Neurological Examination

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General Observations

1. Mental State
2. Language
3. Speech

Cranial Nerves

CN1 – Olfactory Any problems with smell? Not routinely tested

CN2 – Optic

1. Visual Acuity

2. Visual Fields

3. Optic Fundi

Glasses on, Snellen chart at 6m (or handheld chart at 30cm), 6/60 = sees at 6m what normal person can see at 60m), each eye tested separately
Dr and pt 1m apart, Patient covers eye, Dr covers eye, test with wagging moving finger (or pat hin) – 6 quandrants each eye, come from behind patient
Ophthalmoscope
Mildly impaired (cant read newspaper print), impaired

↑ ICP – loss of retinal vessel pulsations, blurring optic disc margin, retinal hemorrhages

CN 3-4-6 Oc-Troc-Abduc

1. Observe
2. Light reflex
3. Eye movements
4. Convergence/Accom
Eye alignment
Ptosis
Pupil size, shape, symmetry
Direct + consensual response (swinging light)
Gearstick ‘H’, hold eyelids up while examining downward gaze

Bring torch closer and closer to patient

Either CN3 (levator palpebrae) or Sym (less severe + smaller muller’s mus) – both maintain eye elev
Anisocoria (diff sized pupils – either one eye sym lesion or other eye parasym lesion)
Abnormal dilation both eyes when shined abnorm eye → relative afferent papillary defect (APD) aka Marcus-gunn pupil
Diploplia, one eye lagging, incomplete range eye mvments, nystagmus
If diplopia – test each eye separately (to exlc mono-ocular diplopia), is it horizontal or vertical, look to see which eye lags
Conjugate lesion = limitation mvment both eyes one direction
Pupil constriction

CN5 – Trigeminal

1. Light touch
2. Pinprick
3. Corneal reflex

4. Muscles of mastication

5. Jaw jerk
V1-3, eyes shut, test each side separately, ask if any differences betw sides
As above
Ensure pt it wont hurt, hold eyelid down, pt looks up + to opp side, gently stroke cornea w wool (not sclera – ie clear surface above iris) – test both eyes
Temporalis wasting, palpate masseters w jaw clenched
Open jaw
Open jaw against resistance
Jaw open and relaxed, index finger under lip, gentle downward tap, variable

Absent reflex (blink) = earliest sign of trigeminal lesion
Direct and consensual reflex – if only the opposite eye, blinks, then facial n impairmed

Jaw deviation to side of weakness

↑ in UMN lesions

CN7 – Facial

1. Observe
2. Expression
3. Power
Asymmetry, drooping, sagging, smoothing of normal face creases, fasciculations
Raise eyebrows, frown, smile showing teeth, puff out cheeks (asym or difficult.)
Resistance to separation – forehead wrinkles, eyes closed, lips shut Part of CN7 nucleus innervating the forehead receives input from both cerebral hemispheres (UMN lesion – upper spared)
Whole side of face paralysed → periph lesion
Side of forehead paralysed but forehead spared → central lesion

CN8 – Vestibulocochlear

1. Hearing
2. Otoscope
3. Tuning fork (256 Hz)
Eyes closed, whisper numbers in ear while masking other ear, progr quieter
Ear canal and eardrum (only if abnormal hearing acuity)
a. Rinne’s Test – tuning fork mastoid bone v air
b. Weber’s Test – tuning fork midline forhead
Exclude otitis media, perforation tympanic membr, occlusion of external auditory meatus
Normal and sensorineural loss air>bone / conductive loss bone>air
Normal L=R / sensorineural deafness (normal ear better) / conductive deafness (abnormal ear better)

CN9/10 – Glossopha/Vagus

1. Speech

2. Swallow
3. Palate
4. Gag reflex
a. “eeee” (vocal cords closed)
b. “british constitution west registry street”
c. Cough
Ask pt if they have trouble swallowing and observe pt swallowing
Observe at rest + phonation (aahh) – use spatula to depress tongue
Keep tongue depressed + light, touch oropharynx w other spatula
Dysarthria, slurred speech (incoordination + weakness of muscles innervated by nucleus ambiguous via CN 9/10)

