Neurology Exam Flashcards
+ Rombergs test
Unsteady both - = cerebellar disease
+Rombergs - steady with eyes open and unsteady with eyes closed
- posterior column lesion
- peripheral neuropathy (in particular with loss of
- vestibular dysfunction
Additional findings in gait exam
Upper limbs:
Arm swing (absent in Parkinson’s disease).
Weakness and posture e.g. in spasticity shoulder adduction, elbow, wrist and finger flexion.
Ability to stand on toes (tests for S1) & heels (tests for L4,5).
Ability to turn around (often requires several small steps in patients with small step gait, may highlight gait difficulties).
Heel to toe test, often not possible.
Causes of an asymmetric gait?
Unilateral spasticity eg. motor stroke (circumduction, ext of hip/kneee/ankle, leg swings out in lateral arc), UL arm adducted + internally rotated, elbow and wrist fleed
Unilateral cerebellar lesions (veering to a side)
Unilateral foot drop eg. common peroneal, L5, unilateral stroke
Causes of foot drop
Common peroneal nerve palsy Sciatic Lumbosacral plexus lesion L4/5 root lesion Peripheral motor neuropathy Distal myopathy MND Precentral gyrus lesion
Causes of bilateral symmetric spastic gait?
Differentials for spasticity (bilateral UMN lesion) - Bilateral stroke - Hereditary spastic paraplegia (HSP) - Spinal cord lesion - Cerebral palsy MS
Bilateral foot drop?
Peripheral sensorimotor neuropathy (CIDP/Charcot)
Marie Tooth (CMT)
Bilateral strokes
MND
Differentials for a parkinsonian like gait?
Parkinson’s- shuffling, stopped posture, loss of swing and tremor UL
Parkinson’s like syndromes - PSP, drug induced
DDx wide based gait?
Cerebellar ataxia
Sensory ataxia
Vestibular ataxia
Frontal ataxic gait (unlikely in ex)
Findings in an UMN lesion?
Absence of muscle atrophy
Absence of fasciculations
Increased tone/spasticity or clasp knife tone
+/- clonus
Weakness: weaker anti-gravity muscles (eg. hip flex < hip ext, hip ext < knee flex, doriflex < plantarflex)
Hyperreflexia
Plantar reflex up going
Findings in a LMN lesion?
Muscle atrophy
Fasciculations
Decreased tone/flaccidity
Pattern of weakness - hip ext < hip flex, knee flex < ext, plantarflex < dorsiflex)
Hyporeflexia or areflexia
Plantar downgoing
Proximal myopathy
Muscle atrophy in affected muscles No fasciculations Normal tone Pattern of weakness - proximal muscles Normal reflexes Plantar reflex down-going
Sensorimotor peripheral neuropathy
Sensorimotor peripheral neuropathy there may be a variable mix of glove/stocking distribution sensory loss and motor weakness in a symmetric distribution
Absent ankle jerks
Findings in cerebellar lesions?
Cerebellar ataxic gait
Abnormal heel to shin test
Abnormal foot tapping
Sensory findings
Note that pinprick/temperature fibres are carried in the spinothalamic column.
Joint position/vibration fibres are carried in the posterior column.
Light touch is a good screen but is non-discriminatory.
Reflexes in LL exam
Knee Jerk (L3,4) Ankle jerk (S1,2) Adductor reflex (L2,3)
Absent reflexes (despite reinforcement) is seen in peripheral neuropathies and chronic demyelinating polyneuropathy (CIDP).
Hyporeflexia is in keeping with lower motor nerve lesions.
Hyperreflexia is in keeping with upper motor nerve lesions.
Patients with myopathies may have reduced reflexes due to loss of muscle bulk.
Power
5 - Normal power 4+ - Submaximal movement against resistance 4 - Moderate movement against resistance 4- Slight movement against resistance 3- Moves against gravity but not resistance 2 - Moves with gravity eliminated 1 - Flicker only 0 - No movement
LL Movement
Hip Flexion - L1/2 Hip Extension - L5/S1 Hip Adduction - L2/3 Hip Abduction - L4/5 Knee flexion - S1 Knee extension - L3/4 Ankle dorsiflexion - L4/5 Ankle plantarflexion - S1/S2 Ankle eversion - L5/S1 Ankle inversion - L5 Big toe extension - L5
UL Movement
Shoulder abduction - C5 Elbow flexion - C5/6 Elbow extension - C7 Finger extension - C7 Finger flexion - C8 Finger abduction - T1
Assessment of Tone
Normal tone. Hypotonia, flaccidity. Hypertonia: Clasp knife spasticity (pyramidal). Lead pipe rigidity (extra-pyramidal). Cogwheel rigidity (extra-pyramidal) Froment's maneuver refers to accentuation of cogwheel rigidity with contralateral arm movements seen in Parkinson's disease
UL Reflexes
Biceps C5
Triceps C7
Brachioradialis C6
Finger jerk C8
Absent reflexes (despite reinforcement) is seen in peripheral neuropathies and chronic demyelinating polyneuropathy (CIDP).
Hyporeflexia in keeping with lower motor nerve lesions.
Hyperreflexia is in keeping with upper motor nerve lesions.
Patients with myopathies may have reduced reflexes due to loss of muscle bulk.
Sensation
See photos - learn dermatomes + nerve distributions
Observation in sensory lesions
Note the presence of atrophy:
Lower motor neuron lesions.
Peripheral nerve, plexus or root lesions.
Myopathies.
Fasciculations:
Lower motor neuron lesions.
Shiny, hairless skin, ulcers - suggest peripheral neuropathy.
Pes cavus (high arch and claw toes) may be seen in:
Charcot Marie Tooth.
Friedreich’s ataxia.
