1. Pathways mediating the superficial sensation.

Forms of sensation
disturbances. Neurological examination.

Superficial sensory pathway of head and face The cell bodies of the first-order
neurons are situated in the trigeminal ganglion whose peripheral processes join the
sensory branches of the trigeminal nerve and terminate in the superficial receptors in
the skin and mucosa of the head and face.
The sensory exam involves evaluation of pain (or temperature), light touch, position
sense, vibration, and discriminative sensations. This portion of the exam is very
subjective, and may become unreliable if repeated in quick succession. Therefore,
your exam should not be rushed, but must proceed efficiently.
2. Pain: complex neurological phenomenon. Nocioceptive and
antinociceptive system. The theory of “gate control”.
The gate control theory of pain asserts that non-painful input closes the nerve "gates" to
painful input, which prevents pain sensation from traveling to the central nervous system.
The gate control theory of pain describes how non-painful sensations can override and
reduce painful sensations.

3. Pathways mediating deep sensation. Types of sensation disturbances.

Neurological examination.

The pathways mediate the deep sensations (including the sensations of the body posture,
movement, vibration and pressure )and fine touch sensation (discriminatory sensation. (1)
Deep sensory and fine touch pathway of trunk and limbs It consists of three orders of
neurons.

1. Cell body in dorsal root

2. Cell body in nucleus gracilis and nucleus cuneatus (dorsal medulla in brainstem)
3. Cell body in thalamus

Signs,symptoms of central sensation impairment

1. pallanesthesia (loss of vibratory sense)
2. Anesthisa
3. hypothesis(lowering sensation because of deep injury of the nerve)
4. Bathyanesthesia (loss of deep joint sense)

● Posterior column loss (loss of joint positions sense and vibration sense with
intact pain and temperature)
● Hemisection of the cord (brown-sequard syndrome loss of joint position sense
on the same side as the lesion and the pain temperature on the opposite side)
● Complete transverse lesion(loss of all modalites a few segments below the
lesion)

Neurological examination=joint position sense,vibration sense

4. Pyramidal pathway: anatomical and physiological peculiarities, signs of

affection.

It originates in the primary motor area & premotor area. Terminates at the
anterior horn cells (A.H.C.) of the different levels of the spinal cord. It supplies
the opposite side of the body.
The corticospinal tract carries motor signals from the primary motor cortex in the
brain, down the spinal cord, to the muscles of the trunk and limbs. Thus, this tract is
involved in the voluntary movement of muscles of the body.

Divided into the anterior corticospinal tract (supplies axial muscles) and the lateral
corticospinal tract (supplies muscles of the limbs).

The anterior corticospinal tract is primarily responsible for gross and postural
movement of the trunk and proximal musculature

The primary responsibility of the lateral corticospinal tract is to control the

voluntary movement of contralateral limbs.

The corticobulbar tract carries efferent, motor, information from the primary motor
cortex to the muscles of the face, head and neck. It does this by synapsing with
motor cranial nerves in the brainstem. Therefore the corticobulbar tract is
responsible for innervating the muscles of the face, head and neck, as well as the
muscles involved in swallowing, phonation and facial expression.

7. Signs of Spinal Cord lesions at different levels: cervical, thoracic,

lumbar.
8. Hemisection of the Spinal Cord (Brown-Sequard Syndrome).

Brown-Séquard syndrome is a neurologic syndrome resulting from hemisection

of the spinal cord. It manifests with weakness or paralysis and proprioceptive
deficits on the side of the body ipsilateral to the lesion and loss of pain and
temperature sensation on the contralateral side
 9. Sphincter disturbances of neurologic origin.

Cauda equina syndrome

Compression of spinal roots L2 and below. Often due to intervertebral disc

herniation or tumor. Cauda equina syndrome typically results from a massive
rupture of an intervertebral disk that is capable of causing compression of two or
more of the 18 spinal nerve roots of the cauda equina.

Classic presentation: Unilateral radicular pain. Low back pain radiating to leg.
Absent knee and ankle reflex. Loss of bladder and anal sphincter control. Saddle
anesthesia. Loss of anocutaneous reflex. Normal Babiniski (the cauda equine
nerves are peripheral nerves although they still in the vertebral canal)

Treatment: emergent surgery and steroids.

10. Extrapyramidal system: anatomy, physiology, syndromes of affection.

It originates from centers situated at various levels of C.N.S. mainly the Basal
Ganglia. It controls the opposite side of the body.

The extrapyramidal tracts include parts of the following:

● rubrospinal tract=fine motor control

● pontine reticulospinal tract.
● Medial reticulospinal tract=contraction-increase tone
● Lateral reticulospinal tract=relaxation-decrease tone
● lateral vestibulospinal tract=balance and posture
● tectospinal tract=head coordination
11. Semiology of involuntary movements: tremor (parkinsonian, attitude,
action), chorea, athetosis, dystonia, iatrogenic dyskinesias, tics, facial
hemispasm, myoclonia, hemibalism.