Dysphagia
Midline palate deviates to normal side
Can be omitted – 20% have absent or minimal reflex
Midline palate lifting, uvula centered

CN11 – Assessory

1. Observation
2. SCM
3. Trapezius
SCM + trapezius
Pt tries to turn head back to midline against resistance
Shoulder shrug
Wasting, fasciculations, abnormal sustained contraction (dystonia or torticullis)
Innervation also C2-4

CN12 – Hypoglossal

1. Tongue Protrusion
2. Observe tongue
3. Tongue movement
4. Rapid tongue movements

Side to side movement
La la la
Deviation – bilat weakness (no protrusion), LMN unilat weakness (tongue protrudes to weak side) – tongue dual innerv
Wasting, fasciculations

NEUROLOGICAL MOTOR EXAM – UPPER LIMBS

Patient exposes shoulder girdle and upper arms
Always ask if patient has any pain before touching them

1. General Inspection Wasting/Muscle bulk
Fasciculations (irreg contractions of small areas of muscle)
Scars
Posture
Abnormal movements Denervated muscle, Primary muscle disease, Disuse atrophy
Causes 1. MND, 2. Motor root compression, 3. Peripheral neuropathy, 4. Primary myopathy, 5. Thyrotoxicosis

Tremor of wrist or arm
2. Upper limb drift Arms shoulder level, palms up, eyes closed, 15secs Affected arm pronates and falls (most sensitive test for upper extremity weakness)
Causes –
1. UMN (pyramidal) weakness (drift usu downwards + starts distally w fingers spreading proximally + slow pronation wrist/elbow
2. Cerebellar disease (drift usu upwards + slow pronation wrist and elbow)
3. Loss of proprioception (searching movement, usu only fingers)
3. Tone (resist passive mvment) - elbow (flex, ext)
- wrist (flex, ext, supination)
Spasticity – tone maximal at start then suddenly decr as mus lengthened (clasp knife effect)
Clonus – sudden stretching spastic mus → reflex contraction (stretch maintained = repetitive beating)
Rigidity – uniform resistance throughout stretching of mus – assoc w cogwheeling (Parkinson’s)
Assess w patient moving other arm up and down
4. Power - Finger flex (C7-8) – Grip dr’s 2 fingers in fist
- Finger ext (C7-8)
- Finger abduction (ulnar n T1)
- Thumb abduction (median n)
- Wrist ext (radial n C7-8)
- Wrist flex (C6-7)
- Elbow flex (biceps musculocutaneous n C5-6)
- Elbow ext (triceps radial n C7-8)
- Shoulder abduction (C5-6)
- Shoulder adduction (C6-8) Grading
- 0 = no contraction
- 1 = flicker/trace
- 2= active movment
- 3 = active mvment against gravity but no resistance
- 4 = active mvment against resistance but reduced power
- 5 = normal
Compare side to side, ask pt to hold while you try to overcome it (“Stop me”), stablise prox joint, always put pt in pos of advantage
If pt v weak, get them to perform active movement first before applying resistance
Asymmetrical Muscle weakness – usu peripheral n, brachial plexus or root compression OR UMN lesion
5. Reflexes Upper
- Brachioradialis (supinator reflex C5-6) → elbow flexion
- Biceps (C5/6)
- Triceps (C7)
Sudden stretching of muscle → evokes brisk contraction of that muscle/mus group
Patient position – elbows flexed + hands lying pronated on lap and not overlapping each other
Reinforcement – jaw clench (arms) or nterlocking and pulling of fingers (legs)
Grading - 0 = no reflex, + = present but reduced, ++ = normal, +++ = brisk normal, ++++ = v brisk and often assoc w clonus
↑ jerk = UMN lesion
↓ or absent jerk = any breach of reflex arc (myopathy (mus), neuropathy (motor n), ant spinal cord (spondylosis), ant horn cell (poliomyelitis) or sensory arc (sensory root or sensory n)
6. Co-ordination Finger-nose-finger
Cerebellar disease
a. Intention tremor – tremor ↑ as target approached
b. Past pointing – overshooting of target to side of cerebellar abnormality
7. Rapid alternating movements
Alternating patty cakes hand on hand
Dysdiadochokinesia = abnormality of rapid alternating movements
Cerebellar disease = slow and clumsy movements
Also affected in extrapyramidal disorders (eg parkinsons) and pyramidal disorders (eg internal capsule infarction)

