The Nervous System

Neurological History
Acute symptoms (mins – hour) suggests vascular or convulsive problem:
- Vascular can be embolism. Infarction or haemorrhage
- Precipitant or warning (aura) might be present
o E.g. aura preceding seizure (localizing – auditory hallucinations or non-localizing -
apprehension)
- Stroke/ CVA = focal problem
- Headaches & migraines:
Subacute onset:
- Inflammatory disorders (meningitis, cerebral abscess, GBS)
Chronic onset:
- Underlying disorder may be related to a tumour or degenerative process.

Metabolic & toxic disorders can be any of the three above.

Risk factors for cerebrovascular disease:

- HPT
- Smoking
- Diabetes
- Family history
- Haematological disease
- Hyperlipidaemia
- Atrial fibrillation, bacterial endocarditis, MI (emboli)

See Qs page 324  Question box 11.1 and 11.2

Headache & Facial Pain

Headache Description
Hemiplegic migraine Sudden onset of weakness on 1 side of body that resolves; and is
followed by a severe h/ache
TIA Sudden onset of weakness on 1 side of body that resolves; NOT
followed by h/ache
Migraine w an aura/ classical Unilateral h/ache preceded by flashing lights/ zigzag lines and assoc
migraine w photophobia
Common migraine Unilateral h/ache w/o an aura
Cluster h/ache Ocular/ temporal pain lasting mins  hours, assoc w lacrimation,
rhinorrhea and flushing of forehead; and occurring in bouts lasting
several weeks a few times a year
 Cervical spondylosis h/ache over occiput assoc w neck stiffness
Coital h/ache During intercourse or orgasm
Raised intracranial pressure Generalized h/ache worse in am & assoc w drowsiness or vomiting
Meningitis Generalized headache assoc w photophobia, fever & a stiff neck of
more gradual onset
Temporal arteritis Persistent unilateral h/ache over temporal area assoc w tenderness
over the temporal artery & blurring of vision
Acute sinusitis h/ache w pain/ fullness behind the eyes or over the cheeks or
forehead
Subarachnoid haemorrhage Usually instantaneous onset of severe headache that is initially
localized but becomes generalized & is assoc w neck stiffness
Idiopathic intracranial HPT Morning h/aches worse w coughing, esp in an obese pt.
Tension-type h/ache Most frequent h/ache. Bilateral; frontal/occipital/ temporal area;
described as a sensation of tightness that lasts for hours. Recurs
often. Usually no assoc symp (no N, V, weakness or parasthesiae)

Faints and fits

- Localized seizures:
o Impaired consciousness = complex seizure
o Unimpaired Consciousness = simple seizure
-  Read Questions Box 11.4 page 326

Other neurological symptoms:

Dizziness
Visual disturbances & deafness
Disturbances of gait
Disturbed sensation or weakness in limbs
 See Table 11.4 page 328 for movement disorders

Past Medical History

- Previous illnesses to be asked about:

o Meningitis/ encephalitis
o Head or spinal injuries
o History of epilepsy/ convulsions
o Previous operations
o Past hx of STDs
- Remember to ask about risk factors!
- Medical history
o See table 11.5 page 328 for referral
Examination:
Basic Outline:

- Higher Centers
- Cranial Nerves
- Motor Examination
o Inspection
o Tone (resistance to passive movement)
o Power
o Reflexes
o Plantar & Babinski
- Sensory Examination
- Cerebellar function
- Get up and Walk (Gait)

General:

- Shake pts. hand

o Ask about handedness
 94% of R handed people & +- 50% of L handed people have a dominant L
hemisphere
 Dominant hemisphere controls language and mathematical function
- Orientation:
o Test orientation by asking pts. name, present location & date
- Head and Neck: p 352
o Inspect and palpate for lumps (e.g. meningioma or sarcoma)
o Auscultate skull by placing diaphragm of stethoscope on the frontal bone, lateral
occipital bones and the bell over each eye
o Ask pt to hold breath
o Bruits can be heard d/t A-V malformation or advanced Paget’s disease
o Auscultate over carotids for a carotid bruit
- Neck stiffness:
o Assess signs of meningism in pt w acute illness/ febrile/ altered mental status
o Process:
 Pt lies flat in bed
 Place examining hand under the occiput and gently flex the neck passively
 Meningism – resistance to neck flexion d/t painful spasm of extensor MM or
the neck.
 Other causes of resistance:
 Cervical spondylosis
 After cervical fusion
 Parkinson’s Disease
  Raised ICP
- From GEMP 2:
o Inspect for involuntary movements (These suggest lesions of extrapyramidal motor
pathways):
 Dystonic twisting
 Intermittent sustained contraction of 1 or more M groups that
cause a twisting/ distortion of that part of body causing an abN
posture
 Choreiform:
 Ceaseless occurrence of rapid, jerky, involuntary movements
 Myoclonic jerks:
 Sudden, severe involuntary contraction of any M group
 Tics:
 Involuntary, compulsive, repetitive, stereotypes movements
 Tremors:
 Rhythmic, oscillatory to and fro movements of M groups