Fundoscopy Findings
Diabetic retinopathy
Non-proliferative:
Cotton-wool spots or soft exudates: are nerve fibre layer infarcts.
Hard exudates are caused by lipid accumulation in or under the retina secondary to vascular leakage.
Intra-retinal haemorrhages and microaneurysms may also be seen.
Proliferative:
Neovascularisation may progress to fibrosis and retinal detachment
Hypertensive retinopathy:
Mild: narrowing of retinal arterioles also referred to as copper/silver wiring. Arteriovenous nicking or “nipping”.
Moderate – Haemorrhages, either flame or dot-shaped, cotton-wool spots, hard exudates, and microaneurysms.
Severe – Some or all of the above, plus papilloedema.
Findings in diabetic neuropathy
Sensory ataxia
Romberg’s test may be +ve
Progressive loss of distal sensation in a globe and stocking distribution and in severe cases - motor weakness may be present
Ankle jerks may be lost
Expected findings in CIDP
Classic form: Symmetric, sensori-motor neuropathy with predominant motor neuropathy that results in both proximal and distal muscle weakness
Less common variants - asymmetric and/or sensory-predominant forms
Reflexes are generally absent or reduced
Typical findings include an ataxia gait with a +ve Romberg, loss of sensation in a glove + stocking distribution, muscle atrophy + weakness + globally absent/reduce reflexes
LL findings in MS
UMN signs, hyper-reflexia, spasticity, up going plantar
Occasionally reflexes are lost due to interruption to afferent motor reflex arce fibres
Cerebellar and sensory finding (which may be patchy) may also be present
Findings in third nerve palsy (. This is the “down and out” eye syndrome. It is characterised by ptosis, a down-and-out pupil, mydriasis, absent light reflex with intact consensual constriction of the opposite eye, and failure of accommodation)
Ptosis, inferolateral displacement of the ipsilateral eye.
Reduced adduction, elevation and depression of the affected eye.
A dilated non-reactive pupil (to direct or contralateral light reflex & accommodation). In diabetic mononeuritis pupillary sparing is often seen.
Causes of third nerve palsy and 4th nerve palsy
Tumours can compress the nerve anywhere along its path.
Cavernous sinus lesions.
Trauma.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the midbrain.
Mononeuritis multiplex e.g. diabetes (often with pupillary sparing).
Intracranial aneurysms, in particular posterior communicating artery aneurysms.
In occulomotor palsy - no direct pupil response but there is an indirect pupil response
Findings in trochlear palsy + causes
Weakness of downward eye movement with consequent vertical diplopia that is worse in the adducted eye position, but improved diplopia with head tilted to contralateral side (look to the nose then down).
Weakness of intorsion, in particular with eye abducted.
6th nerve palsy - findings + causes
Medial deviation of ipsilateral eye.
Inability to look laterally (abduct).
Common causes of palsy:
Tumours can compress the sixth nerve anywhere along its path. Acoustic neuromas can affect the 6th nerve.
Elevated intracranial pressure, a false localising sign.
Trauma.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons.
Mononeuritis multiplex e.g. diabetes.
5th nerve palsy findings + causes
Sensory abnormality with peripheral nerve OR descending nucleus distribution (pain & temperature).
Motor abnormality: asymmetry of jaw on opening or weakness with mastication.
Loss of corneal reflex.
Common causes of palsy:
Tumours can compress the nerve anywhere along its path.
Trauma.
Cavernous sinus lesions can affect the two superior divisions of the trigeminal nerve.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons or along its descending nucleus.
Findings in a 7th nerve palsy
Lower motor neuron lesions:
Weakness of upper and lower facial muscles.
Upper motor neuron lesions:
Weakness of lower facial muscles with sparing of upper facial muscles.
Loss of corneal reflex.
Decreased tearing
Hyperacusis.
Loss of taste sensation on the anterior 2/3rds of the tongue.
7th nerve- UMN and LMN causes
Common causes of lower motor neuron palsy:
Bell’s palsy, idiopathic facial nerve palsy or facial nerve palsy of suspected viral aetiology is the most common cause of peripheral, lower motor neuron facial nerve palsy.
Sarcoidosis.
Herpes zoster infection.
Guillain-Barré syndrome.
Otitis media.
Lesions affecting nucleus of facial nerve in ipsilateral pons, e.g. stroke, acoustic neuroma, demyelinating lesions.
Common causes of upper motor neuron palsy:
Lesion affecting the contralateral upper motor neuron fibres (above nucleus to cerebral motor cortex).
8th (acoustic) nerve palsy - findings + causes
Hearing loss. Vestibular ataxia. Common causes of palsy: Acoustic neuroma. Trauma or inflammatory conditions along it path.
9th (glossopharyngeal) nerve palsy - findings + causes
Loss of taste in the posterior 1/3rd of the tongue.
Loss of pain and touch sensations in soft palate, and pharyngeal walls.
CN IX and CN X travel together, and their clinical testing is not entirely separable.
Vagus nerve - findings in palsy
Uvula deviation towards normal palate, may result from ipsilateral lower motor lesion of the vagus nerve OR contralateral upper motor neuron vagus nerve.
Through the recurrent laryngeal nerve to the vocal cords, hoarseness may develop.
Dysphagia, dysphonia and decreased gag reflex.
Due to its parasympathetic input, cardiac and gastrointestinal abnormalities may be seen with vagal lesions
Common causes of palsy:
Causes of 10th (vagus) nerve palsy
Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla.
Upper motor lesions of the 10th nerve tract, often as a component of a pseudobulbar palsy.
Motor neuron disease.
Accessory nerve- palsy + causes
Paralysis of sternocleidomastoid and trapezius.
Common causes of palsy:
Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla
