophrenia,
patient may be voluble describing their fantastic experiences. Many schizophrenics do
not not stop talking even when told to. Slowing of speech occurs in psychomotor
retardation and is evident when interview is prolonged. Speech may sound like a
foreigner in catatonic patients and in motor aphasia, they may have falsetto tone or
staccato tone or a nasal speech. Some schizophrenics may sound strange may be a
part of their mannerism.

3. Mannerism and Stereotype: The strange use of words, high-flown expressions and
movements and postures that are out-of-keeping with the total situation is regarded as
mannerisms. Mannerisms of speech can be noticed in form of pronunciation. Only a few
words may be mispronounced or there may be a distortion of most words, resembling
paraphasia. Verbal stereotypies are words or phrases that are repeated. They may be
produced spontaneously or be set off by a question. In verbigeration one or several
sentences or strings of fragmented words are repeated continuously.

4. Perseveration: Perseveration can be defined as

a. Compulsive repetition, in which the act is repeated until the patient receives
another instruction
b. Impairment of switching, in which the repetition continues after the patient has
been given a new task
c. Ideational perseveration, in which the patient repeats words and phrases during
their reply to a question.

In some cases there is perseveration of theme rather than the actual words and this can
be regarded as impairment of switching. In other cases the set or attitude is
perseverated and the patient cannot solve a new problem because they cannot break
free from their previous set. Verbal perseveration can occur in schizophrenia and
organic states.

5. Logoclonia and palilalia are special forms of perseveration. In the palilalia, the patient
repeats the perseverated word with increasing frequency, while in logoclonia the last
syllable of the last word is repeated, for example, the patient might say: ‘I am well today-
ay-ay-ay-ay.’ Palilalia and logoclonia occur in organic brain disorders, in particular in
schizophrenia.

6. Echolalia: In echolalia the patient echoes a part or the whole of what has been said to
them. Words are echoed irrespectively of whether the patient understands them or not,
so that the echolalic patient may repeat words and phrases in foreign languages that
they do not know. It has been suggested that echo speech in children is a conditional
reflex that is suppressed when voluntary speech takes over; echolalia could therefore be
seen as the result of disinhibition of a childhood speech pattern. Some individuals,
including children, may echo the last words that have been said to them.

221
Anatomy of Language function (Ropper & Brown 2005):

There are four major areas in most of the persons situated in the left hemisphere. The
entire language zone is situated around sylvian fissure. Two language areas are receptive
and other two areas are executive.

The two receptive areas are closely related and embrace what has been referred to as the
central language zone. The main receptive area, sub-serving
sub serving the perception of spoken and
probably of internal language, occupies the posterior-posterosuperior
posterosuperior temporal area (the
posterior portion of area 22) and Heschl’s gyri (areas 41 and 42). The posterior part of area
22 in the planum temporale is referred to as Wernicke’s area. A second receptive area,
subserving the perception of written
ritten language, occupies the angular gyrus (area 39) in the
inferior parietal lobule, anterior to the visual receptive areas. The supramarginal gyrus,
which lies between these auditory and visual language “centers,” and the inferior temporal
region, just anterior to the visual association cortex, are probably part of this central
language zone as well. Here are located the integrative centers for cross-modal
cross modal visual and
auditory language functions.

The main executive, or output, region, situated at the posposterior

terior end of the inferior frontal
convolution
on (Brodmann’s areas 44 and 45) is known as Broca’s area. It is related to motor
aspects of speech. In some models, visually perceived words are given expression in
writing through a fourth language area, known as as Exner writing area situated in the
posterior part of the second frontal convolution, this concept is still controversial in view of
the fact that widely separated parts of the language zone may cause a disproportionate
disorder of writing. In any case, tthere
here are two parallel systems for understanding the
spoken word and producing speech and for the understanding of the written word and
producing writing. They develop separately but are the integral components of the semantic
system.

Figure 1 Diagram of the brain showing the classic language areas, Ropper & Brown 2004

These sensory and motor areas are intricately connected with one another by a rich
network of nerve fibers, one large bundle of which, the arcuate fasciculus, passe
passes through
the isthmus of the temporal lobe and around the posterior end of the sylvian fissure; other

222
connections may traverse the external capsule of the lenticular nucleus (subcortical white
matter of the insula). Many additional corticocortical connections and other fiber systems
lead into the perisylvian zones and project from them to other parts of the brain.
Furthermore, the visual receptive and somatosensory zones are integrated in the parietal
lobe, and the auditory receptive zones in the temporal lobe.

Of special importance for the production of speech are the short association fibers that join
Broca’s area with the lower rolandic cortex, which in turn innervates the muscles of the lips,
tongue, pharynx, and larynx. The putative Exner writing area is similarly integrated with the
motor apparatus for the muscles of the hand. The perisylvian language areas are also
connected with the striatum and thalamus and with corresponding areas in the minor
(nondominant) cerebral hemisphere through the corpus callosum and anterior commissure.

Wernicke’s and Broca’s zones, has been the most difficult to accept, because it
presupposes a neat separation of sensory and motor functions, which is not in line with
contemporary views of sensorimotor physiology of the rest of the nervous system or with
the recent analyses of language by cognitive neuropsychologists.

Cerebral Dominance and its Relation to Language and Handedness:

The functional supremacy of one cerebral hemisphere is fundamental to language function.

There are many ways of determining that the left side of the brain is dominant:

1. By the loss of speech that occurs with disease in certain parts of the left hemisphere
and its preservation with lesions involving corresponding parts of the right
hemisphere.
2. By preference for and greater facility in the use of the right hand, foot, and eyes.
3. By the arrest of speech with a focal seizure or with electrical or magnetic stimulation
of the anterior language area;
4. By the injection of sodium amytal into the left internal carotid artery (the wada test—a
procedure that produces mutism for a minute or two, followed by misnaming,
including perseveration and substitution, misreading and paraphasic speech—lasting
8 to 9 min in all).
5. By dichotic listening, in which different words or phonemes are presented
simultaneously to the two ears (yielding a right ear–left hemisphere advantage).
6. By observing increases in cerebral blood flow during language processing and
7. By lateralization of speech and language functions following commissurotomy.

Aphasias (Ropper & Brown 2005):

Injury to various part of brain parenchyma may cause different presentation in form of focal
neurological problems, difficulty in articulation, fluency, naming objects etc. The cause
could be in the form of haemorrhagic embolus or other type of traumatic brain injury. The
various manifestations depends on the nature of injury, extent of brain tissue involved and
the associated neurological deficits. However various attempts have been taken to classify
these disorders.

223
 Aphasia Square ( Willams & Wilkins,1997)

Aphasia Square ( Willams & Wilkins,1997).

Speech Comprehensio Repetitio Associated Localization

type of n n signs
aphasia
Broca Nonfluent, Relatively Impaired Right arm and Frontal
(sensory) effortful, preserved face weakness suprasylvian
agrammatical
, paucity of
output but
transmits
ideas
Wernicke Fluent, Greatly None Hemi- or Temporal,
(repetitive) voluble, well impaired quadrantanopia infrasylvian
articulated , no paresis including
but lacking angular and
meaning supramargina
l gyri
Conduction Fluent Relatively None Usually none Supramargina
preserved l gyrus or
insula
Global Scant, Very impaired None Hemiplegia Large
nonfluent usual perisylvian or
separate
frontal and
temporal
Transcortica Nonfluent Good Largely Variable Anterior or
l motor preserve superior to
d Broca’s area
Transcortica Fluent Impaired as Largely Variable Surrounding
l sensory Wernicke preserve Wernicke’s
d area
Pure word- Mildly Impaired Impaired None or Bilateral (or
deafness paraphasic or quadrantanopia left) middle of
normal superior
temporal
gyrus

224
Pure word- Normal but Normal Normal Right Calcarine and
blindness unable to hemianopia; white matter
(and alexia read aloud unable to read or callosum
without own writing (or angular
agraphia) gyrus)
Pure word Mute, but Normal None None Region of
mutism able to write Broca’s area
(aphemia)
Anomic Isolated word Normal various Normal Variable Deep
aphasia finding sites temporal lobe
difficulty

According to David et al (2009) in Wernicke’s Aphasia, words are used wrongly, paraphasic
errors are frequent.

Prognosis: Recovery from aphasia due to cerebral trauma is usually faster and more
complete than that from aphasia due to stroke. The type of aphasia and particularly its initial
severity (extent of the lesion) clearly influence recovery. Global aphasia usually improves
very little, and the same is true of severe Broca’s and Wernicke’s aphasias. The various
dissociative speech syndromes and pure word mutism tend to improve rapidly and often
completely (Ropper & Brown 2005).

Agraphias
Disorders of writing like disorders of speaking, reflect all the basic defects of language. But
there is an obvious difference between these two expressive disorders. In speech disorder,
only final motor pathway coordinating the movements of lips, tongue, larynx, and respiratory
muscles is involved. In contrast, as in Agraphia, if the right hand is paralyzed, one can still
write with the left one, or with a foot, and even with the mouth by holding a pencil between
the teeth (Ropper & Brown 2005).

A lesion in or near the angular gyrus will occasionally cause a disproportionate disorder of
writing as part of the Gerstmann syndrome which is a symptom complex of right-left
confusion and inability to write, calculate, and identify individual fingers.

Quite apart from these aphasic agraphias, in which spelling and grammatical errors are
abounding, there are special forms of agraphia caused by abnormalities of spatial
perception and praxis. Disturbances in the perception of spatial relationships appear to
underlie constructional agraphia. In this circumstance, letters and words are formed
clearly enough but are wrongly arranged on the page. Words may be superimposed,
reversed, written diagonally or in haphazard arrangement, or from right to left, in the form
associated with right parietal lesions, only the right half of the page is used. Usually one
finds other constructional difficulties as well, such as inability to copy geometric figures or to
make drawings of clocks, flowers, and maps, etc.

A third group may be called the apraxic agraphias. Here language formulation is correct
and the spatial arrangements of words are respected, but the hand has lost its skill in
forming letters and words. Handwriting becomes a scrawl, losing all personal character.
There may be an uncertainty as to how the pen should be held and applied to paper;
apraxias (ideomotor and ideational) are present in the right-hander. As a rule, other learned
manual skills are simultaneously disordered.

225
In addition to the neurologic forms of agraphia, described above, psychologists have
defined a group of “linguistic” agraphias, subdivided into phonologic, lexical, and
semantic types.

Subcortical Aphasia (Thalamic and Striatocapsular Aphasias): A lesion of the dominant

thalamus, usually vascular and involving the posterior nuclei, may cause an aphasia, the
clinical features of which are not entirely uniform. Usually there is mutism initially and
comprehension is impaired. During the early phases of recovery, spontaneous speech is
reduced in amount; less often, speech is fluent and paraphasic to the point of jargon.
Reading and writing may or may not be affected. Anomia has been described with a
ventrolateral thalamic lesion (Ojemann). Characteristically, the patient’s ability to repeat
dictated words and phrases is unimpaired (transcortical sensory aphasia). Complete
recovery in a matter of weeks is the rule.

Other Cerebral Disorders of Language (Ropper & Brown 2005):

Speech and language is disturbed in delirium tremens and Alzheimer’s disease. Lesions in
the medio-orbital or superior and lateral parts of the frontal lobes, impair all motor activity to
the point of abulia or akinetic mutism. Deep cerebral lesions, by causing fluctuating states
of inattention and disorientation, induce fragmentation of words and phrases and
sometimes protracted, uncontrollable talking (logorrhea). Severe mental retardation often
results in failure to acquire even spoken language.

Disorders of Articulation and Phonation: Phonation, or the production of vocal sounds, is

a function of the larynx, more particularly the vocal cords. Articulation consists of
contractions of the pharynx, palate, tongue, and lips, which interrupt or alter the vocal
sounds.

Defective articulation (dysarthria) and phonation (dysphonia) are recognized at once by

listening to the patient’s speech during ordinary conversation or read aloud from a
newspaper.

1. Lower Motor Neuron (Neuromuscular) Dysarthria, Atrophic Bulbar Paralysis: This is due
to weakness or paralysis of the articulatory muscles, the result of disease of the motor
nuclei of the medulla and lower pons or their intramedullary or peripheral extensions
(lower motor neuron paralysis).

2. Spastic (Pseudobulbar) Dysarthria: Diseases that involve the corticobulbar tracts

bilaterally—usually due to vascular, demyelinative, or motor system disease
(amyotrophic lateral sclerosis) result in the syndrome of spastic bulbar (pseudobulbar)
palsy.

3. Rigid (Extrapyramidal) Dysarthria: In Parkinson’s disease and other extrapyramidal

diseases associated with rigidity of muscles, one observes a rather different disturbance
of articulation, characterized by rapid mumbling and cluttered utterance and slurring of
words and syllables with trailing off in volume at the ends of sentences. The voice is
low-pitched and monotonous, lacking both inflection and volume (hypophonia). The
words are spoken hastily and run together in a pattern that is almost the opposite of the

226
 slowed pattern of spastic dysarthria. In advanced cases, speech is almost unintelligible,
only whispering is possible.

4. Ataxic Dysarthria: This condition is characteristic of acute and chronic cerebellar lesions.
It may be observed in multiple sclerosis and various degenerative disorders involving
the cerebellum or its peduncles, or as a sequel of anoxic encephalopathy and rarely of
heat stroke. The principal abnormalities are slowness of speech, slurring, monotony,
and unnatural separation of the syllables of words (scanning). The coordination of
speech and respiration is disordered.

5. Acquired Stuttering: This abnormality, characterized by interruptions of the normal

rhythm of speech by involuntary repetition and prolongation or arrest of uttered letters or
syllables, is a common developmental disorder. It may appear in patients who are
recovering from aphasic disorders and who had never stuttered in childhood.

Aphonia and Dysphonia: This is due to disturbance of phonation. Paresis of respiratory

movements, as in myasthenia gravis, Guillain-Barre´ syndrome and severe pulmonary
disease, may affect the voice because insufficient air is provided for phonation. Also,
disturbances in the rhythm of respiration may interfere with the fluency of speech as seen in
extrapyramidal diseases.

With paresis of both vocal cords, the patient can speak only in whispers, which is aphonia.
Since the vocal cords normally separate during inspiration, their failure to do so when
paralyzed may result in an inspiratory stridor. If one vocal cord is paralyzed the voice
becomes hoarse, low-pitched, rasping, and somewhat nasal in quality, which is known as
dysphonia.

Spasmodic dysphonia occurs when a person has increased tone of laryngeal muscles.
Inspiratory stridor is seen in the condition.

Approach towards patient: (Strub and Black, 2000)

The examination of patient should start with complete neurological examination and note for
any focal neurological deficits after detailed history talking including information about
patient’s nationality, native language and education levels (Spillane 1996). These are the
steps to assess the language function.

1. First inquire about the patient’s handedness, because handedness and cerebral
dominance have closed alliance and should be determined before assessing language.
As many left handed patient are taught to use right hand for writing so ask the patient to
show how they hold a knife, throw a ball, and flip a coin. Also ask the patient about the
tendency to use the opposite hand for any skilled movement. In addition family history of
left-handedness or ambidextery is important as it runs in families. Strong exclusive
unilateral handedness is suggestive of strong right or left handedness.

2. Spontaneous speech: Listen carefully to the patient’s spontaneous speech. If the

patient doesn’t speak ask open ended questions regarding uncomplicated issues to
elicit speech production. Note while listening...
a. Is speech output present?
b. Is the speech dysarthric or dysprosodic?

227
 c. Is there evidence of specific aphasic errors (e.g., errors of syntax, word finding
pauses, abnormal words, or paraphasia)?

3. Verbal Fluency: It refers to produce spontaneous speech fluently without undue word
finding pauses or failures in search word. Normal speech requires verbal fluency in
production of responses and formulation of spontaneous conversational speech. This
ability is often impaired after brain injury, especially associated with anterior left cerebral
hemisphere. Two easy tests administered are FAS test and Animal Naming Test
(controlled oral word association test). A time of 60 seconds should be given to recall
name of animals. Normal individual should produce 18-22 animal names with expected
variations being ±5-7. A score of ≤13 in otherwise normal person should raise question
on verbal fluency in the patient. The FAS test consists of 3 separate times word naming
trials using the word F, A & S respectively. The patient is instructed to name as many
words as he can starting with the stipulated letters each in 60 seconds trial. Patient’s
response is to be recorded including any paraphasia and repeated words that were
produced in 3 different trials. Normal range is 36-60 words. Inability to name 12 or more
words is indicative of impaired verbal fluency. Result should be cautiously interpreted in
under 10 year aged and IQ of less than 85.

There are some exceptions to the rule as in some patients we cannot simply classify
them and that also some patient’s dysphasia is initially “non-fluent” only later becoming
“fluent”. (Spillane 1996)
4. Comprehension must be tested in a structured fashion, without reliance on patient’s
ability to answer verbally. Open-ended questions should not be asked as it requires
patient to construct complex verbal answers that test the integrity of entire language
function not verbal comprehension in isolation. Two methods of testing comprehension
are used: pointing commands and questions that can be answered in yes and no.

5. Repetition of spoken language is linguistically and to some extent, anatomically a

distinct function, and is impaired in certain type of aphasia. Testing should present
material in ascending order of difficulty, beginning with single monosyllabic words and
proceeding to complex sentences (shown in appendix I). The examiner must listen for
paraphasias, grammatical errors, omissions, and additions. Normal people and brain
damaged patients without aphasia can accurately repeat sentences of 19 syllables.
Performance is related to intelligence and educational levels but errorless performance
is expected on these specific items.

6. Naming and Word Finding: The ability to name objects is one of the earliest and most
basic language functions. It remains stable over decades. Naming ability is disturbed in
almost all type of aphasias. Impaired naming is called anomia. Word finding difficulty is
closely related to anomia, which is reduced ability to retrieve noun and verbs used in
spontaneous speech. Examiner asks patient to describe pictures which contain certain
items. In 20 items table in Appendix I which are arranged in ascending order of difficulty,
are suggested for evaluating naming ability. Normal score in set of 5 words are 4.5
(±0.8) words. The examiner should note that name for parts of objects are low frequency
words and frequently misnamed or not named by aphasics and patient with dementia.

7. Reading ability is one of the few aspects of higher mental function which is directly
related to education. Patient should be educated at least 3 years of formal education.
Both reading comprehension and read aloud should be tested. Both are usually

228
 defective in same patient but can be disturbed in isolation. Ask to read from a
newspaper starting from simple to difficult word and then questions to be asked what
can be answered as “yes” or “no”, or ask about what was written. Examiner should note
any word or syllable substitution, omissions and defect in comprehention.

8. Writing must be tested the same way as used to test reading. If the patient shows
aphasia, he/she undoubtedly has agraphia. Agraphia is diagnosed when patient
demonstrates basic language errors, gross spelling errors or use of paragraphias (word
of syllable substitution). Second, ask patient to write name of common objects or body
parts. Third, if patient can successfully write body parts or objects ask the patient to
write short sentence about their job, weather or a picture in a magazine. Writing often
shows misalignment, in which written lines slants upwards or downwards. This
misalignment is an error in the mechanics of writing but is not an agraphia per se.

9. Spelling is a little studied higher language function, and tested by asking the patient to
spell dictated words. Gross errors can be detected in bedside testing. If it is important to
establish an actual level of impairment, use standardized tests given in Appendix-II.

Points to be noted in our CRF:

Physical Examination: Speech and language function (Bedside examination as described

in Appendix I) and note any of the following: Dysarthia, Aphasia, Articulation, Fluency,
Repetition, Verbal comprehension, Reading, Writing, Mathematical and musical symbols

Mental status examination: the mental status examination is the part of clinical
assessment that describes the sum total of examiner’s observations and impressions of the
psychiatric patient at same time of interview. (Sadock & Sadock, 2007)
1. Intensity:
a. Audible: If examiner can listen to the voices of the patient, this occurs in
normal conversation.
b. Excessively loud: Intensity of speech is louder than it is required, e.g., excited
patient, mania or hypomania.
c. Abnormally soft: intensity of speech is softer than usually required, e.g., vocal
cord palsy, depression, paranoid whispering.
2. Tone: The tone of normal speech changes according to situation and feeling
associated with the topic of discussion. Monotonous tone is without change in pitch or
lack of modulation, e.g., parietal lobe damage, chronic schizophrenia and depression.
3. Quality: normal speech is soft in quality. It may become hoarse in vocal cord abuse by
repeated talking or shouting as in mania or hypomania.
4. Reaction time: delayed reaction time is called when the time taken from listening and
answering (stimulus → response) is delayed, e.g., hypothyroidism, depression and
schizophrenia.
5. Speed:
a. Very slow: the rate of production and output of speech is slow, e.g.,
depression dementia and hypothyroidism.
b. Rapid: the rate of speech output and production is faster than normal. This is
associated with prolixity and flight of ideas.
c. Pressure of speech: Increased in the amount of spontaneous speech, rapid
loud accelerated speech occurs in mania, schizophrenia and cognitive
disorders. (Sadock & Sadock, 2007)

229
6. Ease of speech
a. Hastent speech is characterized by frequent pauses and breaks. This is a
defect in verbal fluency, may be tested by asking the patient to enumerate the
name of animals in 1 min period, e.g., head injury and stress
b. Mutism: complete loss of speech as described earlier, e.g., stupor, dementia.
c. Slurring: a form of speech in which words are pronounced with prolongation of
syllable, e.g., cerebellar damage.
d. Stuttering / stammering: as described earlier.
e. Whispering: production of sound using breath not using vocal cords, e.g.,
pseudobulbar palsy
f. Muttering: speaking in a low voice not meant to be heard (usually lip
movements), e.g., schizophrenia, dementia.
g. Speaking only when questioned: speech only when very much required, e.g.,
mental retardation and depression.
7. Relevance: Speech is said to be irrelevant when it is grammatically but the meaning of
the speech sample is unrelated to the question asked or the topic of discussion. Eg
schizophrenia, dementia, delirium and drug intoxication.
8. Coherence: Speech is said to be incoherent when it is un-understandable either due to
lack of logical connections between words, phrases or sentences. There may be use of
idiosyncratic words or distorted grammar, e.g., schizophrenia, catatonic excitement
and organic psychoses.
9. Goal direction: Patient speech is understandable, and starts with relevant topic but
soon it loses connection with the topic and move to some other direction. May be
circumstantiality, tangentiality or flight of ideas etc.
10. Productivity:
a. Overabundant: copious pressured speech appears like excessive
uncontrollable talking, e.g., hypomanina, mania.
b. Scant productivity of speech: speech production is less than adequate in
amount. Either the production of speech is less or difficulty in making final
verbalization, e.g., negative schizophrenia, depression and catatonia.
11. Manner:
a. Excessive formal: when patient uses more than required form of formal
gestures (formalities) during interview, e.g., histrionic personality disorder,
hypomanic and dissocial personality disorder.
b. Tensed up: showing features of anxiety as wringing of hand, sweating or
fidgeting etc during conversation, e.g., anxious-avoidant personality
disorder/traits.
c. Inappropriately familiar: patient acts as he is very much used to the present
set of examination situation, e.g., hypomania, histrionic personality disorder
and dissocial personality disorder.
12. Deviation:
a. Rhyming: repeating the sounds of ending of 1 or 2 words, ie i am
going..roeing.....etc, e.g., mania and hypomaina
b. Punning: humorous use of words with similar meanings of words with double
meaning, e.g., mania and hypomania
c. Talking past the point : as described earlier
d. Clang association: association or speech directed by sound of a word rather
than by its meaning. Words have no logical connections. Punning and
rhyming may dominate in the verbal behaviour. Seen most frequently in mania
or schizophrenia

230
 e. Stereotype: as described above.
f. Perseveration: as described above.

Conclusion :

Speech and language are one of the evolutionary gifts that human beings are
endowed with, though means of non-verbal communication are present in the animal
kingdom, especially the non-human primates. This special ability, like other biologic
ones, is also vulnerable to various aberrations, the so-called disorders of speech and
language.
Many neurological diseases present with symptoms and signs that mimic psychiatric
disorders and thus, pose a challenge to the psychiatrist and vice-versa. Hence, one
needs to lay a strong foundation in both of these specialities, be aware of and put to
practice the ways of assessment of these disorders and finally, have a thirst for
keeping abreast with the changing concepts aided by ongoing research. In the context
of psychiatry, disorders of speech and language are more the reflection of the
disorders of thought, especially of the form of thought and hence, one needs to revise
them in that light.
References:
American Psychiatric Association. (1994); Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition-Text Revision. 58-68.
Andreasen, N.C. (1979); Thought, language, and communication disorders: II. Diagnostic significance.
Archives of General Psychiatry, 36, 1325-1330.
Andreasen, N.C., & Grove, W. (1979);Thought, language, and communication in schizophrenia: diagnosis and
prognosis. Schizophrenia Bulletin, 12, 348–372.
Andreasen, N.C., & Grove, W.M. (1986);Thought, language, and communication in schizophrenia: diagnosis
and prognosis. Schizophrenia Bulletin, 12, 348-359
Chaika, E. O. (1974); A linguistic looks at ‘schizophrenic’ language. Brain and Language, 1, 257-276.
Child Development Institute, LLC CA 92868 http://www.childdevelopmentinfo.com/development/
language_development.shtml
th
David A.S., Kopelman M.D., (2009); Lishman’s Organic Psychiatry: A textbook of Neuropsychiatry, 4 edition.
th
51. diagnostic guidelines (10 ed). Geneva: WHO.
Gandotra, S., Paul, I., Biswas, P.S., (2009); Seminar-Disorders of Speech and Language, Central Institute of
Psychiatry.
rd
Hamilton, M. (1984); Fish’s Schizophrenia, 3 ed., pp.38-77, Bristol, John Wright & Sons.
nd
Hamilton, M., (1994); Fish’ Clinical Psychopathology 2 edition, Varghese Publishing House, 56-59, 102, 104-
6.
Kleist, K. (1914) Aphasia and Geisteskrankheit. Munchener Medizinische Wochenschrift, 61, 8-12.
Kleist, K.(1960) Schizophrenic symptoms and mental pathology. Journal of Mental Sciences, 106, 246-255.
Liddle,P.F., Ngan,E.T.C. & Caissie,S.L., et al. (2002) Thought and Language Index: an instrument for
assessing thought and language in schizophrenia, British Journal Of Psychiatry , 181, 326 – 330.
McKenna, P.J. & Oh, T. M. (2005) ;Schizophrenic Speech . 1st Edition Cambridge University Press
st
McKenna, P.J. (1994); Schizophrenia and Related Syndromes. 1 Edition. Oxford University Press.
Newby, D. (1998) 'Cloze' procedure refined and modified: 'modified Cloze', 'reverse cloze' and the use of
predictability as a measure of communication problems in psychosis. British Journal of Psychiatry 172,
136-41.
Oh, T. M., McCarthy, R. A. & McKenna, P. J. (2002) Is there a schizophasia? A study applying the single case
approach to formal thought disorder in schizophrenia. Neurocase, 8, 233–244. on 05/07/2010
Oyebode F, 2008, Sims' Symptoms in the Mind, 4th editin, Disorders of speech and language, 175-76.
Ram, D., Siddiqui, M.A ., Sethy, R.R.(2009); Seminar: Disorders of Thought. Central Institute of Psychiatry.
Ropper AH, Brown RH, Adams & Victors Principal of Neurology 2005, McGraw-Hill, 413-28, fig 23-1 414.
th
Rutter, M., et al (2008) Rutter’s Child and Adolescent Psychiatry. 5 Edition. Blackwell Publishing.
Sadock, B.J., Sadock, V.A., 2007, Kaplan & Sadock’s, Synopsis of Psychiatry Behavioural Science/Clinical
th
Psychiatry, 10 edition, LWW. 232, 281.

231
 th
Spillane, J., 1996, Bikerstaff’s Neurological Examination in Clinical Practice, 6 edition, Blackwell Science,
Wiley-India. 258, 260
th
Strub, R.L., Black, F.W., (2003); Mental Status Examination in Neurology, 4 Edition, 47-56 171-2 185-87.
World Health Organization. (1992);The ICD–10 Classification of Mental and Behavioural Disorders: Clinical
descriptions and diagnostic guidelines (10th ed). Geneva: WHO. A.I.T.B.S. Publishers and
Distributors.

232
CHAPTER-XIII
 DISORDERS OF MEMORY
Introduction
Classification Of Memory
Processes Of Memory Formation
Models Of Memory Processing
Types of memory Disorders
A. Amnesia
B. Paramnesia
C. Hyperamnesia
Clinical Assessment Of Memory

Conclusion

INTRODUCTION
The ability to store and recall information is one of the most amazing capacities of higher
organisms. As human adults, we can remember events that happened in our earliest
childhood. We can recall skills learned far earlier in the past. Our memories encapsulate
encap
our sense of personal identity, our cultural identities, and the meaning of our lives. We can
even be influenced by memories that we cannot explicitly remember. However, we all
remember—of of that there can be no doubt. Whether we remember accurately or o
inaccurately, in detail or in abstract, are questions that researchers have investigated for
many years.

Disturbance of memory is always of significance for the sufferers; sometimes,

sometimes however,
forgetting is equally important and is an active process. The memory disturbance was a
specific feature following head injury and other conditions was recognised in various
writings in mid 19th century. . The earliest detailed study of disordered memory was from a
psychological perspective and subsequently descri described
bed as an eponymous condition,
pointing out that gross disorder of memory may occur in patients in whom other intellectual
functions and judgement are preserved (Oyebode, 2008).

CLASSIFICATIONS OF MEMORY
 BASED ON DURATION BASED ON WORKING CLINICAL
 SENSORY MEMORY DURATION MEMORY DIVISION

 SHORT TERM MEMORY

SENSORY IMMEDIATE
 LONG TERM MEMORY MEMORY MEMORY
 WORKING MEMORY
 CLINICAL DIVISION SHORT
RECENT
TERM
 IMMEDIATE MEMORY MEMORY
MEMORY

 RECENT MEMORY
LONG TERM REMOTE
MEMORY MEMORY

233
  REMOTE MEMORY

SENSORY MEMORY
Sensory memory is the ability to retain impressions of sensory information after the original
stimulus has ceased. It refers to items detected by the sensory receptors which are retained
temporarily in the sensory registers and which have a large capacity for unprocessed
information but are only able to hold accurate images of sensory information momentarily.
Sensory memory corresponds approximately to the initial 200–500 milliseconds after
an item is perceived (Morgan et al., 1993). The two types of sensory memory that have
been most explored are iconic memory and echoic memory. Visual sensory memory is
more commonly referred to as iconic memory and auditory sensory memory is known as
echoic memory. This type of memory cannot be prolonged via rehearsal.

SHORT TERM MEMORY

Short-term memory (or "primary" or "active memory") is the capacity for holding a small
amount of information in mind in an active, readily available state for a short period of time.
The duration of short-term memory is believed to be in the order of seconds. Estimates of
short-term memory capacity are 7 plus or minus 2 units. Short term memory is memory that
holds information received from sensory register for up to about 30 seconds. Short-term
memory is believed to rely mostly on an acoustic code for storing information, and to a
lesser extent a visual code (Morgan et al., 1993).

WORKING MEMORY
The concept of working memory (WM) was initially proposed by Baddeley and Hitch (1974)
and developed by Baddeley (1986), and is characterized by the assumption that short-term
storage of information must be considered as part of a more complex system involved in
the execution of a specific task. Baddeley, (1986) defined working memory as "A system for
the temporary holding and manipulation of information during the performance of cognitive
task such as comprehension, learning and reasoning (Sims, 2003). The information is
stored in the WM as long as necessary and the structure need not be defined only in terms
of the dichotomy between short- and long term information storage. On the contrary, this
system has the ability to store and process information simultaneously (Cornoldi & Vecchi
2003).

LONG TERM MEMORY (LTM)

When memories
have been MEMORY
rehearsed in
short term SHORT
memory, they SENSORY MEMORY TERM LONG TERM MEMORY
MEMORY
are encoded
into long term
memory. Long DECLARATIVE NON-DECLARATIVE
ICONIC ECHOIC
Term Memory MEMORY MEMORY
(LTM), provides
SIMPLE
lasting retention SEMANTIC EPISODIC PROCEDURAL CLASSICAL PRIMING
of information CONDITIONING

234
and skills from minutes to a lifetime and has a limitless capacity. Encoding is the process of
placing information into what is believed to be a limitless memory reservoir or LTM, can
occur for specific stimuli as well as for the general memory (Casey and Kelly, 2007). ). The
storage of material in long-term memory allows for recall of events from the past and for the
utilization of information learned throughout life.

Divisions of Long Term Memory

Long-term memory is commonly divided into two major types -'declarative' and 'non-
declarative (Oyebode, 2008).
Declarative memory also termed as explicit memory, encompasses all the information
that we can consciously describe or report. . It has been further subcategorized into:
(a) Semantic memory which concerns memory for meaning, the storage of abstracts and
general facts.
(b) Episodic memory or autobiographical memory is memories based upon a personal
experience relating to self and is linked to a particular time and place in life.

Non Declarative memory refers to skills, habits or other manifestation of learning that can
be expressed without an awareness of what has been learned. It is heterogeneous
collection of unconscious or implicit memory abilities.
Subtypes - 1. Procedural
2. Simple classical Conditioning
3. Priming
Procedural memory, also known as implicit memory, is memory system that retains
information we cannot readily express verbally- for example, information necessary to
perform skilled motor activities like riding a bicycle (Baron, 2005). Although we retain these
skills and abilities we are often completely unable to introspect upon or describe how we do
them. Procedural memory is very resistant to forgetting and is also resistant to brain
damage that eradicates other forms of memory like seen in anterograde amnesic patients
who forget simple events or verbal instructions after a few moments.

Simple Classical Conditioning is another type of non-declarative memory that

generally occurs in the presence of conscious awareness of conditioned stimulus (CS) and
unconditioned stimulus (UCS) contingency, but can occur without awareness also (Budson,
2001).

Priming When an object has just been perceived or processed, there is a tendency for that
object to be perceived more easily the next time. Such priming operates across a wide
range of sensory and motor systems, occurring at a range of different processing levels
(Baron, 2005). For example, presenting a picture of an airplane will make it easier for a
subject to identify a highly fragmented version of the picture as an airplane when it is
presented shortly afterwards. In general, priming tends to be very specific, as though some
aspect of the perceptual system has been facilitated by being used recently. As mentioned
earlier, priming is usually preserved in amnesic patients. Good explicit learning do not
influence implicit learning, and vice versa. Another feature of implicit learning is the way in
which it appears to bypass conscious awareness.

SEMANTIC MEMORY
Semantic memory refers to a person’s conceptual knowledge about the world. It includes
knowledge of the meaning of words, objects and other stimuli perceived through the

235
senses, as well as a rich abundance of facts and associated information. Semantic memory
is immensely important because it constitutes the knowledge base that allows us to
communicate, use objects, recognize foods, react to environmental stimuli and function
appropriately in the world. Semantic memory does not break down in an all-or-none
fashion. Patients may know some words but not others, may recognize one exemplar of an
object but not another, and may retain partial information about a concept while other
information is lost (Snowden, 2002).

The diagram indicates various neural structures thought to be important for different types
of declarative and non declarative memory.

CLINICAL CLASSIFICATION
For clinical descriptive purposes, memory is often subdivided into three basic types—
immediate, recent, and remote—distinguished by the time interval between presentation of
the stimuli and retrieval. Immediate memory may refer to the registration of information as a
memory trace for several seconds or more, corresponding to both sensory and sometimes
short-term memory described earlier. Recent memory assumes some period of memory
storage, and might include a person’s recall of day-to-day events, and may refer to
information learned hours, days, or even weeks ago. Remote memories typically include
memories of events or knowledge learned years ago, usually pre morbidly or before a brain
injury (Strub and Black 2000 ).

236
PROCESSES OF MEMORY FORMATION
Description of the requirement for memory is chiefly referable to long term memory and can
be subdivided phenomenologically into the following five functions (Oyebode, 2008).
1) Registration or encoding is the capacity to add new information to the memory store.
2) Retention or storage is the ability to maintain knowledge that can subsequently be
returned to consciousness.
3) Retrieval is the capacity to access stored information from memory by recognition,
recall or by demonstrating that a relevant task is performed more efficiently as a result of
prior experience.
4) Recall is the effortful retrieval of stored information into consciousness at a chosen
moment. It requires an active complex search process. It is influenced by primacy and
recency effects.
5) Recognition is the retrieval of stored information that depends on the identification of
items previously learned and is based on either remembering (effortful recollection) or
knowing (familiarity based recollection).

Seven stages in memory: Following Welford, memory can be isolated in seven stages
(Hamilton, 1984).
These are
1) Adequate perception, comprehension and response to the material to be learned.
2) Short-term storage mechanism.
3) Formation of a durable trace.
4) Consolidation in which traces are often modified or simplified by subsequent learning.
5) Recognition that certain material needs to be recalled.
6) Isolation of the relevant memory.
7) Using the recalled material in new situation.

MODELS OF MEMORY PROCESSING

Atkinson-Shiffrin model
Atkinson and Shiffrin considered memory to have three major constituents. In the Atkinson-
Shiffrin theory, memory starts with a sensory input from the environment which is held for a
very brief period in the sensory register
associated with the sensory channels like
vision, hearing and touch etc. information that
is attended to and recognized in the sensory
register is passed on to short term memory
where it is held for about 20-30 seconds.
Some of the information reaching short term memory is processed by being rehearsed and
may then be passed along to long term memory; information that is not processed is lost.
When items of information are placed in long term memory they are organized into
categories. It was assumed that the longer an item is held in the short term memory, the
more likely it is to go into long-term memory (Morgan et al., 1993).

Working memory model- Baddeley and Hitch

237
In 1974 Baddeley and Hitch proposed a working memory model which replaced the concept
of general short term memory with specific, active components. In this model, working
memory consists of three basic stores: the central executive, the phonological loop and the
visuo-spatial
spatial sketchpad. In 2000 this model was
expanded with the multimodal episodic buffer. The
central executive essentially acts as attention. It
channels information to the three component
processes: the phonological loop, the visuo-spatial
visuo
sketchpad, and the episodic buffer. The phonological
loop stores auditory information by silently rehearsing
sounds or words in a continuousus loop: the articulatory
process.

The visuospatial sketchpad stores visual and sspatial

information. The episodic buffer is dedicated to linking information across
across domains to form
integrated units of visual, spatial, and verbal information and chronological ordering
ordering. The
episodic buffer is also assumed to have links to long-term
long term memory and semantical
meaning. The working memory model explains many practical observobservations,
ations, such as why it
is easier to do two different tasks (one verbal and one visual) than two similar
similar tasks (e.g.,
two visual).

Levels of processing model-

model Craik and Lockharts
Craik and Lockhart (1972) argued that the previous view of a short
short-term
term memory store
relying on speech coding and feeding a long
long-term
term memory store was inappropriate. They
suggested that the more deeply information is processed; the more likely it is to be retained
retai
(Baron, 2005). They argued that all of these processes would lead lead to some long-term
long
learning, but that the amount of learning depended on the type of processing, with "deep"
processing in terms of meaning leading to much better retention than "shallow" processing.
Maintenance rehearsal might keep material available, but
but would not enhance long long-term
learning.

MODELS OF MEMORY: A BRIEF CRITICAL APPRAISAL

Atkinson and Shiffrin’’s Model (1968): The model by Atkinson and Shiffrin (1968) was
criticized as being too rigid and simplistic as information must flow in both the directions
since there is good deal of interaction between various stores, for example we tend to pay
attention to relevant information from the sensory register but this relevance must be stored
in a long term way. It also does not take into account the types
types of information taken into
memory as some items seemed to flow into Long Term Memory (LTM) far more readily
than others. It also ignores factors such as the effort and strategy subjects may show while
remembering and why information changes in coding from from one memory store to another
(Hill, 1998).
Craik and Lockharts Model: In the ensuing years researchers while analyzing Craik and
Lockharts deep processing model found out that the complex semantic processing
produced better cued recall than simple seman
semantic
tic processing and called this mechanism as
elaboration. Eyesenck and Eyesenck (1980) found even words processed phonetically
were better recalled if they were distinctive or usually labeled and termed it as
distinctiveness. Tyler et al. (1979) found better
better recall for words presented as difficult
anagrams like OCDTRO than simple anagrams like DOCTRO and termed it Effort. Rogers

238
et al. (1977) found better recall for those questions which have personnel relevance (e.g.
describes you) than general semantic ones (e.g. means) (Hill, 1998).
Baddeley and Hitch Model (1974): There remain problems in defining deep processing and
further clarifying as to why it is so effective as semantic processing does not always lead to
better retrieval. It was the working memory model of Baddeley and Hitch (1974) which then
gave further insights into the memory processing and its revised model of 1990 is currently
the most accepted models in memory processing (Hill, 1998).

NEUROBIOLOGY OF MEMORY
According to current views, information from the senses is temporally stored in various
areas of the prefrontal cortex as working memory. It is also passed to the medial temporal
lobe, and specifically to the parahippocampal gyrus. From there, it enters the hippocampus
and is processed in a way that is not yet fully understood. From the hippocampus it leaves
via the subiculum and the entorhinal cortex and somehow binds together and strengthens
circuits in many different neocortical areas, forming over time stable remote memories that
can now be accessed by many different cues (Ganong, 2005).

midline thalamic nuclei hippocampal region

dorsomedial thalamus
entorhinal cortex
anterior thalamus
perirhinal parahippocampal
mammillary nuclei cortex cortex

frontal sensory
association association
areas areas

Do amnesias of temporal lobe, diencephalic and frontal lobe differ?

The memory deficits differ across patients with either medial temporal, diencephalic, or
frontal pathology. Temporal lobe pathology gives rise to accelerated forgetting, but it is not
observed with diencephalic amnesia. Alternative hypothesis is that the diencephalon and
medial temporal lobes differ in their contribution to context memory. Parkin and others
argued that diencephalic lesions produce larger deficits in temporal order memory, whereas
spatial context deficits are larger for the medial temporal lobe pathology

Pathology to the frontal lobes has been thought to be damaging to executive functions such
as planning, the organization of material, monitoring of responses, the inhibition of
inappropriate responses.

239
Neuroimaging investigations
Functional neuroimaging studies reviewed by Rugg (2002), found frontal activations in
memory encoding and retrieval, where the left frontal region was particularly involved in the
encoding of episodic memories, and the right frontal region was involved in episodic
memory retrieval. Functional MRI (fMRI) study has produced evidence that there is left right
material-specific asymmetries during encoding in both the medial temporal lobes and the
pre-frontal cortex.

REMEMBERING, FORGETTING AND KNOWING

Remembering is an intensely personal experience of the past, those in which we seem to
recreate previous events and experience with the awareness and experiences mentally.
The process of remembering has four parts-registration, retention, retrieval and recall.
Knowing is referred to experience of the past in which we are aware of knowledge that we
process but in a more impersonal way without awareness of reliving them mentally or
familiarity of facts (Kopelman, 2002).
Forgetting refers to the apparent loss of information already learned and stored in long term
memory. Much is forgotten but enough enters so that we have a sketchy record of our lives.
Much of what we think we have forgotten does not really qualify as “forgotten” because it
was never encoded and stored in the first place. (Morgan et al. 2007).

Intereference theory

Forgetting is a result of some memories interfering with others.

Proactive interference: Old memories interfere with ability to remember new memories.
Retroactive interference: New memories interfere with ability to remember old memories.

Intereference is stronger when material is similar.

MEMORY DISORDERS
Memory disorders may affect the ability to recall both past events (retrospective memory)
and future events and intentions (prospective memory).
The two major brain regions that have generally been implicated in human memory
dysfunction include the diencephalon and the hippocampi (Emilien et al., 2004). The
dysmnesic syndromes that involve these structures include impairment of long-term data
storage, disruption of the encoding of short-term into long-term storage, or a loss of
decoding or access to the long-term data storage. Dysmnesia is the preferred term
describing a partial memory loss, in contrast to the term amnesia, which implies a total
memory loss. Amnesia may be viewed as an extreme on a broad continuum of dysmnesic
syndromes where mild dysmnesic illnesses occur more commonly than total amnesia.
There can be varied presentation of memory impairments. A patient can have memory
impairment in single memory domain, e.g. working memory, or can have deficit in different
domains simultaneously.

Memory disorders can be broadly classified into -

AMNESIAS (loss of memory)

240
 PARAAMNESIAS (distortions of memory)
HYPERAMNESIAS
THE AMNESIAS
Amnesia is a general term meaning temporary or permanent impairment of some part of the
memory system. The term amnesia is typically applied to a deficit of long-term episodic
memory, involving an impaired capacity for new learning (anterograde amnesia), and/or a
deficit in access to old memories (retrograde amnesia). The classic amnesic syndrome
involves impaired episodic memory, but with preserved intellect, normal working memory
and access to semantic memory, although new semantic learning is likely to be impaired.
Implicit memory is likely to be preserved, with patients able to acquire motor and perceptual
skills, to show perceptual priming, to be capable of classical conditioning, and of non-
associative learning (Emilien et al., 2004).

Its origin may be organic or psychogenic.

PSYCHOGENIC AMNESIAS
Psychogenic amnesias may appear without any organic disease present but the
presentation of organic brain disease is always modified by psychogenic factors,
(Oyebode, 2008).

Childhood amnesia
Freud used the concept of repression to account for childhood amnesia. He said that we
are unable to retrieve childhood memories because they are associated with the forbidden,
guilt arousing sexual and aggressive urges. These urges and their associations are
repressed and cannot be retrieved; they are forgotten because being aware of them would
result in strong feeling of guilt or anxiety. Another interpretation of childhood amnesia
stresses over difference in the ways young children and older people encode and store
information (Morgan et al., 1993).

Dream amnesia
Freud’s interpretation of dreams was based on
repression. He considered dreams to be
expression of forbidden sexual and aggressive
urges. Other interpretation stresses the
differences in the symbol system used in
dreaming and waking, the memory-symbol
network in waking life are different from those
of dreaming so it is difficult to retrieve dreams
in waking state (Morgan et al., 1993).

Defensive amnesia
This form of amnesia is usually considered to
be a way of protecting oneself from the guilt or
anxiety that can result from intense, intolerable
life situations or conflicts. People with this form
of amnesia may forget their names, place of
living, occupation and many other important
details of their past life. Amnesic episode can
last for weeks, months, or years (Morgan et al.,
1993).

241
Anxiety amnesias
Anxiety amnesia occurs when there is anxious preoccupation or poor concentration in
disorders such as depressive illness or generalized anxiety. More severe forms of
amnesia in depressive disorders resemble dementia and are known as depressive
pseudo dementia. Amnesias in anxiety and depressive disorders are generally caused
by impaired concentration and resolve once the underlying disorder is treated (Casey
and Kelly, 2007).

Katathymic amnesia
It is also known as motivated forgetting. It is the inability to recall specific painful
memories and is believed to occur due to defense mechanism of repression. Though the
term is often used interchangeably with dissociative amnesia, katathymic amnesia is
more persistent and circumscribed than dissociation in that there is no loss of personal
identity (Casey and Kelly, 2007).

Dissociative or hysterical amnesia

This is a sudden amnesia that occurs during periods of extreme trauma and may be
concerned about the stressful or traumatic life events that may last for hours or even
days. The amnesia will be for personal identity such as name, address and history as
well as for personal events, while at the same time the ability to perform complex
behaviors is maintained (Casey and Kelly, 2007). Dissociation may be associated with a
fugue or wandering state in which the subject travels to another town or country, and is
often found wandering and lost. Four types of amnesia are been described.
 Localized amnesia being the commonest type, have inability to recall the events
over circumscribed period of time corresponding to stressor.
 Selective amnesia related to only selective events of a particular period related to
stressful life event without impairment of memory in other events of same time
period.
 Continuous amnesia, inability to recall all the personal events from the time of
stressful situation till present time.
 Generalized amnesia, rarest inability to recall whole life in face of stressful life
event (Ahuja, 1999).

ORGANIC AMNESIAS
Organic impairment of memory is referred to as true amnesia and can affect different
functions of memory. There can be impairment of registration, retention, retrieval or recall,
or recognition.

Acute brain disease In these conditions memory is poor owing to disorders of perception
and attention. Hence there is a failure to encode material in long-term memory. In acute
head injury there is amnesia, known as retrograde amnesia that embraces the events just
before the injury. Anterograde amnesia is amnesia for events occurring after the injury;
these occurred most commonly following accidents and are indicative of failure to encode
events into long-term memory. Blackouts are circumscribed periods of anterograde
amnesia experienced particularly by those who are alcohol dependent during and following
bouts of drinking. They indicate reversible brain damage and vary in length but can span
many hours. They also occur in acute confusional states (delirium) due to infections or
epilepsy (Casey and Kelly, 2007).

242
Subacute coarse brain disease The characteristic feature of this disorder, is an
amnestic state in which the patient is unable to register new memories leading to inability to
learn new information (anterograde amnesia),and the inability to recall previously learned
material (retrograde amnesia). However, memories from the remote past remain intact, as
does recall of over learned material from the past and immediate recall. As improvement
occurs, the amnestic period may shrink and recovery may sometimes be total (Casey and
Kelly, 2007).

Chronic coarse brain disease Patients with a progressive chronic brain disease have
an amnesia extending over many years, though the memory for recent events is lost before
that for remote events. This was pointed out by Ribot and is known as Ribot's law of
memory regression (Casey and Kelly, 2007).

THE AMNESIC SYNDROMES

Korsakoff’s syndrome
Korsakoff ’s syndrome results from prolonged and excessive alcohol intake. The thiamine
(B1) deficiency has a direct effect on the brain, specifically on the medial thalamus and
possibly on the mammillary bodies of the hypothalamus (Victor et al., 1989).The most
common symptoms associated with this syndrome include anterograde as well as
retrograde amnesia, confabulations, and a general sense of apathy. Korsakoff ’s syndrome
has long been recognized the prototype of diencephalic amnesia, although it is now
recognised that Korsakoff ’s syndrome commonly involves cortical atrophy, especially the
frontal lobes and damage to other brain regions (Parkin, 1991 ). In addition to their
Anterograde memory deficit, Korsakoff ’s syndrome patients have severely impaired
retrograde memory. In Korsakoff ’s syndrome memory for events in the more distant past
preserved relative to memory for more recent events (Butters & Granholm, 1987; Parkin,
1991). Patients with Korsakoff’s syndrome have a striking anterograde and retrograde
amnesia, often with marked confabulation but preserved attention, personality, social
functioning, STM, and nondeclarative memory. Korsakoff patients, like other amnesics,
exhibit severe impairments in the ability to learn new information.

Transient global amnesia

In most cases of amnesia, the severity of the memory deficit remains stable over a period of
years, but there are conditions such as transient global amnesia where recovery occurs.
Global amnesia is characterized by a relatively circumscribed deficit in LTM for new
information. It appears that transient global amnesia may be caused by temporary bilateral
dysfunction of medial temporal lobe structures, including the hippocampus, entorrhinal
cortex, and parahippocampal gyrus (Fisher, 1982). This dysfunction is most likely due to
ischaemia, perhaps caused by vertebrobasilar hypoperfusion or migrainous vasospasm of
vertebrobasilar vessels (Caplan et al., 1981; Crowell et al., 1984). This type of amnesia is
characterised by a patient’s inability to learn new material, by their repeated asking of
questions that have been answered and being able to recall events that precede the onset
of the episode. Transient global amnesia occurs in middle aged and elderly men more
commonly than women (Fisher and Adams, 1964). The condition, which is still not clearly
understood, can emerge in times of severe stress, pain, or emotion, and has been
attributed to migraine, epilepsy, drug use, hypoglycaemia, stroke, and neoplasms but is still
not clearly understood. Fortunately, these patients normally improve spontaneously, within

243
a few hours, and are neurologically normal the following day. In the clinic, transient global
amnesia is typically assessed by means of recall and recognition tests that require retrieval
of recently learned information. Patients with global amnesia also manifest retrograde
amnesia. Frequently, remote memories are better preserved than memories for events that
occurred shortly before brain injury.

Visual memory-deficit amnesia

Vision and visual imagery play a central role in a variety of memory tasks (Rubin, 1995).
Biographical memory appears to rely on visual imagery to a much greater extent than other
sensory modalities. A form of amnesia called visual memory deficit amnesia, caused by
damage to areas of the visual system that store visual information, has been described
(Rubin & Greenberg, 1998). Because it is caused by a deficit in access to stored visual
material and not by an impaired ability to encode or retrieve new material, it has the
otherwise infrequent properties of a more severe retrograde than anterograde amnesia with
no temporal gradient in the retrograde amnesia.

AMNESIA IN THE CURRENT NOSOLOGY

Amnesia forms the core component or a part of symptomatology of a number of psychiatric

disorders in the current nosological system. The diagnostic categories in the current
nosological systems with amnesia as the core component of the diagnosis include:
ICD-10: The ICD-10(World Health Organization, 1992), provides two diagnostic categories
for describing amnesic disorder depending on the etiology of the disorders rather than the
symptomatology. The lCD-10 differentiates amnesia due to organic conditions from
amnesia due to use of substance — single or multiple. The diagnostic categories are:
F 04: Organic Amnesic Syndrome not induced by alcohol and other psychoactive
substances
F1x.6: Mental and Behavioral disorder due to use of psychoactive substances — Amnesic
Syndrome.
DSM-IV-TR: The DSM-lV-TR (American Psychiatric Association,1994) categorization of
amnesic disorders bears resemblance to the lCD-10 except for the fact that the two
diagnostic categories are clubbed under one roof as Amnestic disorders with further
categorization into that due to general medical condition, substance induced amnestic
disorder. The amnestic disorders are labeled under axis-I disorders with a description of the
underlying medical condition to be provided under the axis-Ill category wherever applicable.
The diagnostic categories are:
294.0: Amnestic disorder due to a general medical condition
Substance induced persisting amnestic disorder (Specific substances to be coded as 291.1
Alcohol induced persisting amnestic disorder.292.83 Secobarbital induced persisting
amnestic disorder and the likewise).
294.8 Amnestic disorder not otherwise specified.

PARAMNESIA (DISTORTIONS OF MEMORY)

This term was coined by Emil Kraepelin in analogy of terms such as paranoia, paraphasia,
and paraphrenia, as a general term to explain illusions and hallucinations of memory
(Burnham, 1889). This is the falsification of memory by distortion. This can occur in normal
subjects due to the process of normal forgetting or due to proactive and retroactive
interference from newly acquired material and is also seen in persons suffering from
emotional problems or other organic states.

244
It can be divided into Distortions
istortions of recall
Distortions of recognition

DISTORTIONS OF RECALL
Retrospective falsification
Retrospective falsification refers to the
unintentional distortion of memory that occurs
when it is filtered through a person's current
emotional, experiential and cognitive state (Casey
and Kelly, 2007).Though
).Though it can occur in any
psychiatric illnesses, it is often found in those
suffering from depressive
ressive illness and hysterical
personality and is invariably related to the insight
of the patient as well as to suggestibility.

Retrospective delusions
Retrospective delusions are found in some
patients with psychoses who backdate their
delusions in spite of the clear evidence that the
illness is of recent origin (Casey and Kelly, 2007).
Thus, the person will say that they have al always
been persecuted or that they have always been
evil.

Delusional memories
Primary delusional experiences may take the form of memories and these are known as
delusional memories, consisting of sudden delusional ideas and delusional perceptions.
Delusional memories are variously defined, some authorities believing them to be
delusional
usional interpretations of real memories (Pawar & Spence, 2003), while others such as
the Present State Examination (PSE) suggest that they are experiences of past events that
did not occur but which the subject clearly remembers.
remembers. There are two components to a
delusional memory, i.e. the perception (either real or imagined) and the memory.

Confabulation
Confabulation is the falsification of memory occurring in clear consciousness in association
with organic pathology. It manifests itself as the filling
filling-in
in of gaps in memory by imagined or
untrue experiences that have no basis in fact. There are two wo broad patterns,
patterns the
embarrassed type in which the patient tries to fill in gaps in memory as a result of an
awareness of a deficit and fantastic type in which the lacunae are filled in by details
exceeding the need of the memory impairment. The confabulation diminishes as the
impairment worsens.
Some related disorders include
 Pseudologia fantastica
Pseudologia fantastica or fluent plausible lying (pathological lying) is the term used to
describe the confabulation that occurs in those without organic brain pathology such as
personality disorder of antisocial or hysterical type. Typically the subject describes various
major events and traumas or makes grandiose claims claims and these often present at a time of

245
personal crisis, such as facing legal proceedings. Although it seems that the person with
pseudologia believes their own stories and there is a blurring of the boundary between
fantasy and reality, when confronted with incontrovertible evidence these individuals will
admit their lying (Casey and Kelly, 2007). Minor varieties of this occur in those who falsify or
exaggerate the past in order to impress others.
 Vorbeireden or approximate answers
Vorbeireden or approximate answers is seen in patients with hysterical pseudodementia,
named after Ganser who, in 1898 described four criminals showing several common
features (Casey and Kelly, 2007). Prominent features present in such patients include:
clouding of consciousness with disorientation, auditory and visual hallucinations (or pseudo-
hallucinations), amnesia for the period during which the symptoms were manifest,
conversion symptoms and recent head injury, infection or severe emotional stress.
Approximate answers suggest that the patient understands the questions but appears to be
deliberately avoiding the correct answer, for instance, to avoid a court appearance .It is
distinguished from pseudodementia in which consciousness is clear. Many now believe that
the Ganser syndrome is indicative of either an organic or a psychotic state rather than
hysteria as originally believed .Ganser syndrome and malingering/factitious disorder are
often confused in spite of the conscious basis for the latter. Vorbeireden is also found in
acute schizophrenia, usually the hebephrenic type.
 Munchausen's syndrome
It is a variant of pathological lying in which the individual presents to hospitals with bogus
illnesses, complex medical histories and often multiple surgical scars. A proxy form of this
condition has been described in which the individual, usually a parent, produces a factitious
illness in somebody else, generally their child. The diagnosis of Munchausen’s by proxy
is itself a controversial diagnosis (Casey and Kelly, 2007).

