Disease-targeted

Disease-targeted therapy

Where the suppressants treat the symptom, these treat the mechanism — inner-ear fluid in Ménière’s, inflammation in neuritis, migraine biology in vestibular migraine, and sensory–anxiety processing in PPPD.

Ménière’s disease

Ménière’s disease — recurrent spontaneous vertigo, fluctuating sensorineural hearing loss, tinnitus and aural fullness — is attributed to endolymphatic hydrops. Targeted therapy aims to reduce endolymphatic pressure and stabilise inner-ear fluid dynamics.

Betahistine

Betahistine (16–48 mg/day) is the most prescribed long-term prophylactic. A weak H1 agonist and potent H3 antagonist, it improves stria vascularis and inner-ear blood flow and enhances endolymph resorption. A Cochrane review found a reduction in vertigo episodes versus placebo, though the effect on hearing and tinnitus is inconsistent; given its favourable safety profile it is widely used first-line.1,2

Diuretics

Systemic diuretics — typically hydrochlorothiazide with triamterene, sometimes acetazolamide — are used as adjuncts with a low-sodium diet (< 1.5 g/day) on the rationale that reducing fluid volume lowers endolymphatic pressure. The evidence is largely observational and high-quality trials are lacking; monitor electrolytes and renal function.3

Intratympanic therapy

For refractory disease, intratympanic delivery targets the inner ear directly. Intratympanic corticosteroids (dexamethasone, methylprednisolone) reduce vertigo while sparing hearing, with variable durability.4 Intratympanic gentamicin chemically ablates vestibular hair cells, controlling vertigo in over 85% of cases but risking cochleotoxicity and persistent imbalance — so it is carefully titrated and specialist- administered. The choice depends on hearing status, severity, laterality and patient preference.

Vestibular neuritis

Vestibular neuritis is an acute unilateral vestibulopathy — sudden severe vertigo, nausea and imbalance without hearing loss — probably from reactivation of latent HSV-1 in the vestibular nerve, supported by detection of viral DNA in vestibular ganglia.7

Corticosteroids

Steroids are the best-studied agent, reducing nerve oedema and aiding recovery of conduction. The pivotal Strupp et al. trial showed that methylprednisolone significantly improved peripheral vestibular function on caloric testing, while valacyclovir added nothing.5 A typical regimen is prednisone 60 mg/day tapered over 10–14 days, ideally started within 72 hours. The benefit to objective caloric recovery is clearer than the benefit to long-term subjective outcomes, which remains debated.6

Antivirals

Despite the viral hypothesis, antivirals are not supported: valacyclovir conferred no benefit alone or with steroids, and systematic reviews find insufficient evidence for routine use.5 Reserve them for selected cases such as Ramsay Hunt syndrome. Treatment should prioritise early steroids and rehabilitation, and avoid prolonged suppressants.

Vestibular migraine

Vestibular migraine is among the commonest causes of episodic vertigo, diagnosed by Bárány Society / IHS criteria.8 Management parallels migraine: abortive agents for attacks, prophylaxis to cut frequency.

Acute management

Triptans (e.g. sumatriptan, a 5-HT1B/1D agonist) taken early can ease both headache and vestibular symptoms, though efficacy in vestibular migraine is more variable than in migraine with aura; NSAIDs help milder episodes.10

Prophylaxis

  • Beta-blockers — propranolol 40–160 mg/day, modulating adrenergic tone.
  • Calcium-channel blockersflunarizine 10 mg/day, RCT-supported, stabilising vestibular neurons.9
  • Tricyclics — amitriptyline 10–50 mg at night, useful with coexisting tension headache, insomnia or anxiety.
  • Antiepileptics — topiramate 25–100 mg/day (and valproate in selected patients, avoiding pregnancy).

Prophylaxis takes 6–8 weeks to work, requires gradual titration, and is continued for at least 6 months after control with periodic review.

Persistent postural-perceptual dizziness (PPPD)

PPPD is a chronic functional disorder of non-spinning dizziness, unsteadiness and motion/visual hypersensitivity, often triggered by an earlier vestibular insult and perpetuated by anxiety and visual dependence.11

SSRIs and SNRIs

SSRIs/SNRIs are first-line and appear to act directly on vestibulo-visual hypersensitivity as well as comorbid anxiety. Sertraline (50–200 mg/day) and paroxetine (10–40 mg/day) are common SSRIs; venlafaxine (75–150 mg/day) the usual SNRI. A randomised trial of paroxetine showed a 60–70% symptom reduction versus 20–30% on placebo.12 Start low, titrate, and counsel that benefit takes 4–6 weeks; continue 6–12 months. Crucially, medication should be combined with vestibular rehabilitation and cognitive-behavioural therapy.

Key points

  • Ménière’s: betahistine first-line, diuretics adjunctive, intratympanic steroid or gentamicin for refractory disease.
  • Vestibular neuritis: early corticosteroids aid caloric recovery; antivirals are not supported.
  • Vestibular migraine: triptans/NSAIDs acutely; propranolol, flunarizine, amitriptyline or topiramate for prophylaxis.
  • PPPD: SSRIs/SNRIs first-line, alongside rehabilitation and CBT, with benefit over 4–6 weeks.