CLI NI CAL N EUR OS CIE NCE

APPROACH TO NEUROLOGIC DIAGNOSIS

Johnny K. Lokin, MD
First Long Examination: August 20, 2018

• Cerebellar
• Reflexes
Table of Contents o Check for pathologic reflexes | !
• Sensory
I. Neurologic Diagnosis .......................................................... 1 o Very subjective because the threshold of each person
varies | !
A. History ........................................................................ 1
o Usually tested last but in other books like Harrison’s,
B. Physical & Neurological Examination ......................... 1 sensory testing is done after the motor exam | !
C. Ancillary Diagnostic Procedures/Tests ....................... 1 • Test for presence or absence of meningeal irritation | !
II. Fundamentals of Neurological Diagnosis .......................... 1 C. Ancillary Diagnostic Procedures/Tests
III. Neurologic Problem .......................................................... 1 • Specific for the clinical diagnosis | G!
A. Is there a neurologic problem? ................................... 1 • Computed Tomography (CT Scan) – mass lesions, strokes,
1. Focal neurologic deficits ......................................... 1 head trauma, demyelinating disease, brain abscess
2. Increased intracranial pressure (ICP) .................... 2 • Magnetic Resonance Imaging (MRI) – mass lesions,
strokes, demyelinating disease, brain abscess
3. Signs of meningeal irritation ................................... 2 • Electroencephalogram (EEG) – Seizures
B. Where is the neurologic problem? .............................. 2 • Nerve Stimulation Studies (NSS) – neuropathies,
1. Levelize .................................................................. 3 Myasthenia Gravis, Guillain-Barre’ Syndrome
• Muscle biopsy – myopathies
2. Lateralize ................................................................ 3
• Lumbar puncture – CNS infections (meningitis,
3. Localize .................................................................. 3 encephalitis), subarachnoid hemorrhage
C. What is the neurologic problem? ................................ 3 • Serum potassium – hypokalemic paralysis
IV. Focal Neurologic Deficits ................................................. 4 • Total CPK – muscle disease, polymyositis, dermatomyositis
• Angiogram – aneurysm, AV malformation
A. Cerebral Dysfunction/Cerebral Cortical Lesions ......... 4 • Spinal x-ray – Pott’s disease
B. Brainstem Dysfunction ................................................ 4 • Skull x-ray – fracture
C. Cerebellar Dysfunction ............................................... 4 • Transcranial ultrasound – stroke, hydrocephalus, brain
death | !
D. Spinal Cord Dysfunction ............................................. 4
• Serologic test – infectious diseases i.e. HIV, cryptococcal
E. Peripheral nerve dysfunction ...................................... 5 meningitis | !
F. Myoneural Junction Dysfunction ................................. 5 II. Fundamentals of Neurological Diagnosis
G. Muscle Dysfunction .................................................... 5
Essential steps in arriving at a clinical diagnosis:
V. Management ..................................................................... 5 • Clinical information (chief complaint, HPI, past history, family
VI. Summary .......................................................................... 5 history, etc)
• Anatomical diagnosis (PE, knowledge of anatomy &
physiology, etc)
PREVIOUS
REMEMBER TEXTBOOK EDITOR
TRANS
LECTURER • Etiology and differential diagnosis (clinical neurosciences,
etc)
G & ! 4 ! • Ancillary procedures (imaging, electrophysiology, other
related study)
Disclaimer: The contents of this trans did not follow the order of the
powerpoint presentation. The editor rearranged the notes to III. Neurologic Problem
make it more organized and to avoid redundancy. 3 Questions Asked
• Is there a neurologic problem?
I. Neurologic Diagnosis
• Where is the neurologic problem?
A. History • What is the neurologic problem?
• One of the longest history among different medical fields A. Is there a neurologic problem?
(psychiatry is the most extensive) | !
There are more signs and symptoms but the ones presented here
• Diagnosis based almost 90% on clinical history and mental
are the general findings | !
status exam | !
1. Focal neurologic deficits
B. Physical & Neurological Examination
a. Disturbance in higher intellectual functions
• Follow the right sequence | G!
• Mental status § Memory impairment (cognitive changes)
o Not similar with psychiatry which focuses on the mental § Emotional and behavioral changes (organic)
status while neurology focuses more on the neurological § Language disturbance
examination in which mental status is just one of the § Seizure
components | !
b. Cranial nerve deficits
• Cranial nerves (CN 1-12)
• Motor § Diplopia – most common CN defect | G
o Includes testing for muscle strength | ! § Dysphagia

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§ Dysarthria b. (+) Brudzinski’s neck sign

§ Facial numbness
§ Sensory impairment § Flexing the neck will cause the hips and knees to flex | !

c. Weakness or paralysis of extremities | !

