________________________________________________________________________ Dizziness and Vertigo
Betahistine First approved for use in Europe in the 1970s, betahistine has been prescribed to more than 100 million patients with vestibular disorders and is the first-line treatment of Ménière disease in Germany. Betahistine is not approved by the U.S. Food and Drug Administration, but it may be obtained through compounding pharmacies in the United States with a prescription [15; 130]. It reduces vestibular symptoms but seems to differ from vestibular suppressants by promoting ves- tibular compensation. Histamine regulates sensory coding in the peripheral vestibular system. Betahistine (dihydrochloride or dimesylate), a structural analogue of histamine, is a potent histamine H3 receptor antagonist and a weak histamine H1 receptor agonist [15]. Betahistine reduces the frequency and severity of vertigo, nausea, and vomiting in diverse unilateral vestibular etiologies. Central and peripheral histamine receptor activity is a presumed mechanism [130; 131; 132]. Betahistine dose-dependently increases vestibulo-cochlear blood flow, increases central and vestibular system histamine turnover, decreases peripheral vestibular system input, and reduces histamine-induced excitation in vestibular cells through local H3 receptor blockade. These mechanisms are thought to improve vestibular compensation, reduce func- tional asymmetry of vestibular organs, and improve labyrinth microcirculation by rebalancing the production and resorption of endolymphatic fluid [130; 131; 132]. In this course, all discussions of betahistine refer to betahistine dihydrochloride, unless otherwise stated. Antidepressant Drugs Monoamines are the neurochemicals serotonin, norepineph- rine, and dopamine. Dysregulated monoamine neurotrans- mission is implicated in anxiety disorders and depression. A bi-directional relationship between impaired monoamine neurotransmission and vestibular signaling dysfunction is sug- gested, with asymmetric vestibular system release of serotonin, norepinephrine, or dopamine linked to vestibular migraine and other dizziness/vertigo etiologies [50; 61; 120]. Antidepressant drugs include SSRIs (e.g., fluoxetine, escitalo- pram), serotonin norepinephrine reuptake inhibitors (SNRIs) (e.g., venlafaxine, duloxetine), and tricyclic antidepressants (e.g., nortriptyline, imipramine, amitriptyline). They modulate serotonin, norepinephrine, and dopamine neural pathways (with varying specificities) and are first-line treatments for anxiety disorders and depression. These agents are increasingly recommended for use in some vestibular-related disorders [50; 120; 133].
Aminopyridines Aminopyridines are potassium-channel blockers, established as pharmacotherapy for cerebellar diseases that include downbeat nystagmus, upbeat nystagmus, central positional nystagmus, episodic ataxia type 2, and gait disorders in cerebellar ataxia [61]. Aminopyridines used in these disorders are 3,4-diaminopyri- dine (3,4-DAP) and 4-aminopyridine (4-AP). 4-AP crosses the blood-brain barrier more easily and is superior to 3,4-DAP in some cases. Both drugs are well-tolerated and without major side effects apart from nausea, transient paresthesia, or headache [122]. QT Interval Prolongation Some vestibular disorder pharmacotherapies may interact with other medications to risk QT interval prolongation [120]. A prolonged QT interval is a symptom of disordered myocardial repolarization that increases the risk of potentially life-threat- ening ventricular tachycardia (i.e., torsades de pointes) [134]. A complete list of medications that prolong the QT interval is available at https://www.crediblemeds.org. VESTIBULAR REHABILITATION Vestibular rehabilitation, another therapeutic modality broadly used across dizziness and vertigo etiologies, is a specific physi- cal therapy for patients with peripheral or central vestibular disorders. Vestibular rehabilitation reduces symptoms and improves functioning by promoting CNS compensation through exercise-based strategies [135; 136]. Following an acute peripheral vestibular event, clinical recovery occurs in advance of improved peripheral vestibular function. This suggests that most of the early recovery and a substantial portion of total recovery derives from central compensation (long-term changes in neuronal responses to head movements) that is multisensory and is the primary target of vestibular rehabilitation. Early rehabilitation (during a critical period of adaptation and compensation) may be more effective than late intervention. As such, vestibular rehabilitation should begin shortly after symptom onset [135; 137]. Patients typically receive supervised therapy one to two times per week and are taught daily home exercises. The average dura- tion of therapy is 6 to 12 weeks for patients with peripheral vestibular disorder and longer for patients with central ves- tibular disorder or mobility-impairing comorbidities [43; 136].
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Book Code: ANCCTX2027
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