________________________________________________________________________ Dizziness and Vertigo
Spontaneous Chronic Vestibular Syndrome s-CVS conditions include chronic dizziness or vertigo associ- ated with nystagmus, blurred vision, or impaired visual acuity from oscillopsia, originating from cerebellar or brainstem degeneration or atrophy [122]. Other central etiologies of s-CVS include cervical vertigo and Chiari malformations [119]. Several cerebellar syndromes due to neurodegenerative and hereditary diseases can lead to ataxia and postural instability associated with cerebellar oculomotor disorders (e.g., downbeat nystagmus, gaze-evoked nystagmus) [122]. Episodic ataxia type 2, the most frequent inherited cerebellar ataxia syndrome, is characterized by recurrent attacks of dizzi- ness and ataxia lasting several hours, often elicited by physical activity, alcohol consumption, or stress. More than 90% of patients with episodic ataxia type 2 have oculomotor disorders such as downbeat nystagmus [119]. The vertigo symptoms are usually associated with degenerative cervical spine disease and may resemble BPPV due to proprio- ceptive abnormalities related to cervical spine dysfunction. However, cervical vertigo may be triggered by rotating the head relative to the body while upright, as opposed to the vertigo triggered by changes in head position relative to gravity in BPPV [21; 123]. CLINICAL MANAGEMENT Returning to the funnel analogy, a range of possible dizziness and vertigo etiologies (e.g., orthostatic hypotension, vasovagal syncope, head injury, medication side effects/toxicity, posterior circulation TIA/stroke, central paroxysmal positional vertigo, and cardiac arrhythmias) would be excluded or diagnosed. Certain patients would be treated, and others referred to spe- cialists or admitted to an ED. This would include all etiologies categorized as t-AVS. After vestibular disorders have been differentiated and diag- nosed, treatment selection can be divided into approaches that focus on symptom control, those specific to the underlying vestibular etiology, and those aimed at promoting recovery [124]. Therapeutic approaches broadly used across vestibular etiologies are discussed first, followed by treatments specific to acute, episodic, and chronic vestibular syndromes. COMMON PHARMACOTHERAPIES Most pharmacotherapies for dizziness or vertigo related to peripheral or central vestibular, cerebellar, or oculomotor disorders fall into one of seven groups, or the 7 As [61]: • Antiemetics • Anti-inflammatory
• Antidepressants • Anticonvulsants • Aminopyridines
Patients with severe nausea or vomiting greatly prefer non-oral administration [124]. As such, vestibular suppressants are usu- ally administered in non-oral routes initially for rapid symptom control, followed by oral medications. Vestibular Suppressant Medications As discussed, dizziness, vertigo, disequilibrium, and associ- ated symptoms can arise from diverse central or peripheral disturbances of vestibular function. By suppressing vestibular sensory input, vestibular suppressant medications can reduce conflicting sensory input, control undesirable perceptions, and diminish patient distress [13]. Many distressing vestibular-related symptoms are mediated by the vomiting center in the medulla. The vomiting center is activated through neurotransmitter release involving vestibular and CNS (histamine, acetylcholine), visceral (gut) (dopamine, serotonin), and chemoreceptor trigger zone (dopamine, sero- tonin) pathways [125]. These pathways are therapeutic targets of most vestibular suppressants, which are effectively used for symptomatic control in nearly all AVS or EVS subtypes, regardless of underlying etiology. These medications are vari- ously effective for controlling dizziness, vertigo, motion sick- ness, associated symptoms (e.g., nausea, vomiting, diarrhea), and patient distress or anxiety during episodes, which can be severe [21; 126]. Drug classes and agents commonly used as vestibular suppres- sants include antihistamines, benzodiazepines, scopolamine, dopamine antagonists, and ondansetron (Table 2). Antihis- tamines (e.g., meclizine, diphenhydramine, dimenhydrinate) block the release of histamine and acetylcholine and are espe- cially beneficial in vestibular-mediated nausea, vomiting, and motion sickness. Side effects include sedation, confusion, dry mouth, and urinary retention. Meclizine is preferred because it has minimal anticholinergic effects, causes less sedation, and is effective in the treatment of vertigo due to labyrinth dysfunction. It is also the drug of choice in pregnancy [124]. Diphenhydramine is recommended for the treatment of Ménière disease [127]. Benzodiazepines (e.g., diazepam, clonazepam, lorazepam) potentiate the inhibitory effects of the gamma-amino butyric acid system to produce anxiolytic, sedative, muscle-relaxant, and anticonvulsant effects. Benzodiazepines can be highly effective in vertigo unresponsive to antihistamines and for calming intensely distressed patients, but they are sedating and mainly used when antihistamines are inadequate [124]. They also may be used for patients requiring prophylaxis for canalith-repositioning procedures [21].
• Anti-Ménière • Anti-migraine
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Book Code: ANCCTX2027
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