§ Most common focal neurologic deficit
§ May present with hemiparesis, paraparesis or
quadriparesis
§ Lesion of lateral corticospinal tract or motor system
d. Incoordination, poor equilibrium
Figure 3| Brudzinki’s Neck Sign
e. Reflex asymmetry, pathological reflexes (+ Babinski)
c. (+) Kernig’s sign
f. Sensory impairment in trunk and extremities
§ Flexing the patient’s hip 90 degrees then extending the
§ Most difficult to detect because most often subjective | ! patient’s knee causes pain | !

2. Increased intracranial pressure (ICP)

a. Headache / Vomiting / Both | !

b. Papilledema | !
§ Assessed thorugh fundoscopy
§ Venous pulsation cannot be appreciated Figure 4| Kernig’s Sign
§ No well demarcated disk margins

Papilledema Hemorrhagic

c. Diplopia with internal squint

§ Lateral rectus palsy secondary to abducens nerve lesion
§ Can be bilateral in increased ICP | !
§ Abducens nerve is a long intracranial nerve that can Figure 5| Anatomy of the Meninges
easily be compressed | !
• Infection and hemorrhage are the most common causes of
§ Trochlear nerve – longest intracranial nerve | !
meningeal irritation
§ Vagus nerve – longest cranial nerve | !
• Subarachnoid space – usually affected | !
o Rupture aneurysm
o Bacterial meningitis
o Viral meningitis
o Cancer

Figure 2| Right Lateral Rectus Palsy B. Where is the neurologic problem?

d. Altered sensorium • Is it in the cerebral cortex, cerebellum, brainstem, spinal cord,
peripheral nerves, NMJ, or muscle?
§ Deterioration in the level of consciousness i.e.
drowsiness, stupor, coma
e. Bulging fontanel, separation of sutures, rapid enlarging
head size
§ For infants whose fontanels have not closed yet
3. Signs of meningeal irritation
Headache/ vomiting with | G
a. Nuchal rigidity | !
§ Easiest to test in patients whose level of consciousness
is not affected
§ Passive neck flexion causes pain and resistance in the
neck | G

Figure 6| Cranial Nerves

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 APPROA CH TO N E UR OLOG IC DIAGN O SIS

2. Lateralize
o Is the problem left, right, multifocal, or diffuse? | !
3. Localize
o In which particular neuroanatomical area is the lesion? | !

C. What is the neurologic problem?

1. Disease category

Congenital/ Craniostenosis
Developmental Spina bifida
Aneurysm – usually considered congenital but
can be due to wear and tear | !
Arteriovenous malformation

Trauma Epidural
Subdural
Subarachnoid
Intracerebral hemorrhage
Figure 7| Anatomy of the Spinal Cord
Infection Meningitis
1. Levelize Encephalitis
Meningoencephalitis | !
a. Upper motor neuron Brain abscess
§ Cerebrum
§ Brainstem Degenerative Alzheimer’s
§ Cerebellum Parkinson’s disease
§ Spinal cord Amyotropic lateral sclerosis

b. Lower motor neuron Neoplasm Primary or metastatic

§ Anterior horn cell
Vascular Cerebral infarction or hemorrhage
∗ Both LMN and UMN symptoms | !
(most common) Subarachnoid hemorrhage
∗ Prototypical disease: ALS | !
§ Difficult to diagnose because they come in stages
Metabolic/ Hypoglycemia
§ Peripheral nerve Endocrine Hypoxia – secondary; due to decreased cerebral
§ Neuromuscular junction perfusion i.e. those revived after cardiac arrest |
§ Muscle !
Hyponatremia
Hypercalcemia

Intoxication Drug overdose

Chemicals i.e. arsenic | !
Poison

Nutritional Vit B1, B6, B12 deficiency

Deficiency

Figure 8| Lower Motor Neuron Demyelinating Postinfectious/ post vaccinal encephalomyelitis

Multiple sclerosis - prototypical disease for
Lower Motor demyelinating diseases CENTRALLY | !
Lesion Upper Motor Neuron
Neuron
(-)
Atrophy may also be Immunologic Polymyositis
Atrophy found in UMN disease (+) Dermatomyositis
i.e. disuse atrophy in Guillain-Barre
stroke | ! Myasthenia Gravis
Fasciculation (-) (+)
Tone Increased Decreased 2. Helpful from history
Muscles below level of Muscles at level of o Age of onset
Weakness
lesion lesion o Onset and course | !
Superficial (-) § When did the symptoms begin?
(+/-)
reflexes
§ How did it progress?
(-) § Acute, subacute or chronic?
Deep tendon ↑↑↑
hypoactive/non-
reflexes hyperactive o Other medical data
reactive
§ Occupation – e.g. BPO workers who have HIV may
Pathological present with neurologic symptoms | !
(+) Babinski (-) Babinski
reflexes o Family history

