Cranial nerve examination

see also:

• neurology
• anatomy of the autonomic nervous system
• LITFL - the rule of 4 of the brainstem

NB. Myasthenia gravis has the ability to mimic virtually any cranial neuropathy, including isolated third nerve palsies and INO. Myasthenia gravis must remain a possible diagnosis when encountering a third nerve palsy, especially when the course is variable or atypical.

• test esp. if personality change (frontal lobe lesion) or unexplained visual loss (optic chiasm lesion)
• see taste and smell

• Snellen chart at 6m or Rosenbaum pocket card at 1foot
• with corrective glasses otherwise use pinhole if glasses unavailable

• divide field into 4 quadrants (inf, sup, nasal & temporal) - check each eye individually

• spontaneous venous pulsations on fundoscopy viewed in an upright patient indicate normal intracranial pressure and is an important finding, especially if later it is lost.
• papilloedema indicates raised intracranial pressure
• subhyaloid or pre-retinal haemorrhages are diagnostic of SAH
• tenderness of temporal arteries in those over 50yrs suggests temporal arteritis which if untreated may cause optic neuritis and blindness - check ESR.
• revoptom.com - Anterior Ischemic Optic Neuropathy
• revoptom.com - Optic Disc Edema & Papilledema
• revoptom.com - Demyelinating Optic Neuropathy (Optic Neuritis, Retrobulbar Optic Neuritis)

• hold pen or finger in front of pt, ask pt to follow it while you move it horizontally.
• ask pt how many pens he sees - if “two” is it monocular or binocular & note position - see diplopia
• hold pen horizontally & move it vertically

• due to lesion of ipsilateral medial longitudinal fasciculus which normally allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF) -abducens nucleus complex of one side to the oculomotor nucleus of the opposite side.
• failure of an eye to adduct on gaze to opposite side
• results in horizontal diplopia & may cause compensatory nystagmus in the partner eye.
• bilateral lesions in age < 50yrs is almost always due to multiple sclerosis (MS)
• unilateral lesions may also be due to brainstem infarct, brainstem/fourth ventricle tumour, viral infection, trauma, drugs, subdural haematoma, etc.
• myasthenia gravis may mimic INO.
• see revoptom.com for more details.

• marked nystagmus on lateral gaze or any on forward gaze is abnormal
• vertical nystagmus ⇒ brain stem lesion or phencyclidine
• pendular ⇒ usually congenital
• see assessment of vertigo

• complete ptosis, inability to adduct eye & fixed, dilated pupil

• brainstem lesions:
  • brainstem infarct - usually also involves pyramidal & cerebellar pathways ⇒ c/lat. hemiplegia & ipsilat. cerebellar ataxia
  • metastatic disease
  • multiple sclerosis (MS)
• within subarachnoid space (usually produces painful, isolated CIII lesions +/- pupil involvement)
  • post. commun. artery aneurysm or basilar aneurysm - often assoc. with ipsilat. periorbital pain.
    • suspect if either:
      • adult patient of any age presents with a complete or incomplete isolated third nerve palsy with pupillary involvement
      • 15-50yrs age and has a non-pupillary involved isolated third nerve palsy
    • CT or MR angiography ASAP as risk of aneurysm rupture
  • ischaemic neuropathy (eg. vasculopathy)
• aneurysms within cavernous sinus - usually also involve CIV, CV, CVI nerves
• with normal pupil and aged > 55yrs with sudden onset ⇒ isolated CIII lesion due to atherosclerosis, hypertension or diabetes mellitus.
• other causes: tumour, basal meningitis (eg. TB), head injury, toxins (eg. snakebite).
• children < 14yrs are most likely traumatic or congenital.

• failure to adduct eye downwards

• head injury, ischaemia due to atherosclerosis or diabetes; tumour.

• failure to abduct the eye.

• congenital - Duane syndrome
• vascular - brainstem infarction - usually also ipsil. facial palsy & c/lat. hemiparesis.
• cavernous sinus pathology - usually also involves CIII, CIV, CV nerves
• tumour, infection spreading from otitis media, TB meningitis, MS, # base of skull, raised intracranial pressure (ICP).

• if pupil constricts to light, testing for accommodation adds no further information as pupillary reaction to accommodation but not light is rare, seen only in tertiary syphilis
• pupillary size in room light
• unequal pupils may be normal (anisocoria)

• if with abnormal GCS suggests uncal herniation
• consider CIII lesion, eye drops
• Holmes-Adie pupil (slowly constricts with accommodation)

• Horner's syndrome, eye drops.

• suggests prolonged anoxia, anticholinergics or sympathomimetics

• suggests narcotics, organophosphates or pontine haemorrhage (also Argyll Robertson pupils of tertiary syphilis)

• a CNS lesion affecting CV is likely to involve all 3 divisions, thus it is not necessary to test them individually.
• test sensory function by simultaneously pressing sharp object on both cheeks & asked if can feel them as sharp.
• test motor function by asking pt to clench teeth while you palpate masseter muscle tone.

• see also:
  • facial nerve palsy - Bell's palsy
  • taste and smell
• weakness is usually apparent to the patient and not an unexpected finding.
• in subtle cases, weakness is often apparent by:
  • evidence of flattening of nasolabial fold
  • ask pt to show his teeth, whistle & puff (in succession) - smiling itself is not adequate!
• cortical motor fibres to the forehead muscles run from both motor cortices to each CVII nucleus & thus a cortical “central” lesion does not produce paralysis of forehead muscles whereas a peripheral lesion involves the whole ipsilateral face.
• CVII has two main divisions:
  • motor root to ipsilateral facial muscles including forehead, and via nerve to stapedius, the stapedius muscle in the ear (lesion results in hyperaccusis)
  • nervus intermedius:
    • fibres pass through geniculate ganglion
    • supplies taste to ant. 2/3rds tongue via chorda tympani
    • supplies autonomic fibers via:
      • the major superficial petrosal nerve via pterygopalatine ganglion which innervate the nasal, palatine and lacrimal glands.
      • the lingual nerve via teh submandibular ganglion which supplies the sublingual and submandibular salivary glands.
• if the lesion occurs at the level of the nucleus in the brain stem, it usually also involves:
  • CVI as the CVII fibers loop around the CVI nucleus before exiting the pons.
  • long motor tract fibres
• Ramsay-Hunt syndrome:
  • peripheral CVII palsy + herpetic vesicles in ear canal and on tympanic membrane +/- vertigo/tinnitus

• hearing can be rapidly screened by :
  • rub finger/thumb of each hand next to each ear, alternating which hand rubs, ask which is heard.
• if defect, ask patient to hum. In sensorineural defect, humming is heard loudest in normal ear.
• vestibular nerve is generally not tested unless pt is complaining of vertigo or dizziness:
  • Nylen-Barany manouvre

• these are tested together:
  • lightly depress tongue, gag reflex should cause soft palate to retract symmetrically.
• if nerve injury is one sided, palate will retract to normal side.
• compromise of these nerves is extremely rare.

• occasionally damaged during neck injuries
• test trapezius by shrugging shoulders, if equivocal, test sternocleidomastoid contraction.

• ask pt to stick out his tongue, if there is weakness, tongue will deviate to side of lesion.
• see also bulbar palsy