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At least 37 records · Page 2Linked to original sources
PubMed1977

Betahistine hydrochloride (Serc) in cerebrovascular disease: a placebo-controlled study.

A double-blind, placebo-controlled, clinical study was performed to assess the effects of oral betahistine hydrochloride (Serc) on mental impairment and physical disability in patients with established cerebrovascular disease. Fifty-three patients were admitted to the study during 18 months. Forty-five patients completed the study. They received either betahistine 24 mg daily or placebo for eight weeks. Clinical assessments of general functional activity were done and a battery of nine mental function tests was administered pretreatment and at two-weekly intervals during therapy. The results were analysed statistically using distribution-free tests. Significant differences were demonstrated between betahistine and placebo at week 8 of treatment for associate learning, digit retention, general knowledge, orientation, sentence learning and simple arithmetic. These differences were consistently in favour of betahistine at or close to the 5% level of significance. The results of the remaining mental function tests showed no significant differences between betahistine and placebo, but trends were in favour of the former. General functional activity assessments also demonstrated that betahistine-treated patients were significantly better than those on placebo (P less than or equal to 0.05). No untoward side-effects were noted during the study.

Activities of Daily Living↗
PubMed2001

Histamine and betahistine in the treatment of vertigo: elucidation of mechanisms of action.

The aim of this review is to provide clinicians with a picture of the mechanisms by which: histamine and histaminergic agonists act on the vestibular system both peripherally and centrally; and histaminergic agonists and antagonists interfere with the recovery process after peripheral vestibular lesion. We have focused on betahistine, a structural analogue of histamine with weak histamine H(1) receptor agonist and more potent H(3) receptor antagonist properties, to review the currently available data on the role of the histaminergic system in the recovery process after peripheral vestibular deficits and the effects of histamine analogues in the clinical treatment of vertigo. This review provides new insights into the basic mechanisms by which betahistine improves vestibular compensation in animal models of unilateral vestibular dysfunction, and elucidates particularly the mechanisms of action of this substance at the level of the CNS. It is proposed that betahistine may reduce peripherally the asymmetric functioning of the sensory vestibular organs in addition to increasing vestibulocochlear blood flow by antagonising local H(3) heteroreceptors. Betahistine acts centrally by enhancing histamine synthesis within tuberomammillary nuclei of the posterior hypothalamus and histamine release within vestibular nuclei through antagonism of H(3) autoreceptors. This mechanism, together with less specific effects of betahistine on alertness regulation through cerebral H(1) receptors, should promote and facilitate central vestibular compensation. Elucidation of the mechanisms of action of betahistine is of particular interest for the treatment of vestibular and cochlear disorders and vertigo.

Animals↗
PubMed1997

Dose-dependent effect of betahistine on the vestibulo-ocular reflex: a double-blind, placebo controlled study in patients with paroxysmal vertigo.

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.

Adolescent↗
PubMed2003

Evaluation of betahistine for the prevention of seasickness: effect on vestibular function, psychomotor performance and efficacy at sea.

Betahistine was evaluated for the prevention of seasickness in a laboratory and sea study. The effect of 48 mg betahistine on the vestibulo-ocular reflex (VOR) and on psychomotor performance was evaluated in twelve young healthy subjects in a double-blind, placebo controlled, randomized, crossover design. The vestibulo-ocular reflex was evaluated by the Sinusoidal Harmonic Acceleration (SHA) test at frequencies of 0.01, 0.02, 0.04, 0.08 and 0.16 Hz. Psychomotor performance was assessed by both computerized and paper and pencil test batteries. No significant differences in VOR gain or phase were found between betahistine and placebo treatment for any of the frequencies tested. No significant differences were found between treatments for any of the psychomotor performance tests or other possible side effects. The effect of 48 mg betahistine on seasickness severity was evaluated in 83 subjects during a voyage in rough seas. Betahistine had a borderline non-statistically significant effect on the prevention of seasickness in comparison with placebo (p = 0.053), with no notable side effects. Although our results are insufficient to recommend betahistine as an anti-seasickness drug, further studies are required to determine its possible effectiveness in less provocative motion sickness situations.