NEUROLOGICAL MOTOR EXAM – LOWER LIMBS

Patient exposes shoulder girdle and upper arms
Always ask if patient has any pain before touching them

1. Posture + Gait a. Stand (eyes open, feet together)
b. Romberg’s test (eyes closed, feet together)
c. Walking
d. Walk heel to toe

d. Walk on toes (L5-S1)
e. Walk on heels (L4-5) Marked unsteadiness with eyes open → cerebellar or vestibular dysfunction
Positive if pt markedly more unsteady with eyes closed → loss of proprioceptive sensation
Posture, stride length, broadness of base, arm swing, steadiness, smoothness
Impaired with alcohol intox, weakness, poor position sense, vertigo (exclude these before attributing unbalance to cerebellar lesion)
Excludes a midline cerebellar lesion
Screening – plantarflexion weakness
Screening – dorsiflexor strength
2. General Inspection a. Wasting
b. Fasciculations
c. Palpate muscle bulk quads, calves, anterior tibial muscles

Denervated muscle, Primary muscle disease, Disuse atrophy
Causes 1. MND, 2. Motor root compression, 3. Peripheral neuropathy, 4. Primary myopathy, 5. Thyrotoxicosis

3. Tone a. Hand under knee and abruptly pull upwards causing flexion
b. Support thigh, flex and extend knee at incr velocity
c. Clonus of ankle (dorsiflex ankle + knee bent + ext rotate thigh) Spasticity – tone maximal at start then suddenly decr as mus lengthened (clasp knife effect)
Clonus – sudden stretching spastic mus → reflex contraction (stretch maintained = repetitive beating)
Sustained rhythmical contr of muscles when under sudden stretch – due to hypertonia from UMN lesion (↑ reflex excitability)
Rigidity – uniform resistance throughout stretching of mus – assoc w cogwheeling (Parkinson’s)
Assess w patient moving other arm up and down
4. Power a. Hip flex (Iliopsoas femoral n L2-3) – patient lifts leg off ground
b. Hip ext (gluteus maximus gluteal n L4-5) – pull from ball of foot
c. Knee flex (hamstrings sciatic n L5-S1)
d. Knee ext (quadriceps femoral n L3-4) – kicking out
c. Dorsiflex (tib ant peroneal n L4-5)
f. Plantarflex (tib post tibial n S1-2)
Quick Test of Lower limbs “Lift your leg up and don’t let me push down”
“Push your heel down and don’t let me pull it up”
“Bend your knee and don’t let me straighten it”
“Straighten your knee and don’t let me bend it”
“Don’t let me push your foot down”
“Don’t let me push your foot up”
1. stand up tones S1, 2. Stand up on heels L4-5, 3. Squat and stand again

5. Reflexes a. Knee (L3-4)
b. Ankle (S1) – ankle resting on shin + in dorsiflexion
c. Plantar reflex (Babinski - L5-S2)

Run key up lateral aspect sole of foot heel-MTP joint center, Ankle should be in same position as for ankle jerk
Babinski sign = big toe dorsiflexion + other toes fan out → UMN (pyramidal) lesion
6. Co-ordination a. Heel-knee-shin test (lift heel off shin on return to knee)
b. Foot tapping test Cerebellar disease → heel wobbles all over the place, side to side oscillations and overshooting
Dysdiadochokinesia = abnormality of rapid alternating movements
Cerebellar disease = slow and clumsy movements
Also affected in extrapyramidal disorders (eg parkinsons) and pyramidal disorders (eg internal capsule infarction)

