NeurologyTier 1Disease (DEADMAN)

Ophthalmological conditions - nystagmus

Description

Involuntary, rhythmic oscillation of the eyes - a sign, not a diagnosis; localises to the vestibular system, cerebellum, brainstem, or is congenital
Described by the direction of the fast phase (in jerk nystagmus) and by plane (horizontal, vertical, torsional)

Congenital nystagmus - rare, presents infancy
Acquired nystagmus - incidence tracks the underlying cause (vestibular disease common, central causes less common but higher stakes)

Peripheral vestibular

BPPV, vestibular neuritis, Meniere disease - unilateral labyrinthine/vestibular nerve dysfunction

Central

Cerebellar or brainstem stroke, MS demyelination, posterior fossa tumour, Wernicke encephalopathy, drug/alcohol toxicity (phenytoin, lithium, alcohol)

Congenital/infantile

Idiopathic infantile nystagmus, albinism, congenital cataract/other visual pathway disease

Specific patterns worth naming

Downbeat nystagmus - craniocervical junction lesion (Chiari malformation), cerebellar degeneration, drug toxicity (lithium, anticonvulsants)
Upbeat nystagmus - brainstem (medullary/pontine) lesion
Gaze-evoked nystagmus - cerebellar disease, sedative/anticonvulsant drug effect
Internuclear ophthalmoplegia with nystagmus of the abducting eye - MLF lesion (MS in young patients, brainstem stroke in older)

Peripheral vs central - the critical distinction

	Peripheral	Central
Direction	Unidirectional (horizontal/torsional), fast phase away from lesion	Any direction, may be purely vertical or direction-changing
Visual fixation	Suppressed by fixation	Not suppressed, may worsen
Fatigability	Fatigues with repeated positioning (BPPV)	Non-fatiguing
Associated symptoms	Hearing loss/tinnitus (labyrinthine), vertigo proportional to nystagmus	Diplopia, dysarthria, ataxia, other focal signs; vertigo may be mild relative to nystagmus severity
Head impulse test	Abnormal (catch-up saccade)	Normal

Pure vertical or direction-changing nystagmus is central until proven otherwise
Use HINTS in the acute vestibular syndrome to differentiate (see Vestibular neuritis note)

Work-up

Full neurological and cranial nerve exam, cerebellar signs
MRI brain (with attention to posterior fossa/brainstem) if central features or red flags
Audiometry if peripheral/labyrinthine cause suspected
Medication review (anticonvulsants, lithium), alcohol history, thiamine status if malnourished

Treat the underlying cause - nystagmus itself is rarely treated directly except in specific chronic settings
Acute vestibular causes - see BPPV/Vestibular neuritis notes
Wernicke encephalopathy suspected - immediate IV thiamine before glucose
Drug-induced - cease/adjust the offending agent (anticonvulsant level, lithium level)
MS/demyelinating - disease-modifying therapy per MS management, symptomatic nystagmus rarely treated with agents like gabapentin/memantine in refractory cases
Congenital nystagmus - low vision support, correction of refractive error, rarely surgical options for severe cases

Peripheral causes - typically resolve or compensate over days-weeks
Central causes - reflect the underlying disease course (stroke recovery, MS relapse pattern, tumour progression)
Congenital nystagmus - lifelong but often with reasonably preserved visual function; may dampen with age
Oscillopsia (perceived visual movement) from uncompensated nystagmus can be functionally disabling

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