Comparison of UMN and LMN Lesions :

Upper Lower
Fasciculations No Yes
Wasting Only w prolonged disuse Yes
Tone Increased, spastic Decreased, flaccid
Weakness Yes Yes
Reflexes Exaggerated Depressed/ absent
Clonus Yes No
Plantar response Extensor – dorsiflexion Flexor- plantar flexion

Higher Order Functions:

- Speech:
o Free speech
 This will usually occur with history taking but in an OSCE situation, ask the pt
to describe the room, their clothes or daily activities.
o Comprehension:
 Tell pt to complete a task: “Touch your chin, then your nose and then your
ear”
 Ask a patient yes or no Q: “Do you put your shoes on before your socks”
o Test repetition: “Repeat the phrase, no ifs ands or buts”
o Name two objects pointed at
o Abnormalities of speech:
 Dysphasia
 Disorder of the content of speech. Can be:
 o Receptive
o Expressive
 Dysarthria
 No disorder of content of speech but difficulty w articulation
 Dysphonia
 Alteration of sound of voice

Cranial Nerves:

- If possible position pt so that they are sitting over the edge of the bed.
- Careful general inspection for:
o Ptosis
o Proptosis
o Pupillary inequality
o Skew deviation of the eyes
o Facial asymmetry
1. CN I:
a. External appearance of nose:
i. Rash/ deformity
b. Examine nasal vestibule
c. Examined only if pt complains of anosmia (or loss of taste) or if there’s evidence of
frontal/temporal lobe lesion
d. Don’t use pungent substances (ammonia) because they are upsetting and noxious
stimuli are detected by CN V
e. Causes of anosmia:
i. Upper RTI
ii. Smoking
iii. Increasing age
iv. Ethmoid tumour
v. Basal skull fracture or frontal fracture
vi. Congenital
vii. Unilateral occurs w trauma w/o a fracture

2. CN II:
a. Ask about vision. If problems, enquire about:
i. Time course
1. Sudden loss of vision in 1 eye (curtain being drawn down)  embolus to
retina. If vision returns spontaneously = amaurosis fugax. Vision loss =
negative symptom. Visual hallucinations/ aura/ blurry vision/
photophobia = positive symptom
ii. 1 eye/ both
b. Visual acuity
 i. Pt MUST wear their glasses if they are used for reading/ driving
ii. Snellen’s chart
1. Refractive error is confirmed if visual acuity improves w a pin-hole
2. If pt can’t read the letters, proceed w:
a. Counting fingers, then
b. Perception of hand movement, and lastly
c. Light perception
iii. Rapid onset bilateral blindness:
1. Bilateral optic N damage (e.g. w methyl alcohol poisoning)
2. Bilateral occipital lobe infarction
iv. Rapid onset unilateral blindness:
1. Retinal artery/ vein occlusion
v. Gradual onset bilateral blindness:
1. Cataracts
2. Macular degeneration
3. Diabetic retinopathy
c. Visual fields:
i. REMOVE pts. glasses
ii. Pin/ pen must be brought into the visual field from the 4 main directions,
diagonally towards the center of the field of vision
iii. Map out the blindspot:
1. Ask for the disappearance of the pin around the centre of the field of
vision of each eye
iv. Map w fingers if pt finds pin/ pen difficult to see
v. Patterns of visual field loss  pictures page 334; explanation page 335
d. Opthalmoscopy:
i. Loss of normal depression of the optic disc causes blurring at the margins. This =
papilloedema. If present; increased ICP is suspected.
1. Look for pulsations in retinal veins:
a. If present  raised ICP is excluded
b. If absent  does not exclude raised ICP

3. CN III, IV and VI:

a. PSNS stimulation  pupil constriction (miosis); SNS stimulation  dilation (mydriasis)

SR (CNIII) IO (CNIII)