Parkisonion tremor=occurs mostly at rest,hand and voice are affected with tremor
more than legs and head is rarely affected.

● High amplitude with lower,slower frequency

● Remains asymmetrical but beginning of disease is micrographia(very small
handwriting)
● Attitude (essential) tremors
● Slowed movement (bradykinesia).
● Rigid muscles.
● Impaired posture and balance.
● Loss of automatic movements.

Action tremor =occurs voluntary contraction of muscle includes postural

isometric and kinetic tremors.

chorea=irregular,sudden-onset,expensive purposeless movements.

athetosis= slow, involuntary, and writhing movements of the limbs, face,

neck, tongue, and other muscle groups.

dystonia=disorder characterized by involuntary muscle contractions that

cause slow repetitive movements or abnormal postures.
 myoclonus=sudden, brief involuntary twitching or jerking of a muscle or
group of muscles.

Dyskinesias=involuntary, erratic, writhing movements of the face, arms,

legs or trunk. They are often fluid and dance-like, but they may also cause
rapid jerking or slow and extended muscle spasms.

tics=sudden twitches, movements, or sounds that people do repeatedly.

Facial hemispasm=causes involuntary muscle twitches (spasms) on one side

(hemi-) of the face (facial).

hemibalism=relatively rare hyperkinetic movement disorder characterized

by involuntary, violent, coarse and wide-amplitude movements involving
ipsilateral arm and leg.

12. The cerebellum: anatomy, physiology. Semiology of the cerebellum

affection: ataxia, dysmetria, asynergy, dysdiadochokinesis, intention
tremor, speech and writing impairments. Method of clinical examination.

It is composed of the Neo, Archi & Paleo-cerebellum. It coordinates the

movements of the same side of the body.

Truncal ataxia Widebased gait. Can’t stand independently. Falls over when
sitting. Lesion in the vermis.Vermis is centrally located—affects the central
body. Degeneration associated with chronic alcohol use.

ROMBERG TEST Test for sensory (not cerebellar) ataxia. Loss of

proprioception: compensate though vision. How? Feet together, eyes closed:
Positive test: patients will lose balance or fall. If test positive: ataxia is
SENSORY. Cerebellar ataxia occurs even with eyes open.

Dysmetria: Loss of movement coordination. Under or over-shoot intended

position of hand.Causes lateral lesion of cerebellar hemisphere and dentate
nucleus

Asynergy=lack of coordination between muscles, limbs and joints

Dysdiadochokinesia: Can’t make movements exhibiting a rapid change of
motion. Can’t flip hand in palm.

Intention tremor: Can’t get hand to target.Contrast with resting tremor

(Parkinson’s).

Scanning speech: Spoken words are broken up into separate syllables, often
separated by a noticeable pause, and spoken with varying force. “How are
you doing?” “How…are…you…do…ing” It is also a typical symptom of
multiple sclerosis.

Agraphia: is an impairment or loss of a previous ability to write

Specific tests used to evaluate cerebellar function include assessment of gait

and balance, pronator drift, the finger-to-nose test, rapid alternating action, and
the heel-to-shin test.

13. Semiology of gait disturbances. Clinical peculiarities of topic and

etiologic diagnosis.

14. Midbrain: anatomical – physiological peculiarities, signs of affection.

Alternating syndromes.
 The midbrain is the topmost part of the brainstem, the connection central
between the brain and the spinal cord.

There are three main parts of the midbrain - the colliculi, the tegmentum, and
the cerebral peduncles.

The midbrain serves important functions in motor movement, particularly

movements of the eye, and in auditory and visual processing.

Midbrain—nuclei of CN III, IV

15. Pons of Varoli: anatomical – physiological peculiarities, signs of

affection. Alternating syndromes.

Cr 5, 6 & 7 in Pons.

The pons, while involved in the regulation of functions carried out by the cranial
nerves it houses, works together with the medulla oblongata to serve an
especially critical role in generating the respiratory rhythm of breathing.
Active functioning of the pons may also be fundamental to rapid eye
movement (REM) sleep.
16. Medulla: anatomical – physiological peculiarities, signs of affection.
Alternating syndromes.

It plays an essential role in passing messages between your spinal cord and
brain. It's also essential for regulating your cardiovascular and respiratory
systems.
17. Olfactory nerve: anatomical and physiological peculiarities, signs of
impairment.

