Neurological examination

Organisation

• Mental status testing
• Higher cerebral functions
• Cranial nerves
• Limbs
  • Tone, power, reflexes, coordination and sensation

Mental status testing

• Abbreviated or complete MSE
• Orientation to person, place and time
• Attention and memory assessments are key
  • Attention tested by digit repetition
  • Short-term memory tested by three object recall at 5 minutes
    • If unable to immediately recall, suggests attention problem vs. memory

Higher cerebral functions

• Language – Dominant cortex
  • Screening
    • Free speech (describe room)
    • Test comprehension (simple tasks then ‘do you put shoes on before socks?’
    • Test repetition ‘no ifs ands or buts’
    • Name two objects
    • Say “British constitution’
  • If dysphasic in speech, will also be dysphasic in writing and/or drawing

Higher cerebral functions

• Receptive dysphasia (Wernicke) – Fluent
  • Normal grammatical structure, norml rhythm and clearly articulated but peculiar words
  • Best tested by repeating short phrases i.e. ‘no ifs ands or buts’
  • Paraphasic errors
    • Literal i.e. spool instead of spoon
    • Verbal i.e. fork instead of spoon
• Production dysphasia (Broca’s) – Non-fluent
  • Speed of language and ability to find correct words impaired
• Nominal dysphasia
  • Specifically cannot name objects due to lesion at dominant posterior temporoparietal area
• Conductive dysphasia
  • Can follow commands but repeat and name objects poorly
  • Arcuate fasciculus lesions between Broca’s and Wernicke’s

Higher cerebral functions

• Parietal lobe
  • Dominant – Acalculia, agraphia, left-right disorientation, finger agnosia (AALF = Gerstmann’s syndrome)
  • Non-dominant – Tactile extinction (can feel stimulus if one side but not on one side when both sides stimulated), sensory/visual inattention, tactile agnosia, agraphaesthesia (inability to detect number drawn on palm of hand), two-point discrimination defect, dressing and constructional apraxia, spatial neglect is bilateral

Higher cerebral functions

• Temporal lobe
  • Short- and long-term memory
  • Ask to repeat 3 objects immediately (attention) and in 5 minutes (short-term memory)
  • May have confabulation in Korsakoff psychosis
• Frontal lobe
  • Grasp reflex (run finger along palm)
  • Palmomental reflex (ipsilatreal contraction of eye when stroke thenar eminence)
  • Pouting (when tapping on upper lip with tendon hammer)
  • Interpret a proverb ‘a rolling stone gathers no moss’
  • Anosmia

Cranial nerves

• II – Visual fields and RAPD (III efferent parasympathetics)
• III, IV, VI – EOM – SO4LR6AO3
  • VI – Loss of lateral rectus +- medially deviated
  • III – Down and out with pupil dilation + ptosis (levator palpebrae)
  • IV – Loss of superior oblique – Loss of depression in adduction
• V – Corneal sensation (VII efferent) + facial sensation and masseter motor
• VII – Facial motor
• VIII – Vestibular and auditory
• IX and X – Uvula and gag reflexes
• XI – Shoulder shrug
• XII – Stick out tongue and look for asymmetry

Visual fields

• Tunnel vision – Glaucoma, papilloedema, syphilis
• Enlarged blind spot – Optic nerve head enlargement
• Homonymous hemianopia – Optic tract to occipital cortex +- macular sparing
• Upper homonymous quadrantonopia – Temporal lobe lesion
• Lower homonymous quadrantonopia – Parietal lobe lesion

Diplopia testing

• False image is paler and more peripheral
• Therefore, find where diplopia most separate, then get them to close eye
  • If lateral image disappears, this is the pathological eye
  • If medial image disappears, the other eye is the pathological one
  • If side-by-side, must be medial or lateral recti
  • If above one another, could be any of the other 4 so need to work out where most disparate

Abnormalities of conjugate gaze

• Deviation of eyes to left
  • Destructive lesion between left frontal lobes and oculomotor nuclei
  • Destructive lesion on right side of brainstem
  • Irritative lesion e.g. epileptic focus of right frontal lobe
• Supranuclear palsy
  • Loss of vertical and/or horizontal gaze
  • Affects both eyes, with unequal pupils, no diplopia and reflex eye movements still intact (e.g. with neck flexion/extension)
• One-and-a-half syndrome
  • Rare but important cause
  • Due to lesion often in MS, stroke or tumor in dorsal pons
  • Horizontal gaze palsy in one direction and impaired adduction looking other way

