The conditions
Multiple sclerosis
Vertigo is rarely the headline of multiple sclerosis, but it is a common thread through it — and in a young adult, a demyelinating plaque in the brainstem can be the first thing the balance system reports.
Epidemiology
Multiple sclerosis (MS) is a disease in which the body’s own immune system damages the insulation around nerves in the brain and spinal cord. It usually starts in young adults and is more common in women. Vertigo is one of its many possible symptoms.
MS is a chronic immune-mediated demyelinating disease of the central nervous system, with inflammation, demyelination, gliosis and neuroaxonal loss. It typically presents between 20 and 40 years of age with a female preponderance of roughly 2–3 : 1.1 Vertigo is the presenting symptom in around 5% of patients and occurs at some point in about 20%.2
The demographic itself is a diagnostic lever: isolated central vertigo in a young woman, particularly with any history suggestive of prior demyelination (optic neuritis, sensory symptoms, Lhermitte’s), should prompt consideration of MS rather than the stroke that dominates the older population.1 Vertigo may be episodic, chronic, or part of a defined relapse, and its pattern tracks the location of plaques in the brainstem and cerebellum.
Pathophysiology
MS vertigo arises from demyelinating plaques in the central vestibular network — the vestibular nuclei of the medulla, the medial longitudinal fasciculus, the cerebellar peduncles, and the flocculus and nodulus. Disrupted conduction between the vestibular, ocular-motor and cerebellar systems produces vertigo, imbalance and oscillopsia.1
Internuclear ophthalmoplegia — the signature sign
The most characteristic neuro-ophthalmological finding is internuclear ophthalmoplegia (INO), from demyelination of the MLF. The MLF links the abducens nucleus on one side to the contralateral oculomotor nucleus to coordinate horizontal conjugate gaze; a lesion produces impaired adduction of the ipsilateral eye with abducting-eye nystagmus, often with horizontal diplopia. Bilateral INO in a young adult is highly suggestive of MS and, combined with movement-provoked dizziness, points to central vestibular dysfunction.3
Plaques in the cerebellar peduncles add gait ataxia, dysmetria and gaze-evoked nystagmus, while lesions of the nodulus and uvula disrupt velocity storage and graviceptive processing, producing central positional vertigo or lateropulsion. Bilateral MLF disease or cerebellar demyelination can impair the vestibulo-ocular reflex, experienced as blurred vision on head movement and demonstrable on video head-impulse or rotational-chair testing.
Clinical features
The tempo distinguishes MS from stroke. Symptoms tend to be subacute, evolving over hours to days rather than exploding instantly, and they recur and remit over the longer term. Episodes last hours to days. Useful accompaniments — current or in the history — include:
- Internuclear ophthalmoplegia and other ocular-motor signs.
- Central nystagmus — upbeat, downbeat, torsional or gaze-evoked, direction-shifting and non-fatigable.
- Optic neuritis (painful monocular visual loss), sensory disturbance, or limb weakness/spasticity.
- Lhermitte’s sign — an electric-shock sensation down the spine on neck flexion, from cervical-cord demyelination.
Diagnosis
MRI
MRI of brain and spinal cord is the cornerstone. T2/FLAIR sequences show hyperintense lesions in characteristic sites — periventricular, juxtacortical, infratentorial (cerebellum and brainstem) and spinal cord — and gadolinium enhancement distinguishes active inflammatory plaques from chronic ones.5
Supporting tests
- CSF oligoclonal bands — present in ~85–95% of clinically definite MS and absent from matched serum, indicating intrathecal IgG synthesis.6
- Evoked potentials — delayed visual evoked potential P100 latency (prior optic neuritis) or abnormal brainstem auditory conduction support subclinical dissemination.
- Vestibular testing — VNG may show gaze-evoked or direction-changing nystagmus, and VEMPs can reveal central vestibular conduction abnormality; bilateral or asymmetric findings help separate MS from a peripheral vestibulopathy.
The 2017 McDonald criteria
Diagnosis requires dissemination in space and time. Dissemination in space means lesions in ≥2 of the four characteristic locations; dissemination in time can be shown by simultaneous enhancing and non-enhancing lesions or by a new lesion over time. Crucially, the 2017 revision allows CSF-specific oligoclonal bands to substitute for dissemination in time, enabling earlier diagnosis and earlier treatment.4 A first, isolated episode that does not yet meet criteria is a clinically isolated syndrome, requiring follow-up.
Management
Treatment works on three fronts: settle the acute relapse, prevent future lesions, and rehabilitate residual balance impairment.
Acute relapse
A vertigo relapse from a brainstem or cerebellar plaque is treated with high-dose intravenous methylprednisolone (typically 1 g/day for 3–5 days, with or without an oral taper). Corticosteroids hasten recovery by suppressing inflammation and stabilising the blood–brain barrier; they shorten the relapse but do not alter long-term disability.
Disease-modifying therapy
Long-term, disease-modifying therapies (DMTs) reduce relapse rate, slow disability and lower radiological activity. First-line agents include the interferon betas and glatiramer acetate; for highly active disease, monoclonal antibodies such as natalizumab (anti-α4-integrin)8 and ocrelizumab (anti-CD20)7 give stronger control. DMTs do not treat vertigo directly, but by preventing new brainstem and cerebellar plaques they reduce future vestibular relapses.
Symptomatic and rehabilitative care
Vestibular suppressants (meclizine, betahistine, promethazine) may give short-term relief but should not be continued — they blunt central compensation and prolong recovery. The durable treatment is vestibular and balance rehabilitation: gaze-stabilisation, habituation and postural-control exercises drive neuroplastic compensation, reduce falls and improve confidence, with benefit shown even for MS-related fatigue and postural control.9
Key points
- MS vertigo comes from demyelinating plaques in the brainstem and cerebellar vestibular pathways.
- Onset is subacute and the course relapsing — the opposite tempo to stroke.
- Bilateral internuclear ophthalmoplegia in a young adult is a strong pointer to MS.
- Diagnosis uses the 2017 McDonald criteria (dissemination in space and time); CSF oligoclonal bands can replace dissemination in time.
- Treat the relapse with IV steroids, prevent recurrence with disease-modifying therapy, and rehabilitate the balance deficit.