Sensory only

● The axons of olfactory receptor (smell receptor) cells extend directly into the
highly organized olfactory bulb, where information about odours is processed.
● This specialized epithelium contains the cell bodies of bipolar olfactory
neurons from which the olfactory nerve fibers originate and extend apically.
● Exits through cribiform plate
● For smelling
18. Alternating syndromes. General notions. Classification.
Wallenberg syndrome.
Alternating hemiplegia is a rare neurological disorder that develops in
childhood, most often before the child is 18 months old. The disorder is
characterized by recurrent episodes of paralysis that involve one or both sides
of the body, multiple limbs, or a single limb.
Wallenberg syndrome is a condition that affects the nervous system. Signs and
symptoms may include swallowing difficulties, dizziness, hoarseness, nausea
and vomiting, nystagmus , and problems with balance.
Wallenberg's syndrome is a neurological condition caused by a stroke in the
vertebral or posterior inferior cerebellar artery of the brain stem.

19. Optic nerve: anatomical and physiological peculiarities, signs of

impairment.

Sensory only

● Sight. Not really a peripheral nerve (arises from diencephalon)

● Exits through optic canal
19. Oculomotor nerves (III,IV,VI): anatomical – physiological peculiarities,
signs of impairment.

Motor only

● Eye movement (SR, IR, MR, IO). Pupillary constriction (sphincter pupillae:
EdingerWestphal nucleus, muscarinic receptors) Accommodation. Eyelid
opening (levator palpebrae).
● Exits through superior orbital fissure
● Innervation to the pupil and lens (autonomic, parasympathetic) Innervation to
the upper eyelid (somatic) Innervation of the eye muscles that allow for visual
tracking and gaze fixation (somatic)

Myasthenia gravis=autoimmune disorder which cause antibodies to destroy

communication between nerves and muscles
 ● Weakness
● Double vision
● Trouble focusing
● Drooping eyelids

treatment=surgery or drugs such as (pyridostigmine) which increases acetylcholine

to stimulate receptors

20. Trigemenal nerve: anatomical – physiological peculiarities, signs of

impairment.

Sensory and motor

● Mastication (medial and lateral pterygoid, masseter, temporalis).

● Facial sensation (ophthalmic, maxillary, mandibular divisions).
● Somatosensation from anterior 2/3 of tongue.
● Part of corneal reflex (sensory, V1)
 1. Ophthalmic provides sensory innervation to the skin, mucous
membranes and sinuses of the upper face and scalp.Exits through
superior orbital fissure.
2. Maxillary provides sensory innervation to the skin, mucous membranes
and sinuses of the upper face and scalp.Exits through foramen rotunda.
3. Mandibular nerve supplies the teeth and gums of the mandible, the skin
of the temporal region, part of the auricle, the lower lip, and the lower
part of the face also supplies the muscles of mastication and the
mucous membrane of the anterior two-thirds of the tongue.Exits
through the foramen ovale.

Trigeminal neuralgia

1. Produces recurrent, unilateral, shooting pain in the distribution of CN V.

2. Triggered by chewing, talking, touching certain parts of the face.
3. Lasts (typically) for seconds to minutes, but episodes often increase in
intensity and frequency over time.
4. First-line therapy: carbamazepine or anticonvulsants and botox

21. Facial nerve: anatomical – physiological peculiarities, signs of

impairment.

Sensory and motor

● carries nerve fibers that control facial movement and expression.

● The facial nerve also carries nerves that are involved in taste to the anterior
2/3 of the tongue and produce tears (lacrimal gland).
● Exits through internal acoustic meatus

Facial nerve palsy/bell's palsy

inability to move the muscles that control smiling, blinking, and other facial
movements. This condition can affect a person's ability to convey emotion. Most of
the time, facial paralysis is limited to one side of the face.

Treatment

● Corticosteroids, such as prednisone, are powerful anti-inflammatory agents. If

they can reduce the swelling of the facial nerve, it will fit more comfortably
within the bony corridor that surrounds it. ...
● Antiviral drugs. The role of antivirals remains unsettled.
22. The group of bulbar nerves (IX, X, XII): anatomical – physiological
peculiarities, signs of impairment.

Bulbar muscles are supplied by CN in brainstem • V (jaw), VII (face), IX

(swallowing), X (palate), XI (head), XII (tongue).

23. Autonomic nervous system: anatomical – physiological peculiarities

and signs of impairment. Clinical examination and additional
investigations.
autonomic nerve disorder include:

● dizziness and fainting upon standing up, or orthostatic hypotension.

● an inability to alter heart rate with exercise, or exercise intolerance.
● sweating abnormalities, which could alternate between sweating too much
and not sweating enough.

Autonomic testing, also known as autonomic reflex screen or autonomic

response testing, is a non-invasive test that measures how the nervous
system works to control blood pressure, heart rate and sweating.