False memory
False memory is the recollection of an event (or events) that did not occur but which the
individual subsequently strongly believes did take place (Brandon et al, 1998). The
syndrome refers not to distortion of true memories, as in normal forgetting, but to the actual
construction of memories around events that never took place (Casey and Kelly, 2007).
Memory distrust syndrome is a type of false memory which originates from the person's
own fundamental distrust of their memory known as 'source amnesia'. This source amnesia
arises because of difficulty remembering the source from which the information was
acquired, whether from one's own recall or from some external source as recounted by
others.

Screen memory
This is a recollection that is partially true and partially false; the affected individual only
recalls part of the true memory because the entirety of the true memory is too painful to
recall (Casey and Kelly, 2007). It is difficult to find out precisely which elements of such
memories are true and which is false.

Multiple personality disorder (W .H .0, 1992 ; Oyebode,2008)

This disorder is rare, remains controversial due to lack of reliable information, unclear
prevalence, selection bias and psychopathological imprecisions (Oyebode, 2008). The
essential feature is the apparent existence of two or more distinct personalities within an
individual, with only one of them being evident at a time. Each personality is complete, with
its own memories, behaviour, and preferences: these may be in marked contrast to the

246
single premorbid personality. In the common form with two personalities, one personality is
usually dominant but neither has access to the memories of the other and the two are
almost always unaware of each other's existence. Change from one personality to another
in the first instance is usually sudden and closely associated with traumatic events.

Cryptamnesia
Cryptamnesia is described as 'the experience of not remembering that one is remembering,
(Oyebode,2008).For example a person writes a witty passage and does not realize that
they are quoting from some passage they have seen elsewhere rather than writing
something original. There is no indication as to whether this is a common phenomenon or
whether it is associated with any specific psychiatric disorder (Casey and Kelly, 2007).

State-dependent memory
State dependent memory is the recall of events or learned material only when the person is
in the same drug or medication-induced state under which the event was experienced or
the material learned. Patients with psychosis or severe mood disorder experience this
phenomenon and, when well, will not recall dramatic experiences that occurred when ill.
When ill again, the memories are again accessible and recalled (Murphy-Eberenz et al.
2006).

DISTORTIONS OF RECOGNITION
Déjà vu is not strictly a disturbance of memory, but a problem with the familiarity of places
and events. It comprises the feeling of having experienced a current event in the past,
although it has no basis in fact.

Jamais vous is the knowledge that an event has been experienced before but is not
presently associated with the appropriate feelings of familiarity.
Déjà entendu is the feeling of auditory recognition.
Déjà pense, a new thought recognized as having previously occurred, is related to déjà
vu, being different only in the modality of experience. These experiences occur occasionally
in normal persons but they may become excessive in temporal lobe lesions.

Misidentification
This may occur in confusion psychosis and in acute and chronic schizophrenia.
Misidentification may be 1. Positive misidentification and 2. Negative misidentification
Positive misidentification
The patient recognizes strangers as his friends and relatives. Some patients assert that all
of the people whom they meet are doubles of real people. In acute schizophrenia, it can be
based on a delusional perception.

Negative misidentification
The patient denies that his friends and relatives are people whom they say they are and
insists that they are strangers in disguise. Leonhard has suggested that negative
identification could result from an excessive concretization of memory images, so that the
patient retains all the minute details of the characteristics of the people whom he
encounters. When he sees the same person again he compares the new perception with
the exact memory image.

247
The Basic Misidentification Syndromes (Joseph, 1986)
Capgras Syndrome
The essential feature of this syndrome
syndrome is hypoidentification. Patients insists that a
particular person (or persons), usually
usually somebody with whom the patients is emotionally
linked, is not the person he claims to be but is really a double; is often accompanied by
depersonalization and occurs in a paranoid setting. The commonest cause of capgras
syndrome is schizophrenia and d less common causes include involutional depression and
hysteria.

Amphitryon illusion
In
n this patients believe that their
spouses are doubles.

Sosias illusion
In this patients believe that other
people as well as the spouse are
doubles (Hamilton 1984) .

Fregoli syndrome
In fregoli syndrome hyperidentification takes place. The patient identifies a familiar person
(usually his persecutor) in various strangers, who are therefore fundamentally the same
individual.

Syndrome of Subjective Doubles

It is characterized
aracterized by delusions of doubles exclusively of the patient’s own self. The
misidentification can be either hallucinatory or delusional
delusional. There may be hypoidentification
or hyperidentification.

Syndrome of Intermetamorphosis
In this syndrome the patient falsely recognizes the key figure in various others, who are
perceived as taking on the physical appearance of the person who they are believed to be.

Reduplicative paramnesia
In reduplicative paramnesia, patients believe that a physical location has be
been duplicated.
It can occur with other misidentification syndromes. The major difference between
reduplicative paramnesia and Capgras syndrome is that a patient with reduplicative
paramnesia misidentifies a place, whereas a patient with Capgras syndrome mi misidentifies a
person.

HYPERAMNESIA
The opposite of amnesia and paramnesia can also occur and is termed hyperamnesia, or
exaggerated registration, retention and recall. Flashbulb memories are those memories that
are associated with intense emotion. They are unusually vivid, detailed and long
long-lasting.
Flashbacks are sudden intrusive memories that are associated with the cognitive and
emotional experiences of a traumatic event such as an accident. It may lead to acting
and/or feeling that the event is recurring. It is regarded as one of the cha characteristic
symptoms of post-traumatic
traumatic stress disorder but is also associated with substance misuse
disorders and emotional events (McGee, 1984). It is also likely to be a term that is used

248
inaccurately and should not be confused with intrusive recollections, which lack the
emotional familiarity of flashbacks. Flashbacks involving hallucinogenic experiences can
occur in association with hallucinogenic drugs and possibly cannabis use after the short-
term effects have worn off. These incorporate visual distortions, false perceptions of
movement in peripheral fields, flashes of color, trails of images from moving objects, after-
images and halos, as well as classical hallucinations. Eidetic images represent visual
memories of almost hallucinatory vividness that are found in disorders due to substance
misuse, especially hallucinogenic agents(Casey and Kelly, 2007).

AGING AND MEMORY IMPAIRMENT

Both physical and cognitive functions change as we get older. In general, memory
deteriorates, but is to some extent compensated by the increased use of knowledge,
memory aids, and strategies. In the case of working memory, the phonological loop is
reasonably robust, the visuo-spatial sketch pad somewhat less so, while at least some
executive processes tend to decline. In the case of long-term memory, episodic memory
shows a slow but steady decline from the twenties onwards, with memory for names being
particularly sensitive to the effects of ageing. Semantic memory continues to grow, but
speed and reliability of access declines. Implicit learning shows a mixed pattern, with some
types of learning being relatively preserved, but others deteriorating. As age advances, we
find it harder to maintain performance against distraction, particularly under levels of high
arousal. Nutritional factors may also influence the elderly more, as they are less able to
maintain blood glucose level during the gaps between meals, resulting in poorer memory
performance (Baddeley, 1999).

MILD COGNITIVE IMPAIRMENT (Emilien,2004)

A large group of elderly cognitively impaired subjects do not meet the criteria for dementia
or other specific neurological and psychiatric disorders.
Several descriptors including MCI, incipient dementia, and isolated memory impairment
have been used.
The terminology “mild cognitive impairment” refers to subjective memory disturbances
verified by objective deficits of memory at testing.

DEMENTIA
Dementia was initially thought of as a unitary behavioural syndrome, characterised by a
homogeneous decline in intellectual functions, regardless of aetiology.
Dementia is defined as decline of memory and other cognitive functions in comparison with
the patient’s previous level of function, implying a change between two or more assessment
points (McKhann et al., 1984).

ALZHEIMER’S DISEASE
The dementia of AD typically includes anterograde and retrograde amnesia early in its
course.
Deficits in recent memory are typically the first symptoms of AD and may be clinically
reported as misplacing objects, repeating questions and statements, and forgetting names.

249
Impairments in visuospatial memory are often experienced as getting lost. This anterograde
amnesia reflects impaired encoding and consolidation of the material
Several hypotheses have been proposed to account for this impairment of episodic
memory in AD, which might affect both encoding and retrieval of information, and would
result from attentional deficiencies, working memory dysfunction, semantic difficulties, or
neglect of contextual information
It has also been suggested that recent memories are more vulnerable than remote
memory especially in dementia (Ribot law).
In general, remote memory remains relatively intact early in the course of AD. With
disease progression, a slight temporal gradient becomes evident. The remote memory
impairment in AD is a temporal gradient, with recall of recent events being more severely
impaired than recall of more remote events. In moderate to severe AD, the temporal
gradient disappears and patients show marked retrograde amnesia for all decades of life
(Butters et al., 1995). This general pattern of impairment has been demonstrated for
memory for famous faces and public events, visuospatial information, and autobiographical
information.

Semantic memory- Naming

A naming disturbance has been recognised as one of the core clinical features of AD. The
anomia tends to be a relatively early manifestation of the disease. It progressively worsens
over the disease course and is strongly correlated with overall dementia severity.

SEMANTIC DEMENTIA
Semantic dementia is a recently documented syndrome associated with non-Alzheimer
degenerative pathology of the polar and inferolateral temporal neocortex with relative
sparing (at least in the early stages) of the hippocampal complex (Hodges et al., 1992).
Core features of semantic dementia
1. Selective impairment of semantic memory causing severe anomia, impaired spoken and
written single-word comprehension, reduced generation of exemplars on category fluency
tests, and an impoverished fund of general knowledge about objects, persons, and the
meaning of words.
2. Relative sparing of other components of language output and comprehension, notably
syntax and phonology.
3. Normal visuo-perceptual and spatial skills, working memory, and non-verbal problem-
solving abilities.
4. Relatively preserved autobiographical and day-to-day (episodic) memory.
(Hodges et al., 1992).
MEMORY PROBLEM IN PSEUDODEMENTIA
It is important differentiate memory problems commonly seen in elderly patients with
depression and those seen in dementia. With the help of features given below we can
differentiate between the above conditions.
In pseudodementia:-atients generally have prominent depressive symptoms, more
insight into their symptoms and it is usually acute in onset without prior cognitive
disturbances. There is a personal or family histrory of affective episodes, marked
psychomotor retardation with reduced social interaction.Self reproach, diurnal cognitive
dysfunction(worse in the morning).Subjective memory dysfunction in excess of objective
findings.Circumscribed memory dysfunction that can be reversed with proper coaching and
treatment.

250
Meta-memory(Emilien,2004)

Meta-memory is the subjective judgment about one’s own memory capabilities. It is

influenced by the present state of emotion. Patients who are depressed subjectively
experience their performance to be worse than in fact, while those in manias or with the
frontal lobe disinhibited syndrome experience their performance to be better than in fact.
Patients with temporal lobe epilepsy overestimate their memory capacities and their self-
monitoring is less accurate for verbal or non-verbal recall depending on the side of the
seizure focus.

MEMORY DYSFUNCTION IN PSYCHIATRIC DISORDERS

The most common psychiatric disorders in which memory impairment may be seen are
schizophrenia, depression, and anxiety. The objective cognitive impairment is often mild
with alterations in such functions as attention, STM, and speed of processing.

SCHIZOPHRENIA

Memory deficits observed in schizophrenia are not restricted to a single element of memory
but strike different systems, such as declarative memory, short term, and working memory
(Goldberg et al., 1993).There are deficits in long-term memory, including evidence of
impaired retrieval in both recall and recognition. There is also evidence of impaired short
term memory. Furthermore, there is evidence of impairment of working memory and
semantic memory but procedural or implicit memory remains intact (McKenna et al., 2002).
Cognitive impairment is a central manifestation of the schizophrenic illness that impacts on
the quality of life of the patient.

ANXIETY

The presence of distracting, task-irrelevant thoughts is a common feature of anxiety. As

worry occupies some of the limited capacity available to the working memory system, this
negatively impacts tasks that rely heavily on the working memory system. The adverse
effects of anxiety will be evident on tasks carried out in conjunction with a task treated as
more “primary”, as this reduces the capacity available for further tasks.

DEPRESSION

STM or the retention of small amounts of information over very short durations has been
found to be unaffected among depressive patients (Austin et al., 1992; LTM seems to be
more prone to impairment. Depression is associated with a number of deficits in episodic
memory and learning. There is involvement of both explicit verbal and visual memory in
patients with both melancholic (endogenous) and non-melancholic (nonendogenous)
depression (Austin et al., 1999).Impaired delayed memory as opposed to preserved
immediate recall has also been found among depressive patients (Cohen et al.,
1982).People with major depressive disorder, including those who have recently attempted
suicide, have difficulty retrieving specific autobiographical memories in response to cue
words (Williams, 1996).

251
Obsessive compulsive disorder

Obsessive compulsive disorder (OCD) is characterized by recurrent unwanted thoughts and

repetitive, ritualistic behaviors that lead to severe impairments in daily functioning. There
are deficits in learning and memory, especially for non verbal information in OCD patients.
The difficulty in retrieving specific autobiographical memories exhibited by OCD patients
might reflect excessive cognitive capacity consumption due to preoccupation with intrusive
thoughts typical of major depression.
Panic disorder

Patients with panic disorder have a defect in fear-relevant episodic memory, and their panic
attacks arise from automaticity in recollecting fear-relevant emotional–automatic clusters.
The cluster as a component of fear appears to have been dissociated from cognitive
structure, episodic or informative memory trace, or from information structures.
Post-traumatic stress disorder

Post-traumatic stress disorder (PTSD) is a specific anxiety disorder of significant

prevalence and morbidity that develops following exposure to extreme emotional trauma.
Three symptoms clusters characterize the disorder, all of which represent direct or indirect
effects of memory processes:
(1) Persistent re-experience of the traumatic event,
(2) Persistent symptoms of increased arousal,
(3) Persistent avoidance of stimuli associated with the trauma that may include amnesia for
an important aspect of the traumatic event.
Adult PTSD patients often report a wide range of cognitive problems in memory,
concentration, attention, planning, and judgment.
PTSD may be conceived as a clinical condition that involves both memory intensification for
the core traumatic event and memory impairment for the context surrounding the trauma.
The latter comprises dissociation of the experience from ordinary autobiographical memory.
MEMORY DISORDERS IN EPILEPSY
Patients with epilepsy frequently complain of memory difficulties. In some cases this is
secondary to problems of concentration and attention and may therefore not be a memory
defect per se. For patients with temporal lobe abnormalities, memory may be selectively
affected. Seizures may have an acute effect on memory but this is usually transient and
does not affect prospective memory .But poor memory of patients with temporal lobe
epilepsy does not correlate with seizure frequency. In patients who are undergoing
temporal lobectomy careful testing of memory function prior to surgery is mandatory, and
deficits may occur following removal of offending lobe.
DRUG INDUCED MEMORY ALTERATION
Some drugs that may impair or improve memory
Drugs
IMPAIRED MEMORY Type of memory impaired/improved
Lorazepam and diazepam Explicit and Implicit Memory
Methylenedioxymethamphetamine Verbal and visual Memory
(MDMA or “Ecstasy”)

252
 Ethanol and temazepam LTM
IMPROVED MEMORY
Citicoline Facilitates recovery of function and cognition
after traumatic brain injury

Over the past three or four decades, there has been increasing interest in
neuropharmocological regulation of memory. Some drugs have been identified as cognitive
enhancing agents or ‘’SMART DRUGS’’. These groups of drugs have displayed memory-
enhancing effects in experimental settings through diverse mechanism of actions. Important
mechanisms includes cholinergic agonists at the muscarinic and nicotinic receptors,
cholinesterase inhibitors such as physostigmine, CCB’s like nimodipine, neurotransmitters
such as norepinaphrine, GABA-B receptor blockers, peptides like vasopressin corticotropin,
glucose etc(Emilien,2004).
Lithium usually causes mind slowing (bradyphrenia) and cognitive deficits are more when
used along with ECT.
Anticholinergics mainly affect short term memory especially encoding and storage of
information.
Ethanol acute ingestion induces BLACKOUT AMNESIA which refers to profound STM
deficits and it may be associated with hypoglycemia, hypomagnesemia etc. Chronic
ingestion causes korsakoff’s psychosis where we can see the memory deficits as
confabulation as the patient tries to fill the memory gaps with unnecessary details.
Beta blockers may produce poor memory particularly for emotionally valent information.
Corticosteroids causes memory impairment mainly by its deleterious effects on
hippocampus.
Barbiturates tend to impair acquisition and interfere with retention of learned behavior.
Antiepileptic drugs may exacerbate pre existing memory problem by affecting
concentration, attention and psychomotor abilities. Phenytoin and primodone are
associated with cognitive decline.
Topiramate causes word finding difficulties.
Cognitive enhancers (cerebroactive drugs)-There are various drugs claimed to be
having cognitive enhancing property. But as per the Cochrane review there is no definitive
evidence.
Cholinergic activators: Donepezil, Rivastigmine, Galantamine, Tacrine.
Glutamate (NMDA) antagonist: Memantine
Miscellaneous cerebroactive drugs: Piracetam, Pyritinol, Dihydroergotoxine, Piribedil,
Ginkgo biloba.
MEMORY DISTURBANCES AND ECT
Memory disturbances are seen occurring immediately after ECT and includes short lived
impaired learning ability, defective retrievals along with permanent loss of memories of
events (especially autobiographical memories) preceding immediately to ECT treatment.
These deficits are proportional to strength of current, duration of electrical stimulus, number
of sessions given to the individual, the area of the brain where the current pulse is given
(dominant or non-dominant area of the brain) and finally bilaterality of ECT. Therefore ECT
if applied unilaterally, in non-dominant side of the brain not only hastens recovery but also
causes less post ictal amnesia, confusion and memory disturbances. However amidst
various ongoing controversies regarding the ECT generated memory deficits the effects do
not seem to last more than six months and some researchers currently have pointed out
that ECT does not cause more than a temporary disturbance in memory (Oyebode, 2008).
253
CLINICAL ASSESSMENT OF MEMORY

Tests for memory (Strub & Black, 2000)

Valid memory testing presumes that the patient is reasonably attentive, can relate to and
cooperate with the examiner, and has no defect that impairs language comprehension or
expression.

IMMEDIATE RECALL (short term memory)

Immediate memory usually tested by digit repetition.

RECENT MEMORY
Tested for constantly changing facts. Indian adaptation (Pershad & Wig, 1988):
1. कल आपने रात के खाने म या खाया?
2. आज सुबह आपने ना ते म या खाया?
3. इस मिहने का या नाम है?
4. आज कौन-सा दन है?
5. कल आपसे कौन-कौन िमलने आया या कल आप कस कस से िमलने गये?

REMOTE MEMORY
These evaluate the patient’s ability to recall personal and historic events. Personal events
must be verified from a reliable source other than the patient, and performance on the recall
of historic information must be interpreted in light of the patient’s premorbid intelligence,
education, and social experience.

Indian adaptation (Pershad & Wig, 1988). The following items to be enquired-
1. आपक उ कतनी है?
2. आपका ज म कहाँ आ?
3. आपक शादी कब ई?/आपने नौकरी या साय करना कब से चालु कया?/आपने पढ़ना कब छोडा या हाई- कू ल
कब पास कया?
4. आपके सबसे छोटे ब े या भाई बिहन क उ कतनी हौ?
5. आप इस िवभाग म पहली बार अपने इस इलाज के िलये कब आये?
6. िपछिल बार आप इस िवभाग कब आये थे?
Each correct answer to be scored one thus a maximum score of 6. (Pershad & Wig,
1988)

FOUR UNRELATED WORDS

Instructions: Tell the patient, “I am going to tell you four words that I would like you to
remember. In a few minutes, I will ask you to recall these words”. To ensure that the patient
has heard, understood, and initially retained the four words, have him or her to repeat the
words immediately and to correct any errors. Older patients may require several trials to
learn the words.

254
Then he is asked to recall the words at 5, 10 and 30 minutes. To eliminate possible mental
rehearsal, interference should be used between presentation and recall of words.
Scoring: Normal persons accurately recall 3-4 words after a 10-minute delay. In some,
after being reminded of the correct words i.e., by verbal cues, whether he/she recognizes
the appropriate word from the series of words and improve their performance after 10 and
30 minutes may be seen, but patients with dementia cannot improve even on subsequent
trials.

Indian adaptation (Pershad & Wig, 1988)

Set 1 छाता, फू ल, घडी, त वीर, पिसल Set 2 मछली, लप, पया, ताज, िखलैना

VERBAL STORY FOR IMMEDIATE RECALL

Instructions: tell the patient, “I am going to read you a short paragraph. Listen carefully,
because when I finish reading, I want you to tell me everything that I told you.” A short
paragraph is read out to the patient which he is required to reproduce immediately. As the
patient retells the story the number of items recalled is indicated. The normal individual is
expected to produce at least 10 of these items, though this number decreases with age. If
recall is good then he may be asked for another recall after 30 minutes.

Indian adaptation
There are three sentences of increasing length. First sentence is read slowly, distinctly and
at a uniform rate and note down the recalled sentence verbatim or each of the correctly
recalled clauses. One mark for each clause correctly reproduced. (Pershad & Wig, 1988)
1. राम कु स से उठा, दरवाजा खोला और घर चला गया।
2. रोगी को मेज पर िलटाया, उसको देखा, दवा िलखी और कल आने के िलए कहा।
3. मोहन के घर पानी नह था, उसने बा टी उठाई, बाजार के नल पर गया, पानी भरा और वािपस लौट आया।

VISUAL MEMORY (hidden objects) (Strub & Black, 2000)

Five small, commonly used, easily recognizable objects are hidden in the patient’s vicinity
while he is watching. Each item is named while being hidden. Then interfering stimuli is
provided for 5 minutes. After this period he is asked to name and indicate the location of
each hidden object. Finding out fewer than three objects indicates impaired visual memory.

PAIRED ASSOCIATE LEARNING

Instructions: Tell the patient, “I am going to read you a list of words, two at a time. Listen
carefully because I will expect you to remember the words that go together. When the
patient understands the directions, continue as follows: “Now listen carefully to the words as
I read them.” The patient is read out a list of paired words at the rate of one pair every 2
seconds. Then he is given the first words from the pairs, one after another and given 5
seconds for each response. After completion of the first recall list the second presentation
list is provided after a 10 second interval and proceeds in the same way.
A normal person under 70 years is expected to recall the two easy paired associates and at
least one of the hard associates of the first recall trial and to recall all paired associates on
second trial. Some patients can learn the paired words with strong natural associations but
cannot learn the pairs without such associations which indicate an inability to learn new
material that cannot be associated with memories already in storage.

255
Indian adaptation (Pershad & Wig, 1988)

Retention for similar pairs For dissimilar pairs

पेड़ फू ल मेज काला
मीठा नमक न पेड़ ऊँचा
आदमी औरत लप खुरदरा
दन रात ब ा कड़वा
काला सफे द सपना गहरा

EMOTIONAL AND SOCIAL CONSEQUENCES OF MEMORY DISORDERS

These are acquired neuropsychological disorders fall within the domain of psychosocial
functioning. Emotional responses occur within the context of an individual’s personality
structure and their environment underlying stable traits, and transient fluctuations in
emotional affective and mood states, which occur in response to day to day events. Those
with fairly circumscribed memory disorders are well placed to harness their intelligence and
other neuropsychological strengths and implement compensatory strategies to circumvent
the memory disorders. This enables them to access a range of life otherwise it will be
difficult to achieve productive work, independent lifestyles and a regular social life in the
presence of other neuropsychological impairments in addition to memory disorder makes it
difficult to attribute any emotional or social disturbance to the memory disorder itself, as
opposed to some concomitant neuropsychological problem that the person may
experience, such as aphasia, executive impairment, attention deficit and so forth. The
literature regarding emotional and social consequences for people with a range of
neuropsychological problems is relevant and important, given that the majority of adults
who experience acquired memory disorder also have additional neuropsychological
impairments.

MEMORY REHABILITATION
How are the memory difficulties manifested in everyday life?
• What problems cause most concern to the family and the memory-impaired person?
• What do we know about the cultural background and level of support available?
• What coping strategies are used?
• Are the problems exacerbated by depression or anxiety?
• Is this person likely to be able to return to work (or school)?
• Can this person live independently?
• What kind of compensatory aids did this person use premorbidly?
• What kind of memory compensation strategies are being used now?
• What is the best way for this person to learn new information?
Ten Key Memory Tips
Take it easy
1. Try not to do too many things at once.
2. Anxiety and tiredness can affect memory, so try to avoid stressful situations. Be positive
and have regular breaks.

256
3. If you do forget something, don’t get too upset about it. Stay calm and think of
connections that may jog your memory. Be well organized
4. Keep to a fixed routine, with set things at set times of the day and on set days of the
week.
5. Be systematic: Have a place for everything and put everything back in its place.
Put labels on drawers and files.
Concentrate better
6. If you have to do something, do it now rather than later: “Do it or lose it.”
7. Try not to let your mind wander: Keep on track.
8. If you have to remember something such as a message or a name, go over it in your
mind at regular intervals.
9. Try to find meaning in things you have to remember (e.g., by making associations or
linking things together). (Wilson, 2009).
10. Use memory aids

External memory aids are effective in improving everyday memory functioning, and this
benefit is particularly evident in the area of prospective memory.
1. An electronic diary to keep a record of appointments.
2. An alarm which provides auditory cues, with or without text information, at preset, regular
or irregular times.
3. A temporary store for items such as shopping lists, messages, etc.
4. A more permanent store for information such as addresses, telephone numbers, etc.
5. In more expensive models, a communication device that can receive and send
information, such as reminders and factual knowledge.

REFERENCES

Ahuja, N. and Hebbar, S. (1999). Dissociative disorders. In: Vyas, J.N. and Ahuja, N. (Eds.).
Textbook of postgraduate Psychiatry, 2nd edn, 295-320. New Delhi, Jaypee brothers.

American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorder (4th
ed). Washington DC, APA.

Atkinson, R.C. and Shiffrin, R.M. (1968). Human memory: A proposed system and its control
processes. In: Spence, K.W. and Spence, J.T. (Eds.) The psychology of learning and motivation
(Vol.2). New York, Academic press.

Austin, M. P., Ross, M., Murray, C., O’Carrol, R. E., Ebmeier, K. P., & Goodwin, G. M. (1992).
Cognitive function in major depression. Journal of Affective Disorders, 25, 21–30.

Baddeley, A.D. and Hitch, G. (1974), Working Memory. In Bower GA (ed) Recent advances In
Learning and Motivation. 8, 847-89. New York, Academic press.

Baddeley, A.D. (1986), Working Memory. Oxford, Clarendon.,In Oyebode, F. (2008) Sims’
Symptoms in the Mind: An Introduction to Descriptive Psychopathology, 4th Ed. Elsevier Publication,
65-79.

257
Baddeley, A.D. (1999). Aging and memory. In essential of human memory. Taylor and Franscis
Routledge, 251-272.

Baddeley, A.D., Koppelman, M.D., Wilson, B.A. (2002). The handbook of memory disorders 2nd ed.,
pp.145-667, John Wiley & Sons Ltd.

Wilson, B.A. (2009). Memory rehabilitation: integrating theory and practice.1.Memory disorders
2.Memory 3.Memory disordes-patients-Rehabilitation.

Baron, R.A. (2005), Memory of Things Remembered and Forgotten, Psychology, 5th Ed. Pearson,
219-223.

Brandon, S., Boakes, D., Glaser, D., et al (1998) Recovered memories of childhood sexual abuse:
Implications for clinical practice. British Journal of Psychiatry, 172, 296−307.

Budson, A.E., and Price, B.H. (2001). Memory: Clinical Disorders. In: Encyclopedia of life sciences,
Macmillan Publishers Ltd, Nature Publishing Group / www.els.net

Burnham, W.H. (1889). Memory, historically and experimentally considered. III paramnesia.
American Journal of Psychology, 2, 431–494.

Butters, N., and Granholm, E. (1987). The continuity hypothesis: Some conclusions and their
implications for the etiology and neuropathology of alcoholic Korsakoff’s syndrome. In Parsons,
O.A., Butters, N. and Nathan, P.E. (eds.), Neuropsychology of alcoholism: Implications for diagnosis
and treatments. New York: Guilford Press.

Caplan, L., Chedru, F., Lhermitte, F., and Mayman, C. (1981). Transient global amnesia and
migraine. Neurology, 31(9), 1167–1170.

Casey, P.R. & Kelly, B. (2007). Disorders of memory. In: Fish’s Clinical Psychopathology: Signs and
symptoms in psychiatry, 3rd Ed., 55-64. London, RCPsych Publication.

Cornoldi, C. and Vecchi, T. (2003)., working memory. In: visuo-spatial working memory and
individual differences, 6. NewYork, Hove.

Craik, FI. M., and Lockhart, R.S. (1972). Levels of processing: A framework for memory research.
Journal of Verbal Learning and Verbal Behavior, 11, 671-684.

Crowell, G.F., Stump, D.A., Biller, J., McHenry, L.C., and Toole, J.F. (1984). The transient global
amnesia–migraine connection. Archives of Neurology, 41(1), 75–79.

Cohen, G. (2008). Overview: conclusion and speculations. In: Memory in the real world.3rd ed., 381-
408. New York, Psychology Press.

Delis, D.C., Kramer, J.H., Kaplan, E., Ober, B.A. (1996). California Verbal Learning Test. The
psychological Corporation, San Antonio, 1987. As cited in Mayes AR. The Assessment of memory
disorders. In Baddeley AD, Wilson BA, Watts FN. eds. Handbook of memory Disorders, New York:
John Wiley & Sons Inc.

Emilien, G., Durlach, C., Antoniadis, E., Linden, M.V. and Maloteaux, J.M. (2004).
Neuropsychological, Imaging, and Psychopharmacological Perspectives Memory, pp 147-168. New
York , Psychology Press.

258
Fisher, C. M. (1982). Transient global amnesia: Precipitating activities and other observations.
Archives of Neurology, 39(10), 605–608.

Fisher, C. M., and Adams, R. D. (1964). Transient global amnesia. Acta Neurologica Scandinavica,
40(Suppl. 9), 1–83.

Ganong, W.F. (2005). Higher function of the nervous system, conditional reflex, learning and related
phenomenon, In review of medical psychology 22nd ed, 259-270. New York, The McGraw Hill
Company.

Goldberg, T. E., Torrey, E. S., Gold, J. M., Ragland, J. E., Bigelow, L. C., & Weinberger, D. R.
(1993). Learning and memory in monozygotic discordant for schizophrenia. Psychological Medicine,
23, 71–85.

Hamilton, M. (1984). Disorders of memory. In: Fish’s Clinical Psychopathology: Signs and
symptoms in psychiatry, 4th Ed. Bristol, John Wright & sons, 63-69.

Hill, G. (1998) Advanced Psychology through diagrams, 1st ed.,pp.64-72. Oxford University Press

Hodges, J. R., Patterson, K., Oxbury, S., & Funnell, E. (1992). Semantic dementia: Progessive
fluent aphasia with temporal lobe atrophy. Brain, 115, 1783–1806.

Joseph, A.B. (1986), Focal central nervous system abnormalities in patients with misidentification
syndromes. In Christadoulou (ed), Bibliotheca Psychiatrica. 164, 68-79. Basel, Karger.

Ken, A.P. & Larry, R.S. Biology of memory in Kaplan & Sadock Comprehensive Text boom of
psychiatry 8th edition. Lippincott Williams & Wilkins, pp 560-580.

Kopelmem, M.D. (2002). Disorder of memory. Brain;125, 2152-2190.

Lishman, W.A. (2004). Organic psychiatry the psychological consequences of cerebral disorder, 3rd
ed., pp28-31. Blackwell Publishing Company.

McGee, R. (1984) Flashbacks and memory phenomena. A comment on ‘Flashback phenomena −

clinical and diagnostic dilemmas’. Journal of Nervous and Mental Diseases, 172, 273−278.

McKenna, P.J., Ornstein, T., Baddeley, A.D. (2002) Schizophrenia. In Baddeley, A.D., Kopelman,
M.D. and Wilson, B.A. (eds) The Handbook of Memory Disorders, 2nd Ed., Chichester, John Wiley,
413-435.

Morgan, C.T., King, R.A., Weiss, J.R. and Schopler, J. (1993). Memory. In: Introduction to
Psychology, 7th Ed., New York, Tata McGraw-Hill Companies, 181-223.

Murphy-Eberenz, K., Zandi, P.P. and March, D. (2006). Is perinatal depression familial? Journal of
Affective Disorders, 90, 49–55.

Oyebode, F. (2008) Sims’ Symptoms in the Mind: An Introduction to Descriptive Psychopathology,

4th Ed. Elsevier Publication, 65-79.

Parkin, A. J. (1991). Recent advances in the neuropsychology of memory. In: Weinman, J. and
Hunter, J. (Eds.), Memory: Neurochemical and abnormal perspectives. London: Harwood Academic
Publishers.

259
Pawar, A. V. and Spence, S. A. (2003). Defining thought broadcast: Semi-structured literature
review. British Journal of Psychiatry, 183, 287–291.

Pershad, D. and Wig, N.N. (1988). Revised Manual for PGI Memory Scale (PGIMS). Agra, National
Psychological Corporation.

Rubin, D. C. (1995). Memory in oral traditions: The cognitive psychology of epic, ballads and
counting-out rhymes. New York, Oxford University Press.

Rubin, D. C., & Greenberg, D. L. (1998). Visual memory-deficit amnesia: A distinct amnesic
presentation and etiology. In: Proceedings of the National Academy of Sciences of the United
States of America, 95, 5413–5416. Rugg, M.D.(2002). Functional neuroimaging of memory. In:
Baddeley AD, Kopelman MD, Wilson BA, editors. Handbook of memory disorders. 2nd ed.
Chichester (UK): John Wiley. 2002. p. 57-80.

Sims, A., (2003) Disturbance of memory. In: Symptoms in the Mind: An Introduction to Descriptive
Psychopathology, 3rd edn,63-76. Philadelphia, Saunders.

Snowden, J., (2002) Disorders of semantic memory, In: Baddeley, A.D., Kopelman, M.D. and
Wilson, B.A.(eds.). The handbook of memory disorders, 2nded, 293. Wiltshire, John Wiley & sons.

Strub, R.L. and Black, F.W. (2000). The Mental Status Exam in Neurology, 4th edition. 74-92.
Philadelphia, FA Davis.

Victor, M., Adams, R. D. and Collins, G.H. (1989). The Wernicke-Korsakoff syndrome. 2nd Ed.
Philadelphia, FA Davis.

Williams, J. M. G. (1996). Depression and the specificity of autobiographical memory. In D. Rubin

(Eds.), Remembering our past: Studies in autobiographical memory, Cambridge: Cambridge
University Press.

World Health Organization (1992). The ICD-10 Classification of Mental and Behavioural Disorders:
Clinical descriptions and diagnostic guidelines(10th ed). Geneva, World Health Organization.

260
APPENDIX- 1

261
Budson, E.A., Price, B.H. (2001). Memory: Clinical Disorders. ENCYCLOPEDIA OF LIFE
SCIENCES, Macmillan Publishers Ltd. / www.els.net

262
CHAPTER –XIV
 DISORDERS OF EMOTION

 Introduction  The Physiology of Emotions

 What is emotion  Facial Expression as a mirror for Emotion
 Theories of emotion  Gender and Socio Cultural Aspect of Emotions
 Clinical assessment of emotions  Theories of Emotion: Critical Evaluation
 Classification of emotional disorders  Emotions from developmental Perspective
 Conclusion  Neurobiological Basis of Emotions
 Emotional Disorder in Various Psychiatric
Conditions
 Tools to Assess Different Emotions
 Conclusion

INTRODUCTION:
Emotion is a well acknowledged term in day to day life; happiness, fear, anger being very
common examples. Emotion not only affects relationships and health but influences
important decisions too. There are facial expression, body movements, and action that
indicate to others how a person feels. Frowns, smiles, and sad expressions combine with
hand gesture, the turning of one’s body, and spoken words to produce an understanding of
emotion. Indian classical dances like Bharat Natyam, Odisi, Kathak, and Kuchuipudi are a
good example of facial expression of emotion, where emotions are displayed with help of
facial and bodily movements. There is different kind of Emotions, Ekman & Friesen, (1971)
proposed six basic emotions that are expressed in the face, that are- anger, disgust, fear,
happiness, sadness and surprise.

WHAT IS EMOTION?
Emotion is the feeling aspects of consciousness, characterized by a certain physical
arousal, a certain behavior that reveals the emotion to the outside world, and an inner
awareness of feelings.
The word emotion made from the Latin word ‘Emover’ which means ‘to excite’.
According to Kaplan, et al. (2009)Emotion is a “complex feeling state with psychic, somatic
and behavioral component.”.
According to Sims, (2009) “Emotion is often used to refer to spontaneous and transitory
experience similar to but not identical to feeling, as it need not incorporate the physical
accompaniment of experience”.
Taylor & Vaidya (2009) “A mental state or feeling such as fear, hate, love, anger, grief, or
joy, arising as a subjective experience rather than as a conscious mental effort”.
Emotion according to Whybrow (1997) is actually memory and feeling intertwined (Sims,
2009).
According to Fish,(1984) “Emotion is a moved or stirred up state of organism caused by
physiological changes occurring as a response to some event and which tends to maintain
or abolish the causative event.”
Emotion is considered “a drive”. Emotions are communicated non-verbally by different parts
of body, for example eyes, gesture, posture, tone of voice and general appearance
especially the choice of clothes.

Feeling:

263
“Feeling has been used to describe a positive or negative reaction to an experience; it is
marked but transitory.” (Sims, 2009)
Feeling is “the conscious phase of nervous activity”. (Taylor & Vaidya, 2009)
A feeling can be defined as a “positive or negative reaction to some experience or event
and is the subjective experience of emotion.” (Fish, 1984)
Jasper has categorized feelings in following ways:
 Feeling is aspect of conscious personality and defines the self; e.g. my own sadness in
contrast to the sadness of landscape.
 Feeling can be grouped in opposites to some extent; Wundt distinguished excitement
and calm, pleasure and displeasure, tension and relaxation,
 Feeling can be without an object and numerous (i.e. how one feels) or they may be
classified accordingly.
Feeling can be categorized according to the resource. There can be very important feelings
affecting the whole body in which emotion is described as subjectively as being physical but
affecting the whole organism in complete way. It is possibly to evaluate emotion according
to its biological purpose e.g. pleasurable feelings express the progression of biological
purpose. Feeling state is a description of all the different feeling occurring at any one time
and describes the affective state of individual at time. For example state of arousal. Jasper
also emphasized that emotion has been categorized traditionally according to the duration
and intensity. Thus feeling is individual emotional reaction whereas affect is complex but
short-lived emotional perturbation and mood is more prolonged emotional state which
influences or features the mental state.
 Mood:
Mood is the emotional state existing at any given time or as “The dominant hedonic tone of
the moment”. According to DSM IV (A.P.A.1994) “mood is a pervasive and sustained
emotion that colors the perception of the world.”
According to Fish, (1984), mood is often used by psychiatrist for “an emotional state which
usually lasts for some time and which colors the total experience of subject.” In
phenomenology assessment of mood, Jasper (1959) has determined three main aspects:
the involvement of self, the contrast of opposites and the nature of the object of feeling.
Mood is more extended prevailing state or disposition. Mood describes the state of self in
relation to its environment. There is a huge range of variation of what could convincingly be
called normal mood. Pathological mood, that is, mood from which the patients suffer or
mood that cause disturbance or suffering to others, also varies greatly and extent to which it
is acceptable to others in its expression is different in different social context. (Sims, 2009)
 Affect:
Affect is short-lived emotion, is defined as the patient’s present emotional responsiveness.
It is what the examiner infers from the patient’s body language including facial expression
and it may or may not be congruent with mood.
According to DSM IV (A.P.A.1994) “affect is a pattern of observable behavior that is the
expression of a subjectively experienced feeling state (emotion).”
Fish, (1984)describes as “Affects are waves of emotion in which there is a sudden
exacerbation of emotion usually as a response to some event.” Affect are divided into
sthenic and asthenic varieties-
Sthenic affect: Are anger, hate or joy.
Asthenic affect: Are anxiety, horror, shame, grief and sadness.
“Affect is a broad term to cover mood, feeling, attitude, preferences and evaluation.” (Sims,
2009)

264
Affect: The observable behavior seen in the expression of emotion. Affect responds to
changes in emotional states as defined by Tasman .Affect can be expressed in three ways
(Tasman, 2003)
 Autonomic responses that may reflect by sweating, trembling, blushing becoming
flush.
 Speech changes that reflect affect by changes in tone of voice, vocalization and
word selection.
 Body movement that changes in posture, alternation facial expression, reactive
response and grooming movement of body
Affect has three functions (Tasman, 2003)
 Self perception: it is emotional value judgment or affective response associated with
affect.
 Communication: The expression of affect communicates to other emotional response
to events, interaction, behavior, and situations.
 Motivation: Affect precedes a behavioral response or motivates it, like anger is
precursor of aggression.

THEORIES OF EMOTION:
There are various theories to explain emotion, the classification of theories given by
Leventhal and Tomarken (1986) is as follows:
 DARWINIAN EVOLUTIONARY THEORY:
A-McDougall (1923): All human behavior strives for achieving a goal, either to derive
pleasure or to avoid pain. These two basic tendencies in human behavior are termed as
feeling.
B-Izard (1977): Emotions are inherently adoptive and discrete in nature. He proposed ten
primary emotions –anger, contempt, disgust, sadness, fear, guilt, interest, joy, shame, and
surprise.
C-Plutchik (1980): Gave eight primary emotions i.e. anger, fear sadness, disgust, surprise,
expectancy, acceptance and joy. He presented a three dimensional circumplex model
which is a hybrid of both basic complex categories and dimensional model. It arranges
emotion in concentric circle where inner circle are more basic and outer circle are more
complex.
 BODY REACTION THEORIES:
Body reaction theorists believe that a perception of peripheral reactions gives rise to the
experience of emotion.
A-James-Lange (1884): According to this theory we feel emotion as a result of body
response to the event.
B-Cannon-Bard(1928):Experience of emotion and body reaction co-occur in the event of
emotional stimulation.
 COGNITIVE AROUSAL THEORIES:
The cognitive theorists, view emotion as a function of arousal when integrated with
perceptual organization.
A-Schachter-Singer (1964): Emotion is product of interaction between physiological
arousal and cognition.
B-Lazarus (1984): An emotion provoking stimulus triggers a cognitive appraisal which is
followed by the emotion and physiological arousal. He made a strong claim that the
appraisal are both necessary and sufficient for emotion, and sees the identity of particular
emotion as being completely determined by the patterns of appraisal giving rise to them.
 ORIENTAL THEORIES:

265
A-Hindu tradition: Sources of mind (mana), namely, purity (sattva), energy (rajas), and
inertia (tamas), give rise to basic emotion.
B-Buddhist tradition: Pleasure, pain and neutral feeling (positive feeling of indifference)
are basic to human emotion.
C-Jain tradition:
Spiritual pleasure (enjoyment of self) that is not dependent on physical or mental element is
central to human emotion.

 CLINICAL ASSESSMENT OF EMOTIONS:

. Clinical assessment of emotion is divided is mood and affect.

Assessment of Mood on Various Dimensions:

A particular mood is not necessarily abnormal or pathological but must be evaluated in
context of the patient’s entire history and psychiatric mental status examination.
Assessment of mood of any individual is very difficult but there are some dimensions on
which mood can be assessed (Tasman, 2003).
(a) Quality: mood can be characterized as depressed, dysphoric, elevated, and irritable.
Quality of mood can be assessed by asking the patient “how do you feel?” & “And what
is your mood?”
(b) Stability: to what extent does mood remain constant over time? It can be assessed
by asking “do you always feel like this?”
(c) Reactivity: ability to react emotionally to the innate changes in the environment and
it is assessed by asking “Does your mood ever change?” or “When does your mood
change?”
(d) Intensity: A degree to which an emotion is experienced and is clinically assessed by
asking “what is it like to feel this way?” or “on the scale of 0-10 how would you rate your
mood?”
(e) Duration: Duration is regarded as the basis for the experience of the passage of
time. It can be assessed by asking “How long have you felt this way?”
(f) Congruence: whether the emotion shown is congruent with thought content. This is
based on impression of the interviewer.

Assessment of affect
Assessment of affect is difficult solely on the basis of verbatim of an individual because
what person speaks and what emotions he displays or shows might be incompatible. So
we need to assess the affect crossectionally on the basis of certain dimensions (Tasman,
2003).

Quality:
Quality (valence): Happy, sad, and angry. It should be assessed in two forms-
(a) Subjectively: How do you feel in yourself?
(b) Objectively: Observation of interviewer.
There are some qualities of sad and happy mood which are as follows-
Observed depression includes sad, mournful look, tears, gloomy tone of voice, voice
chokes on distressing topic (WHO, 1998).
Dysphoric includes sustained emotional states such as sadness, anxiety or irritability.
(a) Anxiety: Feeling of apprehension caused by anticipation of danger which may be
internal or external or anxiety is an unpleasant affective state with the expectation,
but not the certainty of something untoward happening.

266
 (b) Irritability: It can be defined as liability to outburst or as state of poor control over
aggressive impulses directed toward others; most frequently to those nearest and
dearest.
It is a state in which a person is easily annoyed and provoked to anger.
(c) Sadness: Emotional mood tending toward sorrow. Relative passivity and diminished
muscular tone with weeping characteristics.
Observed Hypo manic - Abnormal cheerfulness & sense of well being.
Elevated: exaggerated feeling of well-being, euphoria, or elation.
(a) Euphoric: increased sense of psychological well-being with cheerful thoughts and
lack of response to depressing influence so that everything is seen in the best
possible light.
(b) Elation: feeling of well-being and euphoria leading to faulty judgment, general over
activity & disinhibited behavior.
(c) Exaltation: feeling of intense elation and grandeur; seen in severe mania.
(d) Ecstasy: intense sense of rapture or blissfulness; seen in delirious and stuporous
mania.
Expansive: lack of restraint in expressing feelings.
Euthymic: mood in normal range implying absence of depressed or elated mood.

Range:
The range of the affect is characterized by the variety of emotional expression. There is
different feeling at different times -
(a) Full range: Patients who appropriately express many different emotions have a full or
broad range of affect.
(b) Restricted range: person shows only a fixed or immobile affect found only in one type of
emotion.

Intensity:
Intensity of affect (the strength of emotional expression) normally varies according to the
situation. Those with limited emotional expression may have blunted or flattened affect –
Flat affect: When no affect is displayed or it is reported as to be flat or absence of
emotional response.” absence of appropriate outward emotional responses.
Blunted affect: as “greatly diminished emotional response” or expressionless face and voice
uniform, whatever the topic of conversation is, the patient is indifferent (whether delusional
or normal) .
Shallow affect: when there is lack of depth in emotion.

Mobility:
The mobility of affect is related to ease and speed with which one move from one to
another type of emotion. Changes in type and intensity of emotional expression normally
occur gradually.
(a) Constricted affect: Reduced mobility is also referred as constricted affect.
(b) Fixed affect: When affect is extremely constricted to one emotion it is called fixed or
immobile emotion.
(c) Labile affect: Pathologically increased mobility of affect is referred to as labile or
rapid shift from one to another without persistence of any one affect.

Reactivity:

267
The reactivity is extent to which the affect changes in response to environment
stimulus.Eg., when patient does not respond to examiner’s provocations like joking, the
affect is nonreactive.

Communicability:
The expression of affect communicates to others, the emotional response to events,
interaction, behavior, and situations.
Appropriateness:
It refers when there is congruence between the expressed quality of emotion and the
situation. Paramimia refers as lack of unity between the various modes of expression of
emotion. Parathymia is a expression of an emotion that is the exact opposite of what is
expected under the circumstances (e.g. laughing at tragic news), or the expression of
emotions that appear unnatural, exaggerated or theatrical.

CLASSIFICATION OF EMOTIONAL DISORDERS:

Some emotional reaction is normal responses of ill person to a primary morbid
psychological experience. We use the term ‘abnormal’ in the sense of “morbid” or of “a
quantitative deviation from mean”. When we speak of “abnormal emotions” means
excessive emotional response or emotional state resulting from “morbid” process in
nervous system. In this discussion the world abnormal will be used for excessive emotional
responses of normal kind and the morbid for those phenomena which is result of a morbid
process within the nervous system.
 Abnormal emotional predispositions
 Abnormal Emotional reactions
 Abnormal expressions of emotion
 Morbid disorders of emotion
 Morbid disorders of the expression of emotion

Abnormal emotional predispositions:

It is believed that abnormal personalities and temperament are determined genetically and
predisposition to emotion disorder is determined by childhood experiences. It may often be true
in hyperthymic, dysthymic, cyclothymic, and irritable temperament which often found in patient
with manic-depressive disease. Examples are:

Hyperthymic personality:
Hyperthymic personality, where person is over cheerful and is not touched by minor
irritation of life. Some people have an increased emotional responsiveness, so that their
mood swings from euphoric to depression with slight change of emotional
environments.Disinhibited behavior easily occurs in such individual who are highly
suggestible.

Emotionally cold personality:

Who has a generally an indifference, lack of emotion, and an absence of finer feelings. It
has been suggested that mental deprivation give rise to affectionless individuals. In
childhood and adolescents there is normally a lack of constancy in emotional feeling and
instinctual life. This is usually associated with a lack of persistence a tendency to egotism,
cruelty, outbursts of emotion and overvalued thinking.

268
Cyclothymia personality:
Cyclothymic personality is characterized by gradual and modest mood swings lasting
weeks or months. When the mood is elevated, the person is extroverted, outgoing, cheerful,
optimistic, impulsive, restless, talkative, and uninhibited. The need for sleep is reduced and
appetitive behaviors increase, the latter often leading to interpersonal and social
indiscretions.

Dysthymic personality:
Who has dysthymic personality is characterized by brooding, anhedonia, self-blame,
passivity, and indecisiveness. Who always looks on the sad side of life and is miserable.

Irritable personality:
The irritable personality has hypercritical, brooding, complaining, dysphoric, restless,
sarcastic, irritable, and choleric. They are easily irritated when things are not happened
according to them.

Abnormal Emotional reactions:

A clear representation of the distinction between normal and abnormal emotional states is
illustrated by the Yerkes−Dodson curve (1908), which shows that up to a certain level of
stress there is no impairment but beyond certain point functioning deteriorates.
Diagnostically, both the ICD−10 Classification of Mental and Behavioural Disorders (World
Health Organization, 1992) and the Diagnostic and Statistical Manual of Mental Disorders
(American Psychiatric Association, 1994) define these abnormal emotional reactions as
anxiety and fear.

Anxiety:
Anxiety is an unpleasant affective state with the expectation, but not the certainty of
something untoward happening but in psychiatry the term anxiety is an uneasy
preoccupation with some personal matter or worrying about something. Sometimes the
anxiety is accompanied by physical symptoms such as palpitations, sweating, difficulty in
breathing, dizziness, etc. In anxiety states it is very common for patients to experience
episodes or attacks of panic. The patients experience feeling of choking or difficulty in
breathing These attacks often constitute basis for agoraphobia. Morbid anxiety is always
accompanied by one or more symptoms e. g. disturbance of sleep, lack of concentration.
Pathological anxiety occurs in situation where there is no real physical or psychological
danger or when the emotional reaction is disproportionate in intensity to actual danger.

Fear:
Which is briefer and to the point. When it is restricted to one object, situation or idea, the
term phobia is used. Phobias are associated with physical symptoms of anxiety and with
avoidance. Most fears are learned responses, such as the person who develops a fear of
dogs after being bitten. Some phobias are secondary to morbid states, most commonly
depressive illness, and others, such as fear of contamination, are regarded as obsession
symptoms. When fear become intense, chaotic motor behavior may occur which is usually
called “panic”.

“Depressive illness is commonly classified into “reactive” and “endogenous”

Endogenous depression:

269
Endogenous is a type caused by an intrinsic biological or somatic process rather than an
environmental influence, in contrast to a reactive depression. The emotional reaction to
chronic frustration and disappointment is depression. It is merely quantitatively different
form mood states which occurs in so-called ‘endogenous depression’

Reactive depression:
Reactive depression, situational depression a usually transient depression that is
precipitated by a stressful life event or other environmental factor ; includes loss of weight,
interest and loss of libido. The typical symptoms of depression are not present but sleep is
definitely disturbed. In this patient is usually are not self-reproachful but tend to blame other
for their illness& often anger and resentment are ill-controlled. But it is different from morbid
depression which is characterized by morbid thinking like suicidal thinking or threats, loss of
judgment, helplessness and hopelessness and psychophysiological disturbance.

Verstimmung:
Verstimmung is German term for means ‘ill- humored mood states’. There is no clear
distinction between ill- humored mood states and depressive mood state. In which persons
are not only unhappy, irritable and angry themselves but also make others unhappy.
The hyperthymic individual is usually euphoric, while the cyclothymic, dysthymic and
irritable personalities have episode of euophoria which are not morbid.

Abnormal Expressions of Emotion:

These refer to emotional expressions that are very different from the average normal
reaction. Excessive emotional response may be the result of learning and of different
cultural norms. So the distaught woman screaming at the death of a loved one may be
reflecting a cultural variant of normal grief.
Dissociation of affect is being an unconscious defense reaction against anxiety.It is a lack
of manifestation of anxiety or fear under conditions where this would be expected. Some
depressed people fail to exhibit any emotion where some would be expected. For example,
the person exposed to extreme stress may fail to show any emotion. There are two form of
dissociation of affect-
Denial of anxiety: The first is plain denial of anxiety. The terrified adolescent who has got
himself into sever trouble may put on bold front and pretended that he is not afraid
.Nevertheless he does experience fear and he is aware of it.
La Belle indifference: Another of dissociation of affect is the La belle indifference of the
conversion hysteria. That is seen in conversion disorder. A defense that may manifest as
lack of emotion is denial. This occurs when the person denies awareness of an event even
though such an event has clearly taken place. The most extreme example of dissociation of
affect is given by David Livingstone of the feeling he had when he was seized by a lion: It is
caused a sense of dreaminess in which there was neither sense of pain nor feeling of
terror, though he was quiet conscious of all that was happening.
Perplexity: Perplexity is a tentative or bewildered, slightly puzzled state that occurs in
anxiety, mild clouding of consciousness and emerging schizophrenia, as new psychotic
experiences are occurring. The emotional state of other persons, but do not experience
their distress.