NEUROLOGICAL EXAM - SENSORY

1. Light touch Touch + pressure – ipsilateral dorsal column + contralat spinothalamic tr Finger touch (do not drag), dermatomal distribution, compare sides as you go
2. Pin-prick Pain + temp – spinothalamic tract Safety pin, alternate sharp and blunt
3. Joint position Proprioception – dorsal column (distal IP joint of pts little finger) Great phalanx or distal IP joint little finger, hold toe/finger from sides (not pulp), up and down
4. Vibration 128Hz tuning fork (bony prominences or soft pulp – distal then prox 1st) Demonstrate upper sternum, perform pulp middle finger or big toe, eyes closed, pt reports when vibration stops
If abnormal, move proximal

ABNORMAL RESULTS

UMN – from motor cortex → pyramidal (corticospinal tract)
LMN – motor neuron innervating skeletal muscles

UMN eg stroke, spinal cord lesions, brain tumors LMN Extra-pyramidal (basal ganglia)
Wasting Normal + Normal
Fasciculation Normal +/- Normal
Tone ↑ (spasticity) Normal or ↓ ↑ (rigidity)
Power ↓ ↓ Normal
Reflexes ↑ ↓ or absent Normal
Plantar Response (normal flexion) Up – abnormal Down - Normal Down - Normal
Rapid Alternating Movements ↓ Normal ↓

UMN Lesions LMN Lesions
Weakness Atrophy
Spasticity Fasciculations
Hyper-reflexia Hypotonia
Babinski reflex Weakness
Hyporeflexia

Myotomes

Hip flexion L2-3 Hip extension L4-5 Inversion L4
Knee extension L3-4 Knee flexion L5-S1 Eversion L5-S1
Dorsiflexion L4-5 Plantarflexion S1-2

Gait Abnormalities
Hemiplegia Foot if plantar flexed and the leg swung in lateral arc
Parkinson’s Hesitation starting, Shuffling, freezing, propulsion, retropulsion
Cerebellar Drunken gait, wide base, staggering toward affected side if there is a unilateral lesion
Posterior column Clumsy slapping down of the feet on a broad base
Foot drop High stepping gait

Sensation Pathways

Pain and Temperature Pathways
Fibers enter the spinal cord and cross a few segments higher to the opposite spinothalamic tract → ascends to brainstem

Vibration and Proprioception (Posterior Columns)
Fibers enter and ascend ipsilaterally in the posterior columns (dorsal columns) to the nucleus gracilis and nucleus cuneatus in the medulla → decussate

Light Touch
Some fibers travel in the posterior columns (ipsilateral) and the rest cross the medulla line to travel in the anterior spinothalamic tract (contralateral).
Light touch is therefore of the least value.

Sensory Abnormality Patterns
1. Dermatome distribution (spinal cord or nerve root lesion)
2. Single peripheral nerve territory
3. Peripheral neuropathy pattern (eg glove and stocking)
4. Hemisensory loss (spinal cord, upper brainstem, thalamic lesions)

NEUROLOGICAL APPROACH

1. Is the legion focal? A focal lesion will generally present unilaterally.

2. Where is the lesion? Analyse cognitive, cranial nerve and motor deficits. Then use sensory examination to confirm site of lesion.

