Dizziness and Vertigo _________________________________________________________________________
Vestibular Migraine and Anxiety Patients with vestibular migraine are more anxious than patients with non-vestibular migraine [168]. Anxiety is so prevalent in vestibular migraine, migraine, and vestibular disorders that a new disorder—migraine-anxiety-related dizzi- ness—was proposed to define the association [48]. The recommended pharmacotherapy for vestibular patients with prominent anxiety, panic attacks, or depression and less prominent nausea is [15]: • Venlafaxine 75 mg/day, OR • A tricyclic antidepressant (e.g., nortriptyline, imipramine, amitriptyline) 50–75 mg/day The established efficacy of venlafaxine in anxiety disorder treatment suggests a potential advantage over other vestibu- lar migraine prophylaxis. One study evaluated patients with vestibular migraine randomized to venlafaxine (37.5 mg/day), flunarizine (10 mg/day), or valproic acid (1,000 mg/day) for three months [169]. Significant decreases in precipitating physical factors and functional consequences of vestibular migraine were noted with all three medications. Improve- ments in emotional consequences of vestibular migraine (with venlafaxine only), vertigo attack severity (with venlafaxine and flunarizine but not valproic acid), and vertigo attack frequency (with venlafaxine and valproic acid but not flunarizine) were also noted. This suggests venlafaxine more effectively reduced emotional distress and anticipatory anxiety related to vestibular migraine attacks, as well as attack frequency and severity [169]. Other Treatment Options Betahistine plus flunarizine leads to greater improvements in vertigo frequency and severity than betahistine alone. Decreases in headache frequency and severity are comparable [170]. Vestibular rehabilitation is effective, with improved symptoms and disability in patients with vestibular migraine as add-on treatment to medical therapy or as stand-alone treatment [48; 163]. Vestibular Paroxysmia With vestibular paroxysmia, the characteristic brevity (seconds up to a few minutes, very seldom many hours) and frequency of recurring vertigo attacks makes the differential diagnosis generally straightforward [45]. The frequent vertigo attacks respond to carbamazepine (200–800 mg/day) or oxcarbazepine (300–900 mg/day), even in the lower dose range. Both drugs are recommended to start with a low dose, slowly progressing to higher doses as necessary [120].
Second-Line Therapies for Carbamazepine/ Oxcarbazepine Intolerance
Alternative drug options include phenytoin, gabapentin, valproate, lamotrigine, topiramate, and baclofen or other non- antiepileptic drugs used in trigeminal neuralgia [45]. Treatment should start with low doses. Options include [120]: • Phenytoin 100 mg once daily, increased up to three times per day • Gabapentin 300 mg once daily, increased to three times daily over four to seven days and further increased with insufficient symptom relief (up to a maximum 1,800 mg) • Valproate dosing proportional to body weight (start with 10 mg per kg body weight, increasing the dose every three days up to 20 mg/kg) Antiepileptic medications can themselves elicit dizziness and should be prescribed cautiously, ideally by specialists who can differentiate possible side effects from dizziness or vertigo sensations per se [120]. Refractory Vestibular Paroxysmia Surgical microvascular decompression of the 8th cranial nerve is used for medically intractable cases or in rare cases with non- vascular compression of the 8th nerve by a tumor or cyst [45].
CHRONIC VESTIBULAR SYNDROMES Context-Specific (Triggered) CVS
Most t-CVS syndromes have been defined too recently for consistently effective therapies to surface. There is some evidence for the treatment of bilateral vestibulopathy, PPPD, depersonalization and derealization disorder, and mal de
débarquement syndrome. Bilateral Vestibulopathy
The primary cause of bilateral vestibulopathy is aminogly- coside ototoxicity, typically gentamicin or streptomycin. In these cases, the ototoxic medication should be stopped or switched to a non-ototoxic drug. Other underlying causes of bilateral vestibulopathy include autoimmune processes, local or systemic infectious/inflammatory processes, bacterial or viral meningitis, bilateral Ménière disease, head trauma, neoplasms, or malformations. The cause should be identified and resolved or symptomatically managed [120]. Vestibular rehabilitation improves dynamic visual acuity, diminishes oscillopsia, and lessens asymmetry of vestibulo- ocular function by promoting adaptation and substitution using vision and proprioceptive cues to stabilize gait and mobil- ity [171]. Vestibular rehabilitation is strongly recommended for patients with bilateral vestibulopathy [15; 120].
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