(d) Morbid Disorders of Emotion:

270
Depressive illness is the most common in this morbid group and mood that is secondary to
bereavement, is described by many patients who can distinguish their understandable
reactions to stressors from the pathologically low mood that is depressive illness. The
morbid sadness in this situation may be associated with thinking which may reach delusion
intensity there is inhibition of thinking, loss of drive and decreased voluntary activity. The
physical and/or psychological slowing that occurs is known as psychomotor retardation.
There may be difficulty making decisions due either to poor concentration or to obsessional
doubting, secondary to the mood state. Some disorders of emotion are as follows-
Anhedonia: This term was originally given by Ribot (1896) refers to loss of capacity to
experience joy and pleasure. There is total inability to enjoy anything in life. It is primary
symptom of depressive illness. Anhedonia is also described as a symptom in schizophrenia
in which is especially likely to be social – absence of ability to feel pleasure in relationship.
Apathy: Apathy may be erroneously confused with dissociation of affect. The apathetic
patient appears listless, does little, makes minimal effort on assigned tasks or needed
chores, and is indifferent to his situation. Will and initiative are lost. Abulia is a synonymous
term. The minimal expression of emotion may be distorted. A proposed mechanism is the
disruption of emotion-cognition processes so that emotional life no longer drives thinking
and the generation of ideas, leading to waning of interests and actions (sometimes referred
to as “psychic akinesia”). Apathy is often used to mean emotional indifference, often with a
sense of futility. According to Tasman (2003) there are three characteristics of emotional
expression of apathy-
(i)Avolition: Avolition is reduced interest and activity associated with an absence of
emotion, interest, and concern. Avolition is associated with schizophrenia and frontal lobe
disease. Such patients have a paucity of ideas and reduced interests, ignore once-
cherished hobbies and skills, are indifferent to their situation, and take little interest in work,
interactions with others, or their medical care. When asked what their typical day is like they
are at a loss to provide details, their day’s empty of activity unless prodded by others.
Prodding may lead to irritability and angry outbursts.
(ii) Alogia: is poverty of speech is manifested by brief, laconic, and empty replies. Fluency
and productivity of speech are reduced.
(iii) Affective flattening: The face appears immobile, unresponsive with poor eye contact
and reduced body language
Organic neurasthenia: is mild anxiety mixed with depression and irritability, occurring in
mild acute and chronic coarse brain disease.
Feeling of a loss of feeling: This is experienced as a loss of feeling, a deficiency that is all
pervasive, affecting all emotions including sadness, joy, anger and so on. It is subjective
experienced of loss of feeling that are formally present rather than objectively observed
absence. Like a religious person can say that he has no longer belief in God. It is described
as loss of feeling of assurance associated with their faith rather than any actual change in
the content of their beliefs. Milder forms are experienced as depersonalization and
deaffectualization.
Vital hypochondriacal depression: It refers as numbed, diminished, made remote from
himself. The patient feels a tight band around his head and there may be a sense of
oppression in the chest associated with anxiety, for which Schneider used the term ‘vital
hypochondriacal depression’. A related and more modern concept is somatisation, or the
presence of somatic features, in which there is misattribution of symptoms as due to
physical illness rather than having a psychiatric cause.
Extreme apathy: Extreme apathy may be a feature of severe depression, schizophrenia or
damage to the frontal lobe. Morbid euphoria and elation classically occur in mania and

271
hypomania but can also be seen in organic states and in schizophrenia, especially the
hebephrenic subtype, where the patient presents as silly and annoying.
Euphoria: It is state of excessive unreasonable cheerfulness; it may be manifested as
extreme cheerfulness. It may seem inappropriate and bizarre. It is commonly seen in
organic states, especially associated with frontal lobe impairment.
Ecstasy: Ecstasy is an exalted state of feeling and is therefore different from the morbid
cheerful mood or elation. It is a state of extreme well-being associated with a feeling of
rapture, bliss and grace. The mind is usually occupied with a feeling of communion with
God or some religious figure. There may be a feeling of being in tune with the whole of
nature and at one with the universe. The person in ecstasy experiences the change in ego
boundaries as voluntary and lacking the interference associated with the former. Time may
be experienced as standing still. Ecstatic states may occur in schizophrenia, in those who
misuse lysergic acid diethylamide, in epilepsy and in mass hysteria associated with
religious services. It may also see in epilepsy and in other organic states like general
paresis. Characteristic of ecstasy is self-referent for example the flowers of spring open for
me .There is very obvious difference between religious experience and ecstasy.
Witzelsucht: Witzelsucht is a happy-go-lucky carelessness and silly facetious humor.
Moria is a synonymous term. The patient cannot refrain from making light of any situation,
makes inane jokes and puns, and can rarely be engaged in a serious conversation.
Witzelsucht is associated with lack of foresight and the ability to plan. It is a sign of frontal
circuitry and cerebellar disease, and is an aspect of the frontal lobe disinhibited syndrome.
Frontal lobe damage with euphoria, often presenting as silliness, lack of foresight and
indifference, is known as moria or Witzelsucht.
Pathological anger: Irritability is associated with several psychiatric syndromes, most
commonly depression and mania. Persons with paranoid, anti-social personality disorder,
and delusions of persecution are typically angered in response to their view of a hostile
world Patients who have abused chemical inhalants are prone to sudden, potentially lethal
violent anger. This irritability is associated with difficulties with speech and language, and
mobility.
Morbid surprise: It is exaggerated startle response characterized by myriad of echo
phenomena including echolalia, echopraxia and echomimia. There is also coprolalia,
automatic obedience and hyper suggestibility. It is seen in latah. (a culture-bound disorder)
Hyperekplexia: It is a heightened startle reflex that occurs either as hereditary neurological
condition involving the inhibiotory glycine receptor or as sympotomatic disorder. In which
surprise stimulus provokes normal startle response. That triggers a focal lobe seizure.
Prosopoaffective agnosia: refers to the selective deficiency in appreciating the emotional
expression displayed in face of others .This is different from prosopagnosia in which
recognition of familiar face and vocal expression of emotion is impaired. It is associated to
frontotemporal dementia.
Receptive emotional dysprosody: refers to the selective deficit in recognizing the
emotional tone in speech. This is often associated with expressive emotional dysprosody,
the impairment of production of emotional tone in speech. Both are found in Parkinson’s
disease.

Morbid Disorders of Emotional Expression:

This differs from abnormal expressions of emotion in that the patient is unaware of the
morbidity in emotional expression even though it is apparent to observer.
 Disturbance in intensity
 Disturbances in the mobility of emotion:
 Disturbances in the variability

272
  Disturbances in appropriateness
 Recognition of emotion

(1)Disturbance in intensity: intensity of emotional expression can be increased as in rage,

panic, and euphoria, or substantially decreased as in stupor, apathy, and emotional
blunting.
(I) Decreased expression: Emotional blunting (affective flattening or stiffening): The term
blunting and flattening are used interchangeably to refer unchanging facial expression,
decreased sponteous movements, poverty of expressive gesture, poor eye contact,
affective unresponsivity or lack of vocal infection. Blunted affect: A lack of emotional
sensitivity or expression in gesture, facial expression, and tone of voice. It is characteristic
of schizophrenia and structural frontal lobe disease. Emotionally blunted persons appear
stiff or still, their faces mask-like and their voice monotone. Chronic schizophrenics typically
have profound loss of emotional expression. In contrast, patients with severe depressive
illness express apprehension and distress unless in a stupor or catatonic state. Kraepelin
emphasized the presence of emotional blunting as characteristic of dementia praecox,
stating that patients have “no desire . . . no visible effort of the will”, being “languid and
expressionless . . . quite dull, experiencing neither fear nor hope nor desires . . . this
peculiar and fundamental want of any strong feeling of the impression of life, with
unimpaired ability to understand and to remember, is really the diagnostic symptom of the
disease before us.” (It shows itself as insensitivity to the subtleties of social intercourse and
is known as inadequacy or blunting of affect and was called ‘parathymia’ by Bleuler. It
manifests itself as social awkwardness and inappropriateness,). Bleuler described
parathymia and paramimia in schizophrenia
Parathymia: Patients react to sad news with cheerfulness or even laughter this patient
may become sad or irritated by events to which other will react with pleasure. The
expression of an emotion that is the exact opposite of what is expected under the
circumstances (e.g. laughing at tragic news), or the expression of emotions that appear
unnatural, exaggerated or theatrical is termed parathymia. The expression is shallow and
flat. Emotional rapport is poor. Bleuler considered this an important sign of schizophrenia.
(Bleuler (1976) Senseless laughing without mirthfulness is considered a sign of
hebephrenia. In milder forms, it shows itself as a insensitivity to the subtleties of social
intercourse. This is known as inadequacy or blunting of affect and was called“parathymia”.
Paramimia: It refers as lack of unity between the various modes of expression of emotion.
For example a woman patient complained bitterly about her voice and body such that her
mouth and forehead manifest disgust, but her eyes expressed happy eroticism. After a few
moments mouth also assumed the expression of happiness while her forehead continued to
appear gloomy and wrinkled.
Flattening affect: is a limitation of usual range of emotion expressed usually by facial
expression but also bodily gesture. Individual does not express very much affect in any
direction, although that which is expressed is appropriate in direction. Both blunting and
flattering can occur in schizophrenia.
Motor aprosodia Motor prosody is the expression of emotion in spoken language, facial
expression, gesture and body language. Receptive prosody is the ability to recognize the
emotional expression of others. Motor aprosodia is associated with disease in the non-
dominant cerebral hemisphere, particularly in frontal circuitry. Motor aprosodia is
descriptively identical to the loss of emotional expression described as emotional
blunting/flat affect. Motor aprosodia is described in autistic spectrum disorders,
schizophrenia, and depression.
(ii) Increased emotional expression:

273
Increased intensity in emotional expression is seen in manic-depressive illness. In mania
elated and euphoric affect and in depression patient has irritable and depressed affect
(2) Disturbances in the mobility of emotion: The disturbance in quality of emotions is as
follows:
(i) Lability of affect: It is defined as rapid and abrupt changes in emotion largely unrelated
to external stimuli. These shifts occur without warning. Those with personality disorder of
the borderline type may also exhibit lability of affect. Affective lability may be morbid when it
occurs in organic states, for example in organic neurashtenia. It is called as compulsive or
“forced affect”. In pathological laughing and crying, there is no or only a mild corresponding
subjective experience. The facial expression and associated movements of the emotion are
exaggerated, and the quality of the emotion can be typical or may seem feigned.
(ii) Incontinence of affect: In affective incontinence there is total loss of control it is also
referred as “forced weeping” or “forced laughing. In emotional incontinence, the observed
emotion is congruent in quality but not in the intensity to the subjective experience, which is
milder.
(iii) Emotional paroxysm: It is also a sudden and brief expression of an emotion, but the
paroxysm is accompanied by the intense corresponding subjective experience. Emotional
incontinence and paroxysms are associated with manic-depression, seizure disorder, and
brain damage from trauma or chronic hallucinogen drug use.
(iv) Smiling depression: The depressed person smiles with the lips and not the eyes, so
that despite their apparent cheerfulness there is hardness and lack of movement of the
muscles around the eyes. Some patients with depression also smile and this may be
mistaken for incongruity of affect or it may even mask the low mood, in the past called
‘masked’ or ‘smiling’ depression.
(3) Disturbances in the variability: The valence of emotional expression normally
changes as circumstances change. Constricted emotional expression (also termed
constricted affect) is the loss of normal variability. Constricted emotional expression is
independent of the quality or intensity of the expressed emotion. For example a manic
patient was laughing and expounding on his “great ideas” about life. Coming to a sad
personal topic, he suddenly burst into tears. The examiner commiserated with the patient,
and then said, “But just before, you were so happy and about to tell me a joke”. The patient,
face still tear-stained, immediately brightened, smiled and began to tell a joke.
(4) Appropriateness of emotion: Normal emotional experience is commonly a response
to what is occurring in the immediate surroundings, or to a recollection. The expressed
emotion is congruent to the situation. In patients with mania and severe depression,
emotional expression may become “stuck” in one valence.
(I)Time, duration and appropriateness to situation: The timing and duration of emotion
are determined whether the emotion is appropriate to context. In pathological grief, the
timing and duration may be altered such as that grief is delayed or prolonged. Delayed grief
is in essence prolongation of initial numb phase. Lability of mood involve both a heightening
or intensification of emotions accompanied by an instability in the persistence of emotions
that communicate itself to the observer as in appropriate to social context.
(5) Recognition of emotion:
(I)Subjective awareness of emotion: The subjective awareness of one’s emotional state
is a human trait. The concept of alexithymia was coined by Sifneos (1972) ,from the Greek
alexis [no words] and thymos [emotion]) was formulated to define a deficit in which the
affected person has reduced capacity to experience, identify, verbalize, think about, and
fantasize emotion. In one, there is an absence of the emotional experience (can’t feel it),
and consequently the absence of the cognition accompanying emotion (can’t describe it or
fantasize about it). A second is a deficit in the cognition of emotion, sparing the capacity to

274
experience emotion. Alexithymia is presumed to be a personality trait.. But it is also
considered an aspect of emotional blunting, and reported in persons with Parkinson’s
disease,
se, depression, anxiety disorder, substance abuse, and eating disorder
sorder.
(ii)Empathy and receptive aprosodia: Empathy is the capacity to experience the
emotional state of others by “putting oneself into their shoes”. Recognizing the emotion
expressed in the other person’s face and body language is a prerequisite for empathy.
Receptive prosody is the capacity to recognize and understand the emotional expression of
others. Poor receptive prosody undermines the capacity for empathy, but they are not
synonymous constructs.
THE PHYSIOLOGY OF EMOTIONSEMOTIONS-
When we are excited, terrified, cheerful, we perceive some changes in the body and
sometimes are unaware of those happenings. Certain instruments gives a great deal of
information about the bodily events in emotion like heart beat variability, blood pressure ,
activity of GI system as well as rate of respiration in emotional states. The bodily changes
that occur in emotion are produced by the activity of autonomic system. The autonomic
nervous system has two parts, ((a) a) sympathetic nervous system and (b) parasympathetic
nervous system. The sympathetic nervous system is active during aroused state and
activity is increased in states of fear, rage etc. The parasympathetic nervous systems are
active during the calm and relaxed
laxed states and thus inhibit the energy consuming processes.
Both systems try to dominate over the other during various emotional states. Interestingly,
in certain emotions, there is a blend of both sympathetic and parasympathetic activity. For
instance, during anger, the heart rate increases (sympathetic) as well as the motility of
stomach increases (parasympathetic). The somatic nervous system also plays a role in
emotions. In flight or fight response, there is both sympathetic arousal plus the periphera
peripheral
nervous system gets activated thereby increase breathing rate, muscle tension, as well as
posture.
The bodily response patterns may be present in a number of emotions and these patterns
are related to facial expressions of emotions. The pattern of changes
changes is as mentioned below
(Ekman et al., 1983)

Facial expression as a mirror for emotions

Within the human face, there is an elaborate network of finely innervated muscles and one
functional role of it includes the facial expression. Face is represented extensively in the
human motor cortex and some investigators believe that facial movements induced i by
emotions are entirely different from the brain areas which control voluntary facial
movements. Voluntary actions are brought about by the cortico
cortico-spinal
spinal system whereas the
facial expressions involve the sub-cortical
sub system. Chronic selective inhibitions
bitions of various
275
sub-cortical systems lead to an expressionless face that occurs in Parkinson’s disease and
in schizophrenia. (Lewis, 2004).

GENDER AND SOCIO-CULTURAL ASPECT OF EMOTIONS

Gender, Emotion and Expression:
Males and females are often socialized to have different motives and goals- depending on
their ages, cultural backgrounds and socialization histories. Interpersonal goals that may
differ for males and females including fulfilling culturally prescribed gender roles, social
motives, and adapting to power and status imbalances between the two sexes .
Intrapersonal processes may also differ for males and females, including the ways in which
anxiety and conflict are regulated and self schemas. Among American samples it was found
that, women are believed to be more emotionally skilled and expressive than men,
especially regarding sending and receiving nonverbal cues, smiling, gazing, and expressing
sadness and fear, whereas males are stereotyped to be more logical and to express more
anger than females. A wide variety of self report measures have indicated that women rate
themselves as more expressive than men. Females also generally report more empathy
and sympathy than do males. Many negative emotions including distress, sadness, disgust,
fear, shame-are also reported more by females than by males. But men express more
anger through vocal, facial, and behavioural modalities than women (Lewis, 2004).

Culture and Emotion:

Emotions vary across cultures. Cross-cultural differences exist in the experience and
expression of emotion. Cultural individualism encourages an independent social
representation of the person. Collectivistic cultures emphasize relatedness, conformity and
harmony in feeling, action and thought. Evidence suggests that emotional experience is
perceived and expressed more intensely in individualistic rather than in collectivistic
cultures. People from an individualistic cultures feel more comfortable expressing negative
emotions than people from collectivistic culture. (Lewis, 2004)

Socio-Economic Status and Emotion

Lower income was related to higher intensity of emotional experience .Studies show that
high income was related to subjective wellbeing or pleasant emotional experience. In less
developed countries social life is more uncontrollable and social stress is stronger, which is
linked to the more intense emotional reaction and at the same time more unpleasant
emotional experience (Lewis, 2004)

TEORIES OF EMOTION: CRITICAL EVALUATION

James- Lange Theory-
The well known trend setter, James Lange Theory, which holds the view that our perception
of the reaction is the basis for the emotion is criticized on the ground that there are different
set of internal and external bodily changes that accompany emotion and every individual
are able to perceive that, although evidences are there for different pattern of bodily
responses in different emotions, question have been raised that in more subtle and less
intense emotions, these bodily patterns can be perceived ; as in general our perception of
bodily changes is not very accurate. Therefore this theory has been criticized (Morgan et al,
1993).

Cannon –Bard Theory

In contrast with James-Lange theory, this theory suggested that bodily reactions and the felt
emotion are independent of each other in the sense that bodily reactions are not the basis

276
of the emotion. Although it is known that the hypothalamus and other lower brain areas are
involved in the expression of emotion but still it is not sure whether perception of lower brain
activity is the basis of felt emotion (Morgan et al, 1993.)

The Schachter-Singer theory

This theory challenges the idea that emotions were natural kinds, without redefining
emotions out of existence .They introduced the idea that a basic biological state (a general
increase in sympathetic nervous system activation) was interpreted as meaningful by
cognitive processes that are contextually driven .Basically this theory described that we feel
emotion due to our interpretation of an aroused bodily state. But growing research
evidence has not supported this theory that aroused subjects who were ignorant or
uninformed about the cause of their arousal reported the aroused state as unpleasant even
when they were in a “happiness-producing situation (Morgan et al, 1993).

Cognitive appraisal theory

Cognitive appraisals are the interpretation and meaning that we attach to sensory stimuli.
The theory says that the emotions we feel result from evaluation of information coming from
the environmental situation and from within the body (Morgan et al., 1993). Rather than
assuming that all the emotions are caused by different kinds of personal significance, it is
also seen that many of them are motivated by different interpersonal functions. Getting
emotional is a process that intimately involves making appraisals, but these appraisals are
often addressed specifically to someone else who sees role in the interaction that requires
consideration before a complete picture of emotion becomes apparent.

EMOTION FROM DEVELOPMENTAL PERSPECTIVE

Emotion in infancy and childhood
Children show some emotions from the time of birth, and during the first one year of life,
they become capable of showing most of the emotion that adult display. By the age of 3
months, infants show evidence of joy, they start to smile and appear to show excitement
and happiness in response to familiar faces. Sadness is also noted when there is
withdrawal from positive events. Anger is reported between 4-6 months. Fearfulness
appears by 7-8 months. Thus basic emotions are present by the age of 8-9 months. Most
infants show anxious reactions by the age of 8 months but separation anxiety decreases
from 30 months onwards.
Between 18-24 months, babies develop self consciousness and self awareness allowing
the individual to develop embarrassment, empathy, envy. At 2-3 years children show pride,
shame, guilt, regret. By this time the child can also name the emotions they perceive in
others. When parents rarely express positive emotion, dismiss their child's feelings as
unimportant and have difficulty controlling their own anger and hostility, children have
continuing problems managing emotion that seriously interfere with psychological
adjustment. By the age of 10, most children shift adaptively between two general strategies
for managing emotion. In problem centered coping, they appraise the situation as
changeable, identify the difficulty and decide what to do about it. If problem solving does not
work, they engage in emotion-centered coping, which is internal private, and aimed at
controlling distress. Children with depression express self criticism and death
wishes;somatic complaints may also be prominent symptoms. The manifestations of mania
involve emotional lability, irritability, increased motor activity, grandiosity and distractibility
(Hurlock, 2001)

Emotion in Puberty

277
Emotion in puberty is characterised by moodiness, sulkiness, temper outburst and the
tendency to cry at the slightest provocation. Depression, irritability and negative moods are
especially common during the premenstrual and early menstrual periods of girls. (Hurlock,
2001)

Emotion in Adolescence
Most of the adolescence experience emotional instability from time to time. Instead of
having temper tantrums adolescents express their anger by sulking, refusing to speak, or
loudly criticizing those who irritate them. If their romance moving along smoothly
adolescents are happy but they become despondent when things begin to go wrong
(Hurlock, 2001).

Emotion in Adulthood
In adulthood people are trying to get the lay of a new land in which they find themselves
likely to be emotionally upset (Hurlock, 2001).

Emotion in geriatric population

Older participants consistently report greater control and regulation of their emotions
through various mechanisms (antecedent-focused emotion regulation, response focused
emotion regulation) which permits them to selectively enhance positive emotions. But
depression is common among elderly person. The prevalence of major depressive disorder
is only about 1 to 2%. Depressed mood, suicidal ideation, guilt are rarely expressed
subjectively. The lifetime prevalence of any DSM -IV -TR mood disorder was 11.9 percent
among those age 60 or older. Disturbances of sleep and appetite, anxiety, apathy and
somatic complaints are common. Depression induced cognitive impairment, also known as
depressive dementia or pseudo dementia is another problem in old person. Anxiety
disorders are also common among the elderly person (Hurlock, 2001).

NEUROBIOLOGICAL BASIS OF EMOTIONS

It is the human brain, after all, that is the biological substrate for emotions, cognitive
abilities, and behaviours that is, everything that humans feel, think, and do. The three
neural systems of most interest in psychiatry are the thalamocortical system, the basal
ganglia, and the limbic system. In the 19th century, William James suggested emotion as
the function of sensory and motor area of neo cortex. Role of Hypothalamus in emotion was
later given by Cannon Bard in 1929. In 1937, James Papez postulated, primarily on the
basis of anatomical data, that these cortical regions were linked to the hippocampus,
mammillary body, and anterior thalamus in a circuit that mediated emotional behaviour.
Mac Lean added structure of amygdala, septal nuclei, OFC, portions of basal ganglia in
papez circuit. The limbic system concept came under light in the 1980’s.
A review by Philips et al, describes the substrates of normal emotion recognition as being
grouped in to two modules, serving three functions that bring about the totality of emotional
states –
1. The ventral stream, as the first functional module involved in two of these functions,
namely a) The identification of emotional salient’s of a stimulus (sub served by the limbic
regions of the amygdala and insular cortex) and b) the generation of the affective state (sub
served by pre frontal regions);
2. The dorsal stream, consisting of the hippocampus, dorsal region of anterior cingulate
cortex, dorso-medial and dorso-lateral which serves as the second functional module
helpful in the regulation of the generated affective state and in a cognitive approach to a
situation rather than a emotional approach.

278
The hypothalamus, a relatively small structure within the diencephalon, is a critical
component of the neural circuitry regulating emotions. (Sadock et al.2009)

RECENT ADVANCES
 The neurotrophic factors are a class of protein molecular signals that were more recently
discovered than the other molecular signals. These proteins are involved in the growth,
differentiation, maintenance, and death of neuronal and glial cells and have been
demonstrated to be involved in processes such as learning, memory, emotion and
complex behaviours.
 A more recently appreciated property of certain neurons and ion channels is the critical
role of pacemaker, or oscillatory, activity in normal maintenance of wakefulness,
attention, and mood.
 The basic process of genetics involves the transcription of DNA into RNA and the
translation of RNA into a protein. A complex system of regulation exists for transcription
and translation.
 Alterations in gene expression occur both during development and in adulthood and may
be the basis of abnormal and normal development and of abnormal and normal
adaptation to stress.
 The fMRI, PET and other techniques can measure and visualize brain function during
increasingly shorter time periods, allowing researchers to ask specific questions about
brain regions and neural networks and their relationships to emotional, cognitive, and
behavioural states and activities.
 A change to previous dogma, it is increasingly becoming accepted that new neurons can
form and function in the adult human brain, especially in regions of the limbic system,
such as the hippocampus (Sadock et al., 2009)

EMOTIONAL DISORDERS IN VARIOUS PSYCHIATRIC CONDITIONS

Most of the psychological disorders have been found to share a common disturbance in
core affective processing.

DISORDERS OF EMOTIONS IN SCHIZOPHRENIA:

The common mood disorders in schizophrenia are elevated mood, depression, anxiety,
perplexity. Elevated mood of the hypomanic variety is not common in schizophrenia,
except some chronic schizophrenics with fantastic thinking. Depression is very common in
the early stages of schizophrenia. Disorders of emotional expressions are prominent than
disorders of mood in chronic schizophrenia. Anxiety is usually associated with persecutory
delusions and hallucinations. The perplexity which often occurs at the onset of illness in
young people is probably partly due to anxiety. The characteristic schizophrenic disorders
of affective expressions are flattening, incongruity and stiffening of affect. Nearly all patients
in the chronic stage of schizophrenia show blunting of affect. (Fish, 1984).
Schizophrenics are non-emotional personalities and harbour differences in inner emotional
feelings and outward emotional expression. It has been proposed that the disorder of limbic
system could be one of the reasons for such split between the perceived emotions and
emotional expression. Disturbance in emotional processing in individuals with
schizophrenia are related to persistent functional disability, and may underlie negative and
deficit symptoms such as avolition and anhedonia.
Individuals with schizophrenia show impairment in processing and facial expression of
emotion in both behaviour and neurocognitive tasks, which are particularly marked for
threat related expressions such as fear. (Mandal et al, 1998).

279
DISORDER OF EMOTION IN BIPOLAR DISORDER
Bipolar disorder is characterised by emotional irritability and fluctuation of mood. One of
the cardinal features of bipolar disorder includes disturbances in positive emotion and
including an abnormally and persistently elevated mood. In hypomania there is elevation of
mood which is somewhat less intense as compared to mania. In cases of acute mania,
there is an intense emotion associated with increased arousal that elicit hyperactivity,
flooded with racing thoughts, and increased energy. (Sadock et al, 2009)
Delirious (Bells) mania: Kraepelin described delirious mania as an uncommon, rapidly
emerging state characterised by extreme excitement, hallucinations and delusions (often
fantastic and grandiose), lability of mood, clouding of consciousnesses and catatonic
features including posturing with waxy flexibility and echolalia and echopraxia.
Cyclothymia: It is characterised by gradual and modest mood swings for weeks or months
characterised by episode of hypomania and mild depression. Kraepelin described four
types of personality disorder: expressive (gloomy), manic (cheerful and uninhibited),
irritable and cyclothymic. He described cyclothymic personality as the alteration of
depressive and manic personalities.
Dysthymia: the most typical feature of dysthymia is the presence of depressed mood. The
term dysthymia which means “ill-humoured”. There are associated feelings of inadequacy,
guilt, irritability and anger, withdrawal from society, loss of interest and inactivity and lack of
productivity.
Melancholia: Is a severe depressive state in which some patients experience dulling of
emotions. In its severe form a pervasive, persisting and unremitting apprehension and
gloom colours, all cognitive processes resulting in a loss of interest, decreased
concentration, poor memory, slow thinking, feeling of failure, low self esteem and suicidal
thoughts.
Depression: In case of depression, Kraepelin suggested that experience of positive
emotions was attenuated in depression. Swartz compared facial electromyographical
activity of depressed and normal control as they imagined positive or negative experiences
in their lives. The group did not differ in EMG response to sad or angry imagery but
depressed participants showed much smaller response with happiness imagery (Taylor,
2009).
Alexithymia: Sifneos (1972) coined the term alexithymia. It is characterised by difficulties
in describing or being aware of one’s emotions or moods and difficulty in elaborate
fantasies. This is common in psycho-somatic disorders, psychogenic pain disorders,
substance use disorders, depression, and PTSD.

DISORDERS OF EMOTIONS IN ANXIETY DISORDERS

Anxiety is the feeling of apprehension caused by anticipation of danger which may be
internal or external. In humans it occurs as a subjective experience of fear. Individuals with
generalised anxiety disorder experience free floating anxiety, worry being the prime
component. Mennin et al. (2002) have developed an emotional dysregulation model in
GAD. Emotions may become dysfunctional in GAD through rapid temporal process of
dysregulation involving
1. Heightened intensity of emotions.
2. Poor understanding of emotions.
3. Negative reactivity of one’s emotional states.
4. Maladaptive emotional management responses.

280
Persons with GAD may also have difficulty in identifying primary emotions such as anger,
sadness, fear, joy, disgust (Mathews, 1998).

DISORDERS OF EMOTIONS IN SUBSTANCE ABUSE

The emotional disturbances are mainly characterised by the inability to identify and express
feelings coupled with vulnerability to experience negative affect. Hostility and features of
alexithymia are also present in patients of substance abuse. (Jaffe et al, 2005).

DISORDERS OF EMOTIONS IN BORDERLINE PERSONALITY DISORDER AND OTHER

PERSONALITY DISORDERS
Emotional dysfunction is the core characteristic of BPD. Several constructs are commonly
used to describe problems in emotional functioning including heightened affect, intensity or
reactivity, negative affectivity and affective instability. In one study, it was found that
individuals with BPD report greater lability in anger and anxiety compared to individuals with
other personality disorders. . Evidence suggests that individuals with BPD exhibits deficit in
emotional awareness and quality, potentially limiting their ability to accurately describe
emotional responses. In a study it was found that the persons with BPD had deficits in
emotional intelligence leading to affective instability, chronic feeling of emptiness and
intense anger. (Gardner, 2009)
In paranoid personality disorder mistrust is predominant and occurs whenever an emotional
reaction is warranted. Similarly narcissistic personality leaves with feeling of superiority and
uniqueness. Individuals with schizoid personality disorder feel emotions but are unable to
produce and express holothymic emotions. On the other hand in dissocial personality
disorder cannot produce empathy and feel emotions. The histrionic personality disorder is
emotionally over-expressive (Linden, 2006).

DISORDER OF EMOTION IN CHILDREN

Children with autism demonstrate a poorer ability to pose emotional expression compared
both to non disordered children and to children with Down syndrome. The deficits are
particularly apparent in social situation where children with autism fail to exhibit “affective
sharing”. Emotion expression deficits have also been identified in children with Down
syndrome. Deficit in emotion processing have been found in patients with autistic spectrum
disorder. They express inappropriate emotion. Sometimes they show negative emotional
response to change. Casey found children with ADHD exhibit more facial expressions
compared to both normal children and children with ODD and MDD. Schlosser found that
children diagnosed with ODD, CD & ADHD expressed more hostility and more surprise.
(Berk, 2006)

ASSESSMENT
Tools to Assess Different Emotions:
Emotion is expression of our own thinking or cognition .Expression of emotion is itself a
technique of assessment of emotion. To assess emotion and its disturbances various
inventories, scales, tests are used. An attempt has been made to throw a light on to them.

Mental Status Examination (MSE):

Mental status examination is the major clinical evaluation or eliciting psychopathology. This
is more structured description and observations of patient’s current state of mind. MSE
covers the various domains of general appearance and behaviour, attitude, motor
behaviour, speech, cognitive functioning, mood and its communicability, appropriateness,

281
depth and so on. All the domains are affected by emotion and specifically if any disturbance
in emotion occurs that certainly and more vividly affects these domains.
Present State Examination (PSE): PSE was developed by eminent psychiatrist John Wing
and colleagues at Maudsley Hospital in Britain in 1960’s. This is another structured
interview schedule for conducting mental status examination based on specific scoring
pattern. PSE is highly influenced by the great Jaspers and Schneider’s phenomenological
approach and was developed for adult population suffering from psychosis or neurosis to
draw an artistic portrait of different aspects of disturbances of emotion with detail, reliable
and adequate information. In the current 9th edition 150 items are there and those items are
rated on a 3 point scale of 0-1-2 with increasing severity. The frequently asked questions
from PSE-9 to elicit numerous kinds of disturbances of emotion are mentioned in the
appendix section.

Schedules for Clinical Assessment in Neuropsychiatry (SCAN):

The SCAN is a semi structured clinical interview tool generally used by trained clinicians to
evaluate and diagnose various psychiatric disorders which include assessment, evaluation,
measurement and classification of adult human behaviour. The SCAN is the accumulated
result of endless effort made by the world Health Organization and The National Institute of
Mental Health. It is necessary to assess disturbances in emotion as to define it specifically
either by some clinical rating scales or other laboratory assessment.
Clinical Rating Scales to Assess Disturbance in Emotion for Bipolar Affective
Disorder
Young Mania Rating Scale (YMRS):
YMRS has been developed by Young et al in the year 1978.It is most frequently used rating
scale to assess manic symptoms. The scale has 11 items and is essentially based on
patient’s subjective report of his or her clinical condition over the previous 48 hours. There
are 4 items that are graded on a 0-8 scale (irritability, speech, thought content and
aggressive behaviour). While remaining 7 items are graded on a 0-4 scale. These items are
given twice the weight of the others to compensate for poor cooperation from severely ill
patients.

The Mood Disorder questionnaire (MDQ)

The 13 items questionnaire rated on a 4 point scale and two additional items which
evaluate level of functional impairment due to manic or hypomanic symptoms. Each ‘yes’
responses are scored as 1 point. This scale was developed by Hirschfeld (2000). It takes 5
minutes to administer.

The Manic State Rating Scale (MSRS)

The 26 items rating scale developed by Beigal et al (1971) and also named as Beigal
Scale. The items are each given a frequency score on a 0-5 scale and intensity score on a
1-5 scale. 11 of the items evaluate grandiosity and paranoid destructiveness .The clinician
needs 15 minutes to administer.
For Depression
The Beck depression Inventory (BDI):
BDI was developed by Beck (1961) to assess severity of depression. It is a self –rated
scale in which individual rate their own symptoms of depression. It includes symptoms of
depression like mood, pessimism, sense of failure, self dissatisfaction, guilt, social
withdrawal and so on. Individuals rate themselves on a 0-3 (0 least 3 most) which gives
score range between 0-63.The scale needs 10 minutes to complete.

282
The Hamilton Rating Scale for Depression (Ham-D)
The HAM-D was developed by Hamilton (1960). The scale consists of 17-21 items to
assess the severity of depressive states, in which 9 items are scored 0-4, whereas further 8
are scored 0-2, items18-21are not regarded as measuring the intensity of depression and
are commonly omitted. The scale takes 30 minutes to complete the full administration.

The Carroll rating Scale for Depression

The test has been adapted as a self rating test of assessing depression. It consists of 52
items. Individual has to endorse yes/no while giving the response to test items, in which 1
point for each item endorsed as ‘yes’ and 0 is given for those items endorsed as ‘no’,
except items 1,7,8,15,25,28,29,32,36,42,,43,44 where ‘no’ responses should be given 1
and items endorsed as ‘yes’ should be given 0 (Carroll,1981).

Assessment Tool for Anxiety

Hamilton Anxiety Scale (Ham-A)
This scale was developed by Hamilton (1969) to quantify the severity of anxiety
symptomatology. It consists of 14 items, which rated on a 5 point scale ranging from 0-4
(severe).The scale measures anxious mood, tension, fear, insomnia, difficulties in
concentration and memories, depressed mood muscular symptoms, sensory symptoms,
cardiovascular symptoms, respiratory symptoms, gastrointestinal symptoms and other
autonomic symptoms.

Beck Anxiety Inventory

This is a self –report inventory developed by Beck, where individual has to assess his/her
own depressive symptoms .The inventory consists of 21 items in which 0-21 scores indicate
very low anxiety ,scores ranged from 22-35 indicative of moderate anxiety and grand total
exceeds 36 is a potential cause for concern.

The State Trait Anxiety Inventory (STAI)

The STAI is developed by Spielberger (1984). It is self report questionnaire consisting 40
items that differentiates between state anxiety (a temporary condition experienced in
specific situation) and trait anxiety. It takes 10 minutes to complete administration of the
test.

Assessment Tool for Grief and Apathy

Grief Resolution Index
This scale consists of 7 items and takes 5 minutes to complete the administration of the
test. The purpose to develop the test was to identify individuals who are experiencing
prolonged distress associated with the death of a spouse. This scale has a good reliability
of .87(Remondet, 1987).

The Apathy Scale

This scale was developed by Glenn (2002) to assess the level of apathy shown by a
patient. It assess the apathy after severe head injury, after stroke, with schizophrenia,
depression or other psychiatric condition and also drug induced apathy.

Assessment Tool for Anger

283
The State-Trait Anger Expression Inventory (STAXI-2). This was developed by
Speilberger (1985) to assess a variety of components of anger in the evaluation of
personality. The STAXI -2 which is based on original STAXI, consisting 44 self administered
questionnaire with a 10 item scale that measures state anger and a 10 item scale that
measures trait anger .Items are rated on a 4 point scale assessing the intensity of anger .It
takes 10-15 minutes for the whole test to complete.

Projective Tests to Assess Emotion

The Rorschach Ink Blot Test
The Rorschach Ink Blot Test was developed by Swiss Psychiatrist Sir Hermann Rorschach
in 1921. It consists of 10 unstructured stimuli. The various variables of this test relates to
emotion although more indirectly. The cluster pertaining to affect in Rorschach Inkblot test
deals with chromatic colour, achromatic colour and shading. The other clusters associated
with determining affect are the affective ratio, weighted sum colour, colour projection, pure
colour, and some other variables which when associated with major colour postulates take
important part in determining emotion. The another significant ratio which has interpretative
usefulness for determining emotion is experience balance, sumc:wsumc(Exner, 2002).

Thematic Apperception Test (Murray and Morgan, 1935)

The TAT was developed by Henry Murray and Morgan in the year 1935.TAT consists of 30
picture cards and 1 blank card. The subject has to project all his thinking, attitude, emotions
to those cards. The numerous kinds of emotions can be elicited from the stories made from
those stimulus cards. The predominant emotions of the individual, several precursors of
emotions and its disturbances all are derived from this test. There are stimulus cards
specified for each emotion –as card 3BM and 14 B-depression, card 10 –love and passion
and so on.

CONCLUSION
Emotion is a fundamental part of human consciousness. This is understandable in so far as
emotion is a perplexing topic because of its heterogeneity, subjectivity and variability.
Research about the emotional disorders is a rapidly expanding area of inquiry. A scientific
understanding of emotional experience requires a rich, context-sensitive description of what
is experienced. Several neuro-imaging studies are being conducted worldwide to concur
the various brain areas responsible to produce various emotional experiences and their
application in various emotional disorders.
To conclude, the truth may well be that; when it comes to “basic emotions” we are not only
basically alike in some ways, but are basically different from each other as well.
- “Let’s not forget that the little emotions are the great captains of our lives and we obey
them without realizing it.” -Vincent van Gogh.

*****************

284
REFERENCES

American Psychiatric Association (1994). Diagnostic and statistical manual of mental

disorder, 4th edition. Text revision.
Baron, R. (2001). Psychology, 5th edition, pearson education publishing.
Beck, A.T., Ward, C.H. (1961). An Inventory for Measuring Depression, Archives of General
Psychiatry, 4, 561-571.
Beigel, A., Murphy, D.L., Bunney, W.E. Jr. (1971). The Manic-State Rating Scale, Arcrives
of General Psychiatry, 25, 256-262.
Berk, L.E. (2006). Child Development, seventh edition. New Delhi: Prentice-Hall of India
Private Limited.
Bhatia, M.S., Jagawat, T., Pradhan, S.C. (1997). Psychiatric interview and examination,
CBS publishing.
Caroll, B.J. (1981). The Caroll Rating Scale for Depression. Development, Reliability and
Validation. British Journal of psychiatry, 138, 194-200.
Carroll, B.J., Feinberg, M., Smouse, P.E. (1981). The Carroll Rating Scale for Depression,
Development, Reliability and Validation, British Journal of Psychiatry,
138,194-200.
Deffenbacher, J.L., Oetting, E.R., Lynch, R.S. (1996). The Expression of Anger and its
Consequences, Behavior, Research and Therapy, 34(7), 575-590.
Dubey, I., Rai, P., Gupta, S. (2009). Seminar-disorder of emotion, Central Institute of
Psychiatry.
Ekman, P., Levenson, R.W., Friesen, W.V. (1983). Autonomic Nervous System Activity
distinguishes among Emotions, Science, 221,1208-1210.
Exner, J.E. (2002). A Primer for Rorschach Interpretation. Ashville: Rorschach Workshops.
Gardner, K.J., Pamela, Q., Tremblay, R. (2009). Emotional functioning of individuals with
borderline personality traits in a non-clinical population, Psychiatry Research,
176, 208-212.
Glenn, M.B. (2002). Cut off score on the Apathy Evaluation Scale in subjects with traumatic
brain injury. 6, 509-518.
Glenn, M.B., Burke, D.T. (2002) Cutoff score on the apathy evaluation scale in subjects with
traumatic brain injury. Brain Injury, 16, 509-516.
Hamilton, M. (1969). The Assessment of Anxiety Scales by Rating, British Journal of
Medical Psychology, 32, 50-55.
Hamilton, M. (1964). Fish’s Clinical Psychopathology. John Wright and Sons Limited.
Hamilton, M. (1984). Fish’s Schizophrenia, third edition. Bristol: John Wright and Sons.
Hamilton, M.A. (1960). A Rating scale for Depression, Journal of Neurology, Neurosurgery
and Psychiatry, 23, 56-62.
Hirschfeld, R.M. (2000). American Journal of Psychiatry,157,1873-1875.
Hurlock, E.B. (1981). Developmental Psychology, A Life-span Approach, fifth edition.
Newdelhi: Tata McGraw-Hill Publishing Company Limited.
Jaffe, J.H., Anthony, J.C. (2005). Substance-Related Disorder An Overview. In: Kaplan and
Sadock’s Comprehensive Textbook of Psychiatry, eighth edition. Philadelphia:
Lippincotts Williams and Wilkins.
Jasper, K. (1962). In genral Psychopathology. Tremedated by Hoenig, J., Hamiltom, M.W.,
Mamhester University press.
Krause, R., Steimer, E., Sanger-Alt, C., Wagner, G. (1989). Facial expressions of
schizophrenic patients and their inter action partners. Psychiatry, 52, 1-12.
Lewis, M., Jones, M. (2004). Handbook of Emotions, second edition. NewYork: London
Press.
285
Linden, M. (2006). Minimal Emotional Dysfunction in Personality disorders, Europeon
Psychiatry, 25,325-332.
Mandal, M.K. (2004). Emotion, East-West Press Private Ltd.
Mandal, M.K., Jain, A., Haque-Nizamie, S., Weiss, U., Schneider, F., (1998) Generality and
specificity of emotion recognition deficit in positive and negative symptom
schizophrenics. Psychiatry Research: In press.
Martin, R.S. (1996). Apathy: Concept syndrome, neural mechanisms and treatment.
Seminars, Clinical Neuropsychiartry, 1, 304-314.
Mathews, A., Mackintosh, B. (1998). A cognitive model of selective processing in anxiety.
Cognitive Therapy and Research, 22, 539–560.
Morgan, C.T., King, R.A., Weisz, J.R. et al. (1993). Introduction to psychology, 7th edition,
Tata Mc Graw hill publication.
Morgan, C.T., King, R.A., Weisz, J.R., Schopler, J. (1993). Introduction to Psychology,
seventh edition. Newdelhi: Tata Mc Graw-Hill Publishing Company Limited.
Murray, H.A. (1935). The Thematic Apperception Test Manual. Cambridge: Harvard
University Press.
Oyebode, F. (2008). Sims Symptom in the mind, 4th edition, affect and emotional disorder.
Remondet, J.H. (1987). Assessing A Widow’s Grief-A short Index. Journal of Gerontol
Nursing, 13, 113-118.
Remondet, J.H., Hanson, R.O. (1987). Assessing A Widows Grief- A Short Index, Journal
Gerontological Nursing,13,30-34.
Rorschach, H. (1921). Psychodiagnostic. Bern, Switzerland: Verlag.
Sadock, B.J., Sadock, V.A., Ruiz, M.D. (2009). Comprehensive Textbook of Psychiatry,
ninth edition. Philadelphia: Lippincotts Williams and Wilkins.
SCAN Glossary (1994). World Health Organisation, American Psychiatric, Washington, DC.
Sifneos, P.E. (1972). Short term Psychotherapy and Emotional Crisis. Cambridge: Harvard
University Press.
Spielberger, C..D. (1984). State-Trait Anxiety Inventory, A Comprehensive Bibiliography.
Palo Alto: Consultant Psychologists Press.
Spielberger, C.D. (1985). “The Experience and Expression of Anger: Construction and
Validation of an Anger Expression Scale,” Anger and Hostility in
Cardiovascular and Behavioural Disorders, New York, NY: Hemisphere/Mc
Graw Hill, 5-30.
Tasman, A. (2003). Psychiatry, 2nd edition, Panther publishing private limited.
Taylor, M.A., Vaidya, N.A.(2009) Descriptive Psychopathology, The Signs and Symptoms
of Behavioral disorders, 199-204, 206-216.
Wing. J. (1960). Present State Examination. Maudsley Hospital ,Britain.
Young, R.C., Biggs, J.T., Ziegler, V.E., Meyer, D.A. (1978) A Rating Scale for Mania:
Reliablilty, Validity, Sensitivity. British Journal of Psychiatry, 133, 429-435. 58.

********************

286
CHAPTER-XV
 DISORDERS OF EXPERIENCE OF SELF AND
CONSCIOUSNESS

INTRODUCTION
Self awareness is contrasted with subject awareness. As we have to differentiate a
number of modes of object awareness, so we have to do the same for self awareness,
since the modes in which the self become aware of itself do not present any single or
simple phenomenon. The formal characteristics of self awareness are activity of self (that
it is I who is thinking, doing, and feeling), the unity of the self (that at any moment of time I
am one person), the continuity of identity of the self (that I am the same person now that
I was in the past and that I will be in the future) and the boundaries of self (that I can
distinguish between myself and the rest of the world as not self) (Jaspers, 1959).

One of the unique characteristic of body is that it is experienced both inside and
outside, in both self and object. For most of the time we are not aware of our body. But
during extreme anxiety, pain, and sexual excitement, there is an awareness of physiological
systems or organs as objects: ‘my heart banging’, ‘my finger throbbing’. For the rest of the
time we assume the parts of the body to be integrated within a self of whom we are not
separately aware, and which we take for granted. It is through our body that we have
contact with the world outside our self. Many terms are used to describe the way person
conceptualizes himself. Self concept refers to the fully conscious and abstract awareness
of oneself; while body image is more concerned with unconscious and physical matters
and includes experiential aspects of awareness. The body schema implies a spatial
element and is more than, and usually bigger than, the body itself and it changes with
changing circumstances. The body cathexis implies the notion of power, force, libido- the
self that make things happen (Oyebode, 2008).

Critchly (1950) has defined body image as the mental idea which one individual
possesses as to his own body and its physical and aesthetic attributes. Schilder (1935) has
claimed that body images are never isolated; they are always encircled by the body images
of others. Body images are more closely bound together in the erogenous zones, and are
social in nature. Our body image and the way other people see us are not dependent on
each other, i.e. a person sees himself and forms his self image in a social setting. He sees
himself in relation to other people, but his view of himself is not actually dependent upon
how another individual sees him but much more on how he believes that person might see
him (Oyebode, 2008).

DISORDERS OF SELF

In descriptive psychopathology the term ego disorders or disorders of self means the
abnormal inner experiences of I-ness and My-ness which occur in psychiatric illness. These
may occur in the patient's state of inner awareness irrespective of any changes he may
show in his attitude to or experience of the world outside himself (Oyebode,
287
2008).According to Jaspers (1959) self-awareness has four formal characteristics. To that
list Scharfetter added a fifth dimension of ego-vitality. Thus, now we have the following
characteristics of self awareness (Oyebode, 2008).

1. The feeling of awareness of being active (ego activity): I know that I am the
sole agent who initiates and executes my thoughts, feelings and actions.
2. An awareness of unity (ego consistency and coherence): I know that I am one
person at any given point of time.
3. Awareness of identity (ego identity): I know that I have been the same person
all the time.
4. Awareness of the boundaries of self (ego demarcation): I am distinct from all
other things and beings and I am aware of the boundary between self and
non-self.
5. The feeling of awareness of being or existing (ego vitality): I know that I am
alive and exist and this is fundamental to awareness of self.
Within these formal characteristics, self-awareness displays a range of developmental
levels from a plain, bare existence to a full life with a conscious wealth of sensitive
experience. In the course of such development, the self grows aware of itself as a
personality. Abnormalities of self awareness show themselves typically as a lack of one or
other of these formal characteristics (Jaspers, 1959).

1. Disorders of awareness of being: ‘I never have to ask myself the question as to

whether I exist’. It is an assumption that I make with unquestioning certainty. I am so sure of
this that it does not even come into the agenda of doubts and uncertainties. My only
knowledge that everything else exists is based upon the premise that we do (Oyebode,
2008).

Self-awareness is present in every psychic event. In the form of “I think” it

accompanies all perceptions, ideas and thoughts. Every psychic manifestation, whether
perception, bodily sensation, memory, idea, thought or feeling carries this particular aspect
of being mine, of having an “I” quality, of personally belonging, of it being one’s own doing
which is termed as personalization. This may be disturbed in various psychological
disorders. If this psychic manifestation occurs with the awareness of their not being mine, of
being alien, automatic, independent, arriving from elsewhere, the phenomenon is called
depersonalization (Jaspers, 1959).

The patient's experience of his very existence may be altered, ‘I do not exist’, and
‘there is nothing here’. This is the core experience of nihilistic delusions which may occur in
affective psychoses. Less pronounced nihilistic ideas (not delusions) are experienced as
depersonalization: an alteration of the way one experiences oneself which is accompanied
by a feeling of an alteration, or loss of significance of self- ‘I feel unreal, a bit woozy, as
though I can't be quite certain of myself any more’ (Oyebode, 2008).

Depersonalization: In depersonalization, there is a change in awareness of one’s own

activity and the patient feels that he is no longer his normal natural self. This is often
associated with a feeling of unreality so that the environment is experienced as flat, dull and
unreal. This aspect of the symptom is known as derealization (Hamilton, 1984). The term
depersonalization was used by Heymans in 1904 and by Dugas and Mautier in 1911 and
288
the term derealization was used by Mapother in 1935. Depersonalization and derealization
go together because the ego and its environment are experienced as one continuous whole
(Oyebode, 2008). In this group of phenomenon there is a cessation of normal sensory
experience of one’s body, inability to imagine and remember and patient complaints of
inhibited feeling and an awareness of one’s behavior becoming automatic (Jaspers, 1959).

Sedman (1972) used the term depersonalization to designate a peculiar change in the
awareness of self, in which the individual feels ‘as if’ he is unreal. It is best to reserve the
use of the word to this as if feeling rather than the experience of unreality that occurs in
psychosis; the ‘as if’ prefix is used by the patient to denote that he is not using those words
literally. He is expressing uncertainty and painting a picture and as if is the best way he can
do it. “’ऐसा लगता है’ क मेरा हाथ टूट गया है।पैर फसल गया है। मुि ड टूट के िगर गया है।“ (CRF no.73360/C). According
to Fewtrell (1986) depersonalization is a subjective state of unreality in which there is a
feeling of estrangement either from a sense of self or from the external environment
(Oyebode, 2008).
A more comprehensive definition has been given by Ackner (1954) in which he has
given some inclusion and exclusion criteria, for a phenomenon to be called
depersonalization.

The positive features are:

o Depersonalization is always subjective; it is a disorder of
experience
o The experience is that of an internal or external change,
characterized by a feeling of strangeness, or unreality.
o The depersonalization experience is very unpleasant.
o Any mental functions may be the subject of this change, but
affect is invariably involved.
o Insight is always preserved.

Excluded from depersonalization are:

o The experience of unreality of self when there is delusional
elaboration.
o The ego boundary disorders of schizophrenia.
o The loss or attenuation of personal identity.

The feeling of unreality is the core of this symptom and it is always an unpleasant
experience. In this it is completely different from ecstatic states. It may be present in
anything from short episodes to a continuous state. When patients first experience these
symptoms they often become frightened and think that it is a sign that they are going mad.
Many patients who complain of depersonalization also state that their capacity for feeling is
diminished or absent. This is a subjective experience because to the outside observer
there is no loss of ability to respond emotionally and appropriately to any given situation. It
is important to remember that depersonalization is not a delusion and it should be
distinguished from nihilistic delusions in which the patient denies that he exists or that he is
alive or that the world or other people exist (Hamilton, 1984).

An emotional crisis or a threat to life may lead to complete dissociation of affect

which can be regarded as an adaptive mechanism which allows the subject to function
289
reasonably without being overwhelmed by emotion. Milder degree of dissociative
depersonalization occurs in moderately stressful situations, so that depersonalization is
quite a common experience. Since dissociative depersonalization is a common experience,
many patients will complain about it when they realize that it is a symptom in which doctors
are interested. Dixon found that nearly one half of series of college students to whom he
administered a questionnaire designed to pick out depersonalization experiences reported
this symptom (Hamilton, 1984).

The phenomenon of depersonalization can occur in normal healthy subjects. Some

people may have feelings of ‘not being quite themselves…. looking in on themselves from
the outside’, and so on, without provocation. Others may have such experiences at times of
powerful emotional stimuli or life crisis of any valence: extreme happiness, falling in love,
loss or bereavement, or intense fear or anger. Depersonalization experiences occurring in
normal healthy people are not experienced as unpleasant but the patients describe them
as intensely unpleasant experiences (Oyebode, 2008).

Depersonalization can be found in anxiety states with phobias (the phobic-anxiety

depersonalization syndrome) occasionally, it is the outstanding symptom in depressive
states. This may give rise to a mistaken diagnosis of schizophrenia, because the
unsophisticated and dull patient may have great difficulty in describing depersonalization
and the examiner is misled by the bizarre description of the symptom (Hamilton, 1984).

2. Disorder of activity of the self: Loss of existence can also be conceived as a

reduction in one’s awareness of performing one’s own actions, an awareness which
normally accompanies every psychic event. In the natural course of our activities we do not
notice how essential this experience of united performance is. This general awareness of
one’s own performance can alter in a number of directions, which are quite
incomprehensible, difficult to imagine and not open to empathy (Jaspers, 1959).

Moving may show abnormality. In schizophrenic passivity experience or delusion of

control patient will have problems in awareness of one’s own performance. Patients feel
themselves inhibited and retarded from outside; when they want to lift something, their hand
is held; some psychic power is at work. They feel as if they were pulled from behind,
immobilized, and made of stone. They suddenly find they cannot go on, as if they were
paralyzed and then suddenly it has all gone again. Their speech is suddenly arrested. They
may have to make involuntary movements “मित दा मुझ से march past करवाित है।” (CRF no.
125697/A); they are surprised to find their hand is led to their forehead or that they have
attacked someone else though they did not intend it. . This is all felt as some alien,
incomprehensible power at work (Jaspers, 1959).

Memorizing and imaging may be changed in that the patient with depression feels he
is unable to initiate the act of memory, or, alternatively, a schizophrenic patient feels that
this occurs if it is not initiated by him but from outside himself (Oyebode, 2008).

Willing may be altered, for example the schizophrenic patient who no longer
experiences his will as being his own. Commonly, neurotic patients describe an inability to

290
initiate activity, a feeling of powerlessness, of being ground down, in the face of life's
vicissitudes (Oyebode, 2008).

Some of these abnormalities of experience of one's own activities are closely

associated with mood state. Sometimes however, it is not the affect associated with the
change of activity, but the belief about the initiation of the activity which is changed. These
are the passivity experiences (Oyebode, 2008).

3. Disorder of immediate awareness of self unity: In health, a person is integrated in

his thinking and behavior, so that he does not have to be aware of his feeling of unity. He
just assumes that he is one person, and he knows his limitations and capabilities. Self is
both the observer and also the object of observation (Oyebode, 2008). The experience of
the basic unity of the self can undergo some notable changes. Sometimes, for instance,
while talking we may notice that we are talking rather like an automaton, quite correctly may
be, but we can observe ourselves and listen to ourselves. Should this dissociation last any
length of time, disturbances will occur in the flow of thought, but for a short time we can
ourselves experience without any disturbance that ‘doubling’ of personality which patients
describe to us in much more elaborate terms(Jaspers, 1959).

Autoscopy (Heautoscopy, phantom mirror image) –It is a complex psychosensorial

hallucinatory perception of one’s own body image projected into the external visual space.
According to Fish (1967): 'In this strange experience the patient sees himself and knows
that it is he'. It is not just a visual hallucination because kinesthetic and somatic sensations
must also be present to give the subject the impression that the hallucination is he. This
perceptual experience may involve several of the modalities of sensation. However,
disturbance in visual perception is an essential feature; it is an abnormality of seeing. The
loss of feeling of familiarity for one self is prominent, self is viewed quite dispassionately
and objectively. This perceptual experience is especially associated with disorders of
parietal lobe (Oyebode, 2008).

Double phenomenon: doppelganger- The double or doppelganger phenomena is an

awareness of oneself as being both outside, alongside, and inside oneself: the subjective
phenomenon of doubling. The experience occurs with different conditions or with no mental
disorder at all. It is cognitive and ideational, rather than being necessarily perceptual
(Oyebode, 2008). “’ऐसा लगता है’ क मै दो हो गयी ँ और मेरी पछाई मेरे सा े आ गयी है।“ (CRF no.73360/A).

Multiple personality (Dissociative identity disorder) - Morton Prince (1905)

described multiple personality disorder in which the patient assumes in series a number of
different personalities. The essence of multiple personality is the embodiment of at least
two personalities (identities). Sometimes these personalities claim to know the other
personalities in the same person and dislike them intensely, and sometimes they deny all
knowledge of them (Oyebode, 2008).

Abse (1982) states that 'one way amnesia' is usual for multiple personality, that is,
personality A is amnesic for the other personality B; but the second B, can discuss the
experiences of A. Usually A is inhibited and depressed and B is free and more elated. The
forms of multiple personality seen in practice are usually–
291
 1. Simultaneous partial personalities
2. Successive well-defined partial personalities
3. Clustered multiple partial personalities (Oyebode, 2008)
In psychogenic and depressive depersonalization the patient may feel that he is
talking and acting in an automatic way. This may lead him to say that he feels as if he is two
persons. Naive or appreciation needing personalities may leave out the 'as if' and they say
that they are two people. The subject with demoniac possession may feel that he is two
people, himself and the devil. Some schizophrenics also feel that they are two or more
people, although this is not common (Hamilton, 1984).

4. Disorder of continuity of identity of self- A feeling of continuity for oneself and

one's role is a fundamental assumption of life without which competent behavior cannot
take place. In health, we have no doubts about the continuity of our self from our past into
our present. However, schizophrenic patients sometimes deny that they have always been
the same person (Oyebode, 2008).Schizophrenics with mild defect states may feel that they
are not the person that they were before the illness. This may be expressed as a sense of
change, but fantastic paraphrenics may claim that they died under their old name and have
come to life as a new person (Hamilton, 1984). This complete alteration in the sense of
identity is exclusively psychotic, there is a break in the sense of identity of self, and there is
a subjective experience of someone completely different (Oyebode, 2008).
A feeling of loss of continuity of lesser intensity without the element of passivity may
be experienced in health and in neuroses and personality disorders. The person knows
that both people, before and after, are truly himself, but he feels very altered from what he
was. It should be stressed that the sense of reality is never lost to the extent that he
actually believes himself to be a different person. In the non psychotic it is more that
thoughts and feelings do not seem to be in keeping with himself as he has come to accept
himself (Oyebode, 2008).

