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Clinical cases

Three vignettes that put the chapter to work — the stroke that hid behind isolated vertigo, the young woman whose vertigo was demyelination, and the slow mass that pretended to be an ear problem.

Case 1 — Posterior-circulation stroke as isolated vertigo

A 62-year-old man with hypertension and a smoking history presents with sudden vertigo, nausea, vomiting and an inability to stand or walk without support. There are no overt motor or sensory deficits and the cranial nerves seem intact. But the truncal ataxia is severe and out of proportion, and oculomotor testing shows direction-changing, non-fatigable nystagmus. HINTS is central: the head impulse is normal, nystagmus changes direction with gaze, and a skew deviation is present.

CT is unremarkable, but MRI with DWI reveals a small acute infarct in the PICA territory, consistent with lateral medullary (Wallenberg) syndrome. He is started on aspirin, monitored for cerebellar swelling, and enrolled in balance and gait rehabilitation; his vertigo gradually resolves and he regains independent walking.

Teaching point: isolated vertigo in an older patient with vascular risk factors can be a posterior-circulation stroke. A normal head impulse in a genuinely vertiginous patient, plus gait failure out of proportion, mandated imaging despite a normal CT.2,1

Case 2 — Multiple sclerosis as recurrent vertigo

A 28-year-old woman reports recurrent episodes of vertigo over several months, often with blurred vision and horizontal diplopia lasting a few days. During this episode she also notices mild right-sided limb numbness. Examination shows horizontal nystagmus, impaired tandem gait, and an internuclear ophthalmoplegia implicating the medial longitudinal fasciculus.

Contrast MRI shows multiple T2/FLAIR hyperintense lesions in the periventricular white matter and brainstem, some enhancing. Lumbar puncture reveals CSF-restricted oligoclonal bands. Under the 2017 McDonald criteria she is diagnosed with relapsing-remitting MS.3 The acute relapse is treated with IV methylprednisolone, she begins a disease-modifying therapy, and vestibular rehabilitation targets gaze stabilisation and balance; over three months she improves.

Teaching point: MS-related vertigo in a young woman can mimic vestibular migraine or a peripheral disorder. Subacute, relapsing vertigo with INO and a demyelinating history should prompt MRI and CSF analysis for early diagnosis and treatment.4

Case 3 — The slow mass behind the imbalance

A 54-year-old presents with two years of gradually worsening unsteadiness, asymmetric right-sided hearing loss and tinnitus, and more recently right facial numbness with a reduced corneal reflex. There is no acute rotational vertigo. Gait is wide-based; there is mild right limb dysmetria.

Contrast MRI shows a vestibular schwannoma at the right cerebellopontine angle, now indenting the brainstem. The slow, compensated loss of vestibular input explains imbalance rather than vertigo; trigeminal involvement signals growth.5 He is referred for skull-base multidisciplinary management.

Teaching point: progressive imbalance with asymmetric hearing loss and cranial-nerve signs is a posterior-fossa mass until proven otherwise — image with contrast-enhanced MRI rather than attributing it to a peripheral vestibulopathy.

Shared clinical pearls

  • Not all vertigo is peripheral — in high-risk patients, assume a central cause until it is ruled out.
  • MRI, not CT, is the imaging modality for both stroke and MS — and a normal early scan does not exclude posterior-fossa stroke.
  • Central vertigo often comes with gait imbalance out of proportion to the spinning.
  • A normal head impulse test in a dizzy patient favours a central cause.
  • Match the tempo to the diagnosis: sudden → stroke; subacute and relapsing → MS; slowly progressive → mass.