Disease-targeted

Pharmacologic management in central vertigo

When the lesion is in the brain, the drug strategy inverts: treat the underlying pathology first, and use vestibular suppressants only briefly and sparingly — they can mask progressive signs and stall recovery.

The governing principle

Central vertigo — from stroke, demyelination, tumour or migraine — is usually accompanied by other neurological signs and demands treatment of the cause rather than the symptom. Suppressants have a supporting, time-limited role; over-reliance can blunt central compensation and obscure a deteriorating picture.1 The full clinical work-up of these conditions is covered in the Central Causes chapter; here the focus is the drugs.

Posterior-circulation stroke

Vertigo may be the presenting feature of vertebrobasilar ischaemia, particularly PICA or AICA infarction. The priority is urgent neuroimaging (MRI with DWI) and the acute stroke protocol — antiplatelet therapy, blood-pressure management, and thrombolysis or thrombectomy in selected patients. Meclizine or lorazepam may be used briefly for acute vertigo and nausea during admission, but long-term use is discouraged because it delays central compensation.1,3

Multiple sclerosis and demyelinating disorders

In MS, vertigo arises from demyelination in the vestibular nuclei, cerebellar pathways or medial longitudinal fasciculus. Acute relapses are treated with high-dose intravenous corticosteroids — methylprednisolone 1 g/day for 3–5 days — to reduce inflammation and stabilise the blood–brain barrier and shorten the relapse.2 Short-term suppressants may help disabling vertigo, with caution to avoid sedation worsening ataxia. For symptomatic nystagmus or internuclear ophthalmoplegia, gabapentin or memantine may be trialled. Long-term disease-modifying therapy is essential for relapse prevention.

Tumours and space-occupying lesions

Vestibular schwannomas, cerebellar astrocytomas and brainstem gliomas may cause progressive vertigo, imbalance and hearing loss; management is by surgery, radiosurgery or surveillance depending on the lesion. Pharmacology is adjunctive: corticosteroids reduce peritumoral oedema and intracranial pressure, and short-term suppressants ease the acute vestibular deafferentation after schwannoma resection, followed by early rehabilitation to drive compensation.3

Vestibular migraine and epileptic vertigo

Central episodic vertigo may reflect vestibular migraine or, rarely, vestibular seizures in temporal-lobe epilepsy. Treat the cause: anti-migraine prophylaxis for the former; antiepileptics — valproate, lamotrigine, levetiracetam — for seizure-related vertigo.

Caution: in central vertigo, lean less on symptomatic suppressants. Indiscriminate use can mask progressive neurological signs and delay diagnosis, and the elderly are especially prone to sedation, falls and cognitive impairment with benzodiazepines and anticholinergics. Keep pharmacology judicious, time-limited and tied to a clear diagnosis.

Key points

  • In central vertigo, treat the underlying pathology — suppressants are supportive and brief.
  • Stroke: acute stroke protocol and imaging first; suppressants only during early admission.
  • MS relapse: IV methylprednisolone 1 g/day for 3–5 days, then disease-modifying therapy.
  • Tumours: definitive treatment is surgical/radiosurgical; steroids reduce oedema, rehab drives recovery.
  • Over-using suppressants can mask progression and delay diagnosis — be especially careful in older adults.