LR (CN VI) MR (CNIII)

Nose

IR (CNIII) SO (CN IV)

b. Examine pupils:
i. Size
ii. Shape
iii. Equality
iv. Regularity
v. Ptosis
vi. Ectropion (drooping lower lid)  common in elderly. Also occurs w CN VII palsy.
Often eye irritation & watering d/t defective tear drainage
c. Light reflex:
i. Direct & consensual light reflex
ii. Afferent = CN II; efferent = CN III
iii. Optic atrophy/ severely reduced visual acuity  Affected eye dilated
paradoxically when light is shone into it. This = afferent pupillary defect.
d. Accommodation
i. Focus far; look close. Pupil constriction w near vision.
e. Eye Movements:
i. Assess voluntary eye movements first:
1. Left
2. Right
3. Up
4. Down
ii. Active movements:
1. H pattern
2. Pt must say if double vision (diplopia) occurs:
a. If present, further testing is needed:
i. False image = paler, less distinct & more peripheral than
the real one.
ii. Ask if images lie side-by-side or one on top of another
1. Side by side  problem w MR or LR
2. On top  problem w SO, IO, SR or IR
a. Ask in which direction there is
maximum image separation 
separation is greatest in the direction in
which the weak M has its purest action.
At this maximum point, cover 1 eye to
see which eye is responsible.
i. Loss of lateral image = covered
eye is responsible.
3. Note if there are problems w movement. Test each eye separately if
there are.
Cranial Nerve Features Aetiology
CN III Complete ptosis (partial ptosis Trauma
occurs w incomplete lesion) Idiopathic
Central Causes:
Divergent strabismus (eye down and - Vascular lesion in brainstem
out) - Tumour
Peripheral Causes:
Dilated pupil unresponsive to light - Compressive lesions (e.g.
(Consensual response in normal eye aneurysm, tumor)
is intact) - Ischaemia or infarct (e.g. DM)

Unreactive to accommodation
Always try exclude a CN IV lesion when a CN III lesion is present:
- Tilt the head to the same side as the lesion
- Affected eye will intort in CN IV is intact
- SIN = Superior oblique INtorts
CN IV Weakness of downward (and Isolated palsy is rare.
outward) movement
Idiopathic
Pt may walk w head tilted towards Trauma
opposite shoulder to allow binocular
vision to be maintained
CN VI Failure of lateral movement Bilateral Lesions:
Trauma
Convergent strabismus Wernicke’s encephalopathy

Diplopia Unilateral lesions:

Idiopathic
Trauma
Abnormalities of conjugate gaze on page 339 - 340

4. Nystagmus:
a. Imbalance between eye MM causes eyes to drift slowly in one
direction. This is corrected by a quick movement (saccadic) back
to original position.
b. Often not detected when eyes are at rest; only detected when
eyes are deviated.
i. Fine nystagmus normal at extremes of gaze  TEST by
asking pt to follow pin out to 30°)
c. Jerky horizontal Nystagmus is d/t:
i. Vestibular lesion
ii. Cerebellar lesion
iii. Toxins (phenytoin and alcohol)
iv. Internuclear ophthalmoplegia
d. Jerky vertical nystagmus d/t:
 i. Brainstem lesion
e. Pendular nystagmus
i. Nystagmus phases are = in duration. Causes:
1. Retinal
2. Congenital
ii. Occurs d/t poor vision or increased sensitivity to light