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§ Stroke, epilepsy, cancer | ! B. Brainstem Dysfunction

o Social history
§ Practices | ! • “Crossed motor/ sensory syndrome” | G
o Ipsilateral cranial nerve deficits
3. Temporal profile o Contralateral hemiparesis with Babinski
• Ipsilateral limb ataxia
o Onset of illness
o If the lesion is found in the cerebellar
o Course of illness
peduncles | G
• Internuclear opthalmoplegia - median
longitudinal fasciculus syndrome
o CNs connected by MLF: III, IV, VI for EOM
and VIII | !
o Allows you to turn your head without losing
balance | !
o When you have a lesion in the MLF, you may
have problems with equilibrium and paresis or
ophthalmoplegia | !
C. Cerebellar Dysfunction
• Hemisphere lesion
o Ipsilateral limb ataxia | G
Figure 9| Temporal Profile § Intention tremor
o Vascular § Dysmetria
§ Fast course and onset | ! § Dysdiadochokinesia
§ Acute onset but the deficits, time, and length of the • Vermis lesion
disease can be protracted | ! o Truncal ataxia – cannot sit up/stand up straight and have
o Toxic and metabolic tendency to fall | !
§ Acute to subacute | ! o No limb ataxia – may be limited or cannot be seen | !
o Infection
D. Spinal Cord Dysfunction
§ Acute to subacute | !
o Neoplasm
Weakness Lower motor neuron at level of lesion especially in
§ Accrue symptoms overtime | !
lumbar lesions | !
4. Type of lesion (distribution) Upper motor neuron below level of lesion – usual
manifestation | !
o Focal
§ Mass lesion (neoplasm, abscess) Objective Diminished/absent sensation below level of lesion
§ Infarction sensory
§ Hematoma
o Multifocal Autonomic Present
§ Multiple tumors disturbances
§ Abscesses
§ Multiple sclerosis
o Diffuse
§ Toxic – metabolic encephalopathy
§ Peripheral neuropathy
§ Myopathy
5. Important diseases | !
o Headache – most common
nd
o Stroke – 2 most common
o Alzheimer’s disease – growing in incidence
o Parkinson’s disease
Figure 12| Spinal Cord Dysfunction
IV. Focal Neurologic Deficits
• Cervical | !
A. Cerebral Dysfunction/Cerebral Cortical Lesions o Sensory deficits from the neck down
• Seizure o Hyperreflexia of BUE and BLE particularly the LE are
• Language disorder – aphasia hyperreflexive with (+) pathologic reflexes
• Organic mental, behavioral, and personality o UE can be hyporeflexive at times
changes – must be non-psychologic | G • Thoracic | !
• Contralateral | G o Reflexes at UE are normal
o Hemiparesis with Babinski & cranial nerve o Deep tendon reflexes (ex. patellar reflex) are hyperactive in
deficits the LE
o Hemisensory deficits o Pathologic reflexes in the LE (ex. positive Babinski sign)
o Homonymous hemianopsia/quadrantinopsia • Lumbar | !
o Normal reflexes on the UE
o Decrease or normal reflexes in the LE
o Seldom to no pathologic reflexes

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E. Peripheral nerve dysfunction

V. Management
• Weakness begins distally and symmetrically | G
• Most common disease entity: Diabetic • Medical
neuropathy | G • Surgical
o Sensory deficits start distally → more VI. Summary
usual
o Autonomic deficits may present later in
the disease but may be predominant
depending on what is root involved
more (sensory or motor)
o Reflexes are initially normal but may
slowly have hyporeflexia and
subsequently arreflexia
• Guillain-Barre Syndrome | !
o A peripheral demyelinating type of
disorder
o Characterized by distal, symmetrical weakness and
sensory deficits | G
o Autonomic deficits are present especially in patients with
predominantly disautonomic syndromes
o Reflexes decreases at a much FASTER rate | G

Weakness Distal, symmetrical

Objective sensory deficits Distal, symmetrical Figure 14| Simplified Approach to Neurologic Diagnosis

Autonomic disturbances May be present

Reflexes Areflexia
- END -
F. Myoneural Junction Dysfunction
• Prototypical disease: Myasthenia gravis | G
o Become weaker as the day goes, but get stronger after
rest | G
o Post-synaptic pathology - autoiummune problem causes REFERENCES
degradation in the conformation of the ACh receptors at
the myoneural junction | G • Lecture
• Also common in patients with malignancies
o Ex. Lambert-Eaton Myasthenic Syndrome
§ Fluctuating weakness | G
§ Stronger when moving around as compared to
Myasthenia gravis
§ Pre-synaptic pathology - antigens coming from the
cancer compete with Ca2+ and occupy calcium channel
receptors | G

Weakness Fluctuating

Objective sensory deficits None

Autonomic disturbances None

Reflexes Normal

G. Muscle Dysfunction

Weakness Proximal, symmetrical

Neuropathy proximal < distal | !

Objective sensory deficits None

Autonomic disturbances None

Reflexes Depending on severity of weakness

More severe à more
hyporeflexive/areflexive | !
Mild to moderate à normal reflexes | !

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