What is the treatment for vestibular paroxysmia?

Treatment of Vestibular Paroxysmia

Sodium channel blockers, specifically oxcarbazepine (300 mg three times daily) or carbamazepine (200 mg twice daily), are the first-line treatment for vestibular paroxysmia, with oxcarbazepine preferred due to better tolerability. 1, 2

First-Line Pharmacotherapy

Oxcarbazepine (Preferred Agent)

• Start with 300 mg once daily for week 1, increase to 300 mg twice daily in week 2, then 300 mg three times daily from week 3 onward 2
• Oxcarbazepine demonstrated significant efficacy in the only randomized, double-blind, placebo-controlled trial (Vestparoxy), reducing the risk of experiencing a day with at least one attack by 33% (relative risk 0.67,95% CI 0.47-0.95, p=0.025) 2
• The number of attacks was reduced by 47% compared to placebo (ratio 0.53,95% CI 0.42-0.68, p<0.001) 2
• Oxcarbazepine has a lower incidence of side effects compared to carbamazepine, making it the preferred sodium channel blocker 3, 4

Carbamazepine (Alternative)

• Use 200 mg twice daily if oxcarbazepine is not available or not tolerated 3, 4
• Carbamazepine is effective but has higher rates of adverse effects and drug interactions compared to oxcarbazepine 4

Augmentation Strategy

Adding Betahistine Mesilate

• Consider adding betahistine mesilate 18 mg twice daily to either oxcarbazepine or carbamazepine for enhanced efficacy 3, 4
• The combination of carbamazepine plus betahistine showed greater reductions in vertigo frequency, duration, and severity scores compared to carbamazepine alone 4
• Higher doses of betahistine (18 mg twice daily) provide better synergistic effects than lower doses (12 mg twice daily) 3
• The combination of oxcarbazepine plus betahistine 18 mg twice daily offers the best balance of efficacy and tolerability 3

Diagnostic Imaging Requirements

Mandatory MRI Evaluation

• High-resolution MRI with constructive interference in steady-state (CISS) or fast imaging employing steady-state (FIESTA) sequences of the cerebellopontine angle is mandatory before initiating treatment 1
• Imaging distinguishes between classical VP (neurovascular cross-compression), secondary VP (space-occupying lesions), and idiopathic VP (no identifiable cause) 1
• Imaging of the posterior fossa including the inner ear must be performed to rule out secondary causes 1

Clinical Characteristics to Confirm Diagnosis

Attack Pattern

• Frequent short attacks of vertigo lasting seconds to minutes (not hours) 1
• Attacks occur spontaneously or can be provoked by head movements or hyperventilation 1
• May be accompanied by unilateral auditory symptoms such as tinnitus or hyperacusis 1

Response to Treatment as Diagnostic Confirmation

• Beneficial response to sodium channel blockers is the most reliable clinical sign for vestibular paroxysmia 1
• Lack of response should prompt reconsideration of the diagnosis 1

Surgical Intervention

Microvascular Decompression

• Reserve microsurgical decompression for patients who cannot tolerate medical therapy or have failed adequate trials of sodium channel blockers 1
• Microvascular decompression is effective in secondary VP with identified compressive lesions 1
• Surgery is the ultimate therapy in classical or idiopathic VP when medication is not tolerated 1

Common Pitfalls

Medication Tolerability

• The most common reason for treatment discontinuation is adverse events from sodium channel blockers 2
• Monitor for hyponatremia, dizziness, and cognitive effects, particularly with carbamazepine 4
• Switch from carbamazepine to oxcarbazepine if hypersensitivity or intolerable side effects occur 3, 4

Duration of Treatment

• Continue treatment for at least 12 weeks to assess full therapeutic response 3, 4
• Long-term maintenance therapy is typically required as vestibular paroxysmia is a chronic condition 1