4. CN V:
a. Pain along N distribution is v common. Tic douloureux (trigeminal neuralgia) = sudden, v
severe shooting pain in 1 of the N divisions. May be precipitated by eating/ brushing
teeth. Caused by pontine lesion or compression of the N by a vascular abN.
i. Common in elderly
ii. When in young females, it suggests Multiple sclerosis
b. Pain d/t sinusitis, dental abscess, malignancy or herpes zoster may be felt along the
distribution.
c. Corneal reflex:
i. Normal response = blinking both eyes
ii. Sensory component = ophthalmic division of CN V
iii. Motor component = CN VII to orbicularis oculi
1. If blinking occurs only w contralateral eye this indicates an ipsilateral CN
VII palsy. Pt feels the sensation but doesn’t blink.
d. Test Facial Sensation:
i. Neurological pin
1. Pt must close eyes
2. Ask pt if it feels sharp/ dull
a. Loss of pain sensation  pt feels it as dull
i. Area of dull sensation should be mapped by testing
sensation progressively – test from dull to sharp area.
ii. Cotton wool
1. Pt keeps eyes closed
2. Pt must say YES each time the touch is felt (DON’T STROKE)
e. Motor division:
i. Inspect wasting of temporal and masseter
ii. Palpate
iii. Get pt to hold mouth open while you attempt to close it. Unilateral motor
division lesion causes jaw to deviate TO affected side.
iv. Jaw jerk/ masseter reflex
f. CN V Palsy:
i. Causes:
1. Central (pons, medulla & upper cervical cord)
a. Vascular lesion
b. Tumour
 c. Syringobulbia (Condition where by fluid filled cavities affect the
brainstem. Usually results congenitally, or d/t trauma or tumor
growth)
2. Peripheral (middle fossa)
a. Aneurysm
b. Tumor (primary or secondary)
c. Chronic meningitis
ii. If there is total sensation loss  lesion is at ganglion/ sensory root
iii. Total sensory loss in one division  postganglionic lesion.
iv. Dissociated sensory loss (loss of pain but preservation of touch) brainstem/
upper cord lesion e.g. syringobulbia, foramen magnum tumor.
v. If touch is lost and pain is intact  abnormality of pontine nuclei e.g. vascular
lesion or tumor.

5. CN VII:
a. Pt may have noticed difficult speaking & keeping liquids in mouth; dry mouth & dry
eyes.
b. Inspect for asymmetry
i. Unilateral drooping of corner of mouth
ii. Smoothing of wrinkled forehead
iii. Symmetry might be maintained w bilateral N palsies
c. Muscle Power:
i. Look up to wrinkle forehead
1. Preserved w UMN lesion d/t bilateral cortical representation. Other MM
usually affected on the side of the UMN lesion
2. In a LMN lesion, all MM of facial expression are affected on side of
lesion
ii. Puff out cheeks
iii. Shut eyes tightly
iv. Show me your teeth
v. Taste on anterior 2/3 of tongue
1. Not routine
d. Causes of a N Palsy:
i. UMN lesion (supranuclear)
1. Vascular lesions
2. Tumour
ii. LMN lesion
1. Pontine causes:
a. Vascular lesions
b. Tumours
c. Syringobublia
d. Multiple sclerosis
 2. Posterior fossa lesions:
a. Acoustic neuroma
b. Meningioma
c. Chronic meningitis
3. Petrous Temporal bone:
a. Bell’s Palsy
i. Commonset cause of facial N palsy
ii. Present in everyone; but not usually visible
iii. When pt attempts to shut eye w a LMN palsy, there is
an upward movement of the eyeball and incomplete
closure of eye lid. See picture page 347
e. Regrowth:
i. Crocodile tears
1. d/t regrowth of fibres meant for the salivary gland to the lacrimal gland.
Thus tear formation when a pt eats.

6. CN VIII:
a. History:
i. Unilateral hearing loss more likely to be d/t N lesion
ii. Timing of deafness
iii. Family history
iv. Occupational/ recreational exposure to loud noise w/o protection
v. Hx of trauma or recurrent ear infxns.
b. Inspection:
i. Hearing aid?  remove
ii. Scars behind ears?
iii. Feel for pre and post auricular nodes.
iv. Inspect external auditory meatus
c. Rinné’s Test:
i. 256Hz vibrating tuning fork on mastoid process. When sound no longer heard,
place by external meatus:
1. Neural deafness:
a. Audible at meatus because air and bone conduction are
reduced equally, so air conduction is better.
i. This = Rinne positive
2. Conductive deafness
a. Nothing audible at meatus.
i. This = Rinne negative
d. Weber’s Test:
i. Vibrating 256 Hz tuning fork placed in centre of forehead.
ii. Normally sound heard incentre of forehead
1. Nerve deafness:
 a. Sound heard better in normal ear
2. Conduction deafness:
a. Sound is louder in abnormal ear.
e. Causes of deafness:
i. Unilateral Nerve deafness
1. Tumours (acoustic neuroma)
2. Trauma (fracture to petrous temporal bone)
3. Vascular disease or internal auditory artery (rare)
ii. Bilateral N deafness:
1. Environmental exposure to noise
2. Degeneration
3. Toxicity (aspirin, streptomycin)
4. Infection (congenital rubella syndrome, congenital syphilis)
iii. Conduction deafness:
1. Wax
2. Otitis media
3. Osteosclerosis
f. Vestibular Examination
i. Hallpike Manoeuvre
1. Positive test:
a. Vertigo and nystagmus (rotatory) towards the affected side
occur for several seconds; and then abate and cant be
reproduced for 10-15 minutes
i. This occurs in BPPV (Benign Paroxysmal Positional
Vertigo)
1. Concretions in semicircular canals.
ii. Causes of abnormalities:
1. Labyrinthine causes:
a. Acute labyrinthitis
b. Motion sickness
c. Streptomycin toxicity
2. Vestibular causes:
a. Vestibular neuronitis