Your doctor might recommend tests to evaluate autonomic functions,

including:

1. Autonomic function tests. ...

2. Tilt-table test. ...
3. Gastrointestinal tests. ...
4. Quantitative sudomotor axon reflex test. ...
5. Thermoregulatory sweat test. ...
6. Urinalysis and bladder function (urodynamic) tests. ...
7. Ultrasound.
24. Anatomical – physiological peculiarities of the hypothalamic region.
Syndromes of hypothalamic dysfunction. Clinical criteria of the
hypothalamic syndromes.

HYPOTHALAMIC SYNDROME

● Diabetes insipidus (loss of ADH).

● Fatigue (loss of CRH low cortisol).
● Obesity.
● Loss of temperature regulation.

Maintains homeostasis by regulating:

1. Thirst and water balance.

2. Controlling Adenohypophysis (anterior pituitary) and Neurohypophysis

(posterior pituitary) release of hormones produced in the hypothalamus.

3. Regulating Hunger, Autonomic nervous system, Temperature, and Sexual

urges (TAN HATS). Inputs (areas not protected by blood-brain barrier): 1.
OVLT (senses change in osmolarity). 2. Area postrema (found in medulla,
responds to emetics)

Other possible tests include: Hormone injections followed by timed blood

samples. MRI or CT scans of the brain. Visual field eye exam (if there is a
tumor

23. Frontal lobe of the cerebral cortex: signs of impairment.

Motor function (initiation of movements), planning movements, thinking, feeling,
imagining, making decisions. Key Areas: Motor cortex, Frontal Eye Fields,
Broca’s speech area, Prefrontal Cortex

Lesion posterior part of middle frontal gyrus:

 1. Irritative: attacks of conjugate eye deviation to the opposite side of the lesion.
2. Destructive: both eyes deviate to side of lesion.

Lesion site anterior ⅔ of frontal lobe:

1. Mentality, personality & behavioral changes: lack of attention & judgment,
disinterest in people & surroundings, lack of personal hygiene, ending in
dementia.
2. Reappearance of primitive reflexes

The frontal lobe, for example, helps govern personality and impulsivity. If damaged,
there might be no "braking mechanism" for self-control. A person may find he cannot
control his anger or aggression. He may also make inappropriate comments to
friends or strangers not realizing they are off color.
24. Speech disturbances in the cerebral cortex lesions. Semiology of
aphasia.

WERNICKE’S SPEECH AREA: Lesions Wernicke’s aphasia.

UW: The middle cerebral artery supplies Broca's area (superior division) and
Wernicke's area (inferior division)this condition is also called sensory aphasia
or fluent aphasia. People who have Wernicke's aphasia can't understand
words.
25. Temporal lobe of the cerebral cortex: signs of impairment.
The temporal lobes are integral to auditory perception, receptive components of
language, visual memory, declarative (factual) memory, and emotion. Patients
with right temporal lobe lesions commonly lose the ability to interpret
nonverbal auditory stimuli (eg, music). Left temporal lobe lesions interfere
greatly with the recognition, memory, and formation of language.
26. Parietal lobe of the cerebral cortex: signs of impairment.
Semiology of apraxias.
Function. The parietal lobe is vital for sensory perception and integration,
including the management of taste, hearing, sight, touch, and smell. It is home
to the brain's primary somatic sensory cortex a region where the brain
interprets input from other areas of the body.
Gerstmann's syndrome is a cluster of symptoms resulting from damage to the
left parietal lobe. People with Gerstmann's syndrome often struggle with
writing, arithmetic, language, and the ability to perceive objects, though the
degree and extent of damage varies from person to person and injury to
injury.
Damage to the left parietal lobe can result in what is called "Gerstmann's
Syndrome." It includes right-left confusion, difficulty with writing
(agraphia) and difficulty with mathematics (acalculia). It can also produce
disorders of language (aphasia) and the inability to perceive objects normally
(agnosia).
Apraxia=is a neurological disorder characterized by loss of the ability to
execute or carry out skilled movements and gestures

27. Occipital lobe of the cerebral cortex: signs of impairment.

Agnosias.

The primary visual cortex

Visual association areas
Lesions in the primary visual cortex lead to a form of cortical blindness; in one
form, called Anton syndrome, patients become unable to recognize objects by
sight and are generally unaware of their deficits, often confabulating
descriptions of what they see.
**Agnosia is the loss of the ability to recognize objects, faces, voices, or places.
It’s a rare disorder involving one (or more) of the senses.
-Hearing (auditory agnosia—the inability to identify objects through sound such
as a ringing telephone)
-Taste (gustatory agnosia)
-Smell (olfactory agnosia)
-Touch (somatosensory agnosia)
-Sight (visual agnosia)
But Visual agnosia results from damage to the occipital lobe .