RESUMO
There have been few investigations on the epidemiology, etiology, and medical management of acute unilateral vestibulopathy (AUV). Short-term pharmaceutical resolutions include vestibular symptomatic suppressants, anti-emetics, and some cause-based therapies. Anticholinergics, phenothiazines, antihistamines, antidopaminergics, benzodiazepines, and calcium channel antagonists are examples of vestibular suppressants. Some of these medications may show their effects through multiple mechanisms. In contrast, N-acetyl-L-leucine, Ginkgo biloba, and betahistine improve central vestibular compensation. Currently, AUV pathophysiology is poorly understood. Diverse hypotheses have previously been identified which have brought about some causal treatments presently used. According to some publications, acute administration of anti-inflammatory medications may have a deleterious impact on both post-lesional functional recovery and endogenous adaptive plasticity processes. Thus, some authors do not recommend the use of corticosteroids in AUV. Antivirals are even more contentious in the context of AUV treatment. Although vascular theories have been presented, no verified investigations employing anti-clotting or vasodilator medications have been conducted. There are no standardized treatment protocols for AUV to date, and the pharmacological treatment of AUV is still questionable. This review addresses the most current developments and controversies in AUV medical treatment.
RESUMO
BACKGROUND: Benign paroxysmal positional vertigo (BPPV) is a common cause of acute dizziness. Medication use for its treatment remains common despite guideline recommendations against their use. OBJECTIVES: The objective was to evaluate the efficacy and safety of vestibular suppressants in patients with BPPV compared to placebo, no treatment, or canalith repositioning maneuvers (CRMs). METHODS: We searched MEDLINE, Cochrane, EMBASE, and ClinicalTrials.gov from inception until March 25, 2022. for randomized controlled trials (RCTs) comparing antihistamines, phenothiazines, anticholinergics, and/or benzodiazepines to placebo, no treatment, or a CRM. RESULTS: Five RCTs, enrolling 296 patients, were included in the quantitative analysis. We found that vestibular suppressants may have no effect on symptom resolution at the point of longest follow-up (14-31 days in four studies) when evaluated as a continuous outcome (standardized mean difference -0.03 points, 95% confidence interval [CI] -0.53 to 0.47). Conversely, CRMs may improve symptom resolution at the point of longest follow-up as a dichotomous outcome when compared to vestibular suppressants (relative risk [RR] 0.63, 95% CI 0.52 to 0.78). Vestibular suppressants had an uncertain effect on symptom resolution within 24 h (mean difference [MD] 5 points, 95% CI -16.92 to 26.94), repeat emergency department (ED)/clinic visits (RR 0.37, 95% CI 0.12 to 1.15), patient satisfaction (MD 0 points, 95% CI -1.02 to 1.02), and quality of life (MD -1.2 points, 95% CI -2.96 to 0.56). Vestibular suppressants had an uncertain effect on adverse events. CONCLUSIONS: In patients with BPPV, vestibular suppressants may have no effect on symptom resolution at the point of longest follow-up; however, there is evidence toward the superiority of CRM over these medications. Vestibular suppressants have an uncertain effect on symptom resolution within 24 h, repeat ED/clinic visits, patient satisfaction, quality of life, and adverse events. These data suggest that a CRM, and not vestibular suppressants, should be the primary treatment for BPPV.