Vestibular Training for Benign Paroxysmal Positional Vertigo: Its Efficacy in Comparison With Antivertigo Drugs

Fujino, Akito; Tokumasu, Kohji; Yosio, Satosi; Naganuma, Hideaki; Yoneda, Satosi; Nakamura, Ken

doi:10.1001/archotol.1994.01880290013003

Cited by 45 publications

(27 citation statements)

References 10 publications

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“…Clinicians may prescribe medications to either 1) reduce the spinning sensations of vertigo or 2) reduce the accompanying motion sickness symptoms. However, none of these vestibular suppressants is as effective as the CRMs for BPPV, and cannot be used as a substitute for the repositioning maneuvers 88,89…”

Section: Treatmentsmentioning

confidence: 99%

Benign Paroxysmal Positional Vertigo

2010

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Benign paroxysmal positional vertigo (BPPV) is characterized by brief recurrent episodes of vertigo triggered by changes in head position. BPPV is the most common etiology of recurrent vertigo and is caused by abnormal stimulation of the cupula by free-floating otoliths (canalolithiasis) or otoliths that have adhered to the cupula (cupulolithiasis) within any of the three semicircular canals. Typical symptoms and signs of BPPV are evoked when the head is positioned so that the plane of the affected semicircular canal is spatially vertical and thus aligned with gravity. Paroxysm of vertigo and nystagmus develops after a brief latency during the Dix-Hallpike maneuver in posterior-canal BPPV, and during the supine roll test in horizontal-canal BPPV. Positioning the head in the opposite direction usually reverses the direction of the nystagmus. The duration, frequency, and symptom intensity of BPPV vary depending on the involved canals and the location of otolithic debris. Spontaneous recovery may be expected even with conservative treatments. However, canalithrepositioning maneuvers usually provide an immediate resolution of symptoms by clearing the canaliths from the semicircular canal into the vestibule.

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Section: Treatmentsmentioning

confidence: 99%

Benign Paroxysmal Positional Vertigo

2010

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“…Although the majority of placebo-controlled, dou-ble-blind studies show that betahistine is effective in the treatment of vertigo, this is not a universal finding (7)(8)(9)(10)(11)(12)(13)(14)(15). The same holds true for the inhibitory effect of betahistine on nystagmus induced by vestibular stimulation (7,11).…”

Section: Int'roductionmentioning

confidence: 99%

Dose-Dependent Effect of Betahistine on the Vestibulo-Ocular Reflex: A Double-Blind, Placebo Controlled Study in Patients with Paroxysmal Vertigo

Kingma

Bonink

Meulenbroeks

et al. 1997

Acta Oto-Laryngologica

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The effect of betahistine on the vestibulo-ocular reflex (VOR) was assessed in 12 patients suffering from paroxysmal vertigo. Only patients who responded to betahistine treatment were admitted to the study in order to increase the probability of quantifying the effect of the drug on vestibular function. Patients received placebo or 16, 32 or 64 mg betahistine orally under double-blind conditions. Vestibular function was tested a few minutes before intake, and 1, 2, 3, 4, 6 and 8 h after intake, by torsion swing stimulus in the dark, visuo-vestibular interaction upon simultaneous visual and vestibular stimulation and high frequency passive head shaking. Betahistine significantly affected the velocity gain of low and high frequency VOR. The reduction in gain was maximal about 4 h after administration of the 16 mg dose in the torsion swing experiment and the 32 mg dose in the head shaking experiment. Above these doses, the effect on velocity gain was less marked. Betahistine had no effect on visuo-vestibular interaction or nystagmus duration during low frequency torsion. These results suggest that betahistine has a complex action on H3 receptors and that the site of action may be in the vestibular nuclei.

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“…BPPV may be originated from any semicircular canal, but the posterior canal is the most frequently affected in the majority of cases. The natural clinical course of BPPV is self-limited and takes from weeks to months, and it normally does not respond to antivertigo drugs [18][19][20] . Advocated treatments are various: maneuvers of canalith repositioningEpley maneuver is the most common one 21 , liberatory maneuvers, Semont 22 maneuver, vestibular habituation training [23][24][25] , and surgical treatments such as singular neurectomy or occlusion of posterior semicircular canal that are reserved to cases non-responsive to clinical treatment 26,27 .…”

Section: Introductionmentioning

confidence: 99%

Restrições posturais não interferem nos resultados da manobra de reposição canalicular

Simoceli

Bittar

Greters

2005

Rev. Bras. Otorrinolaringol.

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Beni gn Paroxysmal Positional Vertigo (BPPV) is a frequentcause of dizziness and despite of the excellent results with its treatment, there is some controversy about management. Aim: To assess the efficacy of Epley Maneuver with and without post-maneuver restrictions. Study Design: Prospective randomized. Material and Method: Fifty patients presenting BPPV of the posterior semicircular canal, treated with Epley Maneuver and divided into two groups: study group -23 patients -with post-maneuver restrictions, and control group -27 patients -without post-maneuver restrictions. Results: No significant difference was found between the studied and the control group. Conclusion: Post-maneuver restrictions do not influence the efficacy of Epley Maneuver for BPPV management.

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Vestibular Training for Benign Paroxysmal Positional Vertigo: Its Efficacy in Comparison With Antivertigo Drugs

Cited by 45 publications

References 10 publications

Benign Paroxysmal Positional Vertigo

Benign Paroxysmal Positional Vertigo

Dose-Dependent Effect of Betahistine on the Vestibulo-Ocular Reflex: A Double-Blind, Placebo Controlled Study in Patients with Paroxysmal Vertigo

Restrições posturais não interferem nos resultados da manobra de reposição canalicular

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