Possession state: There is a temporary loss of both the sense of personal identity
and full awareness of the surroundings. The person acts as if he has, and believes himself
to have been, taken over by another- a spirit, a force, a deity or even another person "मुझपर
कबीस सवार हो जाता है।" (CRF no. 16835/C). This can occur in normal, healthy people in unusual
situations either as a group phenomenon (mass hypnosis) or individually. The difference
between those conditions that constitute disorder and those that may be considered as
being within a cultural or religious context alone is that the former are unwanted, cause
disorders to the individual and those around, and may be prolonged beyond the immediate
event or ceremony at which it was induced (Oyebode, 2008).

Jaspers (1959) differentiated between states of possession presenting with an

altered consciousness, and states of possession in which consciousness remains clear, the
former were usually dissociative (hysterical) in origin whilst the latter were more often
associated with schizophrenia (Jaspers, 1959).

5. Disorder of the boundaries of self: One of the most fundamental of experiences is

the difference between one's body and the rest of the world. This distinction between what
pertains to one's body and what does not, rests firmly on the fact that large and specialized
part of the afferent nervous system has the sole purpose for obtaining information about the
292
body, the part known as the proprioceptive system. Knowledge of what is the body and
what is not is based on the link between information from the extero and the proprioceptors,
a link which is probably learned but which has to be maintained constantly. This can be
demonstrated very easily. Anybody who has had a finger anaesthetized knows that when
touched it feels like a foreign object, i.e. not part his body. The physiological schema of the
body and the continuity and integrity of memory and psychological function is the basis for
awareness of the self (Hamilton, 1984).

Boundaries of self in schizophrenia: In schizophrenia the sense of invasion of self

appears to be fundamental to the nature of the conditions as it is experienced: many but not
all first rank symptoms have in common permeability of the barrier between the individual
and his environment. There is a merging between self and not self (Oyebode, 2008). Most
schizophrenic symptoms are aspects of a breakdown of the boundary between self and the
environment. In the early stages of acute schizophrenia, the patient may experience this
breakdown of the limits of his self as a change in his awareness of his own activity which is
becoming alienated from him (Hamilton, 1984).

Loss of control also occurs in obsessions and compulsions, where the thought or
Impulse to action is experienced as belonging to the patient but occurring against his
wishes, but although he has lost control over his thoughts, actions or feelings, he still
retains the sense of personal possession of the act and we can still find some measure of
comprehension. But the thought-phenomena of schizophrenics is something quite different
in that they talk about ‘thoughts made by others’ and ‘thought-withdrawal’, using words
coined by themselves, which psychopathology has had to take over. Patients think
something and yet feel that some external force has thought it and in some way forced it on
them. The thought arises with a direct awareness that it is not the patient but some external
agent that thinks it. The patient does not know why he/she has this thought nor did he/she
intend to have it. He does not feel master of his own thoughts and additionally overpowered
by some incomprehensible external force. Just as the patients find their thoughts are ‘made’
for them so they feel that these are being withdrawn. A thought vanishes and there arises
the feeling that this has come about from outside action. A new thought then appears
without context. That too is made from outside(Jaspers, 1959).Thought broadcasting can
also be regarded as the result of the breakdown of ego boundaries as the patient knows
that as he thinks the whole world is thinking in unison(Hamilton, 1984).

In the alienation of personal actions which occurs in schizophrenia, the patient has the
experience that his action are under the control of some external power and the patient may
not only lose control over his thought, actions or feelings, but also experiences them as
being foreign or manufactured against his will by some foreign influence. "िसर भा र लगती है और
त डा लगता है। मित दा िसर से CSF िनकाि त है| इसीिलये ऐसा होता है।" (CRF no. 125697/A). Alienation may
affect thought, motor actions and feelings. In case of feeling, it is customary to use the term
'passivity feelings.' The patient knows that his actions are not his own and may attribute this
control to hypnosis, radio waves and so on. One patient expressed his passivity feelings by
saying, 'I am a guided missile.' This patient experienced penile erections during the night
which he knew were produced by the night nurse influencing him with her thoughts as she
sat at her desk some twenty feet away(Hamilton, 1984).
293
 Schneider has believed that when a patient experiences his thoughts, action or
feelings as being foreign, in the absence of coarse brain disease this is a symptom of the
first rank and diagnostic of schizophrenia. Some psychiatrists have called these passivity
experiences 'made' or 'fabricated' experiences because the patient experiences these
phenomena as being made by an outside influence. This term 'made experiences' is also
used for apophanous experiences when the patient knows that all the events around him
are being made for his benefit (Hamilton, 1984).

Another aspect of loss of the boundary with the environment is seen when the
patient knows that his actions and thoughts have an excessive effect on the world around
him, and he experiences activity which is not directly related to him or having a definite
effect on him (Hamilton, 1984). According to rather obscure utterances of schizophrenic
patients seem to identify themselves with the objects of the outer world; they suffer from
what others do. If someone is spinning, they say ‘why are you spinning me?’ or, when a
carpet is beaten, say ‘why are you beating me?’ (Jaspers, 1959)

Disorder of the awareness of the body: The body represents the physical manifestation
of the individual being. The external world is experienced through senses of the body. Since
there is no ready division between the subjective experience of self and of body, it is wise to
discuss disorders of awareness of body along with disorders of experience of self
(Oyebode, 2008). Cutting (1997) classified disorders of awareness of the body under five
subheadings:

(a)Disorders of belief about the body: eg: Hypochondriasis.

(b) Disorders of bodily function: eg: Dissociative disorder.

(c) Disorders of the physical characteristics and emotional value of the body: eg: Body
dysmorphic disorder.

(d) Disorders of the sensory awareness of the body (organic changes in body image).

Hypochondriasis: It describes that awareness in which the person takes undue account
of the symptomatic component of his sensorium. It is rather a symptom than a disease. It
can take different modes of expression: minor pain and discomfort dominate the life of the
subject and occupy his attention; he may have unreasonable fear about the likelihood of
developing serious illness, and feel a need to take excessive precaution; he may
misinterpret benign blemishes as having sinister pathological significance. Such symptoms
are very common and usually transient. Only a selected atypical proportion of these cases
are seen by psychiatrists (Oyebode, 2008).

According to Barsky and Klerman (1983) the word hypochondriasis is used to

describe four quite distinct concepts.

1. It describes a psychiatric syndrome characterized by physical symptoms

disproportionate to demonstrable organic disease, fear of disease and the

294
 conviction that one is sick, preoccupation with one's body and pursuit of
medical care.
2. Psychodynamically it is a derivative of aggressive or oral drives or as a
defense against guilt or low self esteem.
3. Hypochondriasis results from a perceptual amplification and augmentation
and a cognitive misinterpretation of normal bodily sensations.
4. It is socially learned behavior to which the philosophy and practice of the
medical profession lends support.

Dissociative disorder: Dissociative or hysterical symptoms are very common, but the
primary diagnosis of hysteria or dissociative (conversion) disorder is not. The symptoms of
dissociation are psychogenic, causation is thought to be unconscious and these symptoms
carry some sort of advantage to the patient which occur by the mediation of the processes
of conversion or dissociation (Oyebode, 2008).The term conversion refers to the behaviour
of physical illness without evidence of organic pathology; the patient is not aware of
psychogenicity. Dissociation implies 'a narrowing of the field of consciousness with
selective amnesia’. There may be dramatic but essentially superficial changes of
personality, at times taking the form of a fugue (wandering state). Behaviour may mimic
psychosis, or rather the patient's idea of psychosis (Oyebode, 2008). In severe anxiety the
patient may be so preoccupied by his conflicts that he is not fully aware of his environment
and finds that he has only a hazy idea of what has happened in the past hour or so. This
may suggest to the patient that amnesia is a solution of his problems, so that he 'forgets',
his personal identity and the whole of his past as a temporary solution of his difficulties.
This state is known as a hysterical twilight state. Wandering states with some loss of
memory are also called 'fugues'(Hamilton, 1984).Therefore dissociation can be considered
as a form of conversion in which environmental stresses result in illness behaviour in the
psychological, rather than the physical, realm. Thus symptoms of dissociative conversion
may be considered to be motor, sensory or psychological (Oyebode, 2008).

Body dysmorphic disorder (dysmorphophobia): It was first defined by Morselli (1886)

as ' subjective feeling of ugliness or physical defect which the patient feels is noticeable to
others, "ऐसा लगता है क मेरे पेिनस ब त चोटा है। यह वजह से म कु छ नह कर पाऊँगा।" (CRF no 82011/A); although
his appearance is within normal limits (Oyebode, 2008). According to Andreasen and
Bardach (1977), the primary symptom of dysmorphophobia is the patient's belief that he or
she is unattractive. Body dysmorphic disorder occurs most frequently in late adolescence.
Three quarters of patients are females and most are either single or divorced (Oyebode,
2008).

Disorders of the sensory awareness of the body (organic changes in body image):
Disease of the brain and trauma to the brain can alter the body image in a variety of ways.
This is either because of damage of the conceptualized object or damage to the process of
conceptualization itself. Morbid changes in the body image may show enhancement,
diminution or distortion (Oyebode, 2008).

Hyperschemazia: It is pathological accentuation of body image. Pain or discomfort causes

the affected part of the body to loom large. Such a description is frequent following surgery
295
and traumatic injury. It also occurs in partial paralysis (Brown sequard paralysis), multiple
sclerosis and peripheral vascular disease where the affected limb gives the impression of
being heavy and too big. It may also occur in non organic cases like hypochondriasis,
depersonalization states and dissociation (Oyebode, 2008).

Hyposchemazia/Aschemazia – It is diminished or absent body image. This may occur

when afferent and efferent innervation is lost, for example with transaction of the spinal cord
the patient may feel sawn off at the waist. It may accompany the sensory deprivation of
weightlessness, for instance like being under water. Parietal lobe lesions may result in
complicated states of diminution of the body image (Oyebode, 2008). In hemisomatognosia
there is a unilateral misperception of one's own body, the patient behaves as though the
limbs on one side are missing; this may occur as part of an epileptic aura or migraine.
Anosognosia is a form of disturbed body image in which the patient is not only unaware but
may even deny the existence of disability e.g. hemiplegia, paralysis of the limbs and even
blindness. Hemispatial neglect describes those patients, who, when asked to perform a
variety of behavioural tasks in space, neglect the hemispace contralateral to their lesion.
Gerstmann's syndrome comprises finger agnosia, acalculia, agraphia and right/left
disorientation (Oyebode, 2008).

Paraschemazia – It is distortion of the body image which may occur with enhancement or
diminution of the body image. Parts of the body may feel distorted, twisted, separated from
the rest of the body or merged with the external environment. When size is affected, the
body may feel smaller (microsomatognosia) or bigger (macrosomatognosia) (Oyebode,
2008).

DISORDERS OF CONSCIOUSNESS

Understanding consciousness has become the ultimate intellectual challenge of this

millennium. Different schools in philosophy as well as neurosciences have understood the
term consciousness from various angles and defined it in different ways. The American
philosopher, John R Searle defines `consciousness’ as those subjective states of sentience
or awareness that begin when one wakes up in the morning from a dreamless sleep and
continue throughout the day until one goes to sleep at night or falls into a coma, or dies, or
otherwise becomes, as one would say, `unconscious' (Searle, 1994) where as for a
neuroscientist consciousness is entirely due to neurobiological processes and realized in
brain structures. From a clinician’s perspective, consciousness refers firstly to the inner
awareness of experience as opposed to the categorizing of events as they occurs,
secondly, it denotes the subject reacting to the objects which it perceives, imagines or
thinks intentionally, thirdly it refers to a knowledge of a conscious self (Oyebode, 2008).Fish
defines consciousness as a state of awareness of the self and the environment. According
to Scharfetter, consciousness is to know about oneself and the world.

Consciousness is considered as a biological phenomenon. But it has some important

features that other biological phenomena do not have. The most important of these is its
`subjectivity'. There is a sense in which each person's consciousness is private to him, a

296
sense in which he is related to his pains, tickles, itches, thoughts and feelings in a way that
is quite unlike the way that others are related to those same experiences. This
phenomenon can be described in different ways. It can be described as that feature of
consciousness by way of which there is something that it's like or something that it feels like
to be in a certain conscious state. The point can also be put by saying that conscious states
have a certain qualitative character; the states in question are sometimes described as
`qualia'- subjective sensation (Searle, 1994).

In psychic life, everything is connected with everything else and each element is
colored by the state and context within which it occurs. Each single element, every
perception, image or feeling differs according to whether it occurs in a state of clear or
clouded consciousness. There for, it will be of decisive significance in the assessment of all
subjective phenomena to determine whether they are occurring in a state of clear
consciousness or not. Hallucinations and delusions which occur in clear consciousness
cannot be taken as part –symptoms of some transient alteration of consciousness; they
have to be regarded as symptoms of much more profound processes within the psychic life.
One can properly speak of hallucinations and delusions only when there is this clear state
of consciousness (Jaspers, 1959).

Clear consciousness demands that what I think is clearly before me and I know what
I do and wish to do it; that what I experience is my experience, linked to a self and held
together in a context of memory. Before psychic phenomena can be called conscious they
must be remarked by the individual at some stage so that they can be lifted into clear
consciousness (Jaspers, 1959).

In short the whole of psychic life at any given moment is called consciousness, which
is like a stage on which individual psychic phenomena come and go or like a medium in
which they move (Jaspers, 1959)

Loss of consciousness occurs when the inwardness of an experience vanishes.

According to Jaspers (1959), unconscious means firstly something that is not an inner
existence and does not occur as an experience; secondly, something that is not thought of
as an object and has gone unregarded; thirdly, it is something which has not reached any
knowledge of itself.

Before we can discuss the disorders of consciousness we must understand the problem
of attention and orientation.

ATTENTION: According to Jaspers (1959) attention can be defined as the field of clear
consciousness within the total conscious state and it covers three closely connected but
conceptually distinct phenomena, firstly attention as the experience of turning oneself
towards an object, secondly, the degree of clarity and distinctness of the conscious content
(the degree of attention), thirdly, the effect of the above two phenomena on the further
course of psychic life. It is the patient’s ability to attend to specific stimulus without being
distracted by extraneous internal or environmental stimuli (Strub & Black, 2000).There are

297
five aspects of attention: selective attention, attention capacity, sustained attention, divided
attention and alternating attention (Oyebode, 2008).

Selective or focused attention refers to the capacity to highlight the one or two
important stimuli or idea being dealt with while suppressing awareness of competing
distractions. This aspect of attention is called concentration.

Attention capacity refers to fact that only limited amount of cognitive processing
activity can be carried out at any one time.

Sustained attention or vigilance refers to the ability to maintain attentional activity

over a period of time.

Divided attention involves the ability to respond to more than one task at a time or to
multiple parts within a task.

Alternating attention is the ability which allows for shifts in focus of attention and
tasks.

Attention can be active when the subject focuses his attention on some internal or
external event, or passive when the same events attract the subject's attention without any
conscious effort on his part. Active and passive attention are reciprocally related to each
other, since when the subject is more attentive , the greater must be the stimulus that will
distract them(Hamilton, 1984).
Attention is decreased in normal people in sleep, dreams, hypnotic states, fatigue or
boredom. It is pathologically decreased in organic states like head injury, delirium, and
epilepsy raised intracranial tension and brainstem lesions as well as in various psychiatric
disorders (Oyebode, 2008).
Disturbance of active attention presents as distractibility, so that the patient is
diverted by almost all new stimuli and habituation to new stimuli takes longer than usual. It
can occur in fatigue, anxiety, severe depression, mania, schizophrenia and organic states.
In abnormal and morbid anxiety, active attention may be made difficult by anxious
preoccupations, while in some organic states and paranoid schizophrenia, distractibility
may be the result of a paranoid set. In other acute schizophrenias, distractibility may be
regarded as the result of formal thought disorder because the patient is unable to keep the
marginal thoughts, which are connected with external objects by displacement,
condensation and symbolism, out of his thinking, so that irrelevant external objects are
incorporated into his thinking (Hamilton, 1984).

ORIENTATION: It is the ability of a person to gauge accurately time, space and person in
his current setting (Oyebode, 2008). When consciousness is disturbed it affects these three
aspects in that order. When the customary events which mark the passage of time are
missing, it is very easy to become more or less disorientated in time (Hamilton, 1984).
Orientation in time is disturbed quite readily by rapt concentration, strong emotion or
organic brain factors (Oyebode,2008). Orientation for place is retained more easily because
the surroundings provide some clues, and orientation for person is lost with greatest
difficulty because the persons themselves provide the information which identifies them. If a
patient is disorientated for time and place it is customary to say that he is confused
(Hamilton, 1984). Disorientation in time and place, when established clearly, are evidence

298
of an organic mental state and they may be the earliest signs in a dementing process
(Oyebode, 2008).
According to Fish, consciousness can be changed in three ways: it may be dream
like, depressed or restricted (Hamilton, 1984). In another way the disorders of
consciousness can be divided broadly into two categories: quantitative and qualitative
disturbances of consciousness (Oyebode, 2008).

Quantitative disturbances in consciousness are heightened consciousness, clouding

of consciousness, of consciousness lowering or torpor, drowsiness and coma.

Quantitative disturbances in consciousness: Consciousness can be considered as a

continuum from full alertness and awareness to coma. In that sense consciousness may be
regarded as quantitative. Various conditions can produce a variable level of diminution of
consciousness that can range from blunted awareness through lethargy and drowsiness to
loss of consciousness (Oyebode, 2008).

Heightened consciousness: It is a state of over wakefulness .Such states are

described mainly by mystics when they retreat into contemplation, also reported during an
aura in epileptic attack as an unusual brilliant state of narrowed consciousness which one
patient described as if “thinking became absolutely clear” (Jaspers, 1959).

Clouding of consciousness: This represents the lesser stages of impairment of

consciousness with deterioration in thinking, attention, perception and memory. It is usually
featured by drowsiness and reduced awareness of the environment. Although the patients
awareness is clouded, he may be agitated and excitable rather than drowsy (Oyebode,
2008).When there are violent affects, as in anxiety states and deep melancholia as well as
in manic states, it becomes much more difficult to concentrate on anything external,
contemplate anything, reach a judgment, or even think of anything. Answers to simple
questions can only be given after a number of unsuccessful attempts and visible exertion
on the part of the patient. Due to the difficulty in concentration, the contents of delusion-like
ideas go unscrutinised by the patient and there is no reality-judgment concerning possible
sense–deceptions. Consciousness is completely filled by the affect, and judgment and
attitude become very disturbed in an understandable way (Jaspers, 1959).

Drowsiness: This is the next stage of progressive impairment in the level of

consciousness. The patient is awake but drift into sleep in the absence of sensory
stimulation .The patient will be slow in activities, have slurred speech, sluggish in intention
and sleepy on subjective description. There will be an attempt at avoidance of painful
stimuli. Reflexes will be present but reduced, with diminished muscle tone. This state of
consciousness is commonly seen following over dosage with drugs that have a central
nervous system depressant effect (Oyebode, 2008).

Consciousness lowering or torpor: According to Jaspers (1959) these are states

that lie between consciousness and unconsciousness. No fresh psychic events are being
experienced .Perceptions remain as dim as the memories. Very few associations appear
and the act of thought can no longer be performed .All psychic events are slowed down and
299
much more difficult. As a result patients take no part in things, are apathetic, apt to doze
and show no spontaneity; when talked to, their attention is hard to rouse and cannot be
sustained; they cannot concentrate and are easily tired but in pure cases appear perfectly
oriented. There is a tendency to fall into a dreamless sleep or sink in to a state of coma
from which they cannot be roused. This type of consciousness is the result of severe
infections, such as typhoid and typhus (Hamilton, 1984).

Coma: In this state patient is unconscious. In lighter states patient may be

momentarily rousable with strong stimuli. There are no verbal responses or responses to
painful stimuli .The righting response of posture has been lost with greatly reduced reflexes
and muscle tone. Breathing is slow, deep and rhythmic with flushing of face and skin. In
latter stages, the patient is no longer rousable and deeply unconscious (Oyebode, 2008).

QUALITATIVE CHANGES OF CONSCIOUSNESS: Consciousness may also undergo

qualitative changes, with the production of altered states. Here awareness is narrowed
down to a few ideas and attitudes which dominate the patient's mind. There is some
lowering of the level of consciousness, so that in some cases the patient may appear only
slightly bemused and uniformed bystanders may not realize that he is confused.
Disorientation to time and place occurs (Hamilton, 1984). Various organic disturbances in
brain function are recognized which are associated with qualitative impairment of
consciousness. Qualitative disturbances in consciousness can be dream like changes in
consciousness, twilight state, delirium, stupor, fluctuation of consciousness and hypnosis.

Dream like changes in consciousness (oneiroid state): In this state there is some
lowering of the level of consciousness which is the subjective experience of a rise in the
threshold for all incoming stimuli. The patient is disorientated for time and place, but not for
person. The most outstanding feature in this state is the presence of visual hallucinations,
usually of small animals and associated with fear or even terror. The patient is unable to
distinguish between his mental images and perceptions, so that his mental images acquire
the value of perceptions. Occasionally Lilliputian hallucinations occur and are associated
with a feeling of pleasure. Common auditory hallucinations are elementary. Other
hallucinations of touch, pain, electric feelings, muscle sense and vestibular sensations often
occur. The patient remains fearful and often misinterprets the behavior of others as threats.
Usually patient is restless in this state and may carry out the actions of his trade or job. This
is known as occupational delirium .These symptoms are worse at night (Hamilton, 1984). In
the milder type of delirium, known as sub acute delirious state or toxic confusional state the
patient may have a general lowering of consciousness during the day and be incontinent
and confused and at night delirium occurs with visual hallucinations and restlessness. The
sub acute delirium state may progress into an amnestic state, torpor, severe delirium or a
twilight state (Hamilton, 1984).

Twilight state: The term 'twilight state' was introduced by Westphal for conditions in
which there was a restriction of the morbidly changed consciousness, a break in the
continuity of consciousness and relatively well ordered behavior (Hamilton, 1984). It is
characterized by: (i) abrupt onset and end: (ii) variable duration from a few hours to several
300
weeks: and, (iii) the occurrence of unexpected violent acts or emotional outbursts during
otherwise normal, quiet behaviour (Lishman, 1997).Commonest example of twilight state is
the result of epilepsy (Oyebode, 2008).

Delirium: Delirium was defined by Lipowski as ‘a transient organic mental syndrome

of acute onset, characterized by global impairment of cognitive functions, a reduced level of
consciousness, attentional abnormalities, increased or decreased psychomotor activity, and
a disordered sleep-wake cycle’ (Oyebode, 2008). In addition to many of the negative
elements, like clouding of consciousness and disturbed attention, impaired memory and
learning delirium is marked by a prominent disorder of perception like hallucinations; a
kaleidoscopic array of strange and absurd fantasies and delusions, inability to sleep, a
tendency to twitch, tremble, and convulse and intense fear or other emotional reactions.
The patient is inattentive and unable to perceive all elements of his situation. He may talk
incessantly and incoherently and look distressed and perplexed; his expression may be in
keeping with vague notions of being annoyed or threatened by someone. From his manner
and the content of his speech, it is evident that he misinterprets the meaning of ordinary
objects and sounds, misidentifies the people around him, and is experiencing vivid visual,
auditory, and tactile hallucinations, often of a most unpleasant type. The signs of
overactivity of the autonomic nervous system, more than any others, distinguish delirium
from all other confusional states. Tremor of fast frequency and jerky restless movements
are practically always present and may be violent. Sleep is impossible or occurs only in
brief naps. The EEG may show symmetrical, mild generalized slow activity in the range of
five to 10 per second—a state that rapidly returns to normal as the delirium clears (Ropper
& Brown, 2005).

Stupor: Stupor is a name for a symptom complex whose central feature is a

reduction in or absence of relational functions: that is action and speech (Berrios, 1996).It is
distinct from coma and does not lie in a continuum from wakefulness to coma. This term
should therefore be reserved for the syndrome in which mutism and akinesis occur: that is
the inability to initiate speech or action in a patient who appears awake and even alert .It
usually occurs with some of degree of clouding of consciousness. The patient may look
ahead or his eyes may wander, may follow external objects, but he appears to take nothing
in (Oyebode, 2008).
Fluctuation of consciousness: Mild degrees of fluctuation in consciousness may
be observed in the periodic waxing or waning of attention. The crest of the wave of psychic
life never remains at the same height from moment to moment, but changes all the time,
however slightly (Jaspers,1959).Fluctuation in conscious level occurs in health, in sleep and
in fatigue. In epileptic patients normal conscious attention fluctuates much more than in the
case of healthy persons, which can occur before, during or after the seizures (Oyebode,
2008).It also occurs with third-ventricle tumour associated with variation in intracranial
pressure and with drugs like mescaline(Oyebode,2008).

Hypnosis: It is another altered state of consciousness. Hypnosis is related to sleep

and identical in character. During hypnosis a particular type of productivity arises , pictures
are seen and memories are relived(Jaspers,1959).The trance in hypnosis is produced by
one person on another using suggestion with compliance, in a waking
state(Oyebode,2008).There is no known principle on which we can grasp this state, as to
what it really is. We can delineate it only by distinguishing it. It is not an understandable
301
psychic change but a vital event of a peculiar kind which is linked with effective suggestion.
It is primary phenomenon of somato-psychic life, manifesting itself as an alteration of the
conscious state (Jaspers, 1959).

Concept of self:
The term ego is phenomenologically not describable and there has been argument that self
cannot describe itself: that a thing what observes that thing cannot be the same. However,
it is the nature of the self and ego to be experienced as either subject or object: you can
feel how it pains when hurt (subjective) also you can explain how one experiences a pain
(objective) (SIMS, 2003). Thus self serves the ability of a person to view himself in relation
to others. Specifically it is how he believes other people see him. As summarized by
Bahnson(1969) the changeable and amorphous self-image develops with age as in the
diagram.
What exactly is meant by the “self”? It can be defined with its fivefold character
(Ramachandran & Blakeslee, 1998):

 Continuity: these are varied experiences involving a lot of time in life; but only one is
‘I’, who feel of past, present and future.
 Unity or coherence of self: diverse are our sensory experiences, memories, beliefs
and thoughts; but each of us experience ourselves as one single person, as a unity.
302
  Sense of embodiment or ownership: we feel, ‘we’ begin with our bodies.
 Sense of agency: ‘we’ are in-charge of our own actions and destinies. We have a
‘free will’ which formulates our ‘to be done’.
 Self reflection: most elusive of all, the self, almost by its very nature, is capable of
reflection of being aware of itself.
Biological perspective: V S Ramachandran tries to explain the self’s characters through
their biological correlates. He with Hirstein enlisted the following characteristics
(Ramachandran & Blackeslee, 1998):

The embodied self: or the self anchored within a single body, which is similar to body
image.
The Passionate self: the emotional aspect of self mediated by limbic system and
amygdale, an essential aspect of self
The executive self: which is the ‘free will’ allowing to make a choice and give motor
commands, attributed to the anterior cingulated gyrus.
The mnemonic self: organizing yourselves on long strings of personal recollections and
memories present in the memory circuits
The unified self: imposing coherence on consciousness, filling in and confabulation by the
brain process associated with limbic and parts of cingulate gyrus.
The vigilant self: by intralaminar and thalamic nuclei driven by pedunculopontine nuclei
processes the vigilance.
The conceptual and social self: is the same which conceptualizes other abstract concepts
like “love”, “happy” or “Mind”.
Social perspective: The existence of ‘self’ portray itself in the background of ‘non-self’. The
theory of mind or mentalisation implies to the ability of an individual to recognize the state of
mind of others. This awareness of others mental activity opens up a new world for
understanding our own behaviors, beliefs and desires which leads to ‘self’. Deficits in theory
of mind (ToM) is reported in patients of autism, schizophrenia; though controversy
regarding ToM as a trait marker, a state marker and a psychosis induced deficit remains to
be resolved (Zeman.A, 2008).

Disorders of experience of self

Depersonalisation-Derealisation

We never ask ourselves-Do we exist? It is by virtue of assumption, we

unquestionably are sure of our existence. In Depersonalisation and derealisation this basic
experience of existence is altered and the individual may feel going crazy. Thus they will
remain reluctant to report their experiences or will report the associated features like
anxiety, depressive symptoms or somatic concerns. It will be difficult for the doctor to
portray: more important it is extraordinarily difficult also for the patient to describe.
Subjectively patients always experience a change in mood with depersonalisation;
the patient loses the feeling of familiarity he has for himself. He may describe himself as
feeling like a puppet: hollow, detached and strange, on the outside, uninvolved with life;
himself like a ghost- not solid, a stranger to himself. He experiences a loss of emotion.
Similarly, with derealisation he may describe his environment as flat, dim in colour, smaller,

303
cloudy, dreamlike, still, ‘nothing to do with me’, and also lacking in emotional significance
(Sims, 2003).
The localisation of this symptom to an individual organ is called desomatisation.
Different possible parameters are affected here like size or quality, appearing larger or tinier
or empty or detached, or ‘filled with water of foam’ or feeling of being weightless, or his leg
as floating or affected is simply the familiarity of the organ. (Sims, 2003)
All these experiences essentially have the ‘as if’ content though not overtly
expressed in exaggerated reporting of some persons like appreciation needing
personalities or with learning disabilities. Also as Freeman reports depersonalisation is a
common experience occurring in 30-70% of young adults under moderate stressful
situations (Casey and Kelly, 2007) but it is the Ackner who records the experiences to be
reported intensely unpleasant by patients than healthy subjects(SIMS, 2003).
What is not Depersonalisation?
Nihilistic Delusions sometimes called the delusion of depersonalisation are
commonly seen with depression, so as is the depersonalisation which are not delusions in
that they does not deny their existence nor that of world or people around.
Depersonalisation needs also to be distinguished from preoccupation and loss of interest
seen in depression (Hamilton, 1984). Deaffectualisation has been used to describe the
consistent loss of the capacity to feel emotion, so that the person seems unable to cry, love
or hate (Leading article, 1972).
Multiple personality (dissociative identity disorder) is not a phenomenological
description but a simple observation of manifestation of more than one ‘personality’ at
different point of time in a ‘single’ person.
Possession state is where there is temporary loss of sense of personal identity and
person believes as well as ‘acts’ as if taken over by a spirit, deity or another person.
Neglect syndromes or asomatognosia, presenting in inferior parietal lobule and
angular gyrus pathologies, though share the biological experiences of depersonalisation
lack the phenomenal experience of “not able to feel”.
Experience of seeing oneself in others is another variation of self-experience where
a person feels an unpleasant familiarity with another person. This is neither a delusion of
misidentification nor is it depersonalisation, which is an experience within an individual
Schizophrenic passivity experiences included within depersonalisation by
Langfeldt’s (1960) was later criticised and Sedman (1970) distinguished schizophrenic ego
disturbances from depersonalization on phenomenological grounds that is on the
description by the patient of his own internal experience (SIMS, 2003).
Depersonalisation Syndrome is distinct from depersonalisation as a symptom, a
symptom in manic-depressive illness, schizophrenia, agoraphobia, panic disorder, post
traumatic stress disorder & other non psychotic disorders; few personality traits in particular
had been implicated to anankastic traits. The syndrome as enlisted by Sierra and Berrios
(2001) prevails with: emotional numbing, changes in visual perception, changes in
experience of body and loss of feelings of agency; which features in addition to the
symptom itself. Depersonalisation-Derealisation disorder in ICD-10, (ICD 10, WHO, 1992)
views both phenomena simultaneously. But Depersonalisation disorder in DSM-IV
304
distinguishes itself from Derealisation unaccompanied by depersonalisation in Dissociative
disorder NOS. Depersonalisation, as rightly mentioned in Sims (2003) is more often
associated with depression and anxiety but DSM IV classifies depersonalisation disorder
under dissociative disorder, which is psychopathologically misleading.

Etiology

Psychodynamic:
Disintegration of the ego or an affective response in defence of the ego are
explained to be causative mechanisms for these disorders, triggered by conflictual impulses
or overwhelming painful experiences. Stamm attempted to extend the basic theory that
depersonalization appears when ordinary ego defences are disrupted and unable to cope
with powerful aggressive and libidinal drives approaching consciousness. Stewart says that
depersonalization represents a splitting of the ego occurring in predisposed individuals
when circumstances produce dissimilarity between ‘myself as perceived by me’ and ‘myself
as perceived by others’. The predisposition reflects the regressive reactivation of (oral)
infantile experiences of such a nature that instinctual needs acknowledged by the ego are,
either not recognized or are treated as though they do not exist by the mother. all these
theories are in fact theories which explain ‘content' and cannot by their very nature explain
the form of the phenomenon in question. As Jaspers has indicated, psychoanalysis is
concerned with ‘the psychology of a meaningful connections and not with causal
explanation' (Sedman, 1970).

Traumatic stress:
A substantial proportion of the patients (typically one-third to one-half), in clinical
depersonalization case series reports history of significant trauma. Several studies of
accident victims find as much as 60 percent of those with a life-threatening experience
report at least transient depersonalization during the event or immediately thereafter.
Military training studies find that symptoms of depersonalization and derealization are
commonly evoked by stress and fatigue and are inversely related to performance. On the
other hand, nontraumatic stressors, such as interpersonal, financial, or occupational losses,
have been associated with the onset or exacerbation of depersonalization disorder. In
addition, chemical stressors, such as marijuana, hallucinogens, and stimulants, have been
known to precipitate chronic depersonalization in some people. These individuals can be
conceptualized as having a neurobiological or genetic vulnerability to chronic
depersonalization after drug use.
Biological:
Mayer-Gross (1935) said that depersonalization is a non specific pre-formed
functional response of brain occurring after a stressful situation, chemical or psychological.
Hughling Jackson viewed experience of self to be a function of nervous system at higher
level of evolution and depersonalisation to be result of dissolution of higher levels and
uncovering of lower levels (Sedman, 1970).

Temporal and limbic lobe theories stood with long clinical association of these
symptoms in temporal lobe epilepsies after Wilder Penfeilds’ stimulation experiments over
superior temporal and medial temporal gyri produced depersonalisation and derealisation
305
experiences; latest support being from neuromaging techniques which have also pointed
towards anterior cingulate gyrus and medial frontal gyrus.

Seirra and Berrios thus proposed “cortico limbic disconnection” model of

depersonalisation in 1998. Over activation of prefrontal cortex is responsible for emotional
dampening by overly inhibiting the limbic system but disconnection between reciprocal
parts causes’ hyper cognitive state wherein people know what they should feel but because
of hypo emotionality they could not really feel it (Simeon & Abugel, 2006).
The association of depersonalization with migraines and marijuana; its generally
favorable response to selective serotonin reuptake inhibitor (SSRI) drugs; the increase in
depersonalization symptoms seen with the depletion of L-tryptophan, a serotonin precursor:
all these point towards serotoninergic involvement. Depersonalization is the primary
dissociative symptom elicited by the drug-challenge studies. Four groups of chemicals have
reliably elicited depersonalization: cannabinoids, NMDA antagonists like ketamine (the
dissociative anaesthetic), opioid agonists and hallucinogens.
The double phenomenon: doppelganger

Having an awareness of one's double may be perceptual, delusional or, more

commonly, an ‘as if’ description of depersonalization; these forms are phenomenologically
distinct. There is a North European myth, shared by several countries that someone may
see his double (‘wraith, ‘fetch’) shortly before his death, and it has therefore become a
sinister omen (Todd and Dewhurst, 1962).
As a clear hallucination, seeing one's double is rare (autoscopy), but the vague
feeling of being beside oneself, alongside oneself or having another self (the soul-double) is
quite common. There could be six possible psychopathological explanations for the
phenomenon of non-organic, non-psychotic doubling:
1. Fantasy
2. Depersonalization: 'while talking we may notice that we are talking rather like an
automaton, quite correctly maybe, but we can observe ourselves and listen to
ourselves' (Jaspers, 1959).
3. Conflict: 'Two beings live within my breast where reason struggles with passion'
(Jaspers, 1959).
4. Compulsive ideas: repetitive, resisted, self-produced and self-ascribed.
5. Double personality: referring to alternating states of consciousness.
6. Being in two, being doubled: 'When both chains of psychic events so develop together
that we can talk of separate personalities, each with their own peculiar experiences and
specific feeling – associations, and each perfectly alien and apart from the other'
(Jaspers, 1959).
These experiences are not wholly distinct from each other and they do overlap; however,
there are phenomenological differences between them which are important.
A clear complex multimodal (visual, somatic, kinesthetic and even auditory at times)
hallucination of seeing himself is phenomenologically a separate entity, called Autoscopy
(also termed Phantom mirror image, Heautoscopy); rather is a rare experience of

306
hallucinatory perception of one’s own body image with feeling of loss of familiarity with
oneself and often associated with parietal lobe lesion.(Sims, 2003)
Disordered self in Schizophrenia

The fundamental nature of schizophrenia appears to be the experience of invasion of

ego boundary; the first rank symptoms portray merging of self with non-self : Passivity
experiences are those events in the realm of sensation, feeling, drive and volition which are
experienced as made or influenced by others and all passivity experiences falsely attribute
functions which are actually coming from inside the self to non self influences from outside.
Passivity experiences of thinking occur as thought withdrawal, thought insertion or thought
broadcasting. Experiences of auditory hallucinations are also ascribed to the sensory stimuli
outside the self whereas, in fact, they arise inside the self. These auditory hallucinations
comment upon the patient in the third person. Usually we think of our self in the first person
singular. Occasionally we address ourselves as “you”, in the second person, but we do not
think about ourself nor comment on our actions in the third person as “he”: this reveals a
considerable disturbance of the boundaries of self. Similarly hearing one's own thoughts out
loud implies locating one's innermost core experiences in distant space exposes a massive
disturbance of the boundaries of self.
Similarly in delusional percept, a normal perception is correctly perceived and
correctly regarded as being outside self. However, delusional percept is delusional
interpretation of the object of perception, which is actually neutral and irrelevant to self, as
highly relevant with intense personal meaning. This implicates that the meaning of the
perception, although in reality is outside the self, has become incorporated within the self
(Sims, 2003).
However, we need to note that it is the interviewer identifying an ego disturbance or
disorder of the patient's experience of self; the patient himself complains of the upsetting
content not of the disordered form of self-experience. Voices arguing or discussing or
commenting with each other is interpreted by the sufferer as coming from outside himself,
whereas it is actually inside, an interpretation by observer, as a disturbance of ego boundaries
(Sims, 2003).So while studying phenomenology it will be incorrect to explain these
phenomenon under disorders of boundaries of self.
Much of the confusion of role and self-image in schizophrenia appears to show this
loss or inconsistency of boundaries, sometimes described in directly physical and concrete
terms. A patient described the difficulty he had in thinking as being caused by 'a vibration
an inch in front of my toes' (Sims, 2003).
The loss of unity of self in schizophrenia was exemplified by a patient who described
how, every night; he became a horse and trotted down Whitehall. At the same time as this
was happening in his mind, he also believed he was in Whitehall watching the horse. This
type of symptom has been called lability in the awareness of personality and was described
by Bonhoeffer (1907) as occurring in paranoid psychosis (Sims, 2003).
Disorder of the Awareness of the Body
Hypochondriasis

307
 It is the form in psychiatry which plays diagnostic role. One of the exceptions to this
statement will be hypochondriasis, whose content is the excessive concern with health,
either physical or mental. Possible forms of the condition are listed in Table (Sims, 2003).
Psychopathology of hypochondriasis

 Hallucination  Obsessional rumination

 Secondary delusion  Depressive rumination
 Primary delusion  Anxious preoccupation
 Overvalued idea

These forms for content of concern about cancer can include the following:
1. A hallucinatory voice may say: ‘you have cancer, you are moribund’.
2. A secondary delusion associated with affective illness may occur in which the patient
unreasonably believes he has cancer. The belief is understandable in terms of the patient’s
overall depressed mood state. Cotard (1882) described such secondary delusions
associated with affective psychoses ‘she blamed herself and felt guilty. After some months
she entertained hypochondriacal delusions, believing that she had no stomach and that her
organs had been destroyed: she attributed these beliefs to the effects of an emetic which
she had, in fact, been given’. This association of hypochondriacal and nihilistic delusions
with depressive psychosis in the elderly has been called Cotard’s syndrome.
3. The delusion may be primary in nature. A patient with schizophrenia believed that he had
been inoculated under a general anaesthetic with a transmissible cancer because others
believed him to be homosexual,
4. Hypochondriasis often manifests as an overvalued idea. Such a person is constantly
worried and concerned about the risk of illness and the need to take precautions in ways
that his friends find ridiculous, for instance in the lengths that he will go to avoid a possible
carcinogen. He considers it perfectly reasonable that he should take the care to maintain
his health, but he agrees that his measures are excessive. He cannot stop himself, night or
day, from thinking worrying and trying to prevent illness. Such an overvalued idea is found
reasonable, or at least not alien to the person’s nature, but preoccupies the mind to an
unreasonable extent: the whole energy and being becomes directed towards this single
idea.
5. The hypochondriacal idea may take the form of an obsessional rumination in which a
form of words, as ‘I have cancer’, may recur. This though is recognized as being both ‘alien
to my nature’, but also ‘coming from inside myself’. Resistance fails and it occurs
repeatedly.
6. Hypochondriacal Symptoms of a non specific nature can occur without amounting to
delusional level in the course of a depressive illness. Though reassurance helps them, they
continue to report hypochondriacal symptoms in different forms as depressive ruminations.
7. In acute or chronic anxiety, the patient may be prone to multitudinous worries concerning
illness and fears of illness. The normal sensorium is interpreted as symptoms: symptoms

308
are interpreted as serious illness. They will get absorbed in those preoccupations about
illness.
Most hypochondriacal symptoms occur in relation to anxiety and depression (Sims, 2003).
There is a distinction between fearing illness when there are no bodily symptoms and
fears and distress associated with bodily symptoms. This shows the overlap between
illness phobias (unreasonable fear of developing illness) and hypochondriasis
(preoccupation with symptoms).There will also be difficulty in diagnosis when a person with
demonstrable physical pathology complains excessively about his symptoms; his
complaints appear to be out of proportion to the anticipated suffering and disability of the
illness.
Commonest organs implicated are musculoskeletal, gastrointestinal, and central nervous
system
Several mechanisms play their role:

 Misinterpretation of normal bodily sensations

 Conversion of unpleasant affects especially depression into physical symptoms
 The experience of autonomic symptoms: caused by disorder of mood
 A learned behaviour in patients with long standing physical illness (Sims, 2003)

Is hypochondriasis a separate condition – a symptom or a syndrome, a noun or an

adjective? In the older psychiatric classifications, and also surprisingly in both ICD 10
(World Health Organization, 1992) and DSM IV (American Psychiatric Association, 1994),
hypochondriasis or hypochondriacal disorder is given a separate designation. However in
ICD 10 and in the more detailed rubric of DSM IV, hypochondriacal disorder (F45.2 in ICD
10) forms one category of somatoform disorders. In ICD 10 somatoform disorders are part
of ‘Neurotic, stress related and somatoform disorders’ (F40-F48); it is used adjectivally to
describe one type of neurotic disorder.

Hypochondriacal symptoms are present in depression as somatisation;

schizophrenia, in different forms; somatisation disorder with recurrent but frequently
changing complaints; and in children with long term medical treatment as Masquerade
syndrome.

Other disorders of body image

Excessive concern about body appearance with excessive absorption with self and self-
love describes narcissism. But in descriptive psychopathology use of this term is cautiously
restricted to those patients who by themselves consider it to be excessive, so that they get
difficulty in relating with others.
Dislike for body is seen with dysmorphophobia and transsexualism. Preoccupation with
generalised disapproval of body appearance or a physical defect characterises the body
dysmorphophobia with usually gaining the form of overvalued idea. Overvalued idea with
the content of belief that their true gender is at variance from biophysical characteristics
conceptualises the gender identity disorder.
Distortion of body image is usually caused by or resulted from eating disorder. Over
estimation of their size is done, both by obese and anorexic individuals.
309
Dissociative - Conversion - Hysteria
After gaining controversies around it, Hysteria went into the obituary list with finding
synonyms in dissociation and conversion. It is a classification in psychiatry based on
psychodynamic formulation. It is based on the concept that:

 Symptoms are psychogenic

 Causation due to mechanisms in unconscious
 Symptoms carry some benefit to patient
 Mediated through process of dissociation or conversion(Sims, 2003)
Conversion disorders are unexplained physical (usually neurological) symptoms, as
a ‘conversion’ of unacceptable affect or perception of life situation. So is the dissociative
disorder where stressors are converted to illness behaviour rather of psychological
symptoms of consciousness, memory or identity. Conversion and dissociation are also the
common mechanisms of hypochondriasis and psychogenic pain syndromes. But the
question persists to haunt the psychiatrists and physicians: how can one be sure that
disturbance is psychogenic? (Sims, 2003)
ICD 10 (World Health Organization, 1992) uses the rather clumsy term, dissociative
(conversion) disorder, to describe hysteria, whilst DSM IV American Psychiatric
Association, 1994) removes the term altogether by fragmenting it into different parts —
conversion disorder under Somatoform Disorders, and Dissociative Disorders- a separate
generic category: this destruction and division is the worst of all options (Sims, 2003).
Similar is the factitious illness but here is the intentional production or feigning of
symptoms or disabilities in order to gain a goal (gains are emotional and craves attention)
which is not obvious. If the goal is obvious (monetary or other materialistic gain) and
recognizable with knowledge of environmental circumstances then it is called malingering.
Culture Bound Disorders of Body Image
Under psychosocial stress certain predisposed individuals, like those with Histrionic
(hysterical) traits, develop dramatic onset disorders; content of symptoms complying with
local culture. Course of these are usually restricted for 1-3 weeks but may recur further.
Manifestations include grossly unusual behaviour, volatile mood, transient occurrences of
alterations of speech, depersonalization with altered body awareness, and symptoms
somewhat similar to delusions and hallucinations.
Some of the culturally localized disorders of awareness of the body are summarized in
Table.
Culture-bound disorders of body image (Kiev, 1972)

Disorder Diagnostic Site Key symptoms

equivalent

Koro Anxiety state SE Asia Belief that the penis will retract into the abdomen
and cause death.

Frigophobia Obsessive East Asia Morbid fear of the cold preoccupation with loss of
compulsive
310
 neurosis vitality, compulsive wearing of layers of clothes.

Latah Hysteria Malaysia Hypersuggestibility, automatic obedience,

coprolalia, echolalia, echopraxia, echomimia,
altered consciousness, disorganization,
depression and anxiety

Evil eye Phobic Mexico Strong glances are harmful, precautions taken to
neurosis avoid or counteract evil eye.
N. Africa

Voodoo Phobic Haiti Violation of taboo may result in death.

neurosis

Windigo Depressive Canadian Fear of engaging in cannibalism and of

reaction Indians becoming a sorcerer; depression of mood.

Amok Dissociative Malaysia Neurasthenia, depersonalization, rage,

state automatism, violent acts.

Disorders of Consciousness
Jasper (1959) states: Consciousness is a stage on which individual psychic
phenomenon come, play and go.

To the psychologist, consciousness denotes a state of continuous awareness of

one’s self and environment. Knowledge of self includes all “feelings, attitudes and emotions,
impulses, volitions, and the active or striving aspects of conduct,” in short, a near
continuous awareness of one’s own mental functioning, particularly of the cognitive
processes, and their relation to past memories and experience. These can be judged only
by the patient’s verbal account of his introspections and, indirectly, by his actions.
Dimensions of Consciousness

Conscious and unconscious spectrum varies in three mutually exclusive organic

states. This can be even demonstrated by electroencephalogram showing utterly different
images. Phenomenologically three different ways of unconscious experiences are
described:

 Deep sleep: a person in deep sleep is unconscious, unaware of one self and the
surroundings. The continuum moves from wakefulness through different stages to
deep sleep.
 Coma: a person with serious brain disease will be unconscious in a continuum of
clouding, drowsiness, coma ending in death.
 Unconscious mind: a person fully awake will still be unaware of certain parts of his
environment as well as certain things of himself. He will not be vigilant of certain
aspects, which is in a continuum from complete attentiveness, pre-consciousness to
unconsciousness.
311
 2. 3.

Deep sleep Unconscious mind

Stages of Sleep Preconscious – Not Readily available

Reduced Wakefulness

Physiological Attention
Normal awareness
Sleeping
Consciousness

Clouding
Organic
Brain disease
Drowsiness

Stupor

I.

Coma

Death

Conscious mind has a limited capacity (can remember up to seven digits; carry out
only a single task at a time). It is the function of preconscious mind which gives different
meanings to ambiguous stimuli, processes automatically and runs parallel task
simultaneously (Sims, 2003).There are many a mental processes which cannot be
introspected. Amongst such processes, for which there is good evidence of their existence,
frequency and complexity, there are some which have been, or may yet become,
conscious. This is what Freud called the preconscious (Frith, 1979).

Disorders of consciousness are associated with disorders of attention, orientation, attitudes,

thinking, registration and perception (Hamilton, 1984).

312
Delirium
There are many meanings and definitions for this term. Sometimes it embraces all
types of acute organic reaction, sometimes referring to degree of overt disturbance and
sometimes to a clinical picture of specific features. Traditionally it was used to describe a
syndrome of impairment of consciousness along with intrusive abnormalities of perception
and affect resulting in disturbed or disruptive behaviour (David, 2009). The DSM IV
(American Psychiatric Association, 1994) uses the term in a global sense to describe a
disturbance of consciousness that is accompanied by a change in cognition and states that:
it could not be attributed to any pre-existing or evolving dementia. The ICD 10 (World
Health Organization, 1992) uses the term delirium in a generic and global sense: An
etiologically nonspecific syndrome characterized by concurrent disturbances of
psychomotor behavior, consciousness and attention, memory, emotion, thinking, perception
and the sleep-wake cycle.
In delirium consciousness is not only affected quantitatively but also qualitatively.
Awareness though impaired arousal is intact leading to the clinical picture. Delirium tremens
is considered to be a prototype of delirium; occurring in the withdrawal stage of alcohol
abuse, from 24 hours to 7 days after ceasing to drink. They are usually associated with
tactile and auditory hallucinations, sometimes Lilliputian hallucinations (seeing little men)
(Sims, 2003).

Mania a Poutu
A specifically acute alcohol intoxication related twilight state needs to be
differentiated from Delirium tremens, which occurs in withdrawal state. It is a non dose
related pathological reaction to alcohol (Sims, 2003)
Coid (1979) describes its four components:
 Follows alcohol consumption
 Senseless, violent behaviour ensues
 Prolonged sleep follows
 Total or partial amnesia of the behaviour occurs.
Confusion
It is yet another imprecisely defined term on disturbed consciousness. Confusion
indicates that the patient is unable to think with his customary clarity and coherence (David,
2009). Disruption of thought process occurs due to structural brain damage and acute
organic or intoxicated conditions; but this is not wholly restricted to organicity. Functional
psychosis and intense emotional disturbance can also cause a similar picture. Clinical
picture also is varied: it may be the patient’s description of confusion in thinking or a
physician’s observation of disturbed thought process.
Automatism

Automatisms are the automatic actions taking place in the absence of

consciousness. Usually occuring in epilepsy, defined by Delgado-Escueta et al (1982):
313
“a more or less co ordinate involuntary motor activity occurring during state of clouding of
consciousness either in the course of, or after, epileptic seizure, usually followed by
amnesia for the event.”(Duncan et al., 1995)
Twilight state
Twilight state is used for states with interruption in continuity of consciousness. While
Sims (2003) notes the term usually refers to an organic state, Fish objects to it by pointing
to ICD’s inclusion of it under dissociative disorder. Lishman introduces the term describing it
to be a description of variety of syndromes including hysterical states and organic states,
most commonly complex partial seizures. Fish do agree that if one goes strictly according
to Westphal’s definition then commonest to be fulfilled is epilepsy; but argues it to be used
traditionally in other terms too when sub classifications of simple, hallucinatory, perplexed,
excited, expansive, psychomotor and oriented twilights were described. Thus restriction of
consciousness resulting from unconscious motives would be termed as ‘hysterical twilight
states’. Here patient may run away from his conflicts, wanders with some loss of memory or
awareness, also called ‘fugues’. Though all fugues necessarily may not be dissociative: as
seen in depressive guilt and malingering (Casey and Kelly, 2007).
Yet another dissociative state with altered consciousness is Trance. Sims (2003)
explains on trance by contrasting vigilance with absorption. Trance is a state where patient
remains absorbed in a single content. When a person remains absorbed he cannot shift his
attention from that content and thus appears absent minded, whereas a vigilant person can
freely shift his attention from one subject to another. Memory will be retained about the
trance state and the subject of its absorption, which is not so as in case of twilight states.
There are number of objective symptoms for all kinds of clouding of consciousness
(Jaspers, 1959):

 Turning away from reality  Disorientation

 Loss of coherence  Disturbance in registration and
memory

EVALUATION OF CONSCIOUSNESS (Strub & Black, 2000)

First, the intensity of stimulation needed to arouse the patient should be indicated:
(1) calling the patient's name in a normal conversational tone, (2) calling in a loud voice, (3)
light touch on the arm, (4) vigorous shaking of the patient's shoulder, or (5) painful
stimulation. Second, the patient's highest level responses should be described: (1) degree
and quality of movement, (2) presence and coherence of speech, or (3) presence of eye
contact with the examiner. Finally, what the patient does on cessation of stimulation should
be described. This information can be recorded in a single statement. For example:
 Patient lethargic: Patient's name called in a normal tone of voice; patient opened
eyes, pulled self part way up in bed, mumbled "Why you bothering me?" then closed
eyes and went back to sleep.

 Patient stuporous: Did not respond to voice but responded to vigorous shaking of
shoulder, accompanied by loud calling of patient's name, with groan and aimless
movement of left extremities while eyes remained closed.

314
 Teasdale and Jennett have demonstrated the practicality of this type of reporting
system for patients with head injury. They have developed what has become known as the
Glasgow Coma, or Responsiveness, Scale. The response is the patient's best response; it
does not, however, take into account the level of stimulus required for its elicitation (Strub &
Black, 2000).

Glasgow Coma Scale (Jennett and Teasdale)

Category of Response Response Points

Eye opening Spontaneous 4
To speech 3
To pain 2
Nil 1
Best verbal response Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible 2
Nil 1
Best motor response Obeys 6
Localizes 5
Withdraws 4
Abnormal flexion (decorticate) 3
Extends (decerebrate) 2
Nil 1

EVALUATION OF ATTENTION (Strub & Black, 2000)

Observation
Observing the patient's behavior and noting any evidence of distractibility or difficulty
in attending to the examiner. A subjective rating scale of 0 (highly distractible) to 5 (fully
attentive) is useful as a means of quantifying attention over the course of the examination.
History
A simple inquiry as to the patient's ability to concentrate or sustain attention often
provides revealing data.
Digit Repetition

The patient's basic level of attention can be readily assessed by using the Digit
Repetition Test. Adequate performance on this task ensures that the patient is able to
attend to verbal stimulus and to sustain attention for the period of time required to repeat
the digits. In patients with a significant language disorder (aphasia), this task and the "A"
Random Letter Test for sustained attention, which follows, cannot be validly applied to
assess attention.
Sustained Attention
A simple test of sustained attention that can be readily administered at the bedside is
the "A" Random Letter Test. It consists of a series of random letters among which a target
315
letter appears with greater-than-random frequency. The patient is required to indicate
whenever the target letter is spoken by the examiner.
Serial seven subtraction test

Counting backward from 100 by 7s: 100, 93, 86… traditionally included test which if
shows adequate performance indicates excellent attention. But the test had showed limited
validity with the errors getting influenced by intellectual functioning, education, calculation
ability, socioeconomic status..
Conclusion
Assessment of disorders of self and consciousness are necessary to arrive at
diagnosis. It is one area which is always missed until asked specifically. Differentiation of
these phenomena is required to get the clear psychopathology of the patient.

References

 Abse, W. (1982). Multiple personality. In Roy, A. (ed) Hysteria. Chichester: John

Wiley.
 Ackner, B. (1954). Depersonalization I. Aetiology and Phenomenology II. Clinical
syndromes. Journal of Mental Science, 100,839-72.
 American Psychiatric Association (1994). Diagnostic and Statistical Manual of
Mental Disorders, 4th edn. Washington: American Psychiatric Association.
 Andreasen, N.C. & Bardach, J. (1977). Dysmorphophobia: symptom or disease?
American Journal of Psychiatry, 134, 673-5.
 Bahnson, C.B. (1969). Body and self images associated with audio-visual self
confrontation. Journal of Nervous and Mental Disease, 148, 262-80.
 Barsky, A.J. & Klerman, G.L. (1983). Overview: Hypochondriasis, bodily
complaints and somatic styles. American Journal of Psychiatry, 140,273-83.
 Berrios, G. E. (1996).The History of Mental Symptoms: Descriptive
Psychopathology since the Nineteenth Century. Cambridge: Cambridge
University Press.
 Bonhoeffer, K. (1907). Klinische Beitrage zur Lehre von den Degenerations
psychosen. Alt's Samml. Vol. 7, Halle.
 Casey, P & Kelly, B. (2007). Fish’s Clinical Psychopathology: Signs and
Symptoms in Psychiatry, 3rd ed., pp. 75-86. London:Gaskell
 Coid, J. (1979). Mania a potu: a critical review of pathological intoxication.
Psychologicla Medicine, 89, 709-19.
 Cotard, M. (1982). Nihilistic delusions. In Hirsch SR and Shepherd M (eds)
Themes and Variations in European Psychiatry, 1974. Bristol: John Wright.
 Critchley, M. (1950).The body image in neurology. Lancet, 335-341.
 Cutting, J. (1997). Principles of psychopathology. Oxford: Oxford university
press.
 David, S.A. (2009). Basic concepts in Neuropsychiatry. In: Lishman’s Organic
Psychiatry. David, S.A., Fleminger, S., Kopelman, M. D., Lovestone, S., Mellers,
J. DC. (eds). 4th Edn, pp3-28. West Sussex, Wiley-Blackworth.