3. Patterns of weakness
• Lesions of the cortex, internal capsule, brainstem, spinal cord, peripheral nerves, NMJ or muscle
• UMN or LMN pattern

UMN lesions
• Damage to motor pathways anywhere from motor nerve cells of precentral gyrus frontal cortex, through the internal capsule, brainstem and cord to the anterior horn cells in the cord
• Typical characteristics are pyramidal in distbn (weakness involving physiological extensors of the arm and flexors of the legs)
• ↑ tone (spasticity) develops in stronger muscles (arm flexors and leg extensors)
• Hyper-reflexia, Positive babinski +/- clonus (reflex arc remains intact in an UMN lesion → ↑ tone)
• UMN weakness affects mus groups not individual muscles

LMN lesions
• Damage from ant horn cells, nerve roots, plexi or peripheral nerves
• Distbn of weakness corresponds to those muscles supplied by the involved cord segment, nerve root, part of plexus or peripheral nerve
• Relevant muscles show wasting, fasciculations, feel soft and flopping (hypotonia/flaccid)
• Reflexes are ↓ or absent, Plantars remain flexor
• Chief differential is weakness from primary mus dis (symmetrical loss, reflexes lost later in neuropathies, no sensory loss)

Patterns
• Proximal, Distal or Pyramidal
• Cortical lesions → unexpected pattern of weakness involving all movements of hand or foot, normal or ↓ tone (but ↑ reflexes more proximally in arm/leg suggest UMN rather than LMN lesion)
• Internal capsule and Corticospinal brainstem lesions → contralateral hemiplegia w a pyramidal distribution of weakness
o If the hemiplegia occurs w epilepsy, ↓ cognition or homonymous hemianopia → lesion is in a cerebral hemisphere
o A cranial nerve palsy (3-12) contralateral to a hemiplegia implicates the brainstem on the side of the cranial nerve palsy
• Cord lesions → paraplegia (both legs) or quadriparesis/tetraplegia → motor and reflex level (muscles unaffected above lesion, show LMN signs at the level of lesion, show UMN signs below the lesion)
• Peripheral neuropathies → most cause a distal weakness (foot drop, weak hand))
• Mononeuropathy → trauma or entrapment (eg carpal tunnel syndrome)

Sensory Deficits
• Distal sensory loss → neuropathy (may all involve all sensory modalities or be more selective )
• Individual nerve lesions → anatomical territories which are usu more sharply defined than those of root lesions (dermatomes)
• Sensory level → cord lesion (↓ or absent sens below the lesion + normal above)
• Lateral cord lesions → brown-sequard syndr (dorsal column loss on the side of the lesion + spinothalamic loss in other leg)
• Lesions above the brainstem → contralateral pattern of generalised sensory loss
• Cortical lesions → sensory loss is confined to more subtle and discriminating sensory function (eg 2 point discrimination)

Cerebral artery territories
Blood supply to brain – 2x internal carotids, 2x vertebral arteries → basilar art
These 3 vessels → anastomotic ring at base of brain (circle of willis) → 3 cerebral arteries (ACA, MCA, PCA)
ACA → frontal and medial part cerebrum (occlusion → weak, numb contralateral leg, face is spared
MCA → supplies lateral part of hemisphere (occlusion → contralateral hemiplegia, hemisensory loss (face/arms), contralateral homonymous hemianopia due to optic radiation involvement, cogv change incl dysphagia (dom0, visuo-spatial disturbance (non-dom)
PCA → occipital lobe occlusion → contralateral homonymous hemianopia
Vertebrobasilar circulation → cerebellum, brainstem, occipital lobes (occlusion → hemianopia, cortical blindness, diplopia, vertigo, nystagmus, hemi or quadriplegia, unilateral or bilateral sensory sxs, cerebellar sxs, dysarthria, dysphagia, coma)

PE-AnatSpine_Figure10.jpg

DERMATOMES

C4 Posterior aspect shoulders
C5 Shoulder tip and lateral aspect upper arm
C6 Lateral aspect forearm and thumb
C7 Middle finger
C8 Little finger
T1 Medial aspect upper arm and elbow

L2 Superior and Upper anterior thigh
L3 Area around front of knee
L4 Medial aspect leg
L5 Lateral aspect leg and medial dorsum of foot
S1 Heel and sole of foot
S2 Posterior thigh
S3-5 Concentric rings around anus

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