Betahistine in the treatment of Ménière's disease

Abstract

Ménière's disease and related disease of the vestibular system are common and debilitating. Current therapy is multi-modal and includes drug therapy and lifestyle adaptations. Unfortunately many of the drugs used in treatment (particularly those used to control nausea) are sedative and hamper the process of vestibular compensation. Although betahistine (Serc®), BetaSerc®); Solvay Pharmaceuticals) is the mainstay of drug treatment in these illnesses, its efficacy has not, until recently, been evaluated to modern standards. Betahistine is an analog of histamine with weak agonist properties at histamine H1 receptors and more potent anatgonistic effects at histamine H3 receptors. Growing evidence suggests that the mechanism of action of betahistine lies in the central nervous system and in particularly in the neuronal systems involved in the recovery from process after vestibular loss. The histaminergic neurones of the tuberomamillary and vestibular nuclei are implicated. In recent years the clinical efficacy of betahistine has been demonstrated in double-blind, randomized, placebo, and active controlled studies in adequate numbers of patients. Although the results of comparative studies between betahistine and other drugs (flunarizine, cinnarizine, and cinnarizine + dimenhydrate) are equivocal, the efficacy of betahistine is now clear.

Keywords: Ménière’s disease; betahistine; vestibular disorders.

Figure 1

Mean recovery curves illustrating maximal performance of the cat on the rotating beam. Results are expressed in percent of the preoperative maximal performance (on the ordinates) as a function of the postoperative time in days (on the abscissae). The betahistine groups (50 mg/kg and 100 mg/kg) are shown as solid squares and triangles, respectively, and the control group as open circles. Standard errors of the mean are shown as vertical lines. Note the acceleration of the recovery time under betahistine treatment compared with the controls, and the shortened time required to achieve a full compensation (3 weeks instead of 6 weeks).

Figure 2

Quantification of the histidine decarboxylase (HDC) mRNA labeled surface in the right (hatched columns) and left (solid columns) tuberomammillary (TM) nuclei for the two groups of betahistine-treated cats compared with the control, untreated cats (open columns). Note that HDC mRNA labeled surface is significantly increased in the TM nuclei of betahistine-treated cats. ** p < 0.0001.

Figure 3

Percentage improvement in frequency of vertigo attacks – Menière’s disease. Reproduced with permission from Mira E, Guidetti G, Ghilardi L, et al 2003. Betahistine dihydrochloride in the treatment of peripheral vestibular vertigo. Eur Arch Otorhinolaryngol, 260:73–7. Copyright © 2003 Springer.

Figure 4

Percentage improvement in frequency of vertigo attacks – peripheral paroxysmal vertigo. Reproduced with permission from FMira E, Guidetti G, Ghilardi L, et al 2003. Betahistine dihydrochloride in the treatment of peripheral vestibular vertigo. Eur Arch Otorhinolaryngol, 260:73–7. Copyright © 2003 Springer.