316
 Delgado-Escuta, A.V., Bascal, F. E., Treiman, D. M. (1982). Complex partial
seizures on closed circuit television and EEG. Annuals of Neurology. 11, 292-
300.
 Duncan, J. S., Shorvan, S. D., Fish, D. R. (1995). The spectrum of epileptic
seizures and syndromes. In: Clinical epilepsy, pp25-102. New York: Churchill
Livingstone
 Fish, F.J. (1967). Clinical psychopathology. Bristol: John Wright
 Frith, C.D. (1979). Consciousness, Information processing and schizophrenia.
British Journal of psychiatry. 134, 225-235
 Hamilton, M. (1984) Fish’s Clinical Psychopathology: Signs and Symptoms in
Psychiatry, 2nd ed., pp. 82-90. John Wright Publication.
 Jaspers, K. (1959) General Psychopathology (tranl. Hoenig, J. & Hamilton, M.W.
from the German 7th edn, 1963). Manchester: Manchester University press.
 Kellner, R. (1985). Functional somatic symptoms and hypochondriasis. Archives
of general Psychiatry, 42, 821-33.
 Kiev, A. (1972). Transcultural Psychiatry. Harmondsworth: Penguin.
 Langfeldt, G. (1960). Diagnosis and prognosis of schizophrenia. Proceedings of
the royal society of medicine. 52, pp 595-596.
 Leading Article (1972). Depersonalization syndromes. British Journal Medical
Journal, 4, 378.
 Lishman, W.A. (1997). Organic Psychiatry: The Psychological Consequences of
Cerebral Disorder, 3rd edn. Oxford: Blackwell Scientific.
 Moerselli, E. (1886). Sulla dysmorfofobia e sulla tafefobi. Bolletino Accademia
delle Scienze Mediche di Genova VI, 100-119.
 Prince, M. (1905). The dissociation of a personality. New York: Longman.
 Oyebode, F. (2008). Self and Body. In: Sims’ Symptoms in the Mind: An
Introduction to Descriptive Psychopathology, 4th edn, pp. 215-284. Philadelphia,
Saunders.
 Oyebode, F. (2008). Conciousness and cognition. In: Sims’ Symptoms in the
Mind: An Introduction to Descriptive Psychopathology, 4th edn, pp. 39-64.
Philadelphia, Saunders.
 Ramachandran, V.S. & Blakeslee, S (1998). Do Martians see red? In: Phantoms
in the brain. Pp.227-257. London: Harper Collins publishers.
 Ropper, A.H & Brown, R.H (2005). Delirium and other acute confusional states.
In: Adams and Victor’s Principles of neurology. 8th edn, pp 355-366. New York:
McGraw-Hill Company.
 Sinha, V.K., Khan, A.H., Shailly. (2009) Seminar- Disorders of experience of self
and consciousness, Central Institute of Psychiatry.
 Scharfetter, C. (1981). Ego Psychopathology: the concept and its empirical
evaluation. Psychological Medicine. 11, 273-80.
 Scharfetter, C. (1995). The self experience of schizophrenics: Empirical studies
of the ego/self in schizophrenia, Borderline Disorders and Depersonalization.
Zurich: Private Publication.
 Schilder, p. (1935). The Image and Appearance of the human body; studies in
the Constructive Energies of the Psyche. London: Kegan Paul.
 Searle, J.R. (1994). The problem of consciousness. In Revonsuo, A. &
Kamppinen, M. (eds) Consciousness in philosophy and cognitive neuroscience.
Hillsdale: Laurence Erlbaum associates.

317
  Sedman, G. (1970). Theories of depersonalization: a reappraisal. British Journal
of Psychiatry, 117, 1-14.
 Sedman, G. (1972). An investigation of certain factors concerned in the aetiology
of depersonalization. Acta Psychiatrica Scandinavica, 48, 191-219.
 Sierra, M. and Berrios, G.E. (2001). The phenomenological stability of
depersonalization: comparing the old with the new. Journal of Nervous and
Mental Diseases, 189, 629-636.
 Sim, M. (1974). Guide to Psychiatry. Edinburgh: Churchill Livingstone.
 Simeon, D. & Abugel, J. (2006). Feeling Unreal. Oxford: Oxford university Press.
 Sims, A. (2003). Depersonalization. In: Symptoms in the Mind: An Introduction
to Descriptive Psychopathology, 3rd ed, pp. 231-240. Philadelphia, Saunders.
 Sims, A. (2003). Disorder of the Awareness of the Body. In: Symptoms in the
Mind: An Introduction to Descriptive Psychopathology, 3rd ed, pp. 241-271.
Philadelphia, Saunders.
 Sims, A. (2003). The Disordered Self. In: Symptoms in the Mind: An Introduction
to Descriptive Psychopathology, 3rd ed, pp. 241-271. Philadelphia, Saunders.
 Strub, R.L. & Black, F.W. (2000) The Mental Status Examination in Neurology,
4th ed, pp. 29-42.
 Todd, J. and Dewhurst, K. (1962). The significance of the Doppelganger
(hallucinatory double) in folk-lore and neuropsychiatry. Practitioner, 188, 377-82.
 Wing, J.K., Babor, T., Brugha, T. et.al. (1990). SCAN. Schedules for Clinical
Assessment in Neuropsychiatry. Archives of General Psychiatry, 47: 589–593.
 Wing, J.K., Cooper, J.E., Sartorius, N. (1974). Measure and Classification of
Psychiatric Symptoms: An Instructional Manual for the PSE and CATEGO
Programs. Cambridge: Cambridge University Press.
 World Health Organization (1992). The ICD 10 Classification of Mental and
Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva:
World Health Organization.
 Yager, J. & Gitlin, M.J. (2005) Clinical Manifestations of Psychiatric Disorders. In
Sadock, B.J. & Sadock, V.A. (Eds) Kaplan and Sadock’s Comprehensive
Textbook of Psychiatry, 8th edn, pp. 964-1002.
 Zeman, A. (2008) Consciousness: concepts, neurobiology, terminology of
impairments, theoretical models and philosophical background. In: G.B. Young,
E.F.M. & Wijdicks (eds) Handbook of Clinical Neurology. Vol. 90 (3rd series), pp
2-37. Elsevier B.V.

Glossary
 Alloaesthesia- sensory stimulation of one side of the body being perceived on the
contralateral side
 Anosognosia- is a form of disturbed body image in which the patient is not only
unaware but may even deny the existence of disability e.g. hemiplegia, paralysis of
the limbs and even blindness.
 Attention– Attention is the process that controls the focus and flow of information
processing.
 Attentional capacity- involves the idea that a given task makes a demand on a
limited pool of resources.
 Autoscopy (Heautoscopy, phantom mirror image) - It is a strange experience in
which the patient sees himself and knows that it is he. It is not just a visual
318
 hallucination but somatic and kinesthetic components are to be present to give an
impression of ‘I’.
 Body cathexis- implies the notion of power, force, libido-perhaps analogous to
electrical charge; the self that makes thing happen.
 Body image- is an individual's mental representation of his or her own body.
 Body schema- implies a spatial element and is more than, and usually bigger than,
the body itself.
 Concentration- sustained attention to internal stimuli.
 Consciousness- denotes first of all the actual inner awareness of experience,
secondly, it denotes a subject-object dichotomy (i.e. a subject intentionally directs
itself to objects which it perceives, imagines or thinks), thirdly, it denotes the
knowledge of a conscious self (self awareness).
 Déjà entendu- a sense that one has previously heard what is actually being heard for
the first time.
 Déjà pensé- a feeling that one has at an earlier time known or understood what is
being thought for the first time.
 Déjà vu- is the sense that one has previously seen or experienced what is transpiring
for the first time; it is a false impression that the current stream of consciousness has
previously been recorded in memory.
 Delirium- the acute confusional state, is usually characterized by a relatively abrupt
onset and short duration of clouded, reduced, and fragmented attention; impaired
memory and learning; perceptual and cognitive abnormalities, such as hallucinations
and delusions; disrupted sleep; and other autonomic dysfunction.
 Delusion of passivity- When patient explains this foreign control as the result of radio
waves, x-rays, television, witchcraft, and hypnosis.
 Depersonalization- is the term used to designate a peculiar change in the awareness
of self, in which the individual feels as if he is unreal.
 Derealization, a term to denote a change in the awareness of the external world, so
that the environment is experienced as flat, dull and unreal.
 Double phenomenon: doppelganger- The double or doppelganger phenomena are
an awareness of oneself as being both outside alongside, and inside oneself: the
subjective phenomenon of doubling.
 Double Orientation: The situation where a person appears to live in two world
simultaneously-psychotic as well as real.
 Dysmorphophobia – It was first defined by Morselli (1886) as ' subjective feeling of
ugliness or physical defect which the patient feels is noticeable to others, although
his appearance is within normal limits.
 Ego ideals- are fantasies of the optimum person one could ever wish to be.
 Exosomesthesia- Displacement of cutaneous sensation into extra personal space.
 Experience of passivity- when the patient merely asserts that his behavior is
controlled from without and be unable to give any further explanation.
 Extinction- Supression of one or more modality of stimuli from one side of the body.
 Gerstmann's syndrome- comprises finger agnosia, acalculia, agraphia and right/left
disorientation.
 Hemisomatognosia- there is a unilateral misperception of one's own body; the
patient behaves as though the limbs on one side are missing.
 Hemispatial neglect describes those patients, who, when asked to perform a variety
of behavioural tasks in space, neglect the hemispace contralateral to their lesion.

319
  Hyperschemazia – It is pathological accentuation of body image where the affected
limb feels larger and heavier.
 Hypochondriasis – refers to a concern with symptoms and with illness that the
outside observer regards as excessive. It describes that awareness in which the
person takes undue account of the symptomatic component of his sensorium.
 Hyposchemazia/Aschemazia– It is diminished or absent body image.
 Jamais vu- a sense where there is no sense of previously having seen a well-known
object.
 Lycanthropy- A state of possession where patient believes that he has turned out to
be an animal.
 Misoplegia- Hatredness towards a part of body (usually associated with left parietal
lesion)
 Multiple personality (Dissociative identity disorder)- Dual personality is not a
phenomenological description but simply implies that the outside observer (doctor)
sees more than one 'personality' manifested at different times by the same person
(patient).
 Neglect- Inattention to one side of body as well as extrapersonal environment.
 Orientation- refers to one's awareness of time, place and person.
 Paraschemazia– It is distortion of the body image which may occur with
enhancement or diminution of the body image.
 Palinaptia- Experience of tactile sensation outlasting the stimulus.
 Possession state- There is a temporary loss of both the sense of personal identity
and full awareness of the surroundings. The person acts as if he has, and believes
himself to have been, taken over by another- a spirit, a force, a deity or even another
person.
 Selective attention is that component which focuses a metaphorical spotlight on
external or internal mental representation.
 Self concept- refers to the fully conscious and abstract awareness of oneself.
 Self esteem- is believed to reflect how one measure up to the desired self image. It
is a measure of one's self appraisal in relation to one's values and ego ideals.
 Torpor- is a condition in which the patient is drowsy, falls asleep easily and shows a
narrower range of perception and slowed thinking.
 Unconscious- means something that is not an inner existence and does not occur as
an experience; secondly, something that is not thought of as an object and has gone
unregarded; thirdly, it is something which has not reached any knowledge of self.
 Vigilance- sustained attention to external stimuli.

PRESENT STATE EXAMINATION (Wing, 1974)

11. Derealisation and depersonalisation

Have you had the feeling recently that things around you were unreal?
Have you yourself felt unreal, that you were not a person, not in the living world?

12. Other perceptual disorders (not hallucinations)

Do you ever get the feeling that something odd is going on which you can’t explain?

320
Does your imagination sometimes play tricks on you? Is there anything unusual about the
way things look or sound, or smell, or taste? In what way?
Do sounds seem unnaturally clear or loud, or things look vividly coloured or detailed?
Do things seem dark or grey or colorless?
Does the appearance of things or people change in a puzzling way: e.g. distorted shape or
size or colour?
Do you think your own appearance is normal?
Does your experience of time seem to have changed?
Do you feel you have lost your emotions in some way?

SCAN (Wing, 1990)

2.084 Somatoform or hypochondriacal preoccupation
What do you yourself thing is wrong?
How many doctors have you consulted in the past 2 years?
- What investigations were made? With what results?
- How many sets of investigations?
- Why do you think there is something physically wrong?
- Do you think you have a serious disease?
- Have you been dosing yourself with any medications?
- What medication do you take?
- Do you think you have a defect in your appearance or a deformity?

2.086 Somatoform or hypochondriacal belief

Has medical reassurance convinced you that nothing is wrong?
- Have you told the doctors about this? (What do they say?)
- Did you feel relieved when they said nothing was wrong?
- Can’t you stay reassured when the doctor/expert assures you that nothing is wrong?
Trance experience
Have you experienced being in state of altered consciousness or a trainer
- Did you lose your sense of personal identity?
- Were you les aware of your general surroundings?
- Was your attention focused on a single thing?
- Did you repeat the same movements or words?
- Were you “frozen” to a certain position?
- Was it troublesome for you?
- Did you want it to happen?
If trance experience initially welcomed:
- Did the trance continue without your wishing it?
- Did it start at a religious or social occasion?

2.107 Possession experience

Have you had the experience of being taken over by some influence or power?
- By what? A spirit, deity, person?
- Can you describe the experience?
- Did you lose your sense of personal identity?
- Did you want it to happen?

321
CHAPTER-XVI
 MOTOR DISORDERS
_________________________________________________________________

INTRODUCTION:

Motor behaviors are the coordinated patterns of activities to facilitate daily living. They are
the source for monitoring the functioning of living and an agent to facilitate communication.
Abnormal movements have been recognized as aspects of behavioral illness for millennia,
and all severe psychiatric conditions are associated with changes in motor functioning.
These changes vary in intensity and frequency and so help demarcate between normal
phenomena and psychiatric conditions. Motor behavior plays significant role in expression,
whether verbal or non-verbal, and in this way helps to process the information in emotional
tone. When we talk about expressing self, speech becomes a major issue as it is part and
parcel of expression, which is a kin to motor system. So any discussion exclusive for motor
disorder can be a theoretically possible exercise but practically it is not feasible to discern
these intermingled psychic activities.

CLASSIFICATION OF MOTOR DISORDERS:

Motor disorders as a manifestation of disturbances in psychic phenomenon cannot be

concretely classified, as they often blend with neurological problems. Though there are
various classifications of motor disorder, here we will discuss the classification given by
Hamilton (1985).

Classification of Disorders of movement (Hamilton, 1985)

 Disorders of adaptive movements
a) Disorders of expressive movement
b) Disorders of reactive movements
c) Disorders of goal-directed movements
 Disorders of non-adaptive movements
a) Spontaneous movements
b) Abnormal induced movements
 Motor speech disturbances
 Disorders of posture
 Abnormal complex patterns of behavior
a. Non-goal-directed abnormal patterns of behavior
b. Goal-directed abnormal patterns of behavior
 Movement disorders associated with antipsychotic medication

322
DISORDERS OF ADAPTIVE MOVEMENTS
a) Disorders of expressive movement

Expressions are the manifestation of psychic process which usually involves face, arm,
hands and the upper trunk. The concept of catatonia was formulated and the illness named
by the German clinician Karl Ludwig Kahlbaum, who formulated it as “a brain disease with a
cyclic, alternating course, in which the mental symptoms are consecutively, melancholy,
mania, stupor, confusion, and eventually dementia”. The catatonic has a stiff
expressionless face and the expressive movements of the body are scanty. Often the eyes
appear to be lively, so that the patient appears to be looking at the world through the mask.
Currently, catatonia is conceptualized as a syndrome of specific motor abnormalities closely
associated with the disorders in mood, affect, thought, and cognition. Snout spasm’
(Schnauzkrampf), is a disorder of expression, and is best regarded as stereotyped posture
in which “pouting of lips to bring them closer to nose” is seen. It is a common abnormal
facial expression which consists of a marked wrinkling of the nose with pouting of the lips,
so that the lips look very much like an animal snout. Patients with depression tend to have a
limited range of expressive movements. Some might try to mask their depression by
smiling; this is termed ‘smiling depression’. In agitated or anxious depression, the patient
may be restless and apprehensive.
 Veraguth fold: The main fold in upper lid is angulated upwards and backwards at
the junction of the inner third with the middle third of the folds; seen in depression.

 Omega sign: The occurrence of a fold like the Greek letter omega in the forehead
above the root of the nose produced by the excessive action of the corrugator
muscle. It was described by Athanassio; seen in depression.
In mania, expressive movements are exaggerated. In milder ecstatic states the patient may
preach or lecture in a high-flown way. Ecstasy is found in happiness psychosis,
schizophrenia, epilepsy and abnormal personalities with the appropriate religious training.
In ecstasy, psychomotor activity decreases.

b) Disorders of reactive movements

Reactive movements are immediate automatic adjustments to new stimuli, as
needed in response to a threat or while attending to source of a percept. These
movements are affected in the inhibited phase of motility psychosis, obstruction in
catatonia, and Parkinsonism. These movements give an indication of alertness and
get affected in the disturbances of affect and other neurotic conditions too like
disorders under anxiety spectrum. Person with a marked anxiety may react in a way
which is out of keeping with the situation at hand. Increase in startle reflex can also
be seen.

c) Disorders of goal-directed movements

Any kind of movement is initiated to meet the desired end whether related to daily
living as to hold a glass from a table or to complex task of driving which needs the
help from various modalities. These movements are intentional purposeful

323
 movements which are called voluntary movements. Usually all these movements are
carried out without any deliberate awareness on the part of the patient. These
movements reflect personality as well as the current mood state of the subject but
when these voluntary movements are seen in reference to mental illness, they are
often seen to be performed with difficulty. It can be categorized under following
heads:

 Psychomotor retardation
 Obstruction (Blocking or Sperrung)
 Mannerism

 Psychomotor retardation: Psychomotor retardation or psychomotor impairment

comprises a slowing down of thought and a reduction of physical movements in an
individual. The expression varies with the degree of severity of an illness. Examples
of psychomotor retardation may include the following:

 Unaccountable difficulty with carrying out what we usually consider as

"automatic" or "mundane" self-care tasks for healthy people (i.e., without
depressive illness), such as taking a shower, putting on clothes, self-grooming,
preparing food, brushing teeth and exercising.

Obstruction: Also known as Blocking or Sperrung. By definition it is an obstacle which

occurs in catatonia and gives rise to an irregular hindrance to motor or psychic activity. It
can be defined as irregular stroboscopic movement in perception, in which the patient
would not be able to initiate the movement depending upon the will but with the chance
factor. Kleist described that the cardinal feature of the obstruction is the “reaction at the last
moment”. As the severity increases it gradually ascends to akinesia and then even to
stupor. The patient stops suddenly in the course of a movement and is generally unable to
give a reason. This appears to be the motor counterpart of thought block.
“Psychomotor retardation has been compared with the uniform slowing down of a vehicle
produced by the steady application of a brake, while obstruction has been compared with
the effect of putting a rod between the spokes of a moving wheel.”

 Mannerism: Mannerisms are odd, stylized movements, usually specific to the

subject and sometimes apparently suggestive of special meaning or purpose (WHO,
1998).They are repeated movements that appear to have some functional
significance. Unusual repeated performances of a goal directed motor action or the
maintenance of an unusual modification of an adaptive posture are known as
mannerisms (Hamilton, 1985). Example are saluting, holding hands as if they were
handguns, peculiarities in dressing, hair style, etc. So it can be stated that an
ordinary gesture or expression that becomes abnormal through exaggeration or
repetition. So the cardinal feature of mannerism are:
 Unusual repetition
 Exaggeration of normal and adaptive act
 Personal significance

324
  Goal- directed
Though mannerism is of no diagnostic significance in schizophrenia, but it
should always be taken carefully that whether it is resulting from delusional
idea of the patient which is being manifested as a catatonic motor disorder.
Whereas in non psychotics, it is seen when the individual feels the need to be
noticed and lacks self confidence.

DISORDERS OF NON-ADAPTIVE MOVEMENTS

a) Spontaneous movements are automatic movements, balanced by the sympathetic

and parasympathetic nervous systems, and are called involuntary movements. The
pumping of the heart, the breathing and the peristaltic movement of stomach and
intestines are all examples of this 'natural spontaneous movement'. The different
types discussed are:

 Tic is a brief movement that is generally repeated in space (same muscle groups)
but is irregular in times. The characteristic feature of tic is that the movement is
usually preceded by an urge to move, and it can be suppressed for a short time
(about 30-60 sec) by voluntary effort (Joseph & Young, 1999) A tic is a sudden,
rapid, recurrent, non-rhythmic, stereotyped motor movement or vocalization. Motor
and vocal tics may be simple (involving only a few muscles or simple sounds) or
complex( involving multiple groups of muscles recruited in orchestrated bouts or
words and sentences)
 Simple motor tics- are eye blinking, nose wrinkling, neck jerking, shoulder
shrugging, facial grimacing, and abdominal tensing. These tics usually last
less than several hundred milliseconds.
 Complex motor tics- include hand gestures, jumping, touching, pressing,
facial contortion, twirling when walking, and assuming and holding unusual
postures. These tics are longer in duration, lasting seconds or longer
(APA,2000)
Tics generally are experienced as irresistible but can be suppressed for
varying lengths of time.Tics generally decrease or stop during sleep, although
some individuals have occasional tics while asleep or awaken suddenly with a
tic. Tics are regarded as psychogenically determined motor habits, or these
may be manifestations of emotional tension in constitutionally predisposed
individuals
The cardinal features of tics are: Irregular repetition, involuntary, usually
accompanied with premonitory urge, and reduces in sleep.

 Tremor is a repetitive rhythmic movement that is consistent in time and space. The
most common cause is essential tremor; followed by idiopathic parkinsonism (Fink
and Taylor, 2003). Tremor is an involuntary, somewhat rhythmic, muscle contraction
and relaxation involving to-and-fro movements (oscillations or twitching) of one or
more body parts. It is the most common of all involuntary movements and can

325
 affect the hands, arms, eyes, face, head, vocal cords, trunk, and leg. Tremors are
classified as normal (or physiologic) and abnormal (or pathologic). It can be rest
tremor (Parkinson’s disease tremor) or action tremor. Action tremors again can be of
two types: postural tremor (Physiologic tremor, Essential tremor, Drug-induced
tremors) and kinetic tremor (Intention tremor and Task-specific tremor) (Ropper &
Brown, 2005).

 Chorea is a quick, irregular, and predominantly distal involuntary movement. The

term ‘semi purposive’ has been used to facilitate its identification. The word chorea
derives from the Greek word for dance, and often the movements resemble dancing
gestures of the limb (Fink and Taylor, 2003). Chorea is an irregular, rapid,
uncontrolled, involuntary, excessive movement that seems to move randomly from
one part of the body to another. In some cases an attempt to make them move
makes the condition even worse. These jerky movements resemble fragments of
expressive or reactive movements.

 Athetosis is a condition in which the spontaneous movements are slow, twisting and
writhing, which bring about strange postures of the body, especially of the hands
(Hamilton, 1985). This term stems from a Greek word meaning “unfixed” or
“changeable”. The maintained posture is interrupted by relatively slow, sinuous,
purposeless movements that have a tendency to flow into one another (Ropper &
Brown, 2005). It is a term which is now seldom used; such movements are now
referred to as dystonia. Choreoathetosis is a movement of intermediate speed,
between the quick, fleeting movements of chorea and the slower, writhing
movements of athetosis.

 Parakinesia is a term used by Kleist (1943) to describe the occurrence in catatonic

schizophrenic patients of motor activity which is reminiscent of, but somehow
different from chorea, athetosis, and tics. It consists of a continuous irregular
movement of the musculature so that patients with this symptom grimace, twitch,
and jerk continuously. Patients are usually referred to as parakinetic catatonic, and
the older psychiatrist used to call the behavior as ‘clown like’( Hamilton,1985)

 Stereotypy is a repetitive, seemingly driven, and nonfunctional motor behavior

(APA, 2000). They are repeated movements that are regular (unlike tics) and without
any obvious significance (unlike mannerism), for example, rocking to and fro. In
simple stereotypy, the subject performs certain repetitive movements such as
rubbing the head round and round with one hand, audible grinding of the teeth,
nodding the head round and round with a hand. It also includes tics. These
movements do not appear to have any special significance (WHO, 1998). It is

326
 required to be distinguished from agitation. Unlike mannerism, stereotypy is an
abnormal, non- adaptive, non-goal directed and senseless act.

b) Abnormal induced movements: It can be classified under two headings namely:

 Undue compliance on the part of the patient
 Rejection of an environment

Undue compliance on the part of the patient: It is categorized under the following heads
namely-

Automatic Obedience (also called command automatism) is an exaggerated cooperation

with examiner’s request, or repeated movements that are requested once (Bush et al,
1996). The patient carries out every action regardless of the consequences (Hamilton,
1985). How to examine: Reach into pocket and state, ‘stick out your tongue, I want to stick
pin into it’. (Bush et al, 1996)

 Echophenomena: are the spontaneous mimicry of the examiner’s movements or

repetition of his statement
1. Echopraxia is the repetition by imitation of movements of another.
The action is not a willed or voluntary one and has a semiautomatic
and uncontrollable quality (APA, 2000). Raising an arm over the head
is imitated, the patient raising his right arm as the examiner raises his
left. Patients do not know why they make these movements and they
usually give a silly or inadequate reason for it, denying their illness.
Study by Chapman and McGhie on schizophrenic patients revealed
that echopraxia usually happens when the patient is trying to
communicate with another person, and is more common when he
finds it difficult to communicate verbally. Three types of echopraxia
has been mentioned corresponding to the different stages of imitation
in childhood described by Piaget: Completely automatic echopraxia,
Echopraxia to memory images and Voluntary echopraxia.
How to examine: Examiner scratches head in exaggerated manner
while conversing with the patient. (Bush et al, 1996)

2. Echolalia is a pathological, parrot like, and apparently senseless

repetition of a word or a phrase just spoken (APA, 2000). Jasper
(1962) describes it as repetition of everything patient hears in a
parrot-fashion. It can also be present in developmental disorders as
autism. There are two types of echolalia, namely immediate and
delayed echolalia. Immediate echolalia appears to tap into the
person's short-term memory for auditory input. This is defined as the
repetition of a word or phrase just spoken by another person.
Delayed echolalia appears to tap into long-term auditory memory,

327
 and for this reason, may be a different phenomenon from immediate
echolalia. Because it can involve the recitation of entire scripts,
delayed echolalia is often thought to denote evidence of near-genius
intellect. There are two described categories of delayed echolalia: No
communicative repetition and communicative repetition.
The patient echoes a part or the whole of what has been said to him,
irrespective of whether he understands them or not. It could be the
result of disinhibition of a childhood speech pattern.

 Echologia (Kleist, 1943): The patient replies to questions by echoing the content of
the questions in different words.

 Perseveration is a senseless repetition of a goal-directed action, which has already

served its purpose (Hamilton, 1985). It can be understood under phenomenon
categorized as;
1. Pathological repetition of the same response to different stimuli, as in a
repetition of the same verbal response to different questions.
2. Persistent repetition of specific words or concepts in the process of speaking.
Seen in cognitive disorders, schizophrenia, and other mental illness.
Freeman & Gathercole (1966) studied perseveration in schizophrenia, arteriosclerotic
dementia and senile dementia. They described three types of perseveration:
 Compulsive repetition, in which the act is repeated until the patient receives
another instruction. Seen more commonly in schizophrenia.
 Impairment of switching, in which the repetition continues after the patient has
been given a new task. Seen more commonly in dementia.
 Ideational perseveration, in which the patient repeats words and phrases
during their reply to a question.
Manifestation of perseveration when speech is affected, due to coarse brain
disease, can be of two types (Hamilton, 1985)
Logoclonia- The last syllable of the last word is repeated.
Palilalia- Patient repeats the perseverated word with increasing frequency.
Perseveration can be distinguished from stereotypy by the fact that the
stereotypy is an abnormal, non-adaptive act whereas perseveration is a
repetition even when the purpose is served. Stereotypy is non-goal directed
whereas perseveration is goal directed. Stereotypy is spontaneous but
perseveration is an induced movement.

Mitmachen (cooperation) is also a form of an extreme compliance on the part of the

patient. In this despite the instruction to the patient for non-compliance, the patient’s body
can be put in any position without any resistance. It is usually found in catatonia and other
neurological diseases. It occurs when the patient acquiesces in every passive movement of
the body made by the examiner.

328
Mitgehen (going along with) is another kind of excessive compliance in which the
examiner is able to move the patient’s body with the slightest touch, but the body part
immediately returns to the previous position, unlike waxy flexibility. It is also known as the
“anglepoise effect” or “angle poise lamp sign” (Hamilton, 1985). It can be called as an
extreme form of mitmachen.

How to examine: The examiner puts his forefinger under the patient’s arm and raises
gently after stating ‘do not let me raise your arm’, whereupon the arm moves upwards in the
direction of the pressure.

1. Forced grasping is a phenomenon in which the patient forcibly and repeatedly grasps
the hands of an examiner when offered. It is an involuntary flexion of the fingers to
tactile or tendon stimulation on the palm of the hand, producing an uncontrollable grasp;
which is usually associated with frontal lobe lesions. Commonly seen in chronic
catatonia and dementia.

How to examine: It is demonstrated when the examiner offers his hand to the patient and
the patient shakes it. Then the examiner explains that on all future occasions when the
examiner offers his hand the patient should not touch it. After this, the examiner talks to the
patient for a few minutes and then offers the patient his hand. If forced grasping is present,
the patient shakes the examiner’s hand. Despite frequent instructions not to touch the
examiner’s hand the patient continues to do so.

Alternatively, it may be elicited by lightly stroking the patient’s finger tips, despite repeated
instructions not to grasp the examiner’s hands the patient grasp it invariably (Taylor &
Vaidya, 2009).

 Magnet reaction is a reflex in which light finger pressure on a toe pad causes a slow
reflex contraction in the lower extremity, which seems to follow the examiner's hand, as
if drawn by a magnet.

 Negativism: Patient resists examiner’s manipulations, whether light or vigorous, with

strength equal to that applied, as if bound to the stimulus of the examiner’s action.
Negativism occurs when the subject consistently does the opposite of what is asked,
e.g. asked to open the hands, it is closed tighter (WHO, 1998). Negativism may or may
not be associated with a defensive attitude. It can be of two types namely:
 Passive negativism: When the patient does not follow the given command and
resist any kind of interference
 Active or command negativism: When the patient not only resists the command
given, but also does the opposite of what is said.

How to examine: The examiner takes the patient’s hand and arm and moves the patient’s
arm horizontally back and forth, with varying degrees of force.

 Ambitendency is a phenomenon in which the patient alternates between resistance

to and cooperation with the examiner’s instructions; for example, when asked to

329
 shake hands, the patient repeatedly extends and withdraws the hand. Patient
appears “stuck” in indecisive, hesitant motor movements (Bush et al, 1996). It can be
regarded as a mild variety of negativism or as the result of obstruction.

How to demonstrate: The examiner offers a hand, as if to shake hands, and firmly
tells the patient “Don’t shake my hand. I don’t want you to shake it.” The patient
moves their hand towards the examiner’s hand, stops, starts moving the hand, stops,
and so on, until the hand finally comes to rest without touching the examiner’s hand
or at maximum lightly touching the examiner’s hand (Bush et al, 1996; Fink & Taylor,
2003).

“In ambitendency due to obstruction a series of tentative movements is followed by

perseveration of posture. Whereas when ambitendency is result of partial breakdown of the
negativistic attitude such perseveration is not noted.”

DISORDERS OF POSTURE

Abnormality in the posture can be seen under various circumstances. It can be defined
under the grounds of psychiatric conditions as schizophrenia, severe anxiety or due to
personality variables.

 Manneristic posture: A manneristic posture is an odd stilted posture that is an

exaggeration of a normal posture and not rigidly preserved.

 Stereotyped posture: It is an abnormal and non-adaptive posture that is rigidly

maintained.

Psychological pillow is a dramatic posture, in which the supine patient lies with head and
shoulders raised as if resting on a pillow. The patient assumes a reclining posture, with their
head a few inches above the bed surface, and is able to maintain this position for prolonged
periods. The exact point at which a postural mannerism becomes a stereotypy may be
difficult to decide.

 Perseveration of posture: The patient persists with a particular movement that has
lost its initial significance. The patient allows the examiner to put his body into
strange uncomfortable positions and then maintains such postures for at least one
minute and usually much longer (Hamilton, 1985).

 Posturing: Patient is able to maintain the same posture for long periods. The
classic example of posturing is “crucifix”. Other examples are sitting with upper and
lower portions of the body twisted at the right angle, holding finger and hands in odd
position. So it can be called as a spontaneous maintenance of postures for extended
period of time. Bizarre posture can also be seen. This has been kept synonymous
with catalepsy (Bush et al, 1996).

 Waxy flexibility (flexibilitas cerea): The examiner is able to position the patient in
what would be highly uncomfortable postures, which are maintained for a
considerable period of time. During reposturing of patient, patient offers initial
330
 resistance before allowing himself to be repositioned, best felt during reposturing of
patient (Bush et al, 1996).

 Catalepsy: Maintains posture, including mundane (e.g., sitting or standing for

long periods without reacting) (WHO, 1998). It is a condition in which a person
maintains the body position in which he is placed, observed in severe cases of
catatonic schizophrenia. Catalepsy usually lasts for more than one minute and
ends with the body slowly sinking back into the resting position. It is often very
variable and may even disappear for a day or so only to return again. Unlike
waxy flexibility, in catalepsy when the examiner releases the body those
muscles which fixes the body in the abnormal position can be felt to contract.

How to examine:

 Patient must always be told at first that they are not obliged to leave their body in the
position in which it is put by the examiner.
 It has to be evoked by putting the patient’s arm in a comfortable position, and if this
is maintained, the arm is put into a series of unusual positions each of which is more
uncomfortable than the previous one, so that finally the patient will preserve very
strange postures.
 If gentle passive movements fail to elicit catalepsy, it can sometimes be evoked by
moving the arm or limb more firmly into a strange position.

ABNORMAL COMPLEX PATTERNS OF BEHAVIOR

a) Non-goal-directed abnormal patterns of behavior: The two important patterns of

behavior of this type are:

 Stupor: Unresponsiveness, hypoactivity, and reduced or altered arousal during

which the patient fails to respond to queries, when severe, the patient is mute,
immobile, and does not withdraw from painful stimuli (Fink & Taylor,2003).The lack
of responsiveness can be explained on the basis of psychomotor inhibition or
obstruction. Bumke defined stupor as a “state of more or less complete loss of
activity with no reaction to external stimuli”. Stupor can be seen under the conditions
of depression, catatonia, epilepsy, cycloid psychosis and coarse brain disease. It is
further classified as;

 Psychogenic stupor: It may occur in the setting of severe psychological shock.

The patient appears as if ‘paralyzed with fear’ and is unable to retreat from
danger – can be terminated by sedation and reassurance.
 Hysterical stupor: It emerges as an acute psychogenic reaction to severe
trauma and then becomes a goal-directed reaction. It is presented by the subject
for some gains, although he is not fully aware of his hidden motivation. It tends to
occur in appreciation needing personality.

331
  Catatonic stupor: In this muscle tension is permanently increased or it varies
from time to time and is associated with obstruction. Significant features are
“dead-pan” facial expression, changes in muscle tone, catalepsy, stereotypies
and incontinence of urine.

 Excitement: It can characterize as an extreme hyperactivity, constant motor unrest

which is apparently non-purposeful. This is not to be attributed to akathisia or goal-
directed agitation (Bush et al, 1996). It is usually manifested as secondary to other
psychological illness. Psychogenic excitements may be acute reactions or goal-
directed reactions.
 Acute reactions: Predisposed subjects may react to moderately stressful
situations with senseless violence. Chaotic restlessness rather like a ‘storm of
movement’ may occur in susceptible subjects during catastrophes, and in
unsophisticated and mentally subnormal persons subject to mild stress.

 Goal-directed reactions: Excitement is part of attention-seeking behavior. Even

during severe excitement, it is usually possible to make contact with these
patients and interrupt the over activity. They seem eager to be punished and
enjoy a good fight.

 Excitement in depression: Moderately severe agitated depression: takes a

mechanical form; patient wanders about restlessly and bewail his fate
monotonously though in severe agitation the patient wrings his hands
continuously, sits up in bed, rocks to and fro and laments; sometimes picking the
hair, rubbing the face or pulling the hair; the total picture is one of abject misery.

 Catatonic excitement: In such patients body movements are often stiff, stilted
and violence is usually senseless and purposeless (Hamilton,1985)

b) Goal-directed abnormal patterns of behavior: Abnormal patterns of behavior of

this type occur in nearly all psychiatric syndromes:

 Compulsive rituals: These are characteristic of obsessive compulsive disorder, and

are the motor act results from obsessions. Often manifested in the forms of cleaning,
checking and repeating.

 Brutal and aggressive behavior: It is often socially determined. Many a times in

conditions like schizophrenia, it is manifested because of the involvement of
hallucinations, persecution or referential ideas, or assuming others as a part of
delusional system. In mood disorders too, it is very much likely to be manifested
either due to elevation of mood itself or due to accompanied psychosis.

332
  ‘Extended suicide’: It is a condition in which the patient with delusional depression
murders his children in the mistaken belief that they have incurable inherited insanity
or some foul disease. The children are therefore murdered in the mistaken belief that
they would be ‘better off dead’.

 Disinhibition resulting from organic brain disease, mania or schizophrenia may give
rise to promiscuous behavior, leading to increased risk of pregnancy and sexually
transmitted disease.

 Dissociative fugue: It is characterized as a fugue state, formally Dissociative

Fugue, previously called Psychogenic Fugue. It is a rare psychiatric disorder
characterized by reversible amnesia for personal identity, including the memories,
personality and other identifying characteristics of individuality. Dissociative fugue
usually involves unplanned travel or wandering, and is sometimes accompanied by
the establishment of a new identity.

MOVEMENT DISORDERS ASSOCIATED WITH ANTIPSYCHOTIC MEDICATION

Antipsychotic medications have been associated with a range of movement disorders. They
can generally be divided into those that occur acutely and those that occur late in treatment
(tardive). The movement disorders can be grouped into the relatively acute neuroleptic-
induced disorders (acute dystonia, Parkinsonism, and akathisia) and neuroleptic-induced
Tardive Dyskinesia and other tardive phenomena. Neuroleptic malignant syndrome (NMS)
and medication-induced postural tremor are other drug induced movement disorders
warranting our focus.

 Drug induced dyskinesia: It can be applied to any type of involuntary movement

but is most frequently employed for the rather complex choreic and dystonic
movements that occur after the prolonged treatment with neuroleptics. The term
neuroleptic means “that which takes neurons” was coined by Deniker. It occurs in the
form of stereotypy, defined as repetitive, coordinated, seemingly purposeful
movements, other drug –induced dyskinesias are manifested by dystonia, chorea,
tics, tremors and miscellaneous involuntary movements.

 Acute dystonia: Acute dystonic reaction is sustained, repetitive, patterned, muscle

spasm resulting in twisting, squeezing, pulling, and often painful posturing. The
symptoms may occurs within hours after administration of the offending drug and
may be the first extra-pyramidal side effect encountered with the neuroleptic.

 Acute and tardive akathisia: The term akathisia (not sitting) was first introduced by
Haskovec in 1901 to describe individuals unable to remain in a seated position.
Akathisia may occur within the first three months of neuroleptic therapy and may
persist as tardive akathisia even when the offending drug is stopped. It is

333
 characterized by a subjective feeling of restlessness accompanied by motor
stereotypies. The restlessness has been described using such phrases as
“nervousness” (Joseph & Young, 1999).

 Tardive dyskinesia: It is a distortion of voluntary movements with involuntary

muscular activity.The American Psychiatric Association Task Force defines tardive
dyskinesias as abnormal involuntary movement resulting from treatment with a
neuroleptic drug for three months in a patient with no other identifiable cause for
movement disorder (Joseph & Young, 1999). The essential features of neuroleptic-
induced tardive dyskinesia are abnormal, involuntary movement of the tongue, jaw,
trunk, or extremities that develop in association with the use of neuroleptic
medication. The mvements are present over a period of at least 4 weeks and may be
choreiform (rapid, jerky, non repetitive), athetoid (slow, sinuous, continual), or
rhythmic (e.g., stereotypies) in nature. The signs or symptoms develop during
exposure to a neuroleptic medication or within four weeks of withdrawal from an oral
(or within 8 weeks of withdrawal from a depot) neuroleptic medication (APA,
2000).Tardive dyskinesia is often a persistent disorder, but spontaneous remissions
are frequently encountered, particularly in the younger population.

 Tardive tremor: It is a relatively rare form of tardive dyskinesia. This rhythmic

movement is distinguishable from the more common stereotypy in that it consists of
an oscillatory movement rather than coordinator, seemingly purposeful movement
seen in tardive stereotypy. Tardive tremor differs from tremor observed in patients in
parkinsons disease in that it is predominantly postural and kinetic and it is not
necessarily accompanied by other parkinsonian signs.

 Tardive Dystonia: It is a persistent dystonic movement disorder and therefore it

differs from acute transient dystonic reaction. Criteria for its diagnosis include the
presence of chronic dystonia, prior or concurrent neuroleptic use, exclusion of non
causes of secondary dystonia, and a negative family history for dystonia. It is
characterized by sustained, slow or rapid twisting movements involving the face,
neck, trunk, or limbs, tardive dystonia may occur after only three days of
antipsychotic treatment, but usually it follows months of neuroleptic therapy.

 Tardive tourettism: Gilles de la Tourette syndrome is a neurobehavioral disorder

characterized by motor and phonic tics and a variety of behavioral problems (Joesph
& Young, 1999). Motor tics are coordinated involuntary movements occurring in
patterned sequences in a spontaneous, unpredictable, abrupt, and transient manner.
Involuntary vocalizations, repetition of words as phrases (echolalia), use of
obscenities (coprolalia), and mimicking of gestures (echopraxia) often occurs in the
patient with Tourette syndrome.

 Tardive Myoclonus: Myoclonus, a jerk- like contraction of muscle group may be

rhythmic or arrhythmic, arising from cortical, subcortical, and spinal cord structures.
Myoclonus must be differentiated from other movement disorders. Tics differ from

334
 myoclonus in that tics can be voluntarily controlled and are more complex
movements. Dystonic contractions are more prolonged and often twisting whereas
myoclonic jerks are brief and simple. Tremors are oscillatory movements that
differentiate them from rhythmic myoclonus which are secondary to repetitive agonist
muscle contractions. Myoclonus differs from chorea in that chorea is a random flow
of brief contractions.

 Neuroleptic Malignant Syndrome: (NMS) was first described by Delay and Deniker
in 1968, and is believed to be a consequence of impaired hypothalamic and striatal
dopamine transmission or sudden withdrawal from dopamine therapy. NMS is
characterized by hyperpyrexia, muscular rigidity, autonomic dysfunction, and
alternations in consciousness.

 Serotonin Syndrome: Concurrent administration of SSRI with a MAO inhibitor, L-

tryptophan, or lithium can raise plasma serotonin concentrations to toxic levels,
producing a constellation of symptoms called the serotonin syndrome. Serotonin
syndrome is composed of Diarrhea, Diaphoresis, Tremor, Ataxia, Myoclonus,
Hyperactive reflexes, Disorientation, and lability of mood (Sadock and Sadock,
2007).

 Rabbit Syndrome: The rabbit syndrome is another neuroleptic drug induced

disorder. It is probably best conceptualized as an acute EPS phenomenon. It was
first described in 1972 as “perioral muscular movements strikingly imitating the rapid,
chewing-like movements of a rabbit’s mouth.” These movements did not involve the
tongue and were limited exclusively to the territory of the oral and masticatory
muscle. This clinical picture was immediately labeled “the Rabbit syndrome”. The
primary signs of rabbit syndrome involve rapid perioral movements. These are
principally in the vertical plane and do not involve horizontal, or rotator jaw motions.

MOVEMENT DISORDERS DIAGNOSED IN CHILDHOOD AND ADOLESENCE

As such there is no separate classification of motor disorders in either of the classificatory

systems. The different movement disorders are usually the accompanying features of other
major psychiatric disorders, hence a meticulous effort for the motor components shall be
attempted so as to make them stand clear (APA,2000)

1. Developmental coordination disorder: It is a motor skills disorder, defined as

marked impairment in the development of motor coordination being displayed in daily
activities like poor handwriting, clumsiness, dropping things etc. which may be due to
marked delays in achieving motor milestones. It may be manifested in speech and
language, fine motor controls and whole body coordination such as:
 Using a knife and fork, fastening buttons and shoelaces, cooking, brushing one's
teeth, applying cosmetics, styling one's hair, opening jars and packets, locking
and unlocking doors, shaving and doing housework.

335
  Poor timing, poor balance (sometimes even falling over in mid-step), tripping over
one's own feet is also not uncommon, as well as difficulty combining movements
into a controlled sequence.

2. Repetitive behaviors : Usually a salient characteristic of pervasive developmental

disorders, they are basically found in autism, which are categorized in the following
forms:
 Stereotypy: Is defined as repetitive movements like hand flapping, making
sounds, head rolling, or body rocking. Stereotypies are periodic and patterned
and are made worse in fatigue, stress and anxiety, usually begins before the age
of three, involves more of the body, are more rhythmic and less random, and are
associated more with engrossment in another activity rather than premonitory
urges.
 Compulsive behavior: It is a behavior which the individuals perform not
because they want to but because they have to. Compulsive behavior is intended
and appears to follow rules, such as arranging objects in stacks or lines.
 Sameness: It is defined as the resistance to change; for example, insisting that
the furniture not be moved or refusing to be interrupted.
 Ritualistic behavior: Rituals are a set of actions, performed mainly for their
symbolic value. These behaviors involve an unvarying pattern of daily activities,
such as an unchanging menu or a dressing ritual. This is closely associated with
sameness and an independent validation has suggested combining the two
factors.
 Restricted behavior: Is limited in focus, interest, or activity, such as
preoccupation with a single television program, toy, or game.
 Self-injury: Basically defined as the intentional, deliberate act of harming
oneself without aim of suicide. Here it includes movements that injure or can
injure the person, such as eye poking, skin picking, hand biting, and head
banging.

3. Tic disorder: It is a sudden, rapid, recurrent, nonrhythmic stereotyped motor

movement or vocalization. It may be simple (eye blinking, shoulder jerking, clearing
throat, grunting etc) or complex (jumping, stomping, sudden and spontaneous
expression of single word or phrases, eg- speech blocking; or meaningless changes
in pitch or volume of speech eg-palilalia, coprolalia). Four disorders are included in
this:
 Tourette’s disorder: Its essential features are multiple motor tics and one or
more vocal tics. The tics occur many times in a day, recurrently throughout a
period of more than a year, with no tic free period of more than three consecutive
months. The onset is before age 18.
 Chronic motor or vocal tic disorder: It is characterized by single or multiple
motor or vocal tics, but not both, that have been present at some time during the
illness. The severity of symptoms and functional impairment are usually much
less.
 Transient tic disorder: It incorporates single or multiple motor and/or vocal tics
that occur many times a day, almost daily for at least four weeks but not more
than a year. Its course may be indicated by specifying single or recurrent.
 Tic disorder NOS: Includes disorders characterized by tics that do not meet the
criteria for a specific tic disorder.

336
 4. Stereotypic movement disorder: This is an independent disorder under the
heading ‘other disorders of infancy, childhood or adolescence’. It is a disorder of
childhood involving repetitive, nonfunctional motor behavior (e.g., hand waving or
head banging), that markedly interferes with normal activities or results in bodily
injury, and persists for four weeks or longer. The behavior must not be due to the
direct effects of a substance or another medical condition. In cases when mental
retardation is present, the stereotypic or self-injurious behavior must be of sufficient
severity to become the focus of treatment. The behavior is not better explained as a
compulsion (e.g., OCD), a tic, a stereotypy as part of a Pervasive Developmental
Disorder, or hair pulling (trichotillomania). It was formerly popular as
Stereotypy/Habit Disorder that caused impairment to the child

PSYCHOLOGICAL EXPLANATIONS OF MOTOR DIORDERS

 Conversion disorder: A conversion disorder is characterized by the loss of a bodily

function, for example blindness, paralysis, or the inability to speak, the loss of
physical function being involuntary. Whilst "hysterical" blindness, paralysis,
anesthesia, dysphagia, and gait disturbance have been described for many years,
the patient confronts an acute stressor that creates a psychic conflict, and the
physical symptom(s) serve as the resolution for the conflict. The patient may repress
the stressor or be unaware of its impact. The conversion symptoms bind the
individual’s anxiety by preventing activities that may lead to expression of repressed
impulses by keeping conflict out of conscious awareness (primary gain). It can even
be explained on grounds of legitimization of the sick role as a way in which the
individual takes the opportunity to communicate the distress in socially acceptable
device in form of physical symptoms (secondary gain) (Joseph & Young, 1999)
 Stereotypy: Because the motions involved are self comforting the stereotypic
movements may be associated with neglectful situations in which other forms of
comfort are not available. Available hypotheses imply that stereotyped movements
are a way to release tension or express frustration, that they communicate a need for
attention or reinforcement. It is a way of sensory stimulation, for autistic children,
since they remain segregated from the environment. It is common to see children in
crowded orphanages exhibiting such behaviors (APA, 2000).
 Tourette’s syndrome: It may be one set of possible outcomes of narcissistic,
repressed childhood sexuality. Individuals with this syndrome are of a mentally
infantile character, narcissistically fixated, from which the healthy developed part of
the personality can with difficulty free itself. Tics have been reported to increase in
power during early puberty, pregnancy, and childhood, at the time of increased
stimulation of the genital regions (Howard& Kushner, 2000).
 Non epileptic seizures: Viewed as a result of intrinsic emotional problem or to
internalized conflicts, such as family conflicts, or in individuals with inadequate
personalities, adjustment reactions, or who have been victims of sexual or physical
abuse. Such individuals may misinterpret or over interpret the occurrences in the
environment. Such behaviors increase after they have been reinforced by family
members. Individuals having difficulty managing anger or controlling their hostility

337
 toward others may result in such manifestations disturbances in patients (Lesser,
2003).
 Compulsive acts: It arises when unacceptable wishes and impulses coming from
the id are only partially repressed (driven out of consciousness), thus provoking
anxiety and to reduce this, the individual would use the ego defense mechanisms
like regression, isolation, undoing and reaction formation. It may also develop
because of an individual’s feeling of incompetence and inferiority. It may also be
explained as an interplay of classical conditioning and operant conditioning where
the previously neutral stimuli becomes temporally associated with a fearful stimuli
such that the former acquires anxiety provoking properties, resulting in conditioned
fear response. Due to the aversive characteristic of the stimuli, escape or avoidance
responses are developed, negatively reinforced by the removal of anxiety (Cardwell
& Flanagan, 2005).
 Catatonia: Catatonia, long viewed as a motor disorder, may be better understood as
a fear response, akin to the animal defense strategy tonic immobility. This proposal,
consistent with K. L. Kahlbaum's original conception, is based on similarities
between catatonia and tonic immobility (“death feint”) as well as evidence that
catatonia is associated with anxiety and agitated depression. It is argued that
catatonia originally derived from ancestral encounters with carnivores whose
predatory instincts were triggered by movement but is now inappropriately expressed
in very different modern threat situations. Found in a wide range of psychiatric and
serious medical conditions, catatonia may represent a common "end state" response
to feelings of imminent doom and can serve as a template to understand other
psychiatric disorders (Moskowitz, 2004).

CULTURAL VARIANTS OF MOTOR DISORDERS:

Culture influences the experience and expression of distress from its inception. While
Western psychiatry has identified several universal patterns of distress, there are significant
geographical variations in the prevalence, symptomatology, course and outcome of
psychiatric illness. Several syndromes linked to specific cultures are better considered
variations of motor disorders

 Ganser syndrome: Ganser syndrome is a type of factitious disorder, a mental

illness in which a person acts as if he or she has a physical or mental illness when in
truth; he or she has caused the symptoms. It is characterized by the individual
mimicking behavior they think are typical of a psychosis, by providing nonsensical or
wrong answers to questions, and doing things incorrectly. The answers given,
however, are usually so close to the question as to reveal that the patient has
understood the question. Also called nonsense syndrome, balderdash syndrome,
syndrome of approximate answers, pseudodementia or prison psychosis. Although
this disorder was previously classified as a factitious disorder, the American
Psychiatric Association has redefined Ganser's syndrome and placed it in the
category called "Dissociative Disorder Not Otherwise Specified."
 Latah, reported in Arcadian Maine but linked to Malaysia, is characterized by
echolalia, echopraxia, coprolalia (repetitive use of profanity), and automatic
obedience within a manic delirium (shouting, yelling, hitting, jumping, and running).

338
 Its association with an excessive startle response and its sporadic nature suggests
an infectious etiology or manic-depressive illness.
 Amok is a culture-related syndrome associated with south-east Asia, although cases
are reported from North America, Britain, and Europe. It is characterized by sudden,
frenzied, violent, and often murderous attacks on strangers in public settings with
multiple victims. The episode may last hours. Depressive illness or vertigo with visual
hallucinations are common prodromes. “Amoks” that are not themselves killed are
found in stupor and are amnestic for the attack. Systematic examinations of Amok
perpetrators have not been done, but case literature suggests the presence of
catatonic features similar to those seen in Latah. Seizure disorder and psychotic
mood disorder are possible etiologies.
 Lycanthropy, associated with eastern European lore of wolf-men, is the combination
of motor disorders with the delusional belief of being changed into an animal due to
the influence of the devil. Delusional memories of eating children, killing domestic
animals, having coitus with the devil, and interacting with demons were related by
sufferers. Associated manic excitement, or “dancing mania” or tarentism (A nervous
affection producing melancholy, stupor, and an uncontrollable desire to dance. It was
supposed to be produced by the bite of the tarantula, and considered to be incapable
of cure except by protracted dancing to appropriate music) is described. Sufferers
acted as if wild animals. Fink and Taylor (2003) describe a man who was found by
the New York police scurrying around the streets on all fours, roaring, snapping, and
biting at passers-by. In the hospital, the man became mute and immobile with
generalized analgesia and automatic obedience. He said later that he thought he
was a tiger (Taylor & Vaidya, 2009)

EXAMINATION OF NON-CO-OPERATIVE OR STUPOROSE PATIENTS (Kirby, 1921)

The difficulty of getting information from non-co-operative patients should not discourage
the physician from making and recording certain observations. These may be of great
importance in the study of various types of cases and give valuable data for the
interpretation of different clinical reactions. To wait for the clinical picture to change or for
the patient to become more accessible is often to miss an opportunity and leave a serious
gap in clinical observation. Hence such examinations are required which would lead us in
reaching to mental status. Following guide covers the recording in a systematic manner.

1. General reaction and posture

 Attitude- voluntary or passive
 Voluntary postures- comfortable, natural, constrained, awkward.
 What does the patient do if placed in awkward or uncomfortable position?
 Behavior towards physicians and nurses: resistive, evasive, irritable,
apathetic, complaint.
 Spontaneous acts: any occasional playfulness, mischievousness or
assaultiveness. Defense movements when interfered with or when pricked
with pin. Eating and dressing. Attention to bowels and bladder. Do the
movements show only initial retardation or are they consistent throughout?

339
  To what extent does the attitude change? Is the behavior constant or variable
from day to day? Do any special occurrences influence the condition?
2. Facial expression: Alert, attentive, placid, vacant, stolid, sulky, scowling, averse,
perplexed, distressed, etc. Any play of facial expressions or signs of emotions: tears,
smiles, flushing, perspiration. On what occasion?
3. Eyes: Open or close. If closed, resist having lid raised. Movement of eyes: absent or
obtained on request; give attention and follow the examiner or moving objects; or
show only fixed gazing, furtive glances or evasion.
Rolling of eyeballs upward. Blinking, flickering, or tremor of lid. Reaction to sudden
approach to threat to stick pin in eye. Sensory reaction of pupils (dilation of painful
stimuli or irritation to skin of neck)
4. Reaction to what is said or done: Commands: show tongue, move limbs, grasp
with hand (clinging, clutching etc.)
Motions slow or sudden. Reaction to pinpricks, automatic obedience: tell patient to
protrude the tongue to have pin stuck into it.
Ecopraxia: imitation of actions of others.
5. Muscular reactions: Test for rigidity: muscles relaxed or tensed when limbs or body
is moved
Catalepsy, waxy flexibility. Negativism shown by movements in opposite direction or
springy of cogwheel resistance.
Test head and neck by movements forward and backwards and to side.
Test also the jaw, shoulders, elbows, fingers and lower extremities.
Does distraction or commands influence the reactions?
Closing of mouth, protrusion of lips (‘Schnauzkrampf’)
Holding of saliva, drooling.
6. Emotional responsiveness: Is feeling shown when talked to of family or children?
Or when sensitive points in history are mentioned or when visitors come?
Note whether or not acceleration of respiration or pulse occurs; also look for flushing,
perspiration, tears in eyes etc. do jokes elicit any response?
Effect of unexpected stimuli (clap hands, flash of electric light)
7. Speech: Any apparent effort to talk, lip movements, whispers, movements of head.
Note exact utterances with accompanying emotional reaction (may indicate
hallucinations).
8. Writing: Offer paper and pencil, of responsive or partially stuporose patient will often
write when they fail to talk.