HINTS testing

• Horizontal head impulse
  • Rapidly rotate head to one side then the other
  • Inability to maintain visual fixation during head rotation requires rapid corrective jerking (saccade) back to target = positive
  • Suggests peripheral lesions
• Nystagmus
  • Direction changing on testing = Central
  • Spontaneous (at rest) vertical or multidirectional nystagmus = Central
• Skew deviation
  • Cover-uncover test
  • Vertical skew deviation = Central

HINTS testing

• 2009. 101 patients. Acute vestibular syndrome (vertigo, nystagmus, nausea/vomiting, unsteady gait, head-motion intolerance) with 1 or more stroke risk factors
  • AF, DM, eclampsia, hypercoagulable state, dyslipidaemia, HTN, prior stroke or MI, recent cervical trauma, smoking
• Sensitivity 100%; specificity 96% for central lesion on MRI
• Done by neurologists
• No evidence in ED setting
• Provides useful information in workup of the dizzy patient

Nystagmus

• Repeated drift with saccadic correction
• Direction defined as that of the fast saccadic movement
• Often only seen gaze-evoked
• At extremes of gaze, physiological nystagmus is normal
• Jerky horizontal nystagmus
  • Causes include:
    • Vestibular lesion (acute fast phase away from side of lesion; chronic towards side of lesion)
    • Cerebellar lesion (fast phase towards lesion)
    • Toxic
    • Internuclear ophthalmoplegia (nystagmus in abducting eye and failure of adduction of other eye due to medial longitudinal fasciculus in MS or stroke)

Nystagmus

• Jerky vertical nystagmus
  • Brainstem lesion
  • Also seen with phenytoin and alcohol
• Pendular nystagmus
  • Phases are equal in duration
  • May be retinal or congenital

CN V – Trigeminal

• Motor and sensory nuclei in pons
• Trigeminal ganglion at petrous temporal bone then divides into ophthalmic (V1), maxillary (V2) and mandibular (V3) branches
  • Ophthalmic runs through cavernous sinus with third nerve via superior orbital foramen
  • Maxillary vis infraorbital foramen
  • Mandibular via foramen ovale
• Lesions may arise in nuclei, temporal fossa, petrous temporal bone (ganglia) or cavernous sinus
• If all three divisions involved, lesion must be proximal to ganglion
• If dissociated sensory loss (i.e. loss of pain/temperature but retention of light touch) suggests brainstem or upper cord lesion

CN VII – Facial

• Nucleus in pons
• Leaves pons with CN VIII and forms geniculate ganglion after facial canal
• Branch that supplies stapedius comes off in facial canal
• Chorda tympani joins facial nerves in facial canal and supplies sensory taste fibres to anterior 2/3 of tongue
• Exits skull via stylomastoid foramen, passes through parotid gland and supplies muscles to face in 5 divisions (Temporal, zygomatic, buccal, mandibular, cervical)

CN VIII – Vestibulocochlear

• Weber’s test
  • Middle of forehead
  • If heard more on one side = sensorineural loss on other side or conductive loss on that side
• Rinne’s test
  • Mastoid process then when no longer heard move in front of ear
  • If sensorineural loss, can hear again – get reduction in both bone and air conduction equally, so air conduction is better (as is normal)
  • If conductive loss, not heard
• Dix-Hallpike
  • 30 degrees neck extension and 30 degrees rotation towards examiner
  • If positive, get latent period then rotatory nystagmus towards down ear then abates
  • If no latent period, no fatiguability or nystagmus persists = brainstem or cerebellar lesion

Pseudobulbar vs. bulbar palsy

Pronator drift

• Arms outstretched and get inward rolling or downward drift and is a subtle sign of weakness
• Can test in lower limbs also

Muscle strength scale

• 5 – Normal strength
• 4 – Weakness and ability to contract against some resistance
  • Large range and degree of resistance is probably more descriptive
• 3 – Full motion against gravity only (not resistance)
• 2 – Active movement with gravity eliminated
• 1 – Minimal flicker
• 0 – Complete paresis

Post-void residual

• An often forgotten but crucial part of motor examination
• >100mL likely abnormal and >200mL definitely abnormal

Reflexes

• 4 – Hyperreflexic
• 3 – Slightly enhanced
• 2 – Normal
• 1 – Reduced
• 0 – Absent
• Babinski – Normal = downward
• Upward +- fanning of other toes = UMNL
• Clonus indicates hypertonia and hyperreflexia

Gait and station

• Keep cerebellar injury in mind in patients with sudden inability to walk
• May have severe nausea and vomiting and be massively diaphoretic

Unilateral hemisphere lesions

Last Updated on October 28, 2020 by Andrew Crofton