7. CN IX and X:
a. History:
i. No definite symptoms. Possibly difficulty in swallowing dry foods.
ii. Glossopharyngeal neuralgia = tic douloureux of CN IX. Pt experiences sudden
shooting pains that radiate from one side of the throat to the ear.
b. Inspect:
i. Uvula displacement
1. Say “Ah!”
 a. Normally posterior edge of soft palate (velum) rises
symmetrically
b. If uvula drawn to 1 side this indicates a unilateral CN X palsy. Its
drawn to Normal side.
c. Gag reflex:
i. Afferent = CN IX; efferent = CN X
ii. Not a necessary test, instead:
1. Touch the back of the pharynx is touched w a spatula. Pt must say if
they can feel it
2. Normally there is reflex contraction of soft palate.
a. Pt can feel touch but theres no palatal contraction  CN X palsy
iii. Reduced w old age
d. Speech
i. Ask pt to speak to assess hoarseness (Possible unilateral recurrent laryngeal
nerve lesion)
ii. Ask pt to cough (Listen for bovine cough)
e. Taste
i. Not routine to test taste to posterior 1/3 of tongue (CN IX)
f. Palsy:
i. Central causes:
1. Vascular lesions
a. Lateral medullary infarct d/t vertebral or posterior inferior
cerebellar artery disease
2. Tumour
3. Syringobulbia
4. Motor neurone disease
ii. Peripheral
1. Aneurysms at base of skull
2. Tumours
3. Chronic meningitis
4. Guillain-Barre syndrome

8. CN XI:
a. Shrug shoulders
i. Feel the bulk
ii. Attempt to push down
b. Turn head against resistance
i. (Right SCM turns head Left)
ii. Feel bulk
c. Torticollis (overactivity of neck MM) is commoner than M weakness
i. W torticollis the head appears turned to 1 side permanently/ in spasms.
d. Palsy causes:
 i. Unilateral:
1. Trauma involving neck or base of skull
2. Poliomyelitis
3. Basilar invagination
4. Syringomyelia
5. Tumours near jugular foramen
ii. Bilateral:
1. Motor neurone disease
2. Poliomyelitis
3. GBS

9. CN XII:
a. Inspect tongue at rest (i.e. inside mouth)
b. Protrude tounge
i. May deviate towards the weaker/ affected side if there is a unilateral LMN
lesion
ii. Tongue receives bilateral UMN innervation in most people, so an UMN lesion
produces no deviation
iii. Combination of bilateral UMN lesions of CN IX, X & XII = Pseudobulbar palsy
iv. LMN lesion  wasting, fasciculation, weakness.
c. Test movement.
d. Palsy causes:
i. Bilateral UMN lesions:
1. Vascular lesions
2. Motor neuron disease
3. Tumours
a. Metastases to base of skull
ii. Unilateral LMN lesions:
1. Central cause:
a. Vascular lesion (thrombosis of vertebral artery)
b. Motor neuron disease
c. Syringobublia
2. Peripheral causes:
a. Posterior fossa:
i. Aneurysms
ii. Chronic meningitis
iii. Trauma
b. Upper neck
i. Tumours
ii. LA
c. Arnold-Chiari malformation
 i. Congenital malformation at base of skull w herniation of
cerebellum and medulla into spinal canal cause lower
CN palsies, cerebellar limb signs and UMN signs in legs
iii. Bilateral LMN lesions:
1. Motor neurone disease
2. GBS
3. Poliomyelitis
4. Arnold-Chiari malformation

Multiple CN Lesions:

- Unilateral III, IV, V & VI involvement suggests lesion in cavernous sinus

- Unilateral V, VII & VIII involvement suggests a cerebellopontine angle lesion (usually –
tumor)
- Unilateral IX, X and XI involvement suggests a jugular foramen lesion
- Combined bilateral X, XI and XII suggests:
o bulbar palsy if LMN changes are present
o Pseudobulbar palsy if UMN signs are present
o See table page 353
- Weakness of eye and facial MM that worsens w repeated contraction suggests myasthenia.

MOTOR EXAMINATION

General:
- Shake hands:
o Pt that cant relax their hand grip has myotonia (inability to relax M after voluntary
contraction). Commonly d/t dystrophia myotonica
- Exposure of upper or lower limbs
Inspection:
- Abnormal posture
o E.g. hemiplegia d/t stroke
o M wasting
 Indicates denervated M, primary M disease or disuse atrophy
 Try figure out WHICH groups are involved: proximal, distal, symmetrical,
asymm, generalized)
o AbN movements
o Skin
 Scars etc. Catheter?

Upper limbs:
- Ask pt to hold out both hands, arms extended, eyes closed.
 o Pt must turn arms palms upward.
o Observe for drift. Causes of drift:
 UMN weakness
 Arms tend to move in downward direction
 Drifting tends to start distally & move proximally
 +- slow pronation of fingers and elbow
 Cerebellar disease
 Drift is usually upwards
 +- slow pronation of wrist and elbow
 Loss of proprioception
 “searching” movement – typically only affecting fingers
 Can be in any direction

- Tone:
o Tested at wrists and elbows:
 Rotation of wrist – supination & pronation (support elbow w 1 hand)
 Elbow
 Rigidity and spasticity
o Lift arm and drop it
 Falls quickly  hypotonia
o Cogwheel rigidity (Parkinsons)

- Power:

0 Complete paralysis (no movement)

1 Flicker of contraction possible
2 Movement is possible when gravity is excluded
3 Movement is possible against gravity but not if further resistance is added
4 Moderate movement against resistance
5 Normal Power

o Shoulder: see page 357

 Abduction
 Adduction
o Elbow & Wrist:
 Flexion
 Extension
o Fingers:
 Flexion (Squeeze my fingers)
 Extension
 Abduction
 Adduction
 - Reflexes:
0 Absent
1 Present but reduced
2 Normal
3 Increased/ brisk, possibly normal
4 Greatly increased, often associated w clonus

o Biceps Jerk (C5, C6)

o Triceps jerk (C7 C8)
o Brachioradialis (supinator) jerk (C5 C6)
o Finger jerks (C8)
o If reflex appears to be absent, always test using reinforcement maneuver:
 Ask pt to clench teeth tightly
 Talking to pt may provide distraction
o Increased jerk occurs w UMN lesion
o Decreased/ absent jerk occurs w:
 Breach in any part of reflex motor arc:
 M (myopathy)
 Motor N (neuropathy)
 Anterior spinal cord root (spondylosis)
 Anterior horn cell (poliomyelitis)
 Sensory arc (sensory root or sensory nerve)

- Examination of peripheral NN of upper limb:

Nerve Root Value Motor Innervation Characteristic deformity Examination
C5, 6 Triceps Wrist drop Motor
Radial N

Brachioradialis
Extensor MM of Absent elbow extension Sensory:
hand (If lesion occurs above the Pin over the anatomical snuff box
upper 1/3 of the upper
C6-T1 MM of forearm Lesion at wrist (Carpal Pen-touching test (most pts. w CT
Median N

(except flexor carpi tunnel) syndrome have symptoms but

ulnaris & ulnar half normal power & signs)
of flexor digitorum
profundus) Lesion in cubital fossa Oschner’s clasping test
C8 – T1 Motor supply to all Claw hand/ claw-like hand Froment’s sign (Paper)
Ulnar N

the small MM of the (wasting of small MM of

hand (except LOAF), hand w partial clawing.
flexor carpi ulnair & Clawing more pronounced Sensory – pinprick
ulnar half of FDP. w ulnar lesion at wrist)
o Brachial Plexus Lesions:
 Causes of lesions:
 Inflammation/ autoimmune disorders (mostly upper plexus)
 Radiotherapy (mostly upper plexus)
 Cancer (Mostly lower plexus)
 o Local invasion causes lesion
 Trauma
 Shoulder girdle examination:
 See page 367 Table 11.15

Lower Limbs:
- Inspection:
o Same as above.
o Run hand along each shin feeling for wasting of anterior tibial MM
- Tone:
o Test at knees and ankles
o Abruptly pull knee up and drop it
o Supporting the thigh, flex and extend knee w & w/o velocity
o Can examine w pts. legs over the bed:
 Leg is raised by examiner and let go
 Oscillates for up to 6 times
 If hypotonic  oscillations are wider and more prolonged
o Test for clonus:
 Clonus = sustained rhythmical contraction of MM when put under sudden
stretch. D/t hypertonia from UMN lesion
 Sharply dorsiflex the foot w the knee bent and thigh externally rotated.
When clonus is present, recurrent ankle plantar flexion movement occurs.

- Power: page 369

o Hip
 Flexion
 Extension
 Abduction
 Adduction
o Knee
 Flexion
 Extension
o Ankle
 Plantar flexion
 Dorsiflexion
o Tarsal joint
 Eversion
 Inversion
o Quick test for power (if running out of time):
 Ask pt to:
 Stand on their toes (s1)
  Stand up on their heels (L4, L5)
 Squat and stand again (L3, L4)
 This tests ankle, knee and hip power. Inability to perform any of these 
test further
- Reflexes:
o Knee Jerk (L3 L4)
o Ankle jerk (S1 S2)
o Plantar reflex (L4, L5, S1)
 Normal: flexion of big toe at the MTP joint in pts. >1 year.
 Abnormal: extension of big toe (Babinski). This indicates UMN lesion
o Reinforcement maneuvers:
 Interlock fingers and pull apart hard at the moment before the hammer hits
tendon
 Teeth clenching
 Grasping an object/ making fists

o Superficial/ cutaneous reflexes: page 375

 Stimulus = more superficial than the tendon reflexes
 Abdominal reflexes:
 Lightly stroke the abdominal wall diagonally towards the umbilicus
in each of the four quadrants.
 Reflex contractions are absent in UMN lesions & pts. w surgery
interrupting the nerves.
 Reflex contractions disappear in coma, deep sleep and anaesthesia.
 Cremasteric Reflexes
 Saddle sensation and anal reflex.

- Examination of peripheral NN of the lower limb:

o Lateral cutaneous N of the thigh
 Lesion here usually happens because N is entrapped between the inguinal
ligament and ASIS
 Causes sensory loss with NO motor loss
o Femoral N:
 Test findings:
 weakness of knee extension
 slight hip flexion weakness
 adductor strength is preserved
 absent knee jerk
 sensory loss involves inner aspect of thigh and leg
o Sciatic N:
 This N supplies all MM below the knee and hamstrings
 Test findings:
 Loss of power below the knee  footdrop
 Weak knee flexion
 Knee jerk intact
 Ankle jerk and plantar response are absent
 Sensation to posterior thigh, lateral and posterior calf and foot is
lost w a proximal N lesion
o Common Peroneal N:
 Major branch of sciatic N. it supplies anterior & lateral compartment MM of
leg.
 Test findings:
 Foot drop
 Weakness of dorsiflexion and eversion
 All reflexes intact
 +- minimal sensory loss over the lateral aspect of the dorsum of the
foot

SENSORY EXAMINATION:

Upper limb:
- Spinothalamic pathway (pain and temperature)
o Fibres enter the SC and cross a few segments higher to the opposite spinothalamic
tract. This ascends to brainstem.
o Pain:
 Pinprick test
 First show sensation to pt on a normal area – ask pt if it feels sharp or dull
 Begin proximally and test each dermatome
o Temperature:
 Test tubes w hot and cold water
 Tested only in special circumstances.
- Dorsal columns (Proprioception and vibration)
o Fibres enter and ascend ipsilaterally in the posterior columns to the nucleus gracilis
and cuneatus in the medulla where they decussate.
o Vibration:
 128 Hz tuning fork
 Closed eyes
 Place on DIP, pt must say when vibration stops (Dr. deadens tuning fork)
 If this sense is reduced or abent – test over the ulnar head at the wrist, then
the elbows and then shoulders.
 Although tuning fork is always placed over a bony prominence, vibration
sense is equally good in soft tissues
 o Proprioception:
 Use DIP of little finger
 If there is an abnormality, test the wrist and elbows
 As a rule, sense of position is lost before sense of movement, and the little
finger is affected before the thumb.
- Sensory dermatomes of the upper limb:
o See page 363 figure 11.56
 C5 supplies the shoulder tip and outer part of outer arm
 C6 supplies the lateral aspect of the forearm and thumb
 C7 supplies the middle finger
 C8 supplies the little finger
 T1 supplies the medial aspect of the upper arm and elbow

Lower Limbs:
- Procedure:
o Test pain first
o Test vibration over ankles and if necessary on knees and ASIS
o Test proprioception using big toes
o Test light touch
- Rough guide to dermatomes:
o L2 supplies anterior thigh
o L3 supplies the area around the front of the knee
o L4 supplies medial aspect of leg
o L5 supplies lateral aspect of leg & medial side of dorsum of foot
o S1 supplies heel and sole
o S2 supplies posterior aspect of thigh
o S3, 4, 5 supply concentric rings around the anus
- If there is a lesion:
o There is often hyperaesthesia that occurs above the sensory level so the upper level
of this must be determined.