MANAGEMENT

To carry out any psychological intervention, it is a must that there be a good rapport
established with the individual concerned and the therapeutic alliance reimbursed, and step
forth with the requisite therapy as need be.

340
  Psychotherapy

The strategies of psychoanalytic psychotherapy can also be useful which ranges from
insight-oriented (uncovering, evocative or interpretive) techniques to supportive
(relationship oriented, suggestive or repressive techniques). Psychoanalytic psychotherapy,
in its narrowest sense, is the use of insight oriented methods only. It includes a blend of
uncovering and supportive measures. Brief psychotherapy has been found useful in some
cases. It is a time limit psychotherapy that is based on psychoanalysis and psychodynamic
theory. Supportive therapy recognizes the emotional support and a stable caring
atmosphere in the management of the patient. Insight oriented psychotherapy aims at
increasing strong motivation to understand (Sadock & Sadock, 2007). A non-
psychoanalytic, non-interpretative, non confrontational approach that develops an alliance
with the patients and shifts the focus from the physical symptoms to the psychological
environment is preferable (Joseph & Young, 1999)

 Behavioral management

Behavioral assessment has three other goals: (1) to define the target behavioral problems;
(2) to identify the cognitive habits that are maintaining those behavioral problems; and (3) to
make it possible to objectively measure therapeutic progress. To best achieve the latter,
behavior therapy focuses on the present manifestations of the target problems. But to
ensure the most comprehensive therapeutic results, the therapist gets a detailed personal
and medical history

Behavior interventions are directed at the symptoms and the environmental antecedents
and consequences that are thought to sustain the symptoms. Typically the sustaining
reinforcers are thought to be social attention or escape from a noxious activity and are
similar to the concepts of primary and secondary gain. Behavior therapy seeks to
systematically reduce the reinforcement of the symptoms and to reinforce more adaptive
social, emotional, and task oriented behavior (Joseph & Young, 1999). Behavior
modification techniques may be used including habit reversal training (using a combination
of procedures such as awareness training, self monitoring, competing response training
and relaxation training), aversion therapy (punishment procedures like time out, response
cost, loud noise, aversive tastes, mild electric shock), problem solving skills training ,
positive reinforcement, etc (Sadock & Sadock,2007)

 Hypnosis and Abreactive Therapy

A number of case reports suggest that hypnosis, relaxation, or drug –induced altered states
of consciousness are beneficial for patients with acute conversion symptoms (Brooksbank,
1984). Hypnosis is a powerful mean of directing innate capabilities of imagination imagery
and attention (Sadock & Sadock, 2007). By abreactive therapy we understand: how we
forget, how forgetting conflicts cause symptoms, how abreaction in general facilitates

341
recollection, thus replacing a symptom by a conflict, and how 'reverie' (what is usually
called 'free association’) in particular facilitates recollection (Joseph & Young, 1999)

 Milieu and Family Therapy

Family therapy focuses on altering the interaction between or among family members and
seeks to improve their functioning as a unit. The locus of milieu is a living, learning or
working environment (Sadock & Sadock,2007). Clinician can often trace the onset or
maintenance of conversion symptoms to family or environmental dynamics. Consequently,
family therapy or other environmental interventions are often tried and reported to be
sometimes of value in treatment. Helping family to express previously blocked feelings and
modifying family dynamics that reinforce the conversion symptoms are common in
intervention (Joseph & Young, 1999)

ASSESMENT OF MOTOR DYSFUNCTION

 Screening Examination for Motor System Dysfunction (Marsh & Margolis, 2005)

Gait—observe walking, including on tiptoes and heels.

Station—observe balance and ability to arise from chair, pull test
Abnormal movements
At rest—observe for excessive movements, hypokinesia, or dystonic features
Hold arms outstretched
Coordination—rapid finger tapping, finger-to-nose test
Tone—passive movement of limbs and neck

 Combined Rating Scale:

 The Maryland Psychiatric Research Centre Involuntary Movement Scale (IMS),

Cassady et al (1997):
It was primarily intended for rating the severity of tardive dyskinesia and
Parkinsonism in clinical and research patients. It offers ratings in 11 anatomical
areas as well as a rating of gait and respiratory dyskinesias. These anatomical
regions are rated in a total of 28 items.
 The Extrapyramidal Symptom Rating Scale (ESRS), Chouinard et al (1980):

It consists of 12 questionnaire items to identify subjective symptomatology, a

clinician’s examination and scoring of Parkinsonian and dyskinetic movements, and
a clinical global impression of tardive dyskinesia. Parkinsonian signs are scored on
an 8-item scale under which is included akathisia (the subjective part is noted among
the nine parkinsonian symptoms in the questionnaire.)

342
 Schedule for the Assessment of Drug-Induced Movement Disorders
(SADIMoD), Anton et al (2000):

It consists of 8 sub-scales, a 9-item scale for dystonia, an 8-item scale for

Parkinsonism, two 7-item scales for dyskinesias during activity and in rest, a 5-item
scale for ataxia, a 2-item scale for akathisia, a 3-item scale for tremors and a 4-item
scale for sedation, depression, psychosis and anxiety. In the sub-scale for dystonia
the severity score (0±4) is multiplied with a provoking factor (0±4) considering the
conditions of occurrence and a weight factor considering the body part that is
affected. In all other sub-scales a scoring code of 0±4 is applied.

 Abnormal Involuntary Movement Scale (AIMS) , Guy (1976):

The most widely used rating scale for tardive dyskinesia. It rates abnormal
involuntary movements in seven body sites. The orofacial movements, rated on four
separate items; extremity movements, on two separate items; and trunk movements,
on one item. Each item is rated on a 5-point scale (0–4); three separate items score
global severity the subject’s awareness, and incapacitation due to involuntary
movements (each on a 5-point scale). Two additional items cover the subject’s
dental status, as movements in the orofacial area are more obvious in edentulous
patients. There are several versions of guidelines for conducting the AIMS
examination.

 The Smith Tardive Dyskinesia Scale, Smith (1979):

It assesses both tardive dyskinesias and Parkinsonism in a single 24-item scale. The
sub scores for Parkinsonism and tardive dyskinesias can be computed separately.

 The Barnes Akathisia Rating Scale ( BARS), Barnes (1989):

Developed by Braude and Barnes and modified by Barnes. It is the most widely used
a four item scale which includes objective and subjective awareness of restlessness,
patient's distress related to the restlessness (scored 0-3) and a global impression
rating. In a six point scale, the BARS has the advantage over other scale in that it
offers the opportunity to distinguish pseudo-akathisia. Patients are rated in a variety
of positions sitting standing and in settings.

 The Hillside Akathisia Scale (HAS), Fleischhacker et al (1989):

A modification of the Simpson-Angus EPS Scale has two subjective and three
objective items. The scale also rates akathisia in a variety of positions, during
activation (serial calculations and finger tapping), and has a yes-or-no response to
the presence of other neuropsychiatric phenomena (objective). There is an 8-item
global impression scale for akathisia. However, it has Poor reliability rating akathisia
in head, trunk, and in the arms.

343
  Agitated Behavior Scale (ABS), Corrigan (1989):
This scale was developed to allow objective assessment of agitated behavior,
particularly serial assessments for the evaluation of interventions to reduce agitation.
It’s a 14 item scale being rated from 1 to 4 indicating absence or presence of
symptom, where 1 indicates absence, 2- slight, 3- moderate and 4- extreme
agitation.
 Behavioral Activity Rating Scale (BARS), Swift et al (2002) :
The BARS was designed to measure the degree of agitated behavior, rather than the
severity of a specific diagnostic entity in patients with psychosis. The treatment
objective is to reduce activity levels and increase the degree of calm in patients
without causing profound sedation. It’s a 7 point rating scale with 1 indicating ‘difficult
to rouse’ and 7 as violent, requires restraint.
 Rating Scale For Catatonia:

 Bush-Francis Catatonia Rating Scale (BFCRS):

The BFCRS reliably detect and quantify the presence and severity of catatonia in
acutely hospitalized psychiatric patients (Bush et al, 1996a, b). It is a 23-item
catatonia severity rating scale, with each item given a score from 0 to 3 . Fourteen
more commonly used items form a screening instrument .Two or more items indicate
a diagnosis of catatonia.
 The Catatonia Rating Scale (CRS), Braunig et al (2000):
It assesses both frequency and severity of symptoms. As such, it can be used
diagnostically and the score also has the potential to be applied as an outcome
measure to assess change in treatment studies. The CRS is composed of 21 items.
Sixteen items correspond to catatonic motor symptoms and five correspond to
catatonic behaviors. Ratings range from 0 (absent) to 4 (severe). To reach the
diagnostic threshold for catatonia, the presence of four or more symptoms must be
rated at least moderate
 Modified Rogers Scale (MRS), Lund et al (1991) :
To date, this is the most comprehensive rating scale to assess catatonic symptoms
as it includes virtually all motor features described in psychotic patients. The MRS
comprises 36 items grouped into 10 categories of related items mainly suitable for
research; there is no cut off for caseness.
 Northoff Catatonia Scale, Northoff et al (1999):
It has forty items divided among motor, affective, behavioral categories. Caseness is
defined as the presence of at least one item from each category.

CIP STUDIES
 Kumar and Ram (2003) studied drug naive and drug free schizophrenic patients and
found that catatonic signs were present in 37.3% of the patients, it was found to be
more frequent among undifferentiated and catatonic subtypes and most frequent
signs observed were negativism, stupor, mutism, staring, rigidity, posturing,

344
 mitgehen, whereas echolalia, echopraxia, mannerism, gagenhalten, gag reflex,
perseveration and combativeness were absent in sample population.
 Akhtar et al in 1993 studied the efficacy of vitamin E in treatment of tardive
dyskinesia in a double blind placebo control trial and concluded that vitamin E
treatment improves tardive dyskinesia.
 Desarkar et al (2006) reported a case of Aripiprazole induced acute dystonia in an
18 year old male.
 Prakash et al (1992) while comparing vulnerability to develop acute dystonia in
patients of schizophrenia and mania to intra venous haloperidol concluded that both
groups are equally vulnerable to develop neuroleptic induced acute dystonia.
 Jagdeeshan et al(2002) in a paper ‘Catatonia in Obsessive compulsive disorder’
reported that catatonia occurs in a wide range of neuropsychiatric conditions. In his
paper he reported that both the patients have obsessive –compulsive disorder and
catatonic signs. None of these patients had features suggestive of major psychoses
such as delusions or hallucinations
 Praharaj et al (2008) reported a case of olanzapine induced rabbit syndrome and
another case was reported by Praharaj et al (2009) of tardive oculogyric crisis
induced by olanzapine.

CONCLUSION

Even after numerous accounts and controversies regarding the issue of wide spectrum of
various motor disorders, quite often overlapping, it remains a debate to concretize the
etiology of motor disorders, as to being psychogenic or neurogenic. There are many other
diseases that produce involuntary movement disorders, but they are unusual outside the
movement disorder clinic. As a group, these disorders are a particularly rewarding
challenge for the clinician. Both diagnosis and management can exercise the clinician’s
skills but the profuse researches, leading to a better understanding into the phenomenon, is
a continuing source of enlightenment for the clinicians.

345
REFERENCES
Akhtar, S., Jajor, T.R., Kumar, S. (1993). Vitamin E in the treatment of tardive dyskinesia.
Postgraduate Medicine, 39, 124-126.
American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders,
fourth edition-text revised(DSM-IV-TR).New York: APA
Anton, J.M & Loonen ,N. (2000). A schedule for the assessment of drug induced movement
disorders (SADI MOD). Test-retest reliability and concurrent validity. International
Journal of Neuropharmacology, 3, 285-296.
Barnes, T.R. (1989). A rating scale for drug induced akathisia. British Journal of Pharmacology, 154,
672-676.
Braunig, P., Kruger, S., Shugar, G., Hoffler, J., Borner, I. (2000). The catatonia rating scale I:
Development, Reliability and use. Comprehensive Psychiatry, 41, 147–158.
Brooksbank D. (1984). Management of conversion reactions in five adolescent girls. Journal of
Adolescence,21, 359-376
Bush, G., Fink, M., Petrides, G., Dowling, F. (1996) Catatonia I. Rating scale and standardized
examination. Acta Psychiatrica Scandinavica, 93, 129-136.
Cardwell M. & Flanagan, C. (2005). Psychology A2 : A Complete Companion. Nelson Thornes Pub.
Chouinard, G., Ross-Chouinard, A., Annable, L., Jones, B. (1980). Extrapyramidal Symptom Rating
Scale. Canadian Journal of Neurological Science, 7, 234.

Corrigan, J.D. (1989). Development of a scale for assessment of agitation following traumatic brain
injury. Journal of Clinical and Experimental Neurospychology, 11, 261-277.

Desarkar, P., Thakur, A, Sinha, V.K. (2006). Aripiprazole-induced acute dystonia, American Journal
of Psychiatry,23, 163.
Fink, M. & Taylor, M.A. (2003) Catatonia: A Clinician’s Guide to Diagnosis and Treatment.
Cambridge: Cambridge University Press.
Guy, W. (1976) ECDEU Assessment Manual for Psychopharmacology. Washington DC: US
Department of Health, Education and Welfare
Kushner, H.I. (2000). A Cursing Brain? ;The History of Tourette Syndrome. Harvard : Harvard
University Press.
Jaspers, K. (1962). Objective performances of psychic life (motor activity). General
psychopathology. (trans. J. Hoeing & MW Hamilton) Manchester University Press.
Manchester
Joseph, A.B., Young, R.R. (1999). Movement Disorders in Neurology and Neuropsychiatry. 2nd ed.
Malden, MA: Blackwell Science.
Kirby,G.H.(1921) Guides for history taking and clinical examination of psychiatric cases.
In:Slater,E.and Roth,M.(eds.)Clinical Psychiatry. Third Edition. London :Bailliere
Tindall.
Kumar, M.& Ram, D. (2003). Catatonic Signs & symptoms in drug naïve or drug free schizophrenia
patients. (Dissertation). Ranchi University.

346
Lesser, R.P. (2003). Treatment and Outcomes of Nonepileptic Seizures. Epilepsy Currents: Review
and Critical Analysis, 3,198-200.
Lund, C.E., Mortimer, A.M., Rogers, D., McKenna, P.J. (1991). Motor, volitional and behavioral
disorders in Schizophrenia 1: Assessment using the modified Rogers scale. British
Journal of Psychiatry, 158, 323–327.
Moskowitz, A. (2004). ‘Scared stiff’: Catatonia as an evolutionary-based fear response.
Psychological Review, 111, 984-1002

Praharaj, S.K., Jana, A.K., Sarkar, S., Sinha, V.K. (2009). Olanzapine-induced tardive oculogyric
crisis . Journal of Clinical Psychopharmacology , 29, 604-6.

Praharaj, S.K., Sarkar, S., Jana, A.K., Sinha, V.K. (2008). Olanzapine-induced rabbit syndrome.
Southern Medical Journal, 101, 1069-70.

Sadock. B.J., Sadock.V.A. (2007). Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry,

10th ed. New York:Lippincott Williams & Wilkins.
Smith, J.M., Kucharski, L.T., Oswold, W.T.(1979) A systematic investigation of tardive dyskinesia in
schizophrenic inpatients. American Journal of Psychiatry, 136, 918–922.

Swift, R.H., Harrigan, E.P., Cappelleri, J.C., Kramer, D., Chandler, L.P. (2002). Validation of the
behavioral activity rating scale (BARS): a novel measure of activity in agitated
patients. Journal of Psychiatric Research, 36,87-95

Taylor, M.A. & Vaidya, N.A. (2009). Descriptive Psychopathology: The Signs and Symptoms of
Behavioral Disorders. Cambridge: Cambridge University Press.

347
1. Excitement: Extreme hyperactivity, 9. Mannerisms: Odd, purposeful
constant motor unrest which is apparently movements (hopping or walking tiptoe,
nonpurposeful. Not to be attributed to saluting passers-by, exaggerated
akathisia or goal-directed agitation. caricatures of mundane movements).
0 = Absent (Abnormality is inherent in the act itself.)
1 = Excessive motion, intermittent. 0 = Absent
2 = Constant motion, hyperkinetic without 1 = Occasional.
rest periods. 2 = Frequent.
3 = Severe excitement, frenzied motor 3 = Continuous.
activity. 10. Verbigeration: Repetition of phrases or
2. Immobility/Stupor: Extreme sentences.
hypoactivity, immobility. Minimally 0 = Absent
responsive to stimuli. 1 = Occasional.
0 = Absent 2 = Frequent, difficult to interrupt.
1 = Sits abnormally still, may interact briefly. 3 = Continuous.
2 = Virtually no interaction with external 11. Rigidity: Maintenance of a rigid position
world. despite efforts to be moved (Exclude if
3 = Stuporous, not responsive to painful cogwheeling or tremor are present.)
stimuli. 0 = Absent
3. Mutism: Verbally unresponsive or 1 = Mild resistance.
minimally responsive. 2 = Moderate.
0 = Absent 3 = Severe, cannot be repostured.
1 = Verbally unresponsive to most 12. Negativism: Apparently motiveless
questions; incomprehensible whisper. resistance to instructions or to attempts to
2 = Speaks less than 20 words/5 minutes. move/examine patient. Contrary behavior,
3 = No speech. does the opposite of the instruction.
4. Staring: Fixed gaze, little or no visual 0 = Absent
scanning of environment, decreased 1 = Mild resistance and/or occasionally
blinking. contrary.
0 = Absent 2 = Moderate resistance and/or frequently
1=Poor eye contact. Gazes less than 20 contrary.
seconds between shifting of attention; 3 = Severe resistance and/or continually
decreased blinking contrary.
2 = Gaze held longer than 20 seconds; 13. Waxy Flexibility: During reposturing of
occasionally shifts attention. patient, patient offers initial resistance
3 = Fixed gaze, non-reactive. before allowing himself to be repositioned
5. Posturing/Catalepsy: Maintains (similar to that of a bending a warm candle).
posture(s), including mundane (e.g., sitting 0 = Absent.
or standing for long 3 = Present.
periods without reacting). 14. Withdrawal: Refusal to eat, drink and/or
0 = Absent make eye contact.
1 = Less than one minute. 0 = Absent.
2 = Greater than one minute, less than 15 1 = Minimal oral intake for less than one
minutes. day.
3 = Bizarre posture, or mundane maintained 2 = Minimal oral intake for more than one
more than 15 min. day.
6. Grimacing: Maintenance of odd facial 3 = No oral intake for one day or more.
expressions. 15. Impulsivity: Patient suddenly engages
0 = Absent in inappropriate behavior (e.g. runs down
1 = Less than 10 sec. hallway, starts screaming, or takes off
2 = Less than 1 min. clothes) without provocation. Afterwards,
3 = Bizarre expression(s) or maintained cannot explain.
more than 1 min. 0 = Absent
7. Echopraxia/Echolalia: Mimicking of 1 = Occasional
examiner’s movements/ speech. 2 = Frequent
0 = Absent 3 = Constant or not redirectable
1 = Occasional. 16. Automatic Obedience: Exaggerated
2 = Frequent. cooperation with examiner’s request, or
3 = Continuous. repeated movements that are requested
8. Stereotypy: Repetitive, non-goal- once.
directed motor activity (e.g. finger-play; 0 = Absent
repeatedly touching, patting or rubbing self). 1 = Occasional
(Abnormality is not inherent in the act but in 2 = Frequent
its frequency.) 3 = Continuous
0 = Absent 17. Passive obedience (mitgehen):
1 = Occasional. Raising arm in response to light pressure of
2 = Frequent. finger, despite instructions to the contrary.
3 = Continuous. 0 = Absent

348
 3 = Present 3 = Present
18. Negativism (Gegenhalten): Resistance 22. Combativeness: Usually in an
to passive movement that is proportional to undirected manner, without explanation.
strength of the stimulus; response seems 0 = Absent
automatic rather than willful. 1 = Occasionally strikes out, low potential
0 = Absent for injury
3 = Present 2 = Strikes out frequently, moderate
19. Ambitendency: Patient appears “stuck” potential for injury
in indecisive, hesitant motor movements. 3 = Danger to others
0 = Absent 23. Autonomic Abnormality
3 = Present Circle: Temperature
20. Grasp Reflex: Strike open palm of Blood Pressure
patient with two extended fingers of Pulse rate
examiner’s hand. Automatic closure of Respiratory rate
patient’s hand. Inappropriate sweating.
0 = Absent 0 = Absent
3 = Present 1 = Abnormality of one parameter [exclude
21. Perseveration: Repeatedly returns to pre-existing hypertension]
same topic or persists with same 2 = Abnormality of 2 parameters
movements. 3 = Abnormality of 3 or greater parameters
0 = Absent

II. EXAMINATION FOR CATATONIA: From Bush et al., 1996

 The method described here is used to complete Catatonia Rating Scales.

 Ratings are made based on the observed behaviors during the examination, with the exception of
completing the items for ‘withdrawal’ and ‘autonomic abnormality’, which may be based upon either
observed behavior and/or chart documentation.
 Rate items only if well defined. If uncertain, rate the item as ‘0’.

Procedure Examines
1 Observe patient while trying to engage in a conversation. Activity level, abnormal
movements, abnormal speech
2 Examiner scratches head in exaggerated manner. Echopraxia
3 Examine arm for cog wheeling. Attempt to reposition, Rigidity,Negativism,Waxy
instructing patient to “keep your arm loose”. Move arm with Flexibility
alternating lighter and heavier force.
4 Ask patient to extend arm. Place one finger beneath hand Passive obedience
and try to raise slowly after stating, “DO NOT let me raise
your arm”.
5 Extend hand stating, “DO NOT shake my hand”. Ambitendence
6 Reach into your pocket and state, “Stick out your tongue, I Automatic Obedience
want to stick a pin in it.”
7 Examine for the grasp reflex. Grasp Reflex
8 Examine the patient’s chart for oral intake, vital signs, and
unusual incidents.
9 Observe the patient indirectly for a brief period each day

349
350
CHAPTER-XVII
 BASICS OF PSYCHOLOGICAL ASSESSMENTS

INTRODUCTION
A psychological assessment is the attempt of a skilled professional, usually a
psychologist, to use the techniques and tools of psychology to learn either general or
specific facts about another individual, either to inform others of how they function now,
or to predict their behavior and functioning in the future. The point of assessment is
often diagnosis, management plan, placement in job or selection of personnel in military
etc. Psychological assessment is a broad area which includes intelligence, personality,
projective tests, and neuropsychological assessment. (Singh, 1997)

PSYCHOLOGICAL TEST: DEFINITION

“A psychological test is a standardized instrument to measure objectively any
one or more aspects of a total personality by means of samples of verbal or non-verbal
responses or by means of other behaviour” (Freeman ,1965). A psychological (or an
educational) test is a standardized procedure to measure quantitatively or qualitatively
one or more than one aspect of trait by means of a sample of verbal and non-verbal
behavior( Singh,1997). A test is “an organized succession of stimuli designed to
measure quantitatively or to evaluate qualitatively some mental process,trait or
characteristics” (Bean, 1953).

HISTORICAL VIEW
The progress of psychology and psychological test started with Wilhelm Wundt
(1832-1920) who established the first psychological laboratory in 1879, in Leipzig,
Germany. In 1905 Binet and Simon invent the first modern intelligence test. Stern
introduced the concept of IQ, or Intelligence quotient in 1914. In 1917 Robert
Woodworth develops the personal data sheet, the first personality test. These are few
milestones in the field of psychological assessment. Psychological assessment has its
extensive history within the field of mental health also. Psychological testing in its
modern form originated little more than one hundred years ago in laboratory studies of
sensory discrimination, motor skills and reaction time. History of psychological testing is
a captivating story that has a substantial relevance to present day practice.
(Appendix I)

NEED OF A PSYCHOLOGICAL TEST

There are six major uses of psychological tests (Gregory, 2004)-
1. Classification: It encompasses a variety of procedures:
a) Assigning a person to one category rather than other.
b) Placement and screening. Placement is sorting of people into different programs
according to their needs or skills. Screening refers to quick and simple test
procedure
2. Diagnosis and treatment planning: Diagnosis consists of task of determining the
nature and source of person’s abnormal behaviour and classifying the behaviour
pattern within an accepted diagnosis system for best choice of treatment.
3. Self knowledge: Psychological tests can be a potent source of self knowledge.
4. Program evaluation: Another use of psychological test is the systematic evaluation
of educational and social programmes.
5. Research: It plays a major role in the both applied and theoretical branches of
behavioural research.
6. Rehabilitation: Psychological testing has a major role in rehabilitation. It is the
process of assisting someone to improve and recover lost function after an event,
illness or injury that has caused functional limitations.

The more common and evident contributions of psychological assessment in clinical

field can be organized into four general categories (Maruish, 1999).
1. Problem Identification- Problem Identification is the most common use of
psychological assessment.
2. Problem Clarification- Psychological assessment can often assist in the
clarification of three most important types of information, the severity of the problem,
complexity of the problem & degree to which the problem impairs the patient’s ability
to function in one or more life roles.

350
3. Identification of important patient characteristics- Identifying patient
characteristics reveals the strengths and weaknesses of the patient that helps in
achieving the therapeutic goals.
4. Monitoring of progress - The information from repeated assessment during the
treatment process can help the clinician to determine, if the treatment plan is
appropriate for the patient at a given point of time.

BASIC PROCEDURES AND TECHNICAL ASPECTS OF A PSYCHOLOGICAL TEST:

A psychological test requires few basic procedures to be followed for
administration. These procedures make the test scientifically sound. (Gregory2004)

 Essential component of individual testing is that examiner must be familiar with the
material and directions before the administration of test.
 Examiners are urged to establish rapport. In testing rapport is a comfortable warm
atmosphere that serves to motivate examinees and elicit cooperation.
 Another important ingredient of valid testing is sensitivity to disabilities in the
examinee.
Technical Aspect in Psychological Testing:
1. Standardization- Standardization refers to uniformity of procedures in administering
and scoring the test (Anastasi, 1997). Thus a test is said to be standardized if test
administration procedures, materials, instructions, recording and scoring are as
constant as possible at all times(Korchin,1999).
2. Norms- Norms refer to the average performance of a representative sample on a
given test. Test developers are advised to publish norms describing the frequency
distribution of scores, obtained in as broad sample as possible of the relevant
population (APA, 1974).
3. Objectivity- A test is said to be objective when the administration, scoring, and
interpretation are independent of the subjective judgment of the particular examiner.
It means that the assessment must be free from subjective element so that there is
complete interpersonal agreement among experts regarding the meaning of the
items and scoring of the test. (Anastasi, 1997).
4. Reliability- The reliability of an assessment refers to its degree of stability,
consistency, predictability, and accuracy (Groth & Marnat, 2003). It refers to self
correlation of the assessment which shows the extent to which the results obtained
are consistent when it is administered once or more than once on the same sample
with a reasonable time gap. There are four types of reliability:
 Split Half Reliability is known to be the best technique in which the test is given
only once. The items are split in half, and the two halves are correlated. To
determine it, the test is often split on the basis of odd and even items. The
reliability coefficient is the correlation of scores obtains by same person on the
two halves (Groth & Marnat, 2003).
 Interscorer Reliability is one which is obtained by scoring of a test by more than
one expert of a single client
(Groth & Marnat, 2003).
 Test-Retest Reliability which is determined by administering the test and then
repeating it on a second condition. The reliability coefficient is the correlation of
scores obtains by same person on the two different administrations (Groth &
Marnat, 2003).
 Alternate Forms Reliability is determined by administering the parallel forms of
the test on a person. The reliability coefficient is the correlation of scores obtains
by same person on the two parallel forms (Groth & Marnat, 2003).

5. Validity- Validity indicates the extent to which the test measures what it intended to
measure and should also produce information useful to clinician (Groth & Marnat,
2003). The degree of validity of a test depends on the magnitude of the errors
present in the measures obtained from it. Some indication of the validity of a given
test is gained from a study of the correlation between scores on a given test and
scores from other tests designed to measure the same factor. They are of the
following types:

351
  Content Validity refers to the representativeness and relevance of the
assessment instrument to the construct being measured.
 Criterion Validity also known as Empirical Validity is determined by comparing
test scores with some sort of performance on an outside measure. It is further
divided into Concurrent Validity and Predictive Validity.
 Concurrent Validity refers to measurements taken at the same, or approximately
the same time of the test administration (Groth & Marnat, 2003).To determine
concurrent validity, test scores and criterion are obtained simultaneously
(Gregory, 2004).
 Predictive Validity refers to outside measurements that were taken some time
after the test score were derived (Groth & Marnat, 2003).
 Construct Validity refers to the extent of measurement to which the test
measures a theoretical construct or trait (Groth & Marnat, 2003).
 Descriptive Validity requires that the characteristics or variable being measured
is unique to the condition that they are supposed to define.

Psychological Assessment in Different Setup

Psychological referrals are meant to understand the unique problems and demands
encountered in different settings. Psychological tests are generally applied by qualified
persons. Few issues that can affect psychological assessment are:
 In the hand of unqualified persons, psychological tests can harm.
 The selection process is rendered invalid for persons who preview test questions.
 Leakage of item content to the general public completely destroys the efficiency
of a test.
The setups where psychological referrals are frequent are following:
i) Psychiatric Setting: -
Psychological assessments are required in very specific conditions in a
psychiatric setting. When there is a diagnostic dilemma, assessment involving pertinent
tools can provide appropriate information. A psychological assessment is also required
as an aid to psychotherapy (short term and problem oriented) in which understanding
the patient and the problem must be accomplished very quickly (Kaplan & Sadock,
2007). It can be used in pretreatment planning, assessing the progress of a therapy,
evaluating its effectiveness and further provide information about the person’s inner life,
conflicts, hidden desires. Current level of functioning, including the intellectual
functioning is another aspect for which a referral can be made.
ii) General medical Setting:-
It has been seen that as many as two-thirds of patients have primarily
psychosocial difficulties. In disorders such as coronary heart disease, asthma, allergies,
rheumatoid arthritis, ulcers and headaches, (Groth-Marnat, et al, 2003; Pruit, et al,
1999) psychological referral can be made in order to understand the underlying
psychological cause, possible emotional factors and to make treatment plan.
The typical areas of assessment focus primarily on the presence of possible
intellectual deterioration such as memory, sequencing, abstract reasoning, spatial
organization, or executive abilities (Groth-Marnat, 2003). Psychological test profile also
helps to asses various disorders like malingering, conversion disorder, hypochondriasis,
organic brain syndrome, or depression with pseudo-neurological features.

iii) Legal context: -

The use of psychological evaluation in legal settings is being accepted as
relevant information. Psychologists in legal settings are called most frequently when
there is a possibility of deception and malingering. According to American Board of
Forensic Psychology, psychological assessment is mostly used in child custody cases,
competency of a person to dispose of property, juvenile commitment and personal injury
suits, in which the psychologist documents the nature and extent of the litigant’s
suffering or disability (stress, anxiety, and cognitive deficit). In contrast, mental health
professionals are more likely to be called for assessing a person’s competency to stand
trial, degree of criminal responsibility and the presence of mental defectiveness (Groth-
Marnat, 2003).
iv) Educational Context:-
Psychologists are frequently called on to assess children who are having
difficulty in, or may need special placement in the school system. The most important

352
areas of evaluation are learning difficulties, measuring intellectual strengths and
weaknesses, assessing behavioural difficulties, creating an educational plan, estimating
a child’s responsiveness to intervention, and recommending changes in a cchild’s hild’s
program or placement (Sattler, 2001)
v) Psychological clinic:-
clinic
Psychologist often works as consultant to people who are aware of the field of
clinical psychology. Since the referrals made here are volunteered by the patients
themselves, psychologist can acts as the decision maker and proceeds with
psychological interventions best suited for the client.

CLASSIFICATION OF PSYCHOLOGICAL ASSESSMENT

These were the main types of psychological test according to Gregory (2004). On
the basis of the criterion of administrative conditions tests are of two types
types-Individual
Individual
and Group tests. On the basis of criteria of scoring the tests are classified into Objective
and Subjective tests. Where, Intelligence test measures individuals’ ability in relatively
global spheres. Aptitude test measures the capabilities for a relatively specific task or
type of skill. Achievement test measures a person’s degree of learning success and
accomplishments in a subject or task. Creativity tests assess novel original think thinking.
ing.
Personality tests measure the trait, qualities and behaviors. Interest inventory
measures individuals’ preference for certain activity or topics. Neuropsychological
tests measure cognitive, sensory, perceptual and motor performance (Gregory, 2004).
Onn the basis of criterion of time limit in producing the response are the power and
speed test. Power tests are those that have generous time limits so that most
examinees are able to attempt every item. Speed tests are those that have severe time
limits (Appendix-II
II and III).

Brief description of commonly used psychological tests in clinical setting

I. Personality II Intelligence III Neuropsychological
assessment assessment assessment

TESTS OF PERSONALITY ASSESSMENTS

The personality assessment measures trait, temperament, values and many
other facets of personality which determines the overall adjustment of the person. There
are three most common tools or methods of personality assessment. They are
following nature:

A. Objective Test B. Projective Techniques C. Observational Methods

Self Report Inventory and questionnaire) – It is commonly known

A. Objective Test (Self
as personality inventories or paper pencil tests in which the individual describes his/her
own feelings, environment, and reaction of others towards him/her.
Objectivity referred to be fairly clearly structured tests for which scoring would be
identical if performed by competent persons.Objectivity to an approach to personality
testing, disclaimed use of the term but believed what is meant is two
two- fold:
(1) Minimization
nimization of errors of observing and recording
(2) Minimization of variability in the task conditions on separate occasion. It is form of
the personality inventory, the check-list,
check list, and the rating scale. Most of these inventories
or assessment techniques measures traits present in an individual. It may even be
administered on a computer. The important tests are as follows:

1. Eysenck’s Personality Questionnairre (EPQ):

It was developed by Eysenck and Eysenck (1975) to measures 3 dimensions and
contains 19 items. These are:
1. Extraversion and Introversion (E),

353
 2. Neuroticism and Stability (N),
3. Psychoticism and Super ego function (P) of a person.

2. Millon Clinical Multiaxial Inventory-III (MCMI-III):

It was developed by Theodore Millon in 1977.It is designed for adult 18 year and
older. It focuses on personality disorder along with symptoms that are frequently
associated with the disorders. The current version is MCMI-III is composed of 175
items and 28 scales divided into the categories of:

Modifying Clinical Severe Clinical Severe

Indices, Personality Personality Syndromes Syndromes
Patterns, Pathology,

3. Minnesota Multiphasic Personality Inventory-II (MMPI-II) –

It is developed by Hathaway and McKinley in 1940. It measures the surface traits of
an individual. Its re-standardization was done at University of Minnesota Press in
1989 and known as MMPI-II (Graham, 2000).The validity scales of MMPI-II are
VRIN, TRIN, F, FB, FP, L, K and S. Clinical scales are
1) Hypochondriasis (H), 6) Schizophrenia (Sc),
2) Hysteria (Hs), 7) Psychesthenia (Pt),
3) Depression (D), 8)Social introversion(Si),
4) Mania (Ma), 9)Psychopathic deviate (Pd),
5) Paranoia (P), 10)Masculinity- Feminity (Mf).
Two coding type namely Hathaway and Welsh are there. It has been widely used for
detection of malingering, personality disorders, aggression etc. The reasons of
revision are inadequacy of sample, item content, language, poor grammar and
punctuation and in order to enhance the validity of this tool & new validity scales
have been added in MMPI-II.

4. Multiphasic Personality Questionnaire (MPQ):

This test is adapted by H.N. Murthy in 1964 for Indian population. It contains 100
items which are divided into 9 scales namely Hysteria, Anxiety, Depression, Mania,
Psychopathic Deviate, Schizophrenia, K- scale, Repression- Sensitization, Paranoia
(Murthy, 1975).

5. Cattell’s 16pf test:

It is developed by Raymond B. Cattell in 1949, to measure 16 source traits which are
also called 16 personality factors. The test provides scores on 16 primary personality
scales and 5 global personality scales. This test is used to generate personality profile
of the individual and is often used to evaluate employees and to help people select a
career.
It has 5 forms i.e.Forms A,B,C,D,andE

A,B and C,D are parallel form

A,B have 187 item(graduation+)

C,D have 105 item (high school)

E has 128 items(illiterate)

6. Neo-PI-Revised:
This test has been developed by Costa & Mc Crae in the year 1992. Initially it was
designed for use by adults, revised in the year 1992 and made usable for people as
young as 10 years. It contains 240 items that assess 30 specific traits (or facets), 6
for each personality dimension:

1) Neuroticism 2) Extraversion 3) Openness to 4) Agreeableness 5)Conscientiousness

(N), (E), Experience (O), (A), (C).

The items are answered in a 5- point Likert scale, ranging from strongly agreeable to
strongly disagreeable. There are two forms: parallel self report (Form S) and observer
rating (Form R).

354
7. Temperament and Character Inventory (TCI) :
It is developed by Robert Clonninger et al in 1994. It is based on biosocial model of
personality.
It has four temperament dimensions:

1.Novelty 2.Harm 3.Reward 4.Persistence

Seeking, Avoidance, Dependence

Three character dimensions:

dimensions
1. Self 2.Self
Self- – 3.Cooperativeness
Directedness, Transcendence

Four validity scales: Runs, Rarity, True and Like-

Like unlike and alternate versions of self
report, informant ratings and interviewer’s ratings are there (Clonninger et al, 1994).

B. Projective Techniques
The term “Projective test” was popularized by L. K. Frank (1939). In this, the
person whose traits are to be studied is asked to describe an unstructured stimulus or
situation and through his responses, his needs, drives, motives, fears, etc, are revealed.

According to Lindzey (1961):

 Association techniques: The subject is asked to tell or write the association
generated by any verbal, visual or auditory stimulus. e.g., Word association Test,
Rorschach.
 Construction techniques: The subject is required to construct any specific thing
for which the test
test provides a framework. For example, in Thematic Apperception
Test, the subject is asked to write a story on a given picture.
 Completion techniques: Here the subject is supposed to complete a sentence or
give a response to complete a conversation. For e e.g., Sentence Completion
Tests, Rosenzweig Picture Frustration Study.
 Choice or ordering technique:
technique Requires the subjects to arrange materials
according to their choice.
Examples are - Tomkins – Horn Picture Arrangement Test, Szondi Test.
 Expressive techniques:
techniques: Subjects are required to draw something or performs
something. With these creative or artistic works, subjects are considered to be
expressing themselves. e.g., Draw-
Draw A – Person Test, Psycho drama

1. Thematic Apperception Test (TAT) :

It was developed by Henry Murray and his co-worker worker Christiana Morgan in 1943.It
consists of 31 achromatic pictures (one card is a blank card), typically showing
individuals of both sexes and of different age groups involved in various activities.
The test requires the subject
subject to tell a story for each card. The administration of the
cards depends upon the age, sex and the condition of the person to be assessed.
Responses are interpreted under categories like the hero, needs, press, outcome,
conflicts, emotions etc. Many different
different scoring and interpretation system like
Murray’s need - press system, and Bellak’s main theme are available. It can assess
a person’s cognitive style, imaginative processes, family dynamics, defensive
structure, significant people, general intelligence,
intelligence, sexual adjustments and many
more (Ackerman et al, 1999).Various adaptations of TAT exist, including Indian
adaptation by Uma Chowdhury (1960).

355
Test administration The subject is asked to write short stories on the events or
situations depicted on the cards. The story should contain few things. For example,
o What happened in past that has led to the present condition.
o What is happening now
o Who is/are this/these person/people?
o What is/are he/she/they doing?
o What are the predominant emotions?
o What is he thinking?
o What will happen in future?
o The subject is asked to be spontaneous and write the stories as fast as possible.
Test interpretation
Following are the basic interpretive points
• Hero: Hero is the central character of the story. Hero can be male or female.
• Needs: Those internal forces of the person which play important role in
determination of behaviour (e.g., need for achievement, need for nurturance,
need for sex, need for affiliation etc.).
• Press: External forces (environmental factors) that have significant impact on
behaviour.
• Emotions: Predominant emotions.
• Defense mechanism: Defenses used by the individual.
• Need-press interaction: How the needs and presses of the individual are interacting
• Outcome: The outcome of the story is happy or sad. It is also important to note that
the outcome is vague or clear.
• Thema: The basic theme of the story (Need-press-outcome combination).

2. Rorschach Inkblot Test:

It is the most used projective test in clinical setting. It is an associative test, was
developed by Swiss psychiatrist Hermann Rorschach in 1921.
The test consists of 10 symmetrical, ambiguous inkblots in which card numbers
1, 4, 5, 6 and 7 are completely achromatic, card number 2 and 3 are partially
chromatic and card number 8, 9 and 10 are completely chromatic. The test requires
the subject to report what the inkblot looks like to him. The test is divided into three
parts- administration, scoring and interpretation. Administration consists of
introduction, instruction, response and inquiry, the scoring refers to the classification
of responses into categories which revolve around the location of the blot in which
the percept was seen (example: whole, detail etc); the qualitative aspects of the
perception (called determinants) which include shape, color, shading etc and content
of what was perceived (animals, human anatomy etc). Interpretation is aimed to
assess the structure of personality with an emphasis on how individuals construct
their experiences (cognitive structuring) and assign meanings to their perceptual
experiences. The interpretation provide information on certain variables within
specific clusters namely control and stress tolerance, Situation related stress,
affective features, self perception, information processing, mediation, ideation and
interpersonal perception. Rorschach died shortly after the publication of
“Psychodiagnotik” (1921). His work was continued by his colleagues and now six
different scoring and interpretation systems are available namely Beck, Hertz,
Piotrowski, Klopfer, Rapaport and Exner for the Rorschach test (Exner, 2002).
Procedure of administration:
The seating arrangement should be side-by-side. Prepare the subject for overall
assessment process. Cards should be stacked in face-down position. Location sheet
should not be visible during the free association phase.

Instruction: Give the first card in the subject’s hand and ask “what might this be?”
(This is the basic instruction and nothing should be added). If the subject responds
by saying that “this is an ink-blot”, acknowledge it and further say “that is right. This
is ink-blot test, and I want you to tell me what it might be.” On the first card, before
giving any response or after giving one response, if the subject asks “How many
things should I find” the standard answer is “If you take your own time, I am sure you
will find more than one.” If after giving more than one response the subject asks
“How many should I see?” the standard response is “It is up to you.” If the subject
gives more than 6 responses on card number one, the card should be taken back.
Same procedure should be followed if on other cards the number of responses is

356
 more than 5. However, if on card number 1, the subject has given less than 6
responses and on other cards he is giving more than 5 responses, he should be
allowed to do so. Verbatim of all the responses should be recorded. Position of
card should be noted.

Inquiry phase: In this phase examiner should read the responses. The instruction in
the inquiry phase should be “Show me where it is and what there is that makes it to look
like that.”

Location:

W Whole The entire blot is used in the response

D Common detail Frequently identified area
Dd Uncommon detail Infrequently identified area
S Space response White space area is used in the response

Developmental Quality
+ Synthesized More than one percept. At least one
percept has definite form demand
V/+ Synthesized None of the percept has any form
demand
O Ordinary One percept with definite form demand
V Vague One percept without any form
demand
Determinants
1.Form F 6.Shading dimension V
FV
VF
2.Movement M 7.Shading diffused Y
FM YF
m FY
3.Chromatic Colour C 8.Form Dimension FD
CF FC Cn
4.Achromatic Colour C’ 9.Pairs and reflections (2)
C’F rF
F’C Fr
5.Shading texture T
TF
FT
 Blends
• Form quality: +, O, U, -
• Content
• Special scores

Unusual verbalizations
1. Deviant verbalization

a. Neologism b.Redundancy

2. Deviant response
a.Inappropriate b.Circumustantial
phrases response

Inappropriate combinations
1.Incongruous 2. Fabulized 3. Contamination
combinations combinations

Inappropriate logic

Perseveration

357
 1.within card 2. content 3. Mechanical
perseveration perseveration perseveration

Confabulation

Special content characteristics

1. Aggressive 2. Morbid content 3.Personalized

movement content

Special colour phenomenon

1. Colour projection

4. The Sentence Completion Test-:

In this test individuals are required to complete a number of incomplete sentence
stems, presented to them. Test usage surveys consistently find that sentence
completion tests are the most popular personality instruments used by practitioners
(Holaday et al, 2000).Rotter’s Incomplete Sentence Blanks are the commonly used
completion techniques (Gregory, 2004).

5. The Draw A Person Test (DAPT) :

It is an expressive technique developed by Karen Machover. It requires a person to
‘draw a person’ that assess the psychodynamic aspects of personality involved with
the self image and body images. The interpretation of DAPT is essentially qualitative
where a particular ‘body sign’ is associated with certain personality characteristics
(Gregory, 2004).

Personality tests for Children:

1. Children Personality Questionnaire (CPQ) :
It is developed by Raymond B. Cattell and Rutherford B. Porter (1968) for age range
8 to12 years having two part A and B each of 70 items. It measures 14 Primary
Factors and 4 Secondary factors (Cattell & Porter, 1968).

2. Children Self Report and Projective Inventory(CSRPI) :

It was developed by Robert L Ziffer and Lawrence E Shapiro(1992) in which
sentence completion, projective story cards, drawing task, critical items are there to
assess the conflict areas of a child(Ziffer & Shapiro, 1992).

3. Children’s Apprerception Test (CAT) :

It is a direct extension of the TAT, given by Leopard Bellak and Sonya Sorel Bellak in
1961. It consists of 10 pictures, suitable for children 3 to 10 years of age. The
preferred version for younger children (CAT-A) depicts animals in unmistakably
human social setting. A human figure version (CAT-H) is available for older children
(Bellak & Bellak, 1994).

C. Observational Methods
In Observational Method, the person whose personality traits are to be observed
are put either in structured or unstructured situations and observations are made by
the observers (Groth & Marnat, 2003).
1. Interview:
Interview is a face to face interpersonal situation which has a clear sequence and
relevant themes that helps the interviewer to achieve the defined goals (Groth &
Marnat, 2003).
2. Rating Scale:
A rating scale is defined as a technique through which the observer or ratter
categorized the objects, events or persons on a continuum, represented by a series
of continuous numerals. Some commonly used rating scale in clinical practice are
Brief Psychiatric Rating Scale(BPRS), Positive and Negative Syndrome
Scale(PANSS),Young Mania Rating Scale(YMRS),Hamilton Rating Scale For

358
 Depression(HAM-D),Beck Depression Inventory(BDI),Yale Brown Obsessive
Compulsive Scale (Y-BOCS) etc.

Observational method and rating scales for Chidren:

1. Conner’s Rating Scale-Revised:
An instrument devised by C. Keith Conners, which uses observer ratings and self-
report ratings to assess attention deficit/hyperactivity disorder (ADHD) and evaluate
problem behavior in children and adolescents. The instrument offers versions for
parents, teachers, and adolescents (Maruish, 1999).

2. The Child Behavior Checklist (CBCL) :

The Child Behavior Checklist (CBCL) given by Thomas M. Achenbach (1991) is a
device by which parents or other individuals who know the child well, rate a child's
problem behaviors and competencies. It gives profiles for scoring parent’s report on
the Child Behaviour Checklist for ages 4-18yrs., teachers’ reports on the Teacher’s
Report Form for ages 5-18yrs., and self-reports on the Youth Self –Report for Ages
11-18yrs (Maruish, 1999).

3. The Childhood Autism Rating Scale (CARS) :

The Childhood Autism Rating Scale (CARS) was initially developed by Schopler,
Reicher and Renner in 1971 to enable clinicians to help in a more objective
diagnosis of autism in a more readily usable form. It is a 15- item behavioral rating
scale developed to identify children with autism, and to distinguish them from
developmentally handicapped children without the autism syndrome (Schopler et al,
1971).

II. Intelligence Tests

Robert Sternberg (1985) defined intelligence in terms of three characteristics:
1. the possession of knowledge
2. the ability to efficiently use knowledge to reason about the world
3. the ability to employ that reasoning adaptively in different environments

Developmental Quotient (DQ), Intelligence Quotient (IQ), Performance quotient (PQ)

and assessment of adaptive functioning in terms of Social Quotient (SQ) are widely
used concepts in intelligence.

Intelligent Quotient (IQ) - The term Intelligence Quotient (IQ) was devised in 1912 by
William Stern. It is an expression of an individual’s ability level at a given point of time,
in relation to the available age norms. IQ=MA/CA X 100 (Anastasi, 1997).
Basal Level-A level for tests in which subtest items are ranked from easiest to hardest
and below which the examinee would almost certainly answer all questions correctly (
Gregory, 2004).
Ceiling Level-A level for tests in which subtest items are ranked from easiest to hardest
and above which the examinee would almost certainly fail all remaining questions
(Gregory, 2004).
Mental Level- The child’s score on the test can be expressed as mental level
corresponding to the age of normal children whose performance he or she equaled
(Anastasi, 1997). It is also called Mental Age (MA).
Chronological Age- The age from birth to the time of testing is called chronological
age. The mental age does not increase in a rapid orderly fashion after middle teens
(Morgan et al, 1993). Therefore even for adults the chronological age mostly taken to be
16 while calculating the IQ ratio.

General intellectual functioning is determined by the used of standardized tests of

intelligence, and the term significantly sub-average is defined as an intelligence quotient
(IQ) of approximately 70 or below or two standard deviations below the mean for the
particular test. Adaptive functioning can be measured by using a standardized scale.

Classification of Intelligence of IQ IQ Range

Range Classification

359
 a
Profound mental retardation (MR) Below 20 or
25
a
Severe MR 20-25 to 35-40
a
Moderate MR 35-40 to 50-55
a
Mild MR 50-55 to about
70
Borderline 70-79
Dull normal 80 to 90
Bright normal 110 to 120
Superior 120 to 130
Very superior 130 and above

a
According to the fourth edition of Diagnostic an Statistical Manual of Mental Disorder
(DSM-IV)

The most commonly used intelligence tests may be classified into three types:
A. Schedules of develoment and B. Verbal C. Non verbal and
socioadaptive functioning Tests Performance tests

Developmental Schedules for infants and preschool children:

These are most useful as screening instruments for assessing the developmental level
of children up to five years of age.
1. Developmental Screening Test (DST):
The Developmental Screening Test by Bharat Raj (1977) is designed to measure
mental development of children from birth to 15 years of age by a semi-structured
interview with the child and a parent or a person well acquainted with the child.
There are 88 items distributed according to the age scales. It provides
Developmental Age, DA and Developmental Quotient, DQ (Bharat Raj, 1977).

2. Gesell Developmental Schedule (GDS):

It is developed by Arnold Gesell (1880-1961) represents a standardized procedure
for observing and evaluating the course of development in child’s daily life. It
assesses maturity in infants and preschool children in four major developmental
areas namely Motor development, Adaptive behavior, Language development and
Personal social behavior. It provides an estimate of Developmental Age (DA) and
Developmental Quotient (DQ) and can be used for the age range of 1-72months

3. Stanford -Binet test for Intelligence:

Since the inception of the Stanford-Binet, it has been revised several times.
Currently it is in its fifth edition assesses intelligence and cognitive abilities in
children and adults aged 2 to 23 years. It assesses four areas: verbal reasoning,
quantitative reasoning, abstract/visual reasoning, and short-term memory which are
covered by 15 subtests. An initial vocabulary test, along with the subject's age,
determines the number and level of subtests to be administered.Total testing time is
45-90 minutes, depending on the subject's age and the number of subtests given
Hindi adaptation of the third revision by Santosh Kumar Kulshrestha (1971) is having
the age norms of 2 years 6 months to 18 years.
Types of Reasoning
1. Verbal reasoning - Vocabulary absurdities
2. Quantitative – Quantitative Test Number series
3. Abstract Visual – Paper folding copying
4. Short Term Memory – Memory for sentence, order in which familiar objects

360
4. Wechsler Intelligence Scale:
The Wechsler Adult Intelligence Scale (WAIS) is the best standardized and most
widely used intelligence test in clinical practice today. It was constructed by David
Wechsler at New York University Medical Centre and Bellevue Psychiatric Hospital,
in 1939. The original WAIS has gone through several revisions.
There are 11 separate subtests, which include the Verbal scale (6 subtests) and the
Performance scale (5 subtests). Verbal IQ score and performance IQ score together
comprise a full-scale IQ score. The Wechsler Intelligence Scale for Children (WISC)
was originally developed as a downward extension of the Wechsler Adult Intelligence
Scale, for ages of 6 and 16 in 1949. A revised edition WISC-R came in 1974, and the
third edition, the WISC-III in 1991. The current version, the WISC-IV, was produced
in 2003(Gregory, 2004). The Verbal part of WAIS has been adopted for Indian
population by Prasad and Verma for age range 20-69 years known as Verbal Adult
Intelligence Scale (VAIS) in 1988 and the performance part of WAIS has been
adapted for Indian population in 1974. Current version is Wechsler Adult Intelligence
Scale revised in 1997 by Verma.
WAIS Scales
• Verbal WAIS scales
1. Information: 29 questions - a measure of general knowledge.
2. Digit Span: Subjects are given sets of digits to repeat initially forwards then
backwards. This is a test of immediate auditory recall and freedom from
distraction.
3. Vocabulary: Define 35 words. It is a measure of expressive word knowledge. It
correlates very highly with Full Scale IQ
4. Arithmetic: 14 mental arithmetic brief story type problems. Test distractibility as
well as numerical reasoning.
5. Comprehension: 16 questions which focus on issues of social awareness.
6. Similarities: A measure of concept formation. Subjects are asked to say how two
seemingly dissimilar items might in fact be similar.
• Performance WAIS scales
7. Picture Completion: 20 small pictures that all have one vital detail missing.A test
of attention to fine detail.
8. Picture Arrangement: 10 sets of small pictures, where the subject is required to
arrange them into a logical sequence.
9. Block Design: Involves putting sets of blocks together to match patterns on cards.
10. Digit Symbol: Involves copying a coding pattern.
11. Object Assembly: Four small jig-saw type puzzles.
WECHSLER ADULT PERFORMANCE INTELLIGENCE SCALE AND VERBAL
INTELLIGENCE SCALE
• Performance part of WAIS has been adopted for Indian population by
Prabharamalinga Swamy in 1974
• Verbal part of WAIS has been adopted for Indian population by Prasad and Verma
(age range 20-69 years)
Performance Verbal
Picture completion Information
Digit symbol Comprehension
Block design Arithmetic
Picture arrangement Digit span
Object assembly
IMPORTANT POINTS:

 If the difference between VQ and PQ > 20 points – Brain dysfunction indicated

361
  Learning Disability- Picture competition, object assembly ,vocabulary arithmetic,
information

 Weschler Scale – 4 factor

 Verbal – I, S.V.C

 Perceptual organization - PC, PA, BD, OA

 Freedom from distractibility - A, DS

 Processing speed - coding

5. Malin’s Intelligence Scale for Indian Children (MISIC):
Malin’s Intelligence Scale for Indian Children is an Indian adaptation for WISC
constructed by Dr. Arthur J. Malin in 1969, for age range is 6-15.11yrs.The scale
comprises 12 sub tests divided into Verbal and Performance groups. In verbal part,
Information, Comprehension, Arithmetic, Similarities, Vocabulary and Digit Span and
in Performance part, Picture Completion, Picture Arrangement, Block Design, Object
Assembly, Coding, Mazes are there. It also provides the child with a full scale IQ
(Malin, 1969).

Non Verbal and Performance Test:

Performance tests require the subjects to express their answers in the form of drawing,
gestures, activities such as arranging block and puzzles, matching designs and placing
pictures meaningfully.
1. Bhatia’s Performance Test of Intelligence:
The test is developed by C.M. Bhatia in 1955.This test consist of five sub tests –
1. Block Design – 10 cards
2.Pass Along Test (Originally by Alexander) 8 patterns
3. Pattern Drawing Test - (8 patterns)
4. Immediate Memory of Sounds/digits
5. Picture Construction Test – 5 item
The test can be administered on persons of 11 years of the age and above. All five
sub tests are administered in a sequence as given above. The obtained raw score
are converted into mental age (MA) which can be used to calculate I.Q. (Intelligence
Quotient) of a person. This test is not to be use on mentally retarded persons
(Bhatia, 1971).

2. Gesell Drawing Test:

The test developed by Arnold Gesell (1880-1961) has norms for children as young
as 16 months and a ceiling of 7 yrs. There are 5 primary shapes corresponding to
assigned ages, in which the individuals are instructed to copy the shapes.
Draw them one by one 3 trials given

3 yrs.

4 yrs

5 yrs

6 yrs.

362
7yrs

3. Seguin Form Board Test (SFB):

The test given by O. Edward Seguin (1812-1880) is used as a quick measure of
general intelligence in children between 3-11 yrs. In this test the individual is
required to insert ten variously shaped blocks into the corresponding recesses as
quickly as possible (Gregory, 2004).

4. The Vineland Social Maturity Scale (VSMS):

It is developed by Edgar A. Doll in 1935, and has been revised several times since its
first publication. The scale was designed to assess the social competence of individuals
of ages from birth to 25 years and above. The Indian adaptation of VSMS, by A.J.
Malin, has an age range of birth to 15 years. There are eight domains with 89 items,
grouped age wise.Scoring of the items gives the information on social age from which
the social quotient could be calculated (Malin, 1992).

