Where the signs appear

Vestibular migraine is among the most common causes of episodic vertigo, especially in middle-aged women. Most attacks are vestibular without head pain. The puzzling thing for clinicians is that some attacks show central-looking eye signs — without a stroke or MS.

Bárány Society criteria require migraine history plus episodic vestibular symptoms with a migrainous feature (photophobia, phonophobia, aura, throbbing headache) in at least half of attacks.1 Examination during attacks can show spontaneous, positional, or gaze-evoked nystagmus — not BPPV-like — and even subtle skew or pursuit deficits.2,3Imaging is normal; treatment is migraine prophylaxis (triptans for acute, propranolol/topiramate/CGRP-targeted agents for prevention).

The trap is calling a central-looking exam “stroke” when it is migraine, and conversely calling “migraine” when it is a small posterior-fossa infarct. In acute presentations apply HINTS strictly; in episodic ones, hold the clinical context against the criteria. Vestibular migraine often coexists with BPPV and PPPD — beware overlapping diagnoses.

MS commonly involves brainstem pathways that move the eyes. Vertigo with double vision in a young person — particularly when one eye lags behind the other on looking sideways — should make you think of MS.

MS brainstem plaques produce INO (often bilateral — BINO), gaze palsy, skew deviation, and nystagmus, frequently alongside vertigo and oscillopsia.4 MRI shows periventricular, juxtacortical, infratentorial, and spinal-cord plaques distributed in time and space.

Treat brainstem relapses with high-dose corticosteroids; long-term, use a disease-modifying therapy matched to phenotype and activity. Symptomatic aminopyridines may improve gaze stability in patients with chronic downbeat nystagmus or oscillopsia.

Posterior-circulation strokes can present with vertigo as the dominant complaint and only subtle other signs. Missing them risks a second, larger stroke or progressive deterioration. The eyes are usually how they are caught.

Cerebellar infarction — particularly in the PICA territory — can present with isolated vertigo in a meaningful minority of cases.5 Look for gaze-evoked nystagmus, skew deviation, INO, or normal head impulse with spontaneous nystagmus — any of which shift the diagnosis from neuritis to stroke.6 Remember that early DWI-MRI misses small posterior-fossa infarcts in 10–20% of patients,7 so a negative scan in a high- suspicion patient should not be reassuring.

Pathway: HINTS-positive AVS → immediate stroke pathway with vascular imaging (CT angio or MRA) and serial neurological assessment regardless of the first MRI. Posterior-circulation stroke benefits from the same thrombolytic and endovascular pathways as anterior-circulation stroke in the appropriate window — but only if the diagnosis is made.

In Chiari type I the lower part of the cerebellum sits below the base of the skull and crowds the brainstem. The classic presentation is a young adult with cough headache, imbalance, and downbeating eye movements.

The characteristic eye sign is downbeat nystagmus, often maximal in lateral and downgaze. Patients describe imbalance, oscillopsia, suboccipital headache exacerbated by Valsalva, and lower-cranial-nerve symptoms. MRI of the cervical spine and brain shows tonsillar herniation; many Chiari I findings on MRI are incidental and asymptomatic.8

Symptomatic Chiari with brainstem compression, syringomyelia, or disabling downbeat nystagmus is referred for posterior-fossa decompression. Aminopyridine therapy may improve gaze stability while definitive management is planned.9

Wernicke's encephalopathy is a treatable emergency caused by thiamine (vitamin B1) deficiency — typically in malnutrition, alcohol misuse, hyperemesis, or after bariatric surgery. The eye signs come early, and IV thiamine can reverse them.

The classic triad is confusion, ataxia, and ophthalmoplegia/nystagmus. Patients show bilateral abducens palsies, gaze palsies, and gaze-evoked or vertical nystagmus reflecting metabolic lesions of the dorsomedial thalami, mammillary bodies, and periaqueductal grey.10 The full triad is seen in a minority at presentation — only ~16% in classic post-mortem series,11 so any single feature should prompt thiamine.

Treat empirically with high-dose IV thiamine before giving glucose, even when the diagnosis is suspected on a single feature. Delay risks permanent memory loss (Korsakoff syndrome) and death. Re-feeding, magnesium repletion, and ongoing thiamine supplementation complete the regimen.