CEREBELLAR EXAMINATION:

Features of Cerebellar disease: VANISH DDT

Vertigo
Ataxia
- Wide based gait
Nystagmus
Intention Tremor
Slurred Speech
Hypotonia
Dysdiadokinesia
Dysmetria
Titubation

- Process :
o Upper limb:
 Examine rapid alternating movements: (repeat for 10 seconds)
 Pat thighs w palms
 Pat thighs w palms and back of hands
 Oppose each finger to the thumb
 Hand to palm
 Examine point to point movements:
 Finger Nose Finger test
 Rapidly extend arms to shoulder height
o Hypotonia in cerebellar disease causes delay in stopping the
arms
 These tests show signs of intention tremor, past pointing and
overshooting
o Lower Limb:
 Heel shin test
 run up and down shin at a moderate pace.
 Closing eyes during this test makes little difference in cerebellar
diease but if there is posterior column loss then the movements are
made worse w closed eyes
 Toe finger test
 Foot tapping test
o Examine gait
 Examine heel-to-toe test to exclude a midline cerebellar lesion

Examine Gait:

- Expose legs
- Walk and turn around
- Walk on their toes (S1 lesion will make this difficult)
- Walk on their heels (L4/5 lesion will make this difficult)
- Ask pt to squat and then stand up OR to sit in a low chair and then stand
o This tests proximal myopathy
- Test station:
o Romberg’s test
o Stand up w feet together and eyes open
o When pt is stable, make them close their eyes
 o Compare steadiness when eyes are open and closed
o Positive test if pt looks like they are going to fall (normally people can maintain their
position for 60 seconds)
 Test is POSITIVE when unsteadiness increased w eye closure
 Usually occurs w proprioceptive sensation
 Marked unsteadiness w eyes open is seen w cerebellar or vestibular
dysfunction

CEREBRAL HEMISPHERES:

- Parietal, temporal and frontal lobe functions are tested is pt is disoriented, has dysphasia or
if dementia is suspected. If a pt has receptive aphasia these tests cannot be performed.
- Parietal lobe:
o This lobe is concerned w the reception and analysis of sensory information
o Dominant lobe signs:
 Lesion to the dominant lobe in the angular gyrus causes Gerstmann’s
syndrome:
 Acalculia
o Ask pt to perform simple arithmetic (take 7 away from 100,
and again etc)
 Agraphia
o Ask pt to write
 L-R disorientation
o Ask pt to show you their L hand and then their R hand. If
this is done correctly, ask the pt to touch their R ear with
their L hand and vice versa
 Finger agnosia
o Ask the patient to name their fingers.
o Non-dominant and non-localising parietal lobe signs (cortical sensation)
 Graphesthesia (ability to recognize numbers or letters drawn on skin using a
pencil or pointed object)
 Tactile extinction
 Pt closes eyes
 Pt is touched on 1 and and then the other; and then both.
 Ask on which side the touch is felt. Normal response is “both”
 Astereognosis
 Inability w eyes close to recognize an object placed in hand
 Two point discrimination
 Dressing and constructional apraxia:
 Dressing ataxia tested by taking the pts. pyjama top or cardigan and
turning it inside out and asking them to put it back on.
  Constructional ataxia is asking the pt to copy a picture you have
drawn
 Spatial neglect
 Ask pt to fill in the numbers on an empty clock face
o Pts. w R parietal lesion may fill in numbers only on the L side
– the other side of the clock face is ignored.
 Point localization
- Temporal lobe:
o Concerned w short term and long term memory
o Test short term
 Ask pt to remember a name, address and names of three flowers. Ask them
to repeat them immediately.
 Ask them again 5 minutes later.
o Test long term:
 Ask what year certain historic events ended.
o Alert pts. might make up stories to fill in gaps in their memory = confabulation. It is
typical of Korsakoff’s psychosis
 Test for confabulation by asking the pt if they have ever met you before.
 K. psychosis is characterized by retrograde amnesia (memory loss for events
before onset of illness) and an inability to memorize new information

Correlation of Physical signs and neurological disease page 383