5. Behavioural Assessment Scale for Indian Children with Mental Retardation

(BASIC-MR):
This scale, developed by Peshawaria and Venkatesan (1992), is divided into two
parts. Part A which has seven domains with 280 items, deals with skill behaviours,
and Part B which deals with problem behaviours, consisting of 10 domains with 75
items .The information on the scale is collected through direct observation of the
child and by interviewing parents.
III. Neuropsychological Assessment
Neuropsychological assessment as began in the 1950s is a well defined
discipline with the work of Halstead, Reitan, and Goldstein in the United States, Ray in
France, and Luria of the Soviet Union. It is used for screening and assessing the
presence of possible neuropsychological impairment.
1. Bender Visual Motor Gestalt Test (BVMGT) :
It is developed by Lauretta Bender in 1938. It cannot be used with the children below
age 3 years. There are total nine cards in which card A is the orientation card. It
assesses visual acuity and motor functioning. There are several scoring methods
available in which Pascal and Hain’s are most commonly used. In Hain’s method
(1964) of scoring which was followed by Bhargava and Sadhu (1987), the protocol
must be scored on the basis of 15 signs. In this the maximum score is 34. The
score of 9 and above shows severe dysfunction.

2. Wisconsin Card Sorting Test (WCST) :

It is developed by David A. Grant, and Esta A. Berg, in the year 1948 to assess
reasoning ability, set shifting, ability to use feedback and inhibitory control of
influence. In this test there are 4 stimulus cards and 128 total cards which are
divided into two sets of 64. The sorting works on three principles Form, Number
and Colour and one more principle of other. Four shapes are there of triangle,
star, cross and circle. The age range for this test is 6 and ½ to 89 years (Heaton
et al, 1993) .Common scoring points are-
1. Number of sets completed
2. Number of errors
3. Number of perseverative responses
4. Number of perseverative errors
5. Number of nonperseverative errors
6. Conceptual level responses

3. Post Graduate Institute Battery of Brain Dysfunction (PGIBBD):

The test is developed by Dwarka Pershad and Santosh Kumar Verma (1990). It
consists of
1. PGI Memory scale,
2. Revised Bhatia’s Short Battery of Performance test of intelligence,

363
 3. Verbal Adult Intelligence Scale,
4. Nahor Benson Test,
5. Bender Gestalt Test.
This test can be use on anyone within the age range of 20-45 irrespective of their
education and sex (Pershad & Verma, 1990).

4. Wechsler Memory Scale –3rd edition (WMS-III) :

It is given by David Wechsler (1948). The second revision is done in 1987, WMS-R
and now it is in its third revision (1998). It assesses learning, memory, and working
memory in the age range of 16-89 years. This edition retains the index score
configuration of the WMS-R, but scale content, administration and scoring
procedures have been changed. It requires strict and discreet timing for certain
subtests (Wechsler, 1998).

This third edition updates the WMS-R and provides subtest and composite
scores that assess memory and attention functions using both auditory
and visual stimuli.

There are now eight Primary Indexes (Auditory Immediate (was Verbal),
Visual Immediate (was Visual), Immediate Memory (new), Auditory
Delayed (new), Visual Delayed (new), Auditory Reception Delayed (new),
General Memory (only delayed subtest scores), and Working Memory),
which constitute Immediate Memory, General (Delayed) Memory, and
Working Memory (was Attention/Concentration).

This edition retains the index score configuration of the WMS-R, but scale
content, administration and scoring procedures have been changed.

There is one slight change to the optional Information and Orientation
subtest and one item has been deleted and six items added to the Mental
Control subtest.

The Figural Memory, Visual Paired Associated, and card B of Visual
Reproduction subtests have been dropped.

There are slight wording and administration changes in Logical Memory,
and added subtests help to assess various aspects of visual memory.

Requires strict and discreet timing for certain subtests

5. The Luria-Nebraska Neuropsychological Battery (LNNB) :

On the basis of the concept given by A.R. Luria, Anne Lise Christensen developed
this battery which was further adapted in the United States by Charles J. Golden,
Thomas A. Hammeke, and Arnold D. Purisch, in the year 1985. It was designed to
assess neurologically impaired patients for ages 15 and over. It has two forms in
which form I has 269 items and form II has 279 items. It is having 4 scales namely
Clinical, Summary, Localization and Factor.

Clinical Summary Localization Factor

Motor functions Pathognomonic Left frontal Kinsethesis-based Simple phonemic

movement reading

Rhythm Left-hemisphere Left sensorimotor Drawing speed Word repetition

Tactile functions Right Hemisphere Left parietal- Fine-motor speed Reading

occipital polysyllabic words

Visual functions Profile elevation Left temporal Spatial-based Reading complex

movement material

Receptive speech Impairment Right frontal Oral-motor skill Reading simple

material

Expressive speech Right Rhythm and Spelling

sensori pitch
motor

364
 perception

Writing Right Simple Motor writing skill

parietal tactile
-
occipit sensation
al

Reading Arithmetic
Right Streognosis calculation
tempor
al

Arithmetic Visual acuity and naming Number reading

Memory Visual-spatial organization Verbal memory

Intellectual processes Phonemic discrimination Visual and

complex memory

Spelling (Form II only) Relational concepts General verbal

intelligence

Motor writing (Form II only) Concept recognition Complex verbal

arithmetic

Verbal-spatial relationship Simple verbal

arithmetic

6. Cambridge Neuropsychological Test Automated Battery (CANTAB) :

CANTAB developed at University of Cambridge, provide an effective method of
cognitive assessment by assessing
1. General memory and learning,
2. Working memory and executive function,
3. Visual memory,
4. Attention and reaction time (RT),
5. Semantic/verbal memory, and decision making and
6. Response control.
This is a language-independent test which has a touch screen technology that
delivers rapid and non invasive cognitive assessment. It contains 19 tests in
which one can run tests individually or can set up a battery of a number of tests.
ASSESSING SPECIAL POPULATION
To assess the special population, who cannot be properly or adequately,
examined with traditional instruments the performance, non language and non verbal
tests are widely used. Mentally Retarded Persons, Person with Physical Disabilities
comes under this group (Anastasi, 1997).Following tests have been developed for these
populations:
1. Assessment of Disability in Persons Suffering from Mental Retardation
(ADPMR):
Individual tests for intelligence and measure for adaptive behavior in everyday life are
widely used to assess the strengths and deficit areas of mentally retarded persons.
ADPMR is a scale for measuring and quantifying disability in person with mental
retardation, developed by A. Nizamie, V.K. Singh and B.N.P. Sinha in 2005. It
comprised of five areas, namely
,
1.Perceptual- 2. Self- 3.Communication 4. Social 5. 6.Occupational
Motor Care Academic

Rating can be done by direct observation and informant’s information.

2. Indian Disability Evaluation and Assessment Scale (IDEAS):

It is a scale for measuring and quantifying disability in mental disorders. The scale is
developed by The Rehabilitation Committee of the Indian Psychiatric Society in 2002.A

365
scale for measuring and quantifying disability in mental disorders. It is best suited for
the purpose of measuring and certifying disability for the mentally ill population
in India. Patients with the following diagnosis are eligible for the disability benefits-
Schizophrenia Bipolar disorder, Dementia, ObsessiveCompulsive
disorder.

The duration of illness at least 2 years - the number of months the patient was
symptomatic in last 2 years should be determined.
3. Assessment for Person with Physical Disabilities:
It is possible to administer verbal tests on the person with hearing impairment; if the
oral questions are typed on cards. Some of the earliest performance scales, such as the
Pintner-Paterson Performance Scale, The Arthur Performance Scale, and the WISC-R
Performance Scale has been the most widely used in this area. For blind persons oral
tests can be most readily adapted while the performance tests are least likely to be
applicable. The Wechsler scales have been adapted for blind persons and widely used
in western scenario. Person with motor impairment found it difficult to work against the
strict time limit or in strange situation, for them there are steps taken by adapting some
tests, like Porteus Maze Test. Peabody Picture Vocabulary Test is one which is widely
used in this area. (Anastasi, 1997)The assessment of physically disabled children at
an early age is very important in order to provide appropriate educational experiences
from the outset. This helps to prevent the cumulative learning deficits that would
magnify the effects of the disability on intellectual development.

COMPUTERS AND PSYCHOLOGICAL ASSESSMENT

Mental health professionals eagerly embraced technology in their quest to
improve the efficiency and accuracy of testing as the scoring of psychological tests by
hand is a tedious, time consuming, and error prone.The umbrella term Computer
Assisted Psychological Assessment (CAPA) refers to the entire range of computer
applications in psychological assessment. Strong Vocational Interest Blank (SVIB)
development was the first step towards this technical revolution in the field of mental
health. By the 1970s, it was realized that computers could be integrated into the entire
process of psychological assessment. By the 1980s, CAPA was so prevalent that
virtually every psychological test in existence could be interpreted by computers.
Computing in mental health has included not only computer assisted assessment but
also computer interviews, computerized diagnosis, computer aided instruction, clinical
consultation and simulated psychiatric interviews. (Groth & Marnat, 2003).For example,
MMPI, WAIS-R, WISC-R, CANTAB and many more psychological tools has computer
versions.

Issues related to the development of Psychological Tests

A psychological test requires few basic procedures to be followed, in order to
make it ready for administration. The following are the main important aspects which
have to be considered:
 Content: - This is the first question; the author of the test must answer. Which
abilities, aptitudes, or personality traits are to be measured? After having
determined this valuable point, the author of the test is required to search for the
scientific work conducted in that particular area. But Test content has often been
an area of criticism. Items in terms of factual and veridical content can always be
challenged.
 Item analysis:-The quality and merits of a test depends upon the individual items of
which it is composed. Item analysis is thus the most integral part of both the
reliability and validity of the test.
 Target Population:- The next step is to identify the target population on whom the
test has been standardized.
 Problems of reliability:- Variation in human performance is an important problem
which may challenge the reliability of a test. Usually it is more evident in personality
tests than as compared to ability test (Groth & Marnat, 2003). Another problem in
establishing reliability results from the imprecise nature of psychological testing
methods. Ideally a test being used for clinical purpose should have reliability of .90

366
 and for research purpose it should not be less than .70 (Anastasi, 1997; Groth-
Marnat, 2003).
 Validity:- Two types of validities required in clinical testing are incremental validity
and conceptual validity. Incremental validity means that the test should be able to
produce the results which are accurate and could be obtained with greater ease and
less expense. Conceptual validity focuses upon the uniqueness of an individual
(Anastasi, 1997) problems with validity.
 Standardization and Norms:- Standardized procedure is an essential procedure in
any psychological test. A test must possess norms or standards. The norm group is
referred to as the standardization sample. Before the administration of the test, the
user must be aware of the population on which the test has been standardized.
Some of the common criticism of psychological tests has come through the Anti-test
Revolt(Anastasi,1997), they are: One of the major criticisms of psychological tests
has been that they foster a rigid, inflexible, and permanent classification of
individuals

Controversial concepts in psychological testing

 Culture fair vs. culture free test
When psychologists began to develop psychological test for cross cultural purpose,
in the first part of the 20th century, they presumed that it would be theoretically possible
to measure “hereditary intellectual potential” independent of the cultural experiences.
The individual’s behavior was thought to be overlaid with a sort of cultural veneer whose
penetration became the objective of what were called the “culture free tests”.
Subsequent developments laid to demonstration of fallacy of this concept. It was
recognized that hereditary and environmental factors operate jointly at all the stages in
the life of a human being. Since all the behaviour are affected by the cultural milieu in
which the individual is reared and psychological tests measure the behavioural aspect
of an individual, the performance is bound to be affected due to the cultural impact.
Thus the term culture free was replaced by terms as “culture common”, “culture fair” and
“cross- cultural” (Anastasi, 1997).
 Measures of deterioration and premorbid IQ
The deterioration in cognitive functioning with age can be accessed through the
overall scatter between the scores of the Wechsler subtests. Wechsler (1998) proposed
that the relation of Verbal to performance IQ, and Hold to Don’t Hold tests can measure
the deterioration.
Don’t Hold - Digit Span, Similarities, Digit Symbol, and Block Design are those which
normally decline with age
Hold tests - Vocabulary, Information, Object Assembly, and Picture Completion tend
to remain stable through age (Korchin, 1986).

Deterioration Index (DI) =Hold- Don’t Hold

2
Premorbid IQ provides the information with which it is possible to compare the
current performance level of an individual to the premorbid level of functioning.For
estimating premorbid ability, the performances on hold test are considered as they
found to be more resistant to neurological impairment. It can also be assessed by
demographic variables based regression equation developed by Crawford and Allan
(1997), National Adult Reading Test(NART) developed by Hazel Nelson in the 1980s
and published in 1982 or Wechsler Test of Adult Reading (WTAR) developed by
Wechsler, 2001(Groth & Marnat, 2003).But, assessing premorbid I.Q is still remaining
an area of controversy.
 Malingering
Malingering is a medical and psychological term that refers to an individual
exaggerating the symptoms of mental or physical disorders for a variety of
motives,including getting financial compensatio, avoiding work, obtaining drugs, getting
lighter criminal sentences, trying to get out of going to school, or simply to attract
attention or sympathy. Malingering is a constant concern when conducting a
psychological assessment. The detection of malingering requires clinical acumen as
well as sound psychological assessment (Groth & Marnat, 2003).
Malingering occurs usually in one of the following situation:

367
 1. In criminal cases, when mental illness or mental retardation is fiegned in
order to obtain better or safer living conditions or an environment from which
escape is easier, in order to obtain drugs, to avoid trails, or in hopes of
evading responsibility for the crime with which the offender is charged.
2. In personal injury actions and compensation cases
3. In military service or similar special situation where nervous or mental
disease might afford an escape from hazardous or arduous duty.
So, psychological tests are being used frequently to detect malingering
Source of Error in Test Findings
Examiner being the test administrator may not always remain neutral in the test
administration and knowingly or unknowingly may affect the test findings. Some of the
effects caused by the examiner have been identified which are supposed to be taken
care of are:
 Barnum effect: The tendency of individuals and clinicians to readily accept vague
personality descriptions as though they were valid and specific (Cash, Mikulka, 1989).
 Halo effect: It refers to the tendency on the part of the examiner to be unduly
influenced by a single trait which may color the judgment of the examiner about the
person taking the test. It is a tendency to rate a person high or low on all dimensions
because of a global impression is called hallo effect.
 Leniency effect: It refers to the reluctance of many raters to assign unfavorable
ratings. It leads to the bunching of ratings at the upper end of scale. It is also caused by
extraneous factors such as the attractiveness of the examinee.
 Error of central tendency: It refers to the tendency to place people at the middle of
the scale and to avoid extreme position
 Context Error: It refers to the examiner to assess the person in the context of
others rather than based upon objective performance.
Other factors caused by the examiner also have been identified that affects
the psychological assessments are:
 Impact of rapport establishment: Rapport establishment is a comfortable, warm
atmosphere that serves to motivate examinees and elicit cooperation. Initiating a
cordial testing milieu is a crucial aspect of valid testing. A tester who fails to establish
rapport may cause a subject to react with anxiety, passive-aggressive
noncooperation, or open hostility. Failure to establish rapport distorts test findings:
ability is underestimated and personality is misjudged.
 Influence of gender, race, and experience in psychological assessment: A wide
body of research has sought to determine whether certain characteristics of the
examiner cause examinee scores to be raised or lowered on psychological
assessment. Interview and interactive testing procedures create ample opportunity
for an examiner’s age, gender, ethnicity or other characteristics to make
respondents feel more or less comfortable and more or less inclined to be
forthcoming. Examiners accordingly need to be alert to instances in which such
personal qualities may be influencing the nature and amount of the data they are
collecting. Most studies find that sex, experience and race of the examiner make
little, if any, difference. In isolated instances, particular examiner characteristics
might very well have a large effect on examinee test scores. (Gregory 2004)
 Background and motivation of the examinee: Examiner not always is at fault,
psychological assessments are also affected by the examinee. Examinee differ not
only in the characteristics that examiner to assess, but also in other extraneous
ways that might confound the test results. There are multiple factors that play an
important role like interest, motivation, test anxiety, malingering, or cultural
background. Test results might be inaccurate if the examinee has reasons to
perform in an inadequate or unrepresentative manner. A motivation to deceive or to
fake will affect the test findings. (Gregory 2004)

Problem in different domains of psychological testing

An inevitable consequence of the expansion and growing complexity of any
scientific endeavor is an increasing specialization of interests and functions among its
practitioner. Each of the area has some merits and certain limitations. It will be
discussed one by one.

i) Issues in intelligence testing:-

368
 IQ tests are excellent predictors of academic achievement, occupational
performance, and are sensitive to the presence of neuropsychological deficit. However,
certain liabilities are also associated with these successes. They are limited in
predicting certain aspects of occupational success and non-academic skills, such as
creativity, motivational level, social acumen, and success in dealing with people.
Furthermore, IQ scores are not measures of an innate, fixed ability, and their use in
classifying minority groups has been questioned. Finally, there has been an
overemphasis on understanding the end product of cognitive functioning and a relative
neglect in appreciating underlying cognitive processes (Groth-Marnat, 2003).
Currently the test of intelligence based upon the psychometric abilities are showing
shift from the g-factor to the multifactor approach. Tests are being developed based on
the neuropsychological processing model. Conceptualization of intellectual functioning
based on a neuropsychological understanding of how various regions of the brain may
function is valuable, especially if the brain is considered responsible for intelligence in
the first place ( Das, et al, 1994). Test such as the Kaufman Assessment Battrey for
Children ( Kaufman & Kaufman, 1993) and Das- Neilgeri Cognitive Assessment System
(Neilgeri and Das, 1997) are based on the neuropsychological model only. There are a
few problems with intelligence tests which must be addressed:
 Testing persons with physical disability: Although steps have been taken to
develop tests to assess the intelligence of those who are physically disabled but the
assessment of intelligence may not be relevant for the simple reason that every
person presents a unique configuration of types and degrees of abilities, disabilities
and personal characteristics
 Ethnic minorities: Intelligence tests have always been criticized for being limited in
assessing the ethnic minorities. For this reason it is often essential to be aware with
the values and beliefs of the client. The more flexible approach in these cases is to
apply tests which are least affected by cultural variables. Tests such as Ravens
Progressive Matrices or the performance part of other intelligence tests can be used.
 Flynn effect: Flynn effect is the rise of the average intelligence quotient over
generations. Norm revision in every 10 years is an essential part of intelligence
testing. The exposure of children enhances with the change with time, hence the
children tested on older norms would score higher so the intelligence test becomes
somewhat of little use if the norms are not revised after a period of ten years.

Personality testing and related issues

Measuring personality may utilize the format of objective testing, as in a
personality inventory, or of projective tests such as the Thematic Apperception Test or
the Rorschach Inkblot Test. But these days cognitive psychologists are also focusing
upon the biological determinants of personality. For example, recently efforts have been
laid to study individual difference on thought processes using positron emission
tomography (Posner, et al, 2001).
Valuable assessment shows what is special or different about the person being
assessed. Some of the major advantages and limitation of personality assessment
techniques are:-

a) Self report tests: Straightforward to standardize, easy to administer, reliable,

capture views of self well; but limited in richness, easy to fake, depends on self-
knowledge.
b) Projective: One of the few ways to go beyond the surface and assesses those
aspects which may not self-report, may yield insight for further studies; but often
have significant problems of reliability and validity.
In projective and self report techniques, there are some limitations that question the
reliability and the validity of the psychological assessment. For example, limitations
highlight several issues associated with the Rorschach Inkblot Test. It is one of the most
complex test in current use, error can potentially be introduced from many different
directions, including censorship by the subjects, scoring errors (particularly for
infrequently used scorings), poor handling of the subtleties of interpretation, time
required for scoring and interpretation, limited use with children, extensive time required
for training. Like most projective techniques, TAT theoretically offers access to the
covert and deeper structures of an individual’s personality. It is still rated in the top most
frequently used instruments. There has typically been difficulty establishing adequate
internal consistency and test-retest reliability. Because inadequate normative data are

369
generally lacking, clinicians often rely on clinical experience when they interpret the
responses. The standardization in respect to administration and scoring is generally
inadequate. Thus, the effectiveness of the technique is often more dependent on the
clinician’s individual skill than on the quality of the test itself.

iii) Issues in neuropsychological assessment

Neuropsychology is a branch of psychology which studies brain-behaviour
relationship. It also focuses upon the neuropsychological assessment and rehabilitation
(Mitrushina et. al 1999).
With the recent advancement in neuroimaging, there have been several queries
regarding the need for neuropsychological assessment. Some of the main ones are:

i) Do we need neuropsychological assessment in the stage of advanced

functional and structural imaging? Neuroimaging today provides precise
information regarding brain functioning. Still neuropsychological assessment retains
its place as an important tool for brain functioning. There are various indicators of
neuropsychological assessment which makes it relevant even today:
 Detailed neuropsychological assessment can help in establishing the baseline
level of cognitive functioning.
 Neuropsychological assessment provides the nature and extent of cognitive
impairment (Groth & Marnat, 2003).
 Also the deficits observed in neuropsychological testing are used for rehabilitation
and planning of treatment.
 Neuropsychological testing is also used in pre and post assessment of cognitive
functioning after neurosurgery (Stringer & Nadolne 2002)
 At times no abnormality is observed on structural imaging; still the behavioural
changes are observed which may be indicating organicity.
 It is used to assess brain functioning in progressive brain disease.
 It is used to assess the neuropsychological sequel of psychiatric disorders.
ii) Contra-indicators- Neuropsychological findings at times may not be relevant,
even if the assessment prerequisites have been checked. There are several factors
which may render the results of neuropsychological findings as unreliable ( Groth &
Marnat, 2003), some of them are:
 Physical problem may affect the test performance. Also the sensory or motor
difficulties may affect the test findings.
 Current or pre-existing psychiatric disorders or learning disability may affect
psychiatric disorders (Lezak, 1995).
 Congenital & pre-existing neurological conditions including prior brain injury,
insult or epilepsy are also relevant factors that may affect results.
 Language problem may also be an important factor as those who have a different
mother tongue may perform poorly.
 Cultural biasness is observed in some of the test which may affect the test
findings.
 Assessment in sessions may affect the test results for a variety of reasons.

Psychological report writing

Psychological report is the final step in assessment. In general there are few
guidelines to be followed while writing a psychological report. They can be discussed in
the following points:

i) Length: A psychological report along with proper history and behavioral

observation should be around five or seven single spaced pages (Singh 1997).
However the length can substantially vary depending upon the nature of report.
ii) Style: The style of report writing may depend upon the primary training and
orientation of the examiner. The American Psychological Association (1992)
recommends that regardless the form followed in report writing the report should
have accuracy, clarity, integration and readability.
iii) Presenting the test interpretation: There are three ways in which clinician presents
the interpretation of the test. The first one is the hypothesis oriented focuses upon the
referral question. The second one is the domain oriented divided over specific topics
such as abilities, interpersonal relationships, vocational abilities or sexuality. The third

370
 approach is test-by-test interpretation, in which the clinician simply gives relevant
findings according to each test (Tallent, 1992).
iv) Topics: In the case of domain oriented report writing there are a few broad topics
under which the report is written. They are the cognitive function, personality&
interpersonal relationship. Furthermore if the test is for diagnostic clarification then it
must include the diagnostic indicators also.
v) What to include? – The guideline to write a report relates to the needs of the
referral setting, background of the readers, purpose of testing, relative usefulness of
the information, and whether the information describes the unique characteristic of
the person. The clinician should emphasis relative intensity of client’s behaviour.
(APA, 1992). And it is very important that the report writer should always try to avoid
technical words in reports means the terminology should be very simple ( Groth &
Marnat, 2003). And there should be some specific rule regarding the length of
information.
vi) Summary and recommendation: This is the final stage of report writing when the
clinician must give an overall summary of the relevant findings in a brief manner
followed by proper recommendations for future assessment and treatment planning.

Ethical issues: related controversies

Ethical issues are of great relevance in psychological assessment. The American
Psychological Association has published certain ethical guidelines called Ethical
Principal of Psychologists and Code of Conduct (APA, 1992). A special series in the
Journal of Personality Assessment (Russ, 2001) also elaborate about the ethical
dilemmas found in training, medical, school and forensic settings. Some of the main
ethical issues to be considered in psychological assessment are:

i) Developing a professional relationship:

The relationship between the client and the clinician should be completely
professional and well defined. This means that the nature, purpose and conditions of
relationship are discussed and agreed on.
ii) Invasion of privacy:
APA (1992) specifically states that the information obtained through
psychological assessment should never be shared without the permission of the client.
iii) Confidentiality :
Practitioners have a primary obligation to safeguard the confidentiality of
information, including test results that they obtain from clients in the course of
consultations (APA, 1992a).
iv) Informed consent :
Before testing commences, the test user needs to obtain informed consent from
test takers or their legal representatives. The main purpose is to made examinee aware,
in language that they can understand, of the reason for testing.
v) Labeling :
The clinician should always be sensitive to the potential negative impact resulting
from labeling by outside sources and or by self-labeling as well as the possible limiting
effects which labeling might have.
vi) Competency of the clinician:
Another ethical issue which has been focused upon is the competency of the
clinician in proper administration and interpretation of the testing instrument. The
clinician should have the knowledge of the test and their limitations and should be
willing to accept responsibility for competent test use (Turner et al., 2001).
vii) Communicating test results:
The psychologist should give feedback to the client or the referral source
regarding the results of assessment. The information being provided should be clear
and should ideally be in the everyday language.
viii) Maintenance of test security and assessment information:
This specifically means that any copyright material should not be duplicated.
This means the psychologist should make all possible effort to ensure that the materials
are safe and remain in the possession of safe hands only. The security of assessment
results should also be maintained.

Related Controversies:
Psychological assessment has been criticized for violating ethical issues.

371
 It is often sited that psychological tests lead to invasion of privacy. Although
this problem can logically be related to personality test it is often used against any kind
of test.
 Furthermore the problem of confidentiality is another area for which the
psychological tests have been seen through skepticism.
 The “self-fulfilling prophecy” has often been sighted against testing, as it
affects the individual’s self concept and the behaviour of his associates around
him.

Indian Scenario
In India majority of work has been done on adaptation of tests. Tests such as the
PGI Battery of Brain Dysfunction (Prasad &Verma, 1989), Bhatia Battery of
Performance Test of Intelligence (Bhatia, 1955), WISC-R(Verbal scale was also
translated in Hindi by Sharma in 1997).Stanford- Binet Intelligence Test(Kulshreshtha,
1971),Developmental Screening Test (Raj, 1977), Multiphasic Personality
Questionnaire (Murthy, 1975) have been adapted.There has been effort in Central
Institute of Psychiatry to standardize the norms of several tests such as the construct
validity of Luria Nebraska Neuropsychological Battery (LNNB),and standardization of
few subtests of Cambridge Neuropsychological Test Automated Battery
(CANTAB).There is AIIMS Neuropsychological battery which is a Hindi adaptation of
Luria Nebraska Neuropsychological Battery (LNNB). Moreover National Institute of
Mental Health & Neurosciences (NIMHANS) has published the norms of tests like
Stroop test, Trail Making and Wisconsin Card Sorting Test and development of tests in
different areas.Hindi Adaptation of Kaufman Assessment Battery for Children was also
done in Ranchi Institute of Neuro Psychiatry and Allied Sciences (RINPAS). But still,
Indian Psychologist need to take further efforts in order to develop new psychological
tests as well as to prepare norm for Indian population and revising of existing norms.
Future Direction
Professional, moral, ethical, social and even legal issues have interacted to
produce today’s trends in psychological testing. New tests keep coming out all the time,
with no end in sight. There are hundreds of new tests being publishes each year. But
there is safety in predicting continued controversy and disagreement in the testing field,
which will no doubt produce further change. Disagreement and controversy are second
nature to psychologists; because of disagreement, however, new data are sought,
found, and ultimately produce some clarification of old controversies along with band-
new contradictions and battle lines. As a consequence, change will be constant
characteristics of the fields. Improved technology is currently being applied in the testing
field. Because of advances in computer technology, statistical procedures can be
performed with great ease. This technology thus contributes to the current trend toward
better future. Psychologists continue to be optimistic because of the change as
ultimately resulting in more empirical data, better theories, continuing innovations, and
higher standards (Groth-Marnat, 2003). Ideal approaches for Psychological assessment
should be comprehensive and multi-faceted in techniques and theoretical frameworks.
They should also be flexible and adaptable to the unique needs of each individual. And
the test should be more standardized and the norms should not be out dated.

Appendix-I
Intelligence: An integrate or global capacity of the individual to think rationally, to act
purposefully and deal effectively with the environment.
Inventory: In inventory the individual describes his/her own feelings, environment, and
reaction of others towards him/her.
Personality: Personality is a dynamic organization, inside the person, of
psychophysical systems that create a person’s characteristic patterns of behaviour,
thoughts, and feelings.
Diagnosis: Determining the nature and source of a person’s abnormal behavior, and
classifying the behavior pattern within an accepted diagnostic system
Assessment: Appraising or estimating the level or magnitude of some attribute of a
person; testing is one small part of assessment which also incorporates observations,
interviews, rating scales and checklists.
Psychometrics: Psychometrics is the field of study concerned with the theory and
technique of educational and psychological measurement, which includes the
measurement of knowledge, abilities, attitudes, and personality traits. The field is

372
primarily concerned with the construction and validation of measurement instruments,
such as questionnaires, tests, and personality assessments.

Appendix-II: Important Landmarks in psychological Testing(Gregory 2004)

1905 Binet and Simon invent the first modern intelligence test.
1914 Stern introduces the IQ, or Intelligence quotient
1916 Lewis Terman revises the Binet-Simon scales, publishes the Stanford-Binet
revisions appears in 1937,1960 and 1986.
1917 Robert Yerkes spearheads the development of the Army Alpha and Beta
examinations
1917 Robert Woodworth develops the personal data sheet , the first personality test
1920 Rorschach Inkblot test published.
1921 Psychological Corporation –the first major test publisher-founded by Catell,
Thorndike and Woodworth.
1939 Wechsler-Bellevue Intelligence Scale published. Revisions published in
1955,1981,and 1997.

Appendix III: Classification of psychological assessment: Commonly Used

PERSONALITY INTELLIGENCE NEUROPSYCHOLOGICAL CHECKLISTAND
TESTS TESTS TESTS RATING SCALES

CATELL’S 16 PF Developmental Bender Visual Motor Brief Psychiatric

Screening Test Gestalt Test Rating Scale
Multiphasic Gesell Wisconsin Card Sorting Positive and Negative
Personality Developmental Test Syndrome Scale
Questionnaire Schedule
(MPQ)-
Neo-PI-Revised Stanford -Binet test Post Graduate Institute Conner’s Rating Scale
Battery of Brain
Dysfunction
Rorschach Inkblot test Wechsler Wechsler Memory Scale – The Child Behavior
Intelligence Scale 3rd edition Checklist
Thematic Apperception Malin’s Intelligence Luria-Nebraska The Childhood Autism
Test Scale for Indian Neuropsychological Battery Rating Scale
Children
The Draw A Person Bhatia’s Cambridge Young Mania Rating
Test Performance Test Neuropsychological Test Scale
Automated Battery
Children Personality Gesell Drawing Test Trail making Hamilton Rating Scale
Questionnaire For Depression
Children Self Report Seguin Form Board Stroop Beck Depression
and Projective Inventory Test Inventory
Children’s The Vineland Social Boston Aphasia test Beck Scale For
Apprerception Test Maturity Scale Suicidal Ideation
Minnesota Multiphasic Behavioural Alcohol Disorder
Personality Inventory -II Assessment Scale Identification Test
for Indian Children
with Mental
Retardation
Millon Clinical Multiaxial Vinland Social CAGE Questionnaire
Inventory- III Maturity Scale
Temperament and Human Figure Yale Brown Obsessive
Character Inventory drawing test Compulsive Scale
Sentence Completion General Health
Test questionnaire
Zung Depression
Scale
Schedule for the
Assessment of
Positive Symptoms
Schedule for the
Assessment of
Negetive Symptoms

373
 Appendix IV: Other tools for psychological assessment
Name of the Test Development Purpose of Assessment
Checklist for Child Joseph Petty, 1990 Child Abuse
Abuse
Evaluation(CCAE)
NEPSY Marit Korkman, Ursula Kirk, Neuropsychological
Sally Kemp, 1998 Development
Eating Disorder David M. Garner, 1984, 1991, Eating Disorder
Inventory-3 (EDI-3) 2004
Slosson Full Range Bob Algozzine, Ronald C. Full range intelligence
Intelligence Test(S- Eaves, Lester Mann, H. Rober
FRIT) t Vance(ed. By Steven. W.
Slosson),1988, 1993
Kaufman Adolescent Alen S. Kaufman, Nadeen L. Intelligence
and Adult Intelligence Kaufman, 1993
Test(KAAIT)
Test of Memory Tomm N. Tombaugh,1996 Neuropsychological impairment
Malingering(TOMM) & Malingering
NEO PI -R Costa and Mc Crae, 2002. Measure of five domains of
personality
Bayley Scales of Infant Nancy Bayley, 1993 Infant Development
Development
Universal Non Verbal Bruce A. Bracken, R. Steve, Nonverbal Intelligence test
Intelligence Test(UNIT) Mc Callum, 1988
Benton Visual Retention Arthur L. Benton , 1946 (Rev- Visual perception & Visual
Test 5 by Abigail Benton Memory
Sivan,1992)
Defence Mechanism N. R. Mrinal & Uma Measure of Defences
Inventory(DMI) Singhal,1984
Dementia Rating Scale- Paul J. Jurica, Christopher L. Dementia
2(DRS-2) Leitten, Mattis, 1988,2001.
Behavioural Barbara A. Wilson, Nick Executive Function
Assessment of the Alderman, Paul W. Burgess,
Dysexecutive Hazel Emslie, Jonathon J.
Syndrome(BADS) Evans, 1996
The Rivermead Barbara A. Wilson, Janet Memory
Behavioural Memory Cockburn, Alan
Test-II Baddeley,1985,2003
Constructive Thinking Seymour Epstein,2001 Constructive Thinking
Inventory(CTI)
Suicidal Ideation William M. Reynolds,1988 Suicidal Ideation
Questionnaire(SIQ)
Amsterdam Short-term Ben Schmand & Jaap Short- term Memory
Memory Test Lindeboom with collaboration
of Thomas Mertin & Scott R.
Millis,2005
Cognitive Distortion John Briere,2000 Cognitive Distortions
Scales(CDS)
Grade Level Jayanthi Narayan, 1999. Learning Problem in Schools
Assessment Device For
Children With Learning
Problems In
School(GLADS)
Autism Diagnostic Ann Le Couteur, Catherine Autism
Interview– Revised(ADI- Lord, Michael Rutter,2003
R)
Nimhans Bhoomika R. Kar, Shobjini Neuropsychological function
Neuropsychological L.Rao, B.A. Chandramouli, K.
Battery For Children Thennaraus,2004
Objects Sorting Test Craig J. Gonsalvez, Ida P. Thought Deviation
(OST) Barnabas, and Marisa L. Lobo
Raven’s Progressive John C.Ravens.2002 Abstract Reasoning
Matrices
Porteus Maze Test Stanley Portues1952 Non verbal test of intelligence
Preschool Behavior Jaxqueline McGuire and Focusing on children need
Checklist Naomi Richman ,1998 ,parental involvement, change

374
 over time, obtaining resourses
Behaviour rating GenardA.gioia, K. To assess executive function
inventory of Executive Isquith,L.Kenworthy,2004 behavior
Functioning
Childhood Autism Schoper, Riechler and Identify children with autism
Rating Scale Renner ,1971
Children’s Self Report Ziffer and Shapiro,1992 Understanding the inner world of
And Projetive Inventory the child ,social –emotional
functioning
Universal Nonverbal Bruce A. Bacon and To assess the general
Intelligence Test R.S.McCallum intelligence and cognitive ability
Behavior Rating RuttenBerg,Schien and Evaluate the Status of autistic ,
Instrument For Autistic Wenar,2004 atypical or other low functioning
And other Atypical Children
Children-II
Portage Guide to early Doan,Wollenburg and To assess the domain of
education-II Wilson,1976 impaired behavior in a child

375
 Appendix IV: Important findings in different clinical conditions : Kahn and Giffen
(1960)
ORGANIC BRAIN SCHIZOPHRENIA MANIA DEPRESSION ANXIETY Suicidal
PATHOLOGY Ideation
Piotrowski signs on Bender-Gestalt test Rorschach Rorschach Rorschach Rorscha
Rorschach  Complete  Decreased  Less  Average or ch
 Number of deviance from reaction time number of slightly poor  FV
responses less gestalt  More number responses form level
than 15  Complete of responses  Vista  Average
 Response time rotation  Colour responses ≥ number of
greater than 60  Added angles dominated 1 poplar
seconds  Giving new form  FC’+C’F+C’ responses
 Less than two names to the responses >2  High number
human designs  More number  Morbid of texture
movements Rorschach of responses responses > responses (≥
 F+% is less than  Perceptual on chromatic 3 1)
70 disturbances cards as  Form level  High number
 Less than 4  X+%(<70) compared to average or of vista
popular  F+% (<70) achromatic slightly poor responses (≥
responses  X-% (>20) cards 1)
 Persevaration of  Thought  Poor form Thematic
responses at disturbances level (<70)Apperception
least 3 times  special Test
without regard to scores (>4)  Inconclusive
form accuracy (incom,fabcom,alog, ends (I don’t
 Impotence contam, DV, DR) know what
 Perplexity  Perseveration will happen)
 Automatic  Few or no Thematic Usually
phrases that are human Apperception negative
illogical and movement Test outcomes of
irrelevant to the responses  Unorganized the stories
task  Pure colour stories  Indecisivene
responses  Lack of ss (may be
 Rejections coherence a boy or a
 Less number girl)
On Bender-Gestalt of responses  Suicidal
Test Thematic intents
 Serious Apperception Test  Short
disturbance of stories (at
gestalt  Rigidity and times mere
 Modification or refusal to description
substitution of elaborate of pictures)
parts of figure  Negation
 Micrographia or  Déjà vu
macrographia reaction
 Difficulty with  Projection of
angles threatening or
 Partial rotation evil intentions
 Vagueness and and
sketchiness

376
 Loss of detail and homosexual
fragmentation attributes
 Perseveration,  Prolonged
overlapping etc. reaction time
The Draw-A-Person  Grossly
Test disproportion
 Lack of details ate emphasis
 Erasures on relatively
infrequent unimportant
 Figures may be details
large  Frequent
 Lines heavy and perusal of the
simple back of the
 Proportions poor card
 Synthesis weak Draw-a-Person test
 Omissions of  Omission of
parts important
parts
 Bizarre
additions
 Grossly
exaggerated
size
 Presence of
sexual
organs in
drawing

Appendix V: Tentative Guidelines for selecting a test for various purposes

The use of specific psychological test is one of the basic skills of the applied
psychologist. In clinical settings, testing is the unique function of the psychologist.
Test user should:
1. Define the purpose of testing and the population to be selected.
2. Appropriate testing enviorment should be considered as per psychological
testing.
3. Should investigate potential useful sources of information, in addition to
test scores.
4. Read the materials provided by the test developers and avoid using tests
which are unclear or incomplete information are provided.
5. Tests should be selected that are appropriate-for the intended test taking
population considering age, sex, education.
6. Provide evidence that the tests meet its intended purpose(s).
7. Avoid being clerical in approach. Should have one’s own perception and
skills in analysis of results. Should have a holistic approach.

377
 Background Behavioral History of
Assessment Tests
Info Observation head injury

 
Personality Not ESDST,BMVGT,MCMI-III/MMPI-II,
Assesment/diagnosis significant TAT,SSCT,RORSCHACH(Basic tests of
assessment. But, other tests can be used
depending upon the situation)

  
Neuropsychological ESDST,BMVGT,PGIBBD/CANTAB/LNBB
Assessment

 
Intelligence May/Not VSMS,DST/VAIS,WAPIS/
Assessment be Standford-Binent, Bhatia Battery,Seguin
Significant form board, MISIC,SPM

May /Not be 

For therapeutic Past history BPRS /PANSS/ SANS/ SAPS/
purposes. and Significant
According to premorbid  HAM-D /MADRS/ GDS BDI/ YMRS
psychiatric Condition personality  Yale Brown OC Scale
1.Depression  Any scale relevant to the condition
2.OCD and tools of personality assessment
3. Anxiety (TAT, Rorschach etc) if required
4.Substance Related
5. Mania

REFERENCES

Major references
Anastasi, A. & Urbina, S. (1997) Psychological testing (7th ed.). Upper Saddle River, NJ:
Prentice-hall
Gregory, R.J. (2004)Psychological Testing: History, Principles, and Applications.4th
edition. Pearson education.
Groth-Marnat (2003). Current Status and future directions of psychological assessment:
Introduction. Journal of Clinical Psychology, 55, 781–785.
Kaplan, M.R. & Saccuzzo, D.P. (1982) Psychological testing: Principles, Applications, and
Issues, 4th edition. IT publication.
Maruish, M.E. (1999) The use of psychological testing for treatment planning and
outcomes assessment. American Psychiatric Publishing. Washington, DC.
Prasad, D. & Verma, S.K. (2002)The comcept and assessment of intelligence. 2nd edition.
Bhargava book house.
Singh, A.K. (1997) Tests, Measurements and Research Methods in Behavioral Science.
Bharti bhavan publication.

Other references

378
Achenbach, T.M. (1991). Integrative Guide to the 1991 CBCL/4-18, YSR, and TRF Profiles.
Burlington, VT: University of Vermont, Department of Psychology
Ackerman, S.J., Clemence, A.J. & Weatherill, R. (1999) Use of the TAT in the assessment of
DSM –IV cluster B personality disorder. Journal of Personality Assessment, 73,
422-448.
Adams, L.A., Culberton, L.J. (2000) Personality Assessment: Adults & Children, in
Comprehensive Text Book of Psychiatry, (Eds.), Kaplan & Sadock, Washington,
Lippincott: Williams & Wilkins.
Agioia. G., Isquith, K., Kenworthy, L. (2004) Behavior rating inventory of executive functioning
manual.Psychologiacl assessment resource.
Algozzine, B., Eaves, R.C., Mann, L. & Vance, H.R. (1988, 1993) Slosson full range intelligence
test(S-FRIT). New York: Slosson Educational Publication, Inc.
American Psychological Association (1974) Standards for educational and psychological tests
and manuals. Washington, D.C.: American Psychological Association.
American Psychological Association (1992) Ethical principles of psychologists code of conduct.
American Psychologist, 49, 677-680.
Bayley, N. (1993). Bayley scales of infant development (2nd ed.): Manual. San Antonio: The
Psychological Corporation.
Bean, K.L. (1953) Construction of Educational and Personnel Tests. New York: McGraw-Hill
Book Co.
Bellak, L. & Bellak, S.S. (1994) Children’s apperception test (C.A.T.) (4th ed.). Larchmnot, N.Y.:
C.P.S. CO
Benton, A.S. (1992). Benton visual retention test (5th ed.). San Antonio: The Psychological
Corporation.
Beutler , L.E. & Clarkin , I.F. (1990) Systematic treatment selection: Toward targeted
therapeutic interventions. New York: Oxford University Press.
Beutler, L.E. & Harwood, T.M. (2000) Prescriptive Psychotherapy : A practical guide to
systematic treatment selection. New York : Oxford University Press.
Beutler, L.E. & Groth–Marnat, G. (2003) Integrative assessment of adult personality (2ndEds.).
New York: Gilford Press.
Beutler, L.E., Engel, D., Mohr, D., Daldrup, R.J., Bergan, J., Merdith, K. & Merry, W. (1999).
Predictors in differential and self directed psychotherapeutic procedures. Journal
of Consulting and Clinical Psychology, 59, 333-340 in The Use of psychological
testing in treatment planning and outcome assessment (2nd ed.) (Eds.), Maurish,
M. E.
Bhatia, R., Verma, S.K, Pradad, D.,et al, (1971) Bhatia Short Battery of Performance test of
intelligence for adults. Psychologiacal cooperation.
Bracken, B.A., Steve, R. & Callum, Mc. (1988) Universal non verbal intelligence test: examiner’s
manual. Illinoise: Riverside Publishing Company.
Briere, J. (2000) Cognitive distortion scales: professionals manual. Florida Avenue:
Psychological Assessment Resources, Inc.
Briere, J. (2001) Detailed assessment of post traumatic disorder: Professional’s manual. USA:
Psychological Assessment Resources, Inc.
CANTAB (2003) Cambridge Neuropsychological Test Automated Battery. Cambridge:
Cambridge Cognition.
Cash, T.F., Mikulka, P.J. & Brown, T.A. (1989) Validity of Millon’s computerized assessment
system for the MCMI: Comment Moreland and Onstad. Journal of Consulting and
Clinical Psychology, 57 (2), 311-312
Cattell, R.B. & Porter, R.B. (1968) Handbook for the children’s personality questionnaire (The
CPQ). New Delhi: The Psycho Centre. By arrangement with Champaign,
Illinoise, U.S.A: Institute for Personality and Ability Testing.

379
Cattell, R.B., Eber, H.W. and Tatsuoka, M.M. (1970) Handbook for the sixteen personality factor
questionnaire (16 PF). Champaign, III: Institute for Personality and Ability
Testing.
Cesi, S.J. (1990). On Intelligence …more or less: A bio ecological treatise on intellectual
development. Englewood Cliff Prentice Hall
Clonninger, C.R., Przybeck, T.R., Svrakic, et.al, (1994) The temperament and character
inventory (TCI): A guide to its development and use. Washington University, St.
Louis, Missouri: Centre for Psychobiology of Personality.
Cohen, M.J. (1997) Children‘s Memory Scale: Manual. San Antonio: The Psychological
Corporation.
Conner’s, C.K. (1997). Conner’s Rating Scales-Revised. In Maruish, M.E. (1999). Use of
psychological testing for treatment planning and outcomes assessment (pp. 467-
495). Hillsdale, NJ: Lawrence Erlbaum Associates.
Costa, P.T., Jr. & McCrae, R.R. (1992) NEO PI-R professional manual. Odessa, F.L.:
Psychological Assessment Resources, Inc.
Craig, J.G., Barnabas, P.I., Lobo, M.L. (2003). Object sorting test manual. Psychological
assessment resource. Inc
Das, J.P., Naglieri, J.A. & Kirby, J.R. (1994). Assessment of cognitive processes: The PASS
theory of intelligence. Neeham Heights, MA : Allyn & Bacon.
Doan, M.A., Wollenburg, K. & Wilson, E. (1998). Portage Guide to early education.Portage
ptoject.
Dorwart, R.A. (1996). Outcome management strategies in mental health: Applications and
implications for clinical practice. In L. I. Sedner & B. Dickey (Eds.), Outcome
assessment in clinical practice (pp 45- 54). Baltimore : Williams & Wilkins.
Epstein, S. (2001). Constructive thinking inventory: Professional’s manual. USA: Psychological
Assessment Resources, Inc.
Exner, J.E. (2002) The Rorschach: A comprehensive system (4th ed.). New York: Willy.
Eysenck, H.J. & Eysenck, S.B.G. (1975). Manual of the Eysenck Personality Questionnaire.
London: Hodder and Stoughton.
Frank, L.K. (1939) Projective methods for the study of personality. Journal of Psychology, 8,
389-413.
Freeman, F.S. (1965) Theory and practice of psychological testing(3rd ed.).New Delhi: Oxford
and IBH Publishing Co. pvt. Ltd.
Garner, D.M. (1984, 1991, 2004). Eating Disorder Inventory-3. Professional’s manual. USA:
Psychological Assessment Resources, Inc.
Golden, C.J., Purisch, A.D. & Hammeke, T.A. (1991). Luria-Nebraska Neuropsychological
Battery. California: Western Psychological Services.
Graham, J.R. (2000). MMPI-2: Assessing personality and psychopathology (3rd ed.). New York:
Oxford University Press.
Greenspan, S. & Driscoll, J. (1997). The role of intelligence in a broad model of personal
competence. In D.P. Flanagan, J.L. Genshaft, P.L. Harrison (Eds.), Contemprary
intellectual assessment: Theories, tests, and issues (pp. 131-150). New York:
Guilford Press.
Griffin, J.R., Walton, H.N., Christenson & G.N. (2006). Decoding- encoding screener for dyslexia
(DESD): Manual. Los Angeles, California: Western Psychological Services.
Hamilton, M.A., (1960). Rating scale for depression. J Neurol Neursurg Psychiatry. 23: 56-62
Hankes, E. (1946), Handbook for the Strong vocational interest blank. Campbell, D. P.
accessed at http://books.google.co.in/books on 28.06.09.
Heaton, R.K. (1993). Wisconsin Card Sorting Test manual. Odessa: Psychological assessment
resources.

380
Holaday, M., Smith, D.A. & Alissa, S. (2000) Sentence Completion Test: A Review of the
Literature
Jaxqueline, M.G., Richman, N. (1998). Preschool Behavior checklist Manual.Academic therapy
Publication.
Jurica, P.J., Leitten, C.L. & Mattis, S. (1988, 2001). Dementia rating scale-2:Professional’s
manual. USA: Psychological Assessment Resources, Inc.
Kahn, C.T. & Giffen, B.M. (1960), Psychologist and their Test in Psychological Techniques in
Diagnosis and Evaluation ,New York Pergman Press, 8-14.
Kaplan, H.I., & Sadock, V.A. (2007)Synopsis of psychiatry, tenth edition, Lippincott Williams &
Wilkins.
Kar, B.R., Rao, S.L., Chandramouli, B.A. & Thennaraus, K. (2004). Nimhans
neuropsychological battery for children: manual. Bangalore: NIMHANS (Deemed
University).
Kaufman, A.S. & Kaufman, N.L. (1993). Kaufman adolescent and adult intelligence test. USA:
American Guidance Service, Inc.
Kirchner, W.K. (1958). Age difference in short term retention of rapidly changing information.
Journal of experimental Psychology, 352-358.
Korchin, S.J. (1999) Pyschological Testing I, in, Modern clinical psychology. New Delhi: CBS
Publishers & Distributers,194-247.
Korkman, M., Kirk, U. & Kemp, S. (1998). NEPSY: A developmental neuropsychological
assessment. China: PsychCorp.
Krstic, K. (1964). Classics in the History of Psychology .accessed at
psychclassics.yorku.ca/Krstic/marulic.htm on 28.06.09.
Kulshrestha, S.K. (1971) Stanfor–binet intelligence scale: Hindi adaptation of third revision-
Form L-M. Varanasi: Prashad Psycho Corporation.
Lezak, M.D. (1995). Neuropsychological assessment (3 rd ed.) New York: Oxford University
Press.
Lindzey, G. (1961) Projective Techniques and Cross Cultural Research. New York: Appleton –
Century – Crofts.
Malin, A.J. (1969) Malins Intelligence Scale for Children- Manual. Lucknow: Indian
Psychological Corporation.
Malin, A.J. (1992) Vineland Social Maturity Scale and Manual. Indian Adaption. Mysore:
Swayam Sidha Prakashan Mental Retardation, A manual for psychologist.
Secunderabad: National Institute for the Menatally Handicapped.
Millon, T., Millon, C., Davis, R., Grossman, S. (1994). Millon Clinical Multiaxial Inventory-III
anual (3rd ed). Minneapolis: NCS Pearson, Inc.
Mitrushina, M.N., Boone, K.B., D’Ella, L.F. (1999). Handbook of normative data for
neuropsychological assessment Oxford: Oxford University Press: 3-9
Morgan, C.T., King, R.A., Weisz, J.R. et al, (1993). What Psychology is Like, in Introduction to
psychology (7th ed.). New Delhi: Tata McGraw-Hill Publishing Company Limited,
1-34
Morgan, C.T., King, R.A., Weisz, J.R. et al, (1993).Psychological Assessment & Testing, in
Introduction to psychology (7th ed.). New Delhi: Tata McGraw-Hill Publishing
Company Limited, 151-561.
Mrinal, N.R. & Singhal, U. (1984). Manual for defence mechanism inventory (DMI). Agra:
National Psychological Corporation.
Murray, H.A. (1943). Thematic Apperception Test Manual. Harvard: Harvard University Press.
Murthy, H.N. (1975) Development of paranoid, depressive, manic and anxiety scale. Bangalore:
Transactions of All India Institute of Mental Health, 50-90.
Naglieri, J.A. & Das, J.P. (1997). Das- Naglieri Cognitive Assessment System. Itasca, IL :
Riverside.

381
Narayan, J. (1999). Grade level assessment device for children with learning problems in
schools. Secunderabad: NIMH.
Nizamie, A., Singh, V.K. and Sinha, B.N.P. (2002).Indian Disability Evaluation and Assessment
Scale (IDEAS). The Rehabilitation Committee of the Indian Psychiatric Society
Nizamie, A., Singh, V.K. and Sinha, B.N.P. (2005) Assessment of Disability in Person with
Mental Retardation. Jharkhand: Deepshikha Institute for Child Development And
Mental Health.
Owenby, R.L. (1997). Psychological reports: A guide to report writing in professional psychology
(3rd ed.). Brandon, V.T.: Clinical Psychology
Paheswaria, R. & Venkatesan, S. (1992, 1994) Behavioural assessment scales for
Indian children with mental retardation (BASIC-MR). Secunderabad:
National Institute for the Mentally Handicapped with financial assistance
from UNICEF
Pershad, D. & Verma, S.K. (1990). Handbook of PGI battery of brain dysfunction (PGI-BBD).
Agra: National Psychological Corporation.
Petty, J. (1990). Checklist for child abuse evaluation (CCAE): Professional’s manual. USA:
Psychological Assessment Resources, Inc.
Posner, M.L., Petersen, S., Fox, P. & Raichle, M.E. (2001). Localization of cognitive operations
in the human brain. Science, 240, 1627-1631.
Portues.S.(1952)The Portues test manual,George Howrap & co Ltd.
Pruit, J.A., Kalpow, J.C., Epping-Jordan, J.E., et al, (1999)Moving behavioural medicine to the
frontline : A model for the integration of behavioural and medical science in
primary care. Professional Psychology: Research and Practice, 29, 230-236.
Raj, B. (1977). The developmental screening test manual. Mysore: Meera Printers.
Ramalingaswamy, P. (1974). Wechsler adult performance intelligence scale, Form-PR: Manual
of Indian adaptation of WAIS- Performance scale. Delhi: Mansayan.
Ravens, J.C. (1936). Ravens Progressive Matrices manual. Oxford press LTD.
Reitan, R.M. (1958). Validity of Trail Making test as an indicator of organic brain damage,
Perception Motor Skills, 271-276
Reuven, B. (2002). Baron Emotional Quotient Inventory: A measure of emotional intelligence.
United States & Canada: Multi Health Systems, Inc.
Reynolds, W.M. (1988). Suicidal ideation questionnaire: Professional’s manual. USA: Psychological
Assessment Resources, Inc.
Russ, S.W. (2001). Tackling ethical dilemmas in personality assessment. Journal of Personality
Assessment, 77, 255-258.
Sattler, J.M. (2001) Assessment of children: cognitive functions (4th Ed.). San Diego, CA :
Author.
Schmand, B. & Lindeboom, J. (2005). Amsterdam short-term memory test: Manual. Leiden:
PITS.
Schopler, E., Reicher, R.J. & Renner, B.R. (1971) The childhood autism rating scale (CARS).
Los Angeles, CA: Western Psychological Services.
Sheidman, E.S. (1947). Manual for the make a picture story method. UCLA: The Society for
Personality Assessment, Inc.
Sternberg, R.J. (1985). Beyond IQ: A triarchic theory of human intelligence. New York:
Cambridge University Press.
Sternberg, R.J. (1997). Intelligence and lifelong learning: What’s new and how can we use it?
American Psychologist, 52, 1134-1139
Stinger, A.Y. & Nadolne, M.J. (2002). Nueropsychological assessment: Context for contemprary
clinical practice. In G. Groth – Marnat (Ed.), Neuropsychological assessment in

382
 clinical practice : A guide to test interpretation and integration (pp.26-47),
NewYork: Willey.
Tallent, N. (1992). The practice of psychological assessment. Englewood Cliffs, NJ: Prentice-
Hall.
Tallent, N. (1993). Psychological report writing (4th ed.). Englewood Cliffs, NJ: Prentice-Hall
Thorndike, R.L., Haegen, E.P., Sattler, J.M. (1986). Stanford- Binet Intelligence Scale (4th ed.)
Itasca, IL : Riverside.
Tombaugh, T.N. (1996). Test of memory malingering (TOMM). New York: Multi- Health Systems
Inc.
Turner, S.M., DeMers, S.T., Fox, H.R. & Reed, G.M. (2001). APA’s guidelines for test user
qualifications. American Psychologist, 56, 1099-1113.
Uma Choudhary (1960) Indian Adaptation of TAT. New Delhi: Manasayan
Wechsler, D. (1998). Wechsler Memory Scale III. Texas: The Psychological Corporation.
Wilson, B.A., Alderman, N., Burgess, P.W., Emslie, H. & Evans, J.J. (1996). Behavioural
assessment of the dysexecutive syndrome (BADS): Manual. UK: Harcourt
Assessment. The Psychological Corporation.
Wilson, B.A., Cockburn, J. & Baddeley, A. (1985, 2003). The rivermead behavioural memory
test-ii: manual (2nd ed.). United kingdom: Harcourt Assessment.
Young, R.C., Biggs, J.T., Ziegler, V.E., Mayer, D.A. (1978). A rating scale for mania; reliability ,
validity & sensitivity. Br. J. Psychiatry.
Ziffer, R.L. & Shapiro, L.E. (1992) Children’s self-report and projective inventory. United States:
Psychological Assessment Services.

****************

383
CHAPTER-XVIII
 BASICS OF PSYCHOTHERAPY

 INTRODUCTION
 HISTORICAL PERSPECTIVE
 WHAT IS PSYCHOTHERAPY?
 AIMS OF PSYCHOTHERAPY
 TYPES OF PSYCHOTHERAPY
 SCHOOLS OF PSYCHOTHERAPY
 PHASES OF PSYCHOTHERAPY
 MODALITIES OF PSYCHOHERAPY
 ETHICS IN PSYCHOTHERAPY
 NONSPECIFIC FACTORS IN PSYCHOTHERAPY
 CLIENT AND THERAPIST VARIABLES IN EFFECTIVENESS OF PSYCHOTHERPY
 PSYCHOTHERAPY AND MEDICATION
 ECLECTISM IN PSYCHOTHERAPY
 PSYCHOTHERAPY FOR CHILDREN
 LIMITATIONS OF PSYCHOTHERAPY
 PSYCHOTHERAPY IN INDIA
 CONCLUSION

INTRODUCTION

Helping another person in distress can be one of the most important human activities. As a
social being, humans are dependent on each other for maintenance of their biological and
psychological well being. When this is threatened in any way, they typically turn to each other
for help. Learning how to help people with psychological problems has been a challenge for
any mental health professional. In mental health care, psychotherapy has been a vital
treatment since the development of the great innovative and technical approaches embodied
by psychoanalysis and behaviorism at the beginning of the 20th century. Therapy researches
continue to make progress in the study of long- term maintenance of treatment gain and
many different approaches have been developed to alleviate personal misery.

HISTORICAL PERSPECTIVE
Psychotherapy is a technical term used in clinical fraternity to treat sufferings of an emotional
nature using the theories and principals of Psychology. Though not very structured and
manualized as psychotherapy is today, we get reflections in philosophical writings in epics
and so on about the concepts that were quite psychotherapeutic. For example, in Indian
philosophy spiritual health has been emphasized since thousands of years. If we trace the
history of Psychotherapeutic concepts in India, we find it as old as ‘Vedas’ and ‘Upanishad’.
The three main systems are Atharva veda , Ayurveda Charaka, Sushruta, Vagabhatta, and
Yoga. Perhaps, one of the first indications we get from Mahabharata in which Shree Krishna
helped Arjun to come out from his sadness and guilt feelings to perform his duty of Kshatria
dharma which was led down by the contemporary society to protect the rules and
regulations. Elements of psychotherapy are implied in the statement of ‘Charaka’. “As
384
regards the mental derangement resulting from an excess of desire, grief, delight, envy, or
greed, it should be allayed by bringing the influence of its opposite passion to bear on the
prevailing one and neutralize it”.

WHAT IS PSYCHOTHERAPY?
Traditionally, the term psychotherapy has been used to refer to the treatment of mental
disorders by means of psychological techniques, in a patient-therapist relationship. It is a
process in which a trained professional enters a relationship with a patient for the purpose of
helping the patient with symptoms of mental illness, behavioural problems or for helping him
towards personal growth.
Wolberg (1988) conceptualizes psychotherapy as an endeavour to alter the behaviour and
change the attitude of a maladjusted person towards a more constructive outcome. He
defines psychotherapy as, “, a form of treatment for problems of an emotional nature in
which a trained person deliberately establishes a professional relationship with a
patient with the object of…

 removing, modifying or retarding existing symptoms,

 mediating disturbed patterns of behavior, and
 promoting positive personality growth and development.

AIMS OF PSYCHOTHERAPY

Psychotherapy is more than a talk between two people regarding some problem. It is a
collaborative undertaking, started and maintained on a professional level towards specific
therapeutic objectives. These are:
 REMOVING EXISTING SYMPTOMS:
To eliminate the symptoms that are causing distress and impediments is one of the prime
goals in psychotherapy.
 MODIFYING EXISTING SYMPTOMS:
Certain circumstances may militate against the object of removing symptoms (e.g.
inadequate motivation, diminutive ego strength or financial constraints); the objective can be
modification rather than cure of the symptoms.
 RETARDING EXISTING SYMPTOMS:
There are some malignant forms of problems e.g. dementia where psychotherapy serves
merely to delay an inevitable deteriorative process. This helps in preserving patient’s contact
with reality.
 MEDIATING DISTURBED PATTERNS OF BEHAVIOUR:
Many occupational, educational, marital, interpersonal, and social problems are emotionally
inspired. Psychotherapy can play vital role from mere symptom relief to correction of
disturbed interpersonal patterns and relationships.
PROMOTING POSITIVE PERSONALITY GROWTH AND DEVELOPMENT:
Deals immaturity of the normal person and characterlogical difficulties associated with
inhibited growth. Here psychotherapy aims at a resolution of blocks in psycho-social
development to a more complete creative self-fulfillment, more productive attitudes, and
more gratifying relationships with people.

 It also aims at…

 Strengthening the patients motivation to do the right things
385
 Reducing emotional pressure by facilitating the expression of feeling
 Releasing the potentials for growth
 Changing maladaptive habits
 Modifying the cognitive structure of the person
 Helping to gain self knowledge
 Facilitating interpersonal relations and communications

TYPES OF PSYCHOTHERAPY

 Supportive Therapy
The main objective of supportive psychotherapy is to bring the patient to an emotional
equilibrium as rapidly as possible, with amelioration of symptoms, so that he can function at
a level approximating his norms. An effort is made to strengthen existing defenses as well as
to elaborate new and better mechanisms of maintaining control. There is no intent to change
personality structure, although constructive characterological alterations may develop as a
consequence of treatment when mastery has been restored.
 Re-educative Therapy
The objective in re-educative therapy is modification of behaviour directly through positive
and negative reinforcers, and /or interpersonal relationships, with deliberate efforts at
environmental readjustment, goal modification and the living up to existing creative
potentialities.
 Reconstructive Therapy
Reconstructive psychotherapy is more or less traditionally rooted in the theoretical soil of the
dynamic model of personality. The objective of reconstructive psychotherapy is to bring the
individual to an awareness of crucial unconscious conflicts and their derivations. It strives not
only to bring about a restoration of individual to an effective life functioning through resolution
of disabling symptoms and disturbed interpersonal relationships but it attempts also to
promote maturation of emotional development with creation of new adaptive potentialities.
(Wolberg,1988)
OBJECTIVES APPROACHES
TYPE OF TREATMENT
SUPPORTIVE  Strengthening of existing Guidance, Environmental Manipulations,
THERAPY defenses Externalization of Interests,
 Elaboration of new and Reassurance, Pressure, Persuasion,
better mechanisms of Emotional Catharsis and
maintaining control Desensitization, Prestige Suggestion,
 Restoration to an adaptive Suggestive Hypnosis, Inspirational
equilibrium Group Therapy, Supportive Adjuncts
(somatic therapy, muscular relaxation).
RE-EDUCATIVE  Deliberate efforts at Behaviour Therapy, Relationship
THERAPY Readjustment Therapy, Attitude Therapy, Client-
 Goal Modification Centered Therapy, Directive Therapy,
 Living up to existing Therapeutic Counseling, Case work
creative potentialities, with Therapy, Rational Emotive Therapy, Re-
or without insight in to educative Group Therapy, Marital
Therapy, Family Therapy, Psycho-
386
 conscious conflicts. drama, Semantic Therapy, Existential
Therapy, Strategic Therapy, Cognitive
Therapy.

RE-CONSTRUCTIVE  Insight in to Freudian Psychoanalysis, Ego-Analysis,

THERAPY unconscious conflicts, with Kleinian Analysis, Object relation
effort to achieve extensive Therapy, Neo-Freudian Psychoanalysis
alterations of character (Adler, Jung, Stekel, Rank, Frenczi,
structure Reich, Fromm, Sullivan, Horney, Rado),
 Expansion of Psychoanalytic Oriented
personality growth with Psychotherapies, Transactional
development of new adaptive Approaches, Existential Therapy,
potentialities Analytic Group Therapy.

SCHOOLS OF PSYCHOTHERAPY

 Psychodynamic Therapy
Psychodynamic theory begins with contribution of Sigmund Freud with the focus on
increasing ego strength and /or reducing the pressure of denied impulses, so that the patient
will be free to run his own life. Psychodynamic therapy is based upon the assumption that
problems occur because of unresolved -- usually unconscious -- conflicts, often originating
from childhood. The goal of this type of therapy is for the patient to understand and better
cope with these feelings by talking about the experiences which led to them, central task of
psychoanalyst is to bring out the hidden unconscious wishes and conflicts which underlie
present symptoms and behaviour through free association in which patient has to tell
everything that comes to his mind.
This therapy also focuses on dream analysis, because according to this therapy, during
sleep there is profound relaxation of normal ego controls than is possible in free association
and hence unconscious processes are freer to operate in sleeping than in waking thought.
Consequently dream provides a potentially rich source of information about unconscious
needs. The analysis of transference is also the core of psychoanalytic therapy. In which the
patient held strong personal feelings toward the analyst which simply could not be
understood in terms of actual events of therapy or the analyst’s character or behaviour. This
transference can be positive (like admiration, love and respect) as well as negative (hate,
contempt or anger). Freud believed that such reactions were not only barriers to therapy but
they might indeed be vehicle of therapeutic change. The essential fact about transference is
that it brings hidden and repressed feelings and conflict into the present where they can be
examined, understood and resolved.
 Behaviour Therapy
Behaviour therapy is a type of psychotherapy that focuses on changing undesirable
behaviours. It involves identifying objectionable, maladaptive behaviours and replacing them
with healthier types of behaviour. Behaviour therapy deals with changing and eliminating
unwanted behaviour. It is based upon the principles of classical conditioning developed by
Ivan Pavlov and operant conditioning developed by B. F. Skinner.
Classical conditioning

387
It is a learning process that occurs through associations between an environmental stimulus
and a naturally occurring stimulus. In classical conditioning, learning that takes place when a
conditioned stimulus is paired with an unconditioned stimulus.
Operant conditioning
Operant conditioning or instrumental conditioning is a method of learning that occurs through
rewards and punishments for behaviour. Through operant conditioning, an association is
made between behaviour and a consequence for that behaviour.

 Simple Extinction: Since learned behaviour pattern tend to weaken and disappear
over time if they are not reinforced, the simplest way to eliminate a maladaptive pattern is
often to remove the reinforcement for it. This is especially true in situations where
maladaptive behaviour is being reinforced unknowingly by others.
 Aversive Conditioning: If a response is followed by pain or punishment, its strength
should be weakened. Thus, behaviour change can be achieved by conditioning an aversive
response to an undesirable behaviour, a principle applied by every parent who has ever
spanked a child. In clinical practice, aversion technique can be used to eliminate addictions
and destructive or deviant behaviours and even with sexual problems. Sometimes aversion
relief conditioning can also be used in which the stimulus associated with termination of pain
can be positively reinforced.

 Response shaping: Positive reinforcement is often used in response shaping, it

means establishing a response that is not initially in the individual’s behaviour repertoire. In
shaping behaviour successive approximation is reinforced in order to increase the likelihood
of behaviour.

 Assertive Training: It is an interpersonal behaviour involving the honest and

relatively straight forward expression of thoughts and feelings. It should be socially
appropriate and when a person is behaving assertively, the feelings and welfare of others are
taken into account. It includes any therapeutic procedure aimed at increasing the client’s
ability to engage in assertive behaviour. Behavioural goals include an enhanced ability to
express negative feelings like anger, resentment or positive feelings like joy, love, praise.
Increased assertiveness is assumed to benefit client in two ways: First, it is thought that
behaving in a more assertive fashion will instil in a client a greater feeling of well being.
Second, it assumes that by behaving in a more assertive manner, the client will be better
able to achieve significant social (as well as material) rewards, and thus obtain more
satisfaction in life.

 The Token Economy: One of the most recent and promising application of operant
conditioning approach is the token economy programs used to modify the behaviour of
institutionalized psychotic patients. The focus of using tokens rather than using primary
reinforces is that they bridge the delay between the occurrences of the desired behaviour
and the ultimate reinforcement. Thus as the patient makes his bed, sweeps the floor or takes
on a job responsibility, he immediately receives the requisite tokens. The goal of token
economy program is to develop behaviour that will lead to social reinforcement from others,
to enhance the skill necessary for the individual to take a responsible social role in the
institution eventually, to live successfully outside the institution. Although token economy can
be used even with those outside the institution, especially with children for increasing
desirable behaviour.

388
 Modelling: Response shaping can be tedious and time consuming, especially when
complex responses are to be learned, such responses can be acquired much more readily if
the subject observes a model and is then reinforced for imitating the models behaviour.
Albert Bandura developed this form of behaviour modification based on social modelling. As
a therapeutic measure, Bandura points three ways in which modelling can influence
behaviour:
1. It can serve as a basis for learning new skills and behaviour.
2. It can serve to eliminate fears and inhibitions and,
3. Finally, it can facilitate pre-existing behaviour patterns.

 Systematic Desensitization: This technique is developed by Joseph Wolpe and aims

specifically at the alleviation of maladaptive anxiety. The technique involves the pairing of
relaxation with imagined scene depicting situations that the client has indicated cause him
or her feel anxious. The therapist usually operates on the assumption that if the client is
taught to experience relaxation rather than anxiety while imagining such scene, the real
life situation will cause much less discomfort.

Systematic desensitization is a technique which is used to help people manage and

eventually conquer phobias. The goal of the treatment is to allow the patient to experience
situations which would normally result in anxiety, fear, and stress without tension. Systematic
desensitization is based on the principle of reciprocal inhibition. The principle states that two
incompatible responses cannot occur at the same time and that the stronger of the two will
replace the weaker. The first step in the technique involves developing relaxation exercises.
Learning to relax is important, as when someone is in a deep state of relaxation, it is more
difficult to experience fear and anxiety. The therapist usually works with the patient in the
office, and the patient practices exercises at home until he or she can relax easily.
Then, the patient and the therapist discuss the phobia, and come with a hierarchy of fears.
For example, someone who is afraid of planes might experience relatively low levels of
tension when exposed to a cartoon drawing of a plane, with high levels of fear and stress
when asked to imagine him or her actually seated in a plane which is getting ready to take
off.

 Implosive Therapy: Another method of behaviour therapy is Implosive therapy. Like

systematic desensitization, this approach regards neurotic behaviour as involving the
conditioned avoidance of anxiety arousing stimuli, and the client is asked to imagine and
relive aversive scenes associated with his anxiety. In this case, rather than trying to banish
the anxiety from the treatment sessions, the therapist deliberately attempts to elicit a massive
flood or “implosion” of anxiety. With repeated exposure in safe setting, the stimulus loses its
power to elicit anxiety and the neurotic avoidance behaviour is extinguished. But because of
its flooding of anxiety at the same time, it’s unethical and used less frequently.

 Cognitive Therapy
Cognitive therapy, a system developed by Aron Beck, stresses the importance of belief
systems and thinking in determining behaviour and feelings. The focus of cognitive therapy is
on understanding distorted beliefs and using techniques to change maladaptive thinking.
The central insight of cognitive therapy as originally formulated over three decades ago is
that thoughts mediate between stimuli, such as external events, and emotions. As in the
figure below, a stimulus elicits a thought -- which might be an evaluative judgment of some
kind -- which in turn gives rise to an emotion. In other words, it is not the stimulus itself which
389
somehow elicits an emotional response directly, but our evaluation of or the thought about
that stimulus. Two ancillary assumptions underpin the approach of the cognitive therapist:
1) The client is capable of becoming aware of his or her own thoughts and of changing them,
and
2) Sometimes the thoughts elicited by stimuli distort or otherwise fail to reflect reality
accurately.

Stimulus Thought Emotion

Cognitive therapy suggests that psychological distress is caused by distorted thoughts about
stimuli giving rise to distressed emotions. The theory is particularly well developed in the
case of depression, where clients frequently experience unduly negative thoughts which
arise automatically even in response to stimuli which might otherwise be experienced as
positive. For instance, a depressed client hearing "please stop talking in class" might think
"everything I do is wrong; there is no point in even trying". The same client might hear
"you've received top marks on your essay" and think "that was a fluke; I won't ever get a
mark like that again", or he might hear "you've really improved over the last term" and think "I
was really abysmal at the start of term". Any of these thoughts could lead to feelings of
hopelessness or reduced self esteem, maintaining or worsening the individual's depression.
Cognitive therapy makes the assumption that thoughts precede moods and that false self-
beliefs lead to negative emotions. It aims to help the patient recognize and reassess his
patterns of negative thinking and replace them with positive thoughts that more closely
reflects reality. It also aims to help the client to become aware of thought distortions which
are causing psychological distress. The objective is not to correct every distortion in a client's
entire outlook -- and after all, virtually everyone distorts reality in many ways -- just those
which may be at the root of distress. The therapist will make every effort to understand
experiences from the client's point of view, and the client and therapist will work
collaboratively with an empirical spirit, like scientists, exploring the client's thoughts,
assumptions and inferences. The therapist helps the client learn to test these by checking
them against reality and against other assumptions.

 Cognitive-Behaviour Therapy
The roots of cognitive behaviour therapy could trace to the development of behaviour therapy
in the early 20th century and the development of cognitive therapy and subsequent
amalgamation of these two approaches.
The term Cognitive-Behaviour Therapy shares three fundamental propositions:
1. Cognitive activity affects behaviour
2. Cognitive activity may be monitored and altered
3. Desired behaviour change may be affected through cognitive change

390
 Thought Emotion

Behavior

Cognitive behaviour therapy is a form of psychotherapy that emphasizes the important role of
thinking in how we feel and what we do. The task of Cognitive Behavior Therapy is partly to
understand how the three components of emotion, behaviour and thought interrelate, and
how they may be influenced by external stimuli -- including events which may have occurred
early in the client's life.

 Exposure and Response Prevention

It is a type of Behaviour Therapy as well as Cognitive Behaviour therapy. The principal focus
is on:
 Deliberate exposure to all previously avoidable situations
 Direct exposure to feared stimuli (including thoughts)
 Prevention of compulsive rituals and neutralizing behaviours including covert ones
(i.e. response prevention)

 Rational Emotive Behavioral Therapy

Rational Emotive Behavioral Therapy was founded by Albert Ellis in 1955.
Rational emotive behavioural therapy ('REBT') holds that humans are prone to adopting
irrational beliefs and behaviours which stand in the way of achieving their goals and
purposes. Often, these irrational attitudes or philosophies take the form of extreme or
dogmatic 'musts', 'shoulds', or 'oughts'; they contrast with rational and flexible desires,
wishes, preferences and wants. The presence of extreme philosophies can make all the
difference between healthy negative emotions (such as sadness or regret or concern) and
unhealthy negative emotions (such as depression or guilt or anxiety).
REBT employs the 'ABC framework' -- depicted in the figure below -- to clarify the
relationship between activating events (A); our beliefs about them (B); and the cognitive,
emotional or behavioural consequences of our beliefs (C). The ABC model is also used in
some renditions of cognitive therapy or cognitive behavioural therapy, where it is also applied
to clarify the role of mental activities or predispositions in mediating between experiences
and emotional responses.

(B) Beliefs (C) Consequences

(A) Activating
Event  Evaluations Emotions
 Actual event  Rational Behaviours
391
 Irrationals Other thoughts
 Clients
The figure below shows how the framework distinguishes between the effects of rational
beliefs about negative events, which give rise to healthy negative emotions, and the effects
of irrational beliefs about negative events, which lead to unhealthy negative emotions.

 Humanistic psychotherapy
Humanistic therapy is an approach where the main emphasis is on client’s subjective,
conscious experiences. The therapist’s focus is more on what clients are experiencing in
the present. The major form off humanistic therapy is client –centered
centered therapy which was
developed by Carl Rogers. Three interrelated attitudes on the part of the therapist are
central to the success of the client –centered therapy. The clientt determines the general
direction
ion of therapy, while the therapist seeks to increase the client’s insightful
insightful self
understanding through informal clarifying questions.

 Existential Psychotherapy
Existential approaches to psychotherapy have tended to emerge at times, and in regions of
the world, where there was a groundswell of interest in existential philosophy. Victor
Frankel and Rollo May were the major contributors
contributors in the field of existential therapy.
Existentialism is a philosophy concerned with the meaning of human existence. They
believe that people are free
ree to choose among alternatives available to them in living and
have a large role in shaping their own personal destinies. According to Frank Frankel the
problems of moral conflicts falls under Logotherapy. In therapy, the patient has to find his
meaning of life for himself. This meaning iiss different for each individual
individual, where his
uniqueness, his destiny, his heritage all come together to give a new meaning to his life.

 Gestalt therapy
Perls’s Gestalt therapy was born in Germany and was profoundly influenced by the
gestalt psychologists Wertheimer, Koffka, Kohler, Lewin and Goldstein. The Gestalt
theory emphasizes Organization and relatedness, which is in contrast with
reductionism of Wundt -Tichner
Tichner and mechanical behaviorism of Watson. Perls
applied this theory to human life, integrating the various aspects dynamic, affective,
cognitive and social in one whole and then understanding it as a total unity.

 Interpersonal Therapy
Interpersonal therapy was given by Gerald L. Klerman and Myrna Weissman based on the
ideas of Harry Stack Sullivan. This is a type of therapy which focuses on past and present
social roles and interpersonal interactions. During treatment, the therapist generally chooses
one or two problem areas in the patient's
patient's current life to focus on. Examples of areas covered
392
are disputes with friends, family or co-workers, grief and loss and role transitions, such as
retirement or divorce.

PHASES OF PSYCHOTHERAPY
Beginning Phase:
The beginning stage of therapy has for its principle objective the establishing of a working
relationship with the patient. Without such mutuality, there will be no therapeutic progress.
Because the working relationship is so vital to success in a therapy, all tasks must be
subordinated to the objective of its achievement. To ensure an adequate working relationship
the patient must be motivated by
 Clarifying and removing misconception about therapy
 To convince the patient that the therapist understands his sufferings and is capable of
helping him
 Defining the objective of the therapy
Middle Phase:
Once the therapeutic relationship is consolidated, and the patient has accepted a more
active role of working on his problem, then it’s time to enter middle stage of treatment. This
has as one of its objectives the revelation of the causes and consequences of the patient’s
disorder. Middle phase is further divided into:
 EARLY MIDDLE PHASE:
Main objective of early middle phase is to delineate and explore environmental frustrations and
maladaptive interpersonal drives through interviewing, and to probe unconscious conflicts that
mobilize anxiety and vitiate basic needs.
 LATE MIDDLE PHASE:
Main objective of a therapist in late middle phase is to help the patient to make changes in
the maladaptive behaviour and give incentive for those changes. He also helps the patient in
dealing with forces that block action, mastering the anxieties surrounding normal life goals,
correcting remediable environmental distortions, adjusting to irremediable conditions, making
adjustment to those symptoms and abnormal character patterns that for one reason or
another cannot be removed during present therapeutic effort.
Terminal Phase:
Theoretically, psychotherapy is never ending since emotional growth can go on as long as
one lives. In a more usual and limited sense, psychotherapy should be terminated when the
stated goals are reached. The terminal phase necessarily begins with therapist and patient
taking stock of his/her current status and future prospects and deciding whether goals are
closely enough approached. Although termination can occur even before the goals are
reached. The conditions under which termination of therapy is indicated are:
 Achievement by the patient of planned treatment goals
 Decision by the patient or therapist to terminate on the basis of incomplete goals
 The reaching of an impasse in therapy or the development of stubborn resistances
that cannot be resolved
 Counter-transference the therapist is unable to control, and
 Occurrence of physical reasons, such as moving of the residence of patient or
therapist

393
How does it work and for how long?
According to Frank (1973) therapeutic changes occur in phases and it starts with restitution
of well – being (remorlization), followed by a relief of symptoms (remediation) and finally
result in an improvement in functioning (rehabilitation). Obviously, in order for a therapy to
cross through all these phases adequate number of sessions will be required. But what is
that optimal number? Though it is tough to give ‘a size that fits all’ number; however, based
on the number of sessions proposed about various techniques such as CBT and IPT, it
seems 8 to 12 weeks of twice weekly sessions are required followed by maintenance
treatment at long-intervals. It is to be noted that if the patient is not responding to therapy
after many sessions the therapist should reevaluate the suitability of the therapeutic
technique chosen. Likewise, even if the patient has responded well, too many sessions
might prove counterproductive or resulting in diminishing returns.

MODALITIES OF PSYCHOTHERAPY

 Individual Therapy
This modality involves one-on-one work between patient and therapist. It allows the patient to
have the full attention of the therapist, but is limited in that it does not allow the therapist an
opportunity to observe the patient within social or family relationships.
 Group Therapy
Group therapy generally involves anywhere from three to fifteen patients. It offers patients
the opportunity to give and receive group support in coping with their particular issues as well
as to observe how they interact in group settings. It may also be a less expensive alternative
to individual therapy. It is a treatment in which carefully selected persons who are
emotionally ill meet in a group guided by a trained therapist and help one another effect
personality change.
 Family Therapy
This approach is most useful when it is necessary to work on dynamics within the family
group. Family therapy is an intervention that focuses on altering the interaction among family
members and attempts to improve the functioning of the family as a unit of individual
members of the family. The therapist conducting family therapy attempts to interrupt rigid
intergenerational patterns that cause distress within or between individuals. Family therapy
addresses the concerns of any family member, yet it is most likely to influence children,
whose daily reality is directly affected by family context.
 Couple's Therapy
Couple or marital therapy is a form of psychotherapy designed to psychologically modify the
interaction of two persons who are in conflict with each other over one parameter or a variety
of parameters- social, emotional, sexual, or economic. In couples therapy a trained person
establishes a therapeutic contract with a patient-couple and, through definite type of
communication, attempts to alleviate the disturbance, to reverse or change maladaptive
patterns of behaviour, and to encourage personality growth and development.

ETHICS IN PSYCHOTHERAPY

394
The psychotherapist must respect and protect civil and human rights and the central
importance of freedom of inquiry and expression in therapeutic effort. They strive to help the
public in developing informed judgments and choices concerning human behaviour. This
Ethics Code provides a common set of principles and standards upon which psychotherapist
build their professional relationship with the patient. (APA, 1992)
1. When obtaining informed consent to therapy, therapist informs clients/patients early
in the therapeutic relationship about the nature and anticipated course of therapy,
fees, and involvement of third parties.
2. When the therapist is a trainee and the legal responsibility for the treatment provided
resides with the supervisor, the client/patient, as part of the informed consent
procedure, is informed that the therapist is in training and is being supervised and is
given the name of the supervisor.
3. When therapist agree to provide services to several persons who have a
relationship (such as spouses, significant others, or parents and children), they take
reasonable steps to clarify at the outset, which of the individuals are clients/patients
and what relationship the therapist will have with each person. This clarification
includes the therapist's role and the probable uses of the services provided or the
information obtained.
4. If it becomes apparent that therapist may be called on to perform potentially
conflicting roles (such as family therapist and then witness for one party in divorce
proceedings), he/she should take reasonable steps to clarify and modify, or withdraw
from, roles appropriately.
5. When therapist provide services to several persons in a group setting, they describe
at the outset the roles and responsibilities of all parties and the limits of
confidentiality.
6. In deciding whether to offer or provide services to those already receiving mental
health services elsewhere, therapists carefully consider the treatment issues and the
potential client's/patient's welfare. Therapists should discuss these issues with the
client/patient or another legally authorized person on behalf of the client/patient in
order to minimize the risk of confusion and conflict, consult with the other service
providers when appropriate, and proceed with caution and sensitivity to the
therapeutic issues.
7. Therapists do not engage in sexual intimacies with current therapy clients/patients.
They should not engage in sexual intimacies with individuals they know to be close
relatives, guardians, or significant others of current clients/patients. They should not
accept as therapy clients/patients persons with whom they have engaged in sexual
intimacies.
8. When entering into employment or contractual relationships, therapist make
reasonable efforts to provide for orderly and appropriate resolution of responsibility
for client/patient care in the event that the employment or contractual relationship
ends, with paramount consideration given to the welfare of the client/patient.
9. Therapist terminate therapy when it becomes reasonably clear that the client/patient
no longer needs the service, is not likely to benefit, or is being harmed by continued
service.
10. Therapist may terminate therapy when threatened or otherwise endangered by the
client/patient or another person with whom the client/patient has a relationship.
11. Except where precluded by the actions of clients/patients or third-party payers, prior
to termination therapists provide pretermination counselling and suggest alternative
service providers as appropriate.
395
 NONSPECIFIC FACTORS IN PSYCHOTHERAPY

Psychotherapy attempts to alleviate emotional sufferings and enhance personality

adjustment through planned psychological interventions. But it is not the only medium
through which such benefits may be achieved. There are varieties of forces which serve to
ameliorate neurotic symptoms and sometimes under fortunate circumstances leads to
personality growth. Among the coincidental factors associated with psychological changes
are:
1. “Spontaneous” remission or cures
Spontaneous cure occurs more frequently than one can admit because both physical and
emotional difficulties are associated with periods of exacerbation and periods of remission,
and without any cause they vanish on their own. Sometimes the most pernicious form of
psychoses show tendency toward spontaneous remission. Although we have a tendency to
focus only on the evil consequences and forget that constructive regenerative influences may
be coincidently present. This indicates that the individual has healing forces within himself
that are capable of altering a presumably fatal illness.
The exact mechanisms involved in spontaneous recovery or cure are not exactly known but
a number of operative factors suggest that:
i. Life circumstances may change and open up opportunities for gratification of
important but vitiated needs, normal and neurotic.
ii. Provocative stress sources may disappear as a result of the removal of the initiating
environmental irritant or because the individual extricates himself from it.
iii. Crumbling and shattered defenses, whose failure promotes adaptive collapse, may
be restored to their original strength, or be reinforced by new, more adequate and
less disabling defenses. The return of sense of mastery in the course of buttressing
failing defenses will help to return the individual to functional equilibrium.
2. Influences that automatically arise out of any “helping” situation
A brief contact with an intelligent authority in which an emotionally disturbed person can
confide brings about relief which may satisfy the ambitions of both sufferer and helping
agency. The factors which influence helping relationships are:

i. The Placebo Effect:

An individual who is suffering from physical or emotional problem and seeking help may
attach himself or herself to the instrument or person in whom he has trust. His conviction
regarding the infallibility of the object or the person may be great enough to induce a
cessation of the symptoms. When this occurs solely on the basis of conviction or trust, it’s
called placebo influence. In medical profession, placebo effect is recognized as a potent
healing force.

ii. The Relationship Dimension:

Every helping situation is characterized by a special kind of relationship that develops
between the therapist and subject. Implicit, if not explicit, the individual has understanding
and trust that the therapist has knowledge, skill and desire to help him overcome the
problems for which he has sought the professional help. The more bewildered and helpless
the person, the greater the reliance he places on the expert individual. It is a most important
factor in the psychotherapeutic situation, particularly at the beginning of treatment and later
when reaching the goal.
396
iii. The Factors of Emotional Catharsis:
Sometimes a sheer act of talking can provide an individual with considerable emotional relief.
It exposes suppressed attitudes and the ideas that the person has been keeping from
himself, at the same time releases tension, softens inhibitions and liberates conscious and
unconscious conflicts that have been held in check. In the unburdening process, there is
often a relief of guilt feelings in relation to past experiences, particularly sexual acting-out,
hostile or aggressive outburst and competitive strivings.
iv. The Factors of Suggestion:
In any helping relationship many forces are operative, including the need to identify oneself
with helping personage who serves as a model. There is then an unqualified tendency to
assimilate the percepts and injunctions of the helper purely on the basis of suggestion. There
are a number of variables that appear to regulate the forcefulness of suggestion (Wolberg,
1962):
 The significance to the individual of the suggesting agency.
 Significance to the subject of the specific content of offered suggestions from the
helping agency.
 Degree of anxiety that is mobilized in the subject by his acceptance of a specific
suggestion or by the relationship itself.
v. Group Dynamics
Group exerts a powerful influence on the individual. They may be responsible for significant
changes among the constituent members. The effect of alcoholic anonymous on victims of
alcohol dependence syndrome, and of the more recent on drug addicts, are examples of how
even serious personality defects may be benefitted through constructive group adventures

CLIENT AND THERAPIST VARIABLES IN EFFECTIVENESS OF

PSYCHOTHERAPY

CLIENT VARIABLES: A client variable can be seen as a moderator or mediator of

change. A moderator variable can affect the relationship between the predictor variable and
dependent variable. In contrast mediator variable is a mechanism through which
independent variable affect the dependent variable. There are various sociodemographic
variables of client that may affect the outcome of psychotherapy. For example, studies have
shown that CBT is more effective in reducing the depressive symptoms in older patients
(Arean et al., 1993; Kemp et al., 1992). Likewise, socioeconomic status (SES) has been
found to be related to continuation of psychotherapy. A positive relationship between higher
social status and length of stay in treatment has been found (Berrigan et al., 1981). Even
gender can be a determinant of the outcome of psychotherapy. Thase et al (2000) found
across various studies that women who were manifesting more severe depression did
better in interpersonal therapy than they did in cognitive therapy.
THERAPIST VARIABLES: Similar to client’s variables there can be many therapist’s
variable’s that can affect the outcome of psychotherapy. For example, therapist’s age,
emotional well being, aptitude and similar other variables can have some effect on the
outcome.

The practice of psychotherapy requires that the therapist possesses special personality
characteristics that will enable him to establish and to maintain the proper kind of relationship
with his patient.

397
Empathy
 The most important characteristic of the good therapist is his capacity to empathize with
others. Empathy is the power or state of imagining oneself to be another person and so of
sharing his ideas and feelings. It enables the therapist to appreciate the turmoil the
patient experiences in his illness and the inevitable resistance he will manifest towards
change. Lack of empathy interferes with the respect the therapist needs to display
towards the patient, with the interest to be shown in his welfare, with the ability to give
him warmth and support when needed, with the capacity to concentrate on his production
and to respond appropriately.
 Empathy should not be mistaken for sympathy or a tendency to overprotect the patient.
Empathy means tolerance of patients making mistakes, of using his own judgment and of
developing his individual sense of values. This means that the therapist must not harbor
preconceived notions as to the kind of person he wants the patient to be.
Unconditional Positive Regard
 The second feature of a therapist which Carl Rogers regarded as essential is
‘Unconditional Positive Regard.’ synonymous with this are acceptance or warmth.
 By Unconditional Positive Regard Carl Rogers wished therapist to ‘prize the person’- to
respect people for what they are, for their uniqueness and for their individuality. With this
feature therapist begins their relationship with a person by directly communicating that he
accepts them, no matter how they might speak or what they might have done. The aim of
this condition is to create a climate within which the person in need can feel safe.
Genuineness
 The simplest way of defining genuineness is to regard it as open communication. Instead
of person in need trying to guess, what therapist really means, or trying to decode the
differences between what he says and the image his body communication provides them
with, there is a directness and openness about the way therapist communicates. By being
genuine the therapist does not pretends to be ‘super –helper’ but encourages the person
in need to stop pretending, denying, hiding or concealing their thoughts and feelings – he
encourages a direct and open communication.
Flexibility
Rigidity in therapist is a destructive force in psychotherapy. It prevents the therapist from
coordinating his approach with the exigencies of the therapeutic situation. Flexibility is not
only essential in the execution of technical procedure, but in other aspects of therapy; such
as, the defining of goals and setting of standards. Flexibility is also necessary in
interpreting the value system of the culture, in order to permit the relaxation of certain
austere demands in the face of which a change in patient’s severity of conscience may be
thwarted.
Objectivity
Awareness of his own feelings and emotional problems helps the therapist to remain
tolerant and objective in the face of irrational controversial and provocative attitude and
behaviour manifested by the patient. No matter what the patient says or thinks, it is urgent
that the therapist has sufficient control over his feelings so as not to become judgmental
and, in this way, inspires guilt in the patient. Objectivity tends to neutralize untoward
emotions in the therapist, particularly, over-identification, which may stifle the therapeutic
process and hostility which can destroy it. Objectivity enables the therapist to endure
attitudes, impulses and actions at variance with accepted norms. It permits the therapist to

398
respect the patient and to realize his essential integrity, no matter how disturbed or ill he
may be.

Sensitivity
It is essential for the therapist to perceive what is happening in the treatment process from
the verbal and non-verbal behaviour of the patient. Not only must the therapist attuned to
the content of the patient’s communication, but he must be sensitive to the mood and
conflicts that underlie the content. He must be aware also of his own feelings and attitudes,
particularly those nurtured by his personal problems and emotional limitation that is inspired
by contact with the patient. These qualities presuppose a superior intelligence and judgment
with the ability to utilize one’s intelligence in practical life problems.
PSYCHOTHERAPY AND MEDICATION (Kay, 2001)
The treatment of patients with psychotherapy and medication simultaneously is a common
practice throughout the world. Most mental health professionals regardless of disciplines,
emphasize the importance of psychotropic medication, in conjunction with psychotherapy.
In fact, psychotherapy and pharmacotherapy are complementary to each other from various
perspectives. For example,
 Pharmacotherapy can make amenable for psychotherapy. A patient in severe
depressive or anxiety state may not show interest in psychotherapy; however, after
some improvement with medication they can reach a stage where psychotherapy
can be started as they become amenable to discuss their problems.
 Medication can increase self-esteem by decreasing feeling of hopelessness, futility
and passivity as well as enhancing the acceptability of treatment.
 Medication, for some patients works as placebo effect allowing more substantial
therapeutic alliance.
 Medication may not only increase the likelihood but also the speed and magnitude of
response to psychotherapy.
 On the other hand psychotherapy when added to an ongoing pharmacotherapy may
have following benefits-
 Psychotherapy promotes improved adaption and coping.
 Psychotherapy improves compliance with pharmacotherapy
 Psychotherapy, even in patients with most severe disorder, decreases the likelihood
of recurrence of symptoms
 Psychotherapy decreases relapses when medications are stopped

LIMITATIONS OF PSYCHOTHERAPY (Wolberg, 1988)

Failures in psychotherapy are generally the product of mismanagement of therapeutic

relationship. Most commonly patient is pushed toward reconstructive goals that are beyond
his competence. There are some factors or conditions that prevent the person to benefit
from therapy. They are as follows-
(a) Resource limitation.
(b) An inability to tolerate anxiety with severe disintegration reaction.
(c) Serious maladjustment since childhood.
(d) Another factor is that the person has been in psychotherapy for a number of years,
particularly with series of therapist without achieving any benefits.

ECLECTICISM IN PSYCHOTHERAPY
399
Eclecticism as the selection of orderly combinations of compatible features from diverse
sources sometime from incompatible theories and systems; the effort to find valid element
from all doctrines and theories and to combine them into a harmonious whole…It is
distinguished from unsystematic and uncritical combination, for which the name is
syncretism. Thorne was first to adapt term eclecticism to designate a detailed,
systematically developed position. The objective of any eclecticism is to develop a single
comprehensive system of psychotherapy including philosophical and theoretical foundation.
Current eclecticism neglect theory and there is little concern with research support
(Patterson, 1989). Goldfried (1982) proposed that integration should be attempted at the level
of strategies rather than at level of techniques. But focusing of strategies rather than
theories does not avoid the theoretical incompatibility because strategies involve the goals,
and goals involve theory.
PSYCHOTHERAPY FOR CHILDREN

The differences between adult and child psychotherapy stem from many factors such as the
nature of the problems exhibited by children, children’s dependence on adults, assessment
issues, patient-therapist relationship etc. For example, most of the problems encountered in
the child are present in the normal course of development in lesser levels (e.g. aggression,
hyperactivity, anxiety), and it is a special challenge to decide whether and when to
intervene (Kazdin, 2003). Similarly, unlike the treatment of adults, child therapy ends by
returning the patient not to his own care alone but to that of the parents. Thus the aim is not
only to have children look at themselves more squarely, but to promote a more open
relationship between children and parents that can meet their emotional needs as they
grow up in a better way (Wolff, 2000). Furthermore, children’s dependence on adults makes
them particularly vulnerable to multiple influences over which they have little control, like
parental mental health, marital and family functioning, stress in the home, difficult living
circumstances, etc. (Kazdin, 2003). The whole problem gets compounded due to the fact
that often children are not able to give clear accounts of their problems that aggravate the
dependence on parental and other authority figure’s accounts and, at times, these accounts
are highly colored by reporter’s own psychopathology and perception. Finally, the therapist-
patient relationship is, somewhat, blurred in child psychotherapy.

PSYCHOTHERAPY IN INDIA:

CULTURE AND PSYCHOTHERAPY

Efficacy of western psychotherapy in Indian culture has aroused attention and concern of
many leading psychiatrists. The first issue is that there is a difference in the way people
from Western and Eastern cultures perceive the outer world and the self. Westerners are
inductive and analytic. In contrast, the Easterner’s perception is deductive, and harmony is
highly valued. The self is perceived as ‘us’ in the collective consciousness. Both Mahal
(1975) & Neki (1977) agree that the West fosters individual independence while Indian
culture fosters social dependence and both arrived at the conclusion that Western
psychotherapy is not adequately applicable in Indian culture. In recent times Western
psychiatrists have found our traditional meditation technique and Yoga to be useful. In
Indian literature varieties of practice have been mentioned for the cure of psychological
disorders. Yoga an ancient Indian system of thought as well as practice is very pertinent to
400
the treatment and prevention of psychological disorders as well as maintenance and
promotion of physical and psychological well- being. Neki (1977) described the concept of
Guru-Chela relationship which is the culturally more appropriate and suitable framework for
psychotherapy in India. Hoch (1977) found some similarities in Indian traditional healing
technique and western psychotherapies. The original meaning of health i.e. “swasth” (self-
reliant or self- supporting) almost sounds similar to the perceived western idea of individual
independence.
One of the basic components of outcome of psychotherapy is the therapist’s ability
to keep track of communication between client and therapist. ‘Intercultural therapies’
already specifically acknowledge this, and include a mutually respectful exploration of the
therapy and of perceived problems and solutions, so that a framework is found within which
the therapist and patient can work. There are some recommendations for culturally capable
practice in psychotherapy. Therapists should consider their preconceptions about the race
and ethnicity of the patient and of that person’s family and recognize that an individual may
be quite different from other members of the same racial and ethnic group.

STATUS OF PSYCHOTHERAPY IN INDIA

In India, the Psychoanalytical movement was started by Giridra Sekhar Bose. He founded
the Indian Psychoanalytical Society in 1922. He proposed that repression results from
psychological opposition of infantile wishes and not due to social and biological factors as
suggested by Freud.
The first discontent of the practice of Western Psychotherapy in India was struck by Surya
and Jayaram in 1964. They emphasized the importance of local language and situational
direct support rather than intrapsychic explanations. A group of Psychotherapists from
NIMHANS (National Institute of Mental Health and Neuro-Sciences, Bangalore) have
attempted to develop techniques that can be used by a variety of mental health
professionals. Similarly the analysis of therapeutic relationship in Indian setup has led to
particular concept known as Guru-Chela relationship. The concept implies that in the
therapy the therapist should be more active and assume responsibility for the decision
making (Neki, 1984). Surya and Jayaram (1996) have also highlighted that Indian patient
readily accepts the dependency relationship and seek support.

CURRENT ISSUES IN PSYCHOTHERAPY

In spite of the fact that many Psychotherapists are interested, inclined and committed to
Psychotherapy, there seems to be a general decline in interest in Psychotherapy. In India,
this has been attributed mainly to impracticability of psychotherapy of western origin,
individualistic and unsystematic nature of psychotherapy, insufficiency of practical training,
belief that a psychotherapist should adhere to a specific school of Psychotherapy and less
number of researches. Shamsundar (1997) has appealed for establishment of an official
forum for the promotion of the cause of psychotherapy in India. He has highlighted some
objectives of the forum such as: (a) exchange of information among therapists related to
training, learning and practice of psychotherapy, (b) easy accessibility of psychotherapy
training facilities, various short and long term courses should be started, (c) something
similar to Continuing Medical Education Programmes, every year programmes should be
organized, where psychotherapists from smaller and remote centre will have the
opportunity to discuss their therapy material among peers, (d) a national journal on
psychotherapy should be started.

401
CONCLUSION
Psychotherapy is a complicated process and almost 100 years have passed since the use
of systematic therapeutic approach. The interplay between scientific confirmation of
particular strategies and the actual implementation of a given therapeutic technique is not
always isomorphic. Also, how theory drives practice and ultimately the empirical
confirmation of such practice is not always clear cut. Moreover, how cultural, financial,
legislative, and forensic and ethical issues act in confluence further complicate the field of
psychotherapy. However, it is these very intricacies and complexities which make
psychotherapy such an interesting field. Psychotherapy can help one to gain better
understanding of his condition or situation, identify and change behaviours or thoughts that
negatively affect one’s life, explore relationships and experiences, and find better ways to
cope and solve problems, learn to set realistic goals for life and feel better about self.

REFERENCE

American Psychological Association. (1992). Ethical principles of psychologists and code of

conduct. American Psychologist, 47, 1597-1611.
Arean, P.A., Joshep,T.X. (1993). Comparative effectiveness of social problem- solving
therapy and reminiscence therapy as treatment for depression in older adults.
Journal of Consulting and Clinical Psychology, 61, 1003-1010.
Beck, A.T. (1976). Cognitive Therapy and the Emotional Disorders. New York, International
University Press.
Berrigan, L.P., Garfeild, S.L. (1981). Relationship of missed psychotherapy appointments to
premature termination and social class. The British Journal of Clinical
Psychology, 47, 882-897.
Bloch, S. (1996). An Introduction to Psychotherapies (3rd ed.). New York: Oxford Medical
Publication.
Chambless, D.L., Barker,M.J., Baucom,D.H. (1998). Update on Empirically validated
therapies, II. The Clinical Psychologist, 51, 1-10.
Coleman, J. C. (1988). Abnormal psychology and modern life. D.B. Taraporevala Sons &
Co. Private limited, Scott Foresman and Company. New York.
Ferri, F. F. (2008). "Major Depression." Ferri's Clinical Adviser. Ed. Mitchell D. Feldman.
(10th ed.) Philadelphia: Mosby Elsevier.
Frank, J.D. (1973).A comprehensive study of psychotherapy. John Hopkins University
Press. As citied in Lambert, J.M., (2004). Bergin & Garfield’s Handbook of
Psychotherapy and Behavioural change.(5th eds), John and Willy sons.
Gorfrield., M.R.(1982). Toward the delineation of therapeutic change principle. American
Journal of Psyhchologist, 35, 991-999.

Gupta, U., Gupta, B.S. (2006). Effect of Yoga Based Meditation on Psychophysiological
Health of Coronary Patients. Indian Journal of Psychiatry, 33, 21-27.
402
Houch, E.M. (1977). Psychotherapy for literate, new dimension in psychiatry- a world view.
John Willy & Sons Inc. U.S.A. As citied in : Shamasundar, C. (1978) What
kind of psychotherapy in Indian setting? Indian Journal of Psychiatry, 21, 34-
38.
Jacobson, J. L., Jacobson, A. M. (2001). Psychiatric Secrets. (2nd eds). Philadelphia, PA :
Hanley & Belfus, Inc.
Kaslow, N.J., Thompson, M.P. (1998). Applying the criteria for empirically supported
treatments to studies for psychosocial intervention for child and adolescent
depression. Journal of Clinical Child Psychology, 27, 146-155.
Kay, J. (2001). Integrated treatment: an overview. In. Kay, J. (ed.) Integrated treatment for
psychiatric disorders: Review of Psychiatry. American Psychiatric Press, pp 1-
29. As cited in : Gabbard, G.O., Beck, J.S., Holnes, J.(2007). Oxford
Textbook of Psychotherapy.Oxford University Press Inc., New York.

Kazdin, A.E. (2003). Research design in clinical psychology (4th ed.). Needham Heights,
M.A.: Allyn & Bacon. Wolfe, D. A. (2000). Child Abuse(2nd ed.).
Newbury. Park, CA: Sage.
Kemp, B.J., Corgiat, M., Gill, C. (1992). Effects of brief cognitive behavioral psychotherapy
with older patients with and without disabling illness. Behavioural Health and
Aging, 2, 21-28.
Korchin, S.J. (1999). Modern Clinical Psychology, Principles of Intervention in the clinic and
community. CBS Publishers & Distributers. New York.
Kumar, D., Ram, D. (2002). Psychotherapy: Current Trends. Eastern Journal of Psychiatry,
5, 12-18.
Lambert, J.M., (2004). Bergin & Garfield’s handbook of psychotherapy and Behavioural
change. (5th eds), John Willy & Sons.USA.

Mahal, A.S. (1975). Psychiatry in India. Indian Journal of Psychiatry, 17, 77-79.
Neki J.J. (1977). Psychotherapy in India. Indian Journal of Psychiatry, 19, 1-12.
Neki J.S. (1973). Guru–Chela relationship possibility of therapeutic paradigm. American
Journal of Orthopsychiatry, 43, 755-765.
Neki, J.S. (1975). Psychotherapy in India: past, present and future. American Journal of
Psychotherapy, 29, 92-98.
Ollandick, T.H., King, N.J. (1998). Empirically supported treatment for children with phobic
and anxiety disorder., Journal of Clinical Child Psychology, 35, 156-167.
Pampallona, S., Bollini, P., Tibaldi, G., Kupelnick, B., Munizza, C. (2004). Combined
pharmacotherapy and psychological treatment for depression: a systematic
review. Archives of General Psychiatry, 61, 714-719.
Pathak, B.N. (1999). Cognitive Therapy in Generalized Anxiety Disorder. Indian Journal of
Psychiatry, 26, 156-165.

403
Patterson, C.H. (1989).Psychotherapy. Foundation for a systematic eclectic psychotherapy.
In understanding the psychotherapy: fifty year of client-centered theory &
practice. American Psychologist, 26,427-435.
Pelham, W.E., Jr., Wheeler, T., Chronis, A. (1998). Empirically supported psychosocial
treatment for attention deficit hyperactivity disorders. Journal of Clinical Child
Psychology, 27, 190-205.
Rimm, D.C., Master, J.C. (2003), Behavior Therapy, Techniques and Empirical Findings,
(2nd ed.). Academic Press, New York, San Francisco, London. Vol- 6, pp 107-
114.
Sadock, B.J. Sadock, V.A. (2003). Synopsis of psychiatry, behavioural sciences and clinical
psychiatry (9th ed.) Lippincott Williams & Wilkins.Philadelphia.USA.
Seligman, M. (1991). Learned optimism. New York: Knopf. As citied Kumar, D., Ram., D.
(2002). Psychotherapy: Current Trends. Eastern Journal of Psychiatry, 5, 12-
18.
Seligman, M. (1994). What you can change & what you can't. New York: Knopf. As citied
Kumar, D., Ram., D. (2002). Psychotherapy: Current Trends. Eastern Journal
of Psychiatry, 5,12-18.
Seligman, M. (1995). The effectiveness of psychotherapy: The consumer reports study.
American Psychologist, 50, 965-974.
Shamasundar, C. (1978). What kind of psychotherapy in Indian setting? Indian Journal of
Psychiatry, 21, 34-38.
Shamsundar, C. (1997). The need for a national forum for psychotherapy. Indian Journal of
Psychiatry, 39, 267-269.
Stuart, R.J., Blecke, D., Renfrow, M. (2006). Cognitive Therapy for Depression. American
Family Physician, 73, 83-86.
Surya, N.C., Jayaram, S.S. (1996). Some basic consideration in practice of psychotherapy
in Indian setting. Indian Journal of Psychiatry, 38, 10-12.
Thase, M.E., Frank, E., Yonkers, K.A. (2000). Gender difference in response to treatment of
depression. Gender and its effects on psychopathology American Journal of
Psychiatry, 34, 103-129.
Verma, S.K., Kaur, H. (1999). Human values and mental health. Indian Journal of
Psychiatry, 26, 144-147.
Wolberg, L.R. (1962). The Technique of Psychotherapy (2nd ed.), Grune & Stratton, Inc.
USA.
Wolberg, L.R. (1988). The Technique of Psychotherapy (1st ed.), Grune & Stratton, Inc.
USA.

404
Appendix
EVIDENCE-BASED PSYCHOTHERAPIES IN DIFFERENT DISORDERS:
The evidence-based psychotherapies are cornerstone of modern scientific psychotherapy
practice. It is the result of various factors such as emphasis on use of therapeutic technique
that has proven its worth, third-party payment system in psychotherapy and so on. In 1995
a task force constituted by the Division 12 of the American Psychological Association
(popularly known as D12 TF), for the purpose of dissemination of psychological services,
reviewed and evaluated existing psychotherapies on certain criteria (given in Table- 1 by
Chambless et al., 1998).

Table-1
I At least two good between group design experiments demonstrating efficacy in one or more of the
following ways:
A. Superior (statistically significantly so) to pill or psychological placebo or to another
treatment.
B. Equivalent to an already established treatment in experiments with adequate sample sizes.
OR
II
A Large series of single case design experiments (n >9) demonstrating efficacy. These experiments
must have:
A. Used good experimental designs and
B. Compared the intervention to another treatment as in IA
FURTHER CRITERIA FOR BOTH I AND II:
III. Experiments must be conducted with treatment manuals.
IV. Characteristics of the client samples must be clearly specified.
V. Effects must have been demonstrated by at least two different investigators or investigating
teams.
Probably Efficacious Treatments
I. Two experiments showing the treatment is superior (statistically significantly so) to a waiting-list
control group.
OR
II. One or more experiments meeting the Well-Established Treatment Criteria IA or IB, III, and IV,
but not V.
OR
III. A small series of single case design experiments (n >3) otherwise meeting Well-Established
Treatment

405
 Table :2
EXAMPLES OF EMPIRICALLY VALIDATED TREATMENTS (Chambless, 1998)
DISORDERS WELL-ESTABLISHED TREATMENTS
 Cognitive behavior therapy for panic disorder with and without
agoraphobia
 Cognitive behavior therapy for generalized anxiety disorder
ANXIETY AND STRESS  Exposure treatment for agoraphobia
 *Exposure/guided mastery for specific phobia
 Exposure and response prevention for obsessive-compulsive
disorder
 Stress Inoculation Training for Coping with Stressors
DEPRESSION  Behavior therapy
 Cognitive therapy
 Interpersonal therapy
HEALTH PROBLEMS:  Behavior therapy for headache
 Cognitive-behavior therapy for bulimia
 *Multi-component cognitive-behavior therapy for pain
associated with rheumatic disease
 *Multi-component cognitive-behavior therapy with relapse
prevention for smoking cessation
PROBLEMS OF  Behavior modification for enuresis
CHILDHOOD:  Parent training programs for children with oppositional
behavior
MARITAL DISCORD  Behavioral marital therapy

DISORDERS PROBABLY EFFICACIOUS TREATMENTS

ANXIETY  Applied relaxation for panic disorder

 Applied relaxation for generalized anxiety disorder
 *Cognitive behavior therapy for social phobia
 *Cognitive therapy for OCD
 *Couples communication training adjunctive to exposure for
agoraphobia
 *EMDR for civilian PTSD
 Exposure treatment for PTSD
 *Exposure treatment for social phobia
 Stress Inoculation Training for PTSD
 Relapse prevention program for obsessive-compulsive
disorder
 *Systematic desensitization for animal phobia
406
  *Systematic desensitization for public speaking anxiety
 *Systematic desensitization for social anxiety
CHEMICAL ABUSE  Behavior therapy for cocaine abuse Brief dynamic therapy for
AND DEPENDENCE opiate dependence
 *Cognitive-behavioral relapse prevention therapy for cocaine
dependence
 Cognitive therapy for opiate dependence
 Cognitive-behavior therapy for benzodiazepine
 withdrawal in panic disorder patients
 *Community Reinforcement Approach for alcohol dependence
 *Cue exposure adjunctive to inpatient treatment for alcohol
dependence
 *Project CALM for mixed alcohol abuse and dependence
(behavioral marital therapy plus disulfiram)
 *Social skills training adjunctive to inpatient treatment for
alcohol dependence
DEPRESSION  Brief dynamic therapy
 Cognitive therapy for geriatric patients
 Reminiscence therapy for geriatric patients Self-control therapy
 *Social problem-solving therapy
HEALTH PROBLEMS  Behavior therapy for childhood obesity
 *Cognitive-behavior therapy for binge eating disorder
 *Cognitive-behavior therapy adjunctive to physical therapy for
chronic pain
 *Cognitive-behavior therapy for chronic low back pain
 *EMG biofeedback for chronic pain
 *Hypnosis as an adjunct to cognitive-behavior therapy for
obesity
 *Interpersonal therapy for binge-eating disorder
 *Interpersonal therapy for bulimia
 *Multi-component cognitive therapy for irritable bowel
syndrome
 *Multi-component cognitive-behavior therapy for pain of sickle
cell disease
 *Multi-component operant-behavioral therapy for chronic pain
 *Scheduled, reduced smoking adjunctive to multi-component
behavior therapy for smoking cessation
 *Thermal biofeedback for Raynaud’s syndrome
 *Thermal biofeedback plus autogenic relaxation training for
migraine
MARITAL DISCORD:  Emotionally focused couples therapy
 for moderately distressed couples
 Insight-oriented marital therapy
PROBLEMS OF  Behavior modification of encopresis
CHILDHOOD:  *Cognitive-behavior therapy for anxious children (overanxious,
separation anxiety, and avoidant disorders)
 *Exposure for simple phobia
 Family anxiety management training for anxiety disorders

407
 SEXUAL  *Hurlbert’s combined treatment approach for female
DYSFUNCTION: hypoactive sexual desire
 *Masters & Johnson’s sex therapy for female orgasmic
dysfunction
 *Zimmer’s combined sex and marital therapy for female
hypoactive sexual desire
OTHER  Behavior modification for sex offenders
 Dialectical behavior therapy for borderline personality disorder
 *Family intervention for schizophrenia
 Habit reversal and control techniques
 *Social skills training for improving
 social adjustment of schizophrenic patients
 *Supported employment for severely mentally ill clients

408