Adult↗
PubMed2002

Fixed combination of cinnarizine and dimenhydrinate versus betahistine dimesylate in the treatment of Ménière's disease: a randomized, double-blind, parallel group clinical study.

In a randomized, double-blind clinical study, we evaluated the efficacy and tolerability of the fixed combination of cinnarizine, 20 mg, and dimenhydrinate, 40 mg (Arlevert [ARL]) in comparison to betahistine dimesylate (12 mg) in 82 patients suffering from Ménière's disease for at least 3 months and showing the characteristic triad of symptoms (paroxysmal vertigo attacks, cochlear hearing loss, and tinnitus). The treatment (one tablet three times daily) extended to 12 weeks, with control visits at 1, 3, 6, and 12 weeks after drug intake. The study demonstrated for both the fixed-combination ARL and for betahistine a highly efficient reduction of vertigo symptoms in the course of the 12 weeks of treatment; however, no statistically significant difference between the two treatment groups could be established. Similar results were found for tinnitus (approximately 60% reduction) and for the associated vegetative symptoms (almost complete disappearance). Vestibulospinal reactions, recorded by means of craniocorpography, also improved distinctly, with a statistically significant superiority of ARL versus betahistine (p < .042) for the parameter of lateral sway (Unterberger's test). The caloric tests (electronystagmography) showed only minor changes for both treatment groups in the course of the study. A statistically significant improvement of hearing function of the affected ear (p = .042) was found for the combination preparation after 12 weeks of treatment. The tolerability was judged by the vast majority of patients (97.5%) in both groups to be very good. Only one patient (betahistine group) reported a nonserious adverse event, and two betahistine patients did not complete the study. In conclusion, the combination preparation proved to be a highly efficient and safe treatment option for Ménière's disease and may be used both in the management of acute episodes and in long-term treatment. Efficacy and safety were found to be similar to the widely used standard therapy with betahistine.

Adult↗
PubMed2004

[Delirium in a 73-year-old man after many years of unwise use of betahistine].

A 73-year-old man was admitted because of delirium that had already persisted for 5 days. The physical examination and extensive tests did not reveal any somatic pathology. The only drug he used was betahistine, taken for several years because of supposed Ménière's disease. After withdrawal of betahistine and treatment with haloperidol the patient recovered completely within a few days. A new delirium was induced when, after discharge from the hospital, betahistine was restarted because of dizziness. There was again a complete remission after betahistine was stopped and haloperidol was restarted. Betahistine is not known to induce delirium, but an investigation in side-effects databases did reveal several cases in which delirium might have been present, even though the term was not actually used. In this case, delirium was possibly caused by the combination of an elevated betahistine plasma level and a damaged blood-brain barrier due to cerebral infarctions, which were revealed by CT and MRI.

Aged↗
PubMed1991

Betahistine dihydrochloride versus flunarizine. A double-blind study on recurrent vertigo with or without cochlear syndrome typical of Menière's disease.

This study was designed to compare the efficacy and safety of betahistine dihydrochloride and flunarizine. All patients included in this multicenter, double-blind, randomized trial showed a specific pattern of vertigo, i.e. recurrent paroxysmal vertigo with or without the cochlear symptoms typical of Meniere's disease. Fifty-five patients were treated for 2 months (28 in the betahistine group and 27 in the flunarizine group). Analysis of intra-group symptom changes demonstrated a greater efficacy for betahistine. Statistically significant decreases in duration and severity of attacks, and in the presence of vegetative symptoms were seen in the betahistine group after the first and second months of treatment, whereas in the flunarizine group this was the case only at the end of the first month of treatment. Furthermore in the betahistine group, statistically significant decreases occurred for the other major criteria, including number of attacks, evidence of vestibular dysfunction, and presence of cochlear symptoms. Adverse effects were similar to those reported in previous studies of both products: stomach pains only with betahistine, and drowsiness, asthenia, and depression with flunarizine.

Betahistine↗
PubMed1990

[Trimetazidine versus betahistine in Ménière's disease. A double blind method].

The efficacy and acceptability of trimetazidine (60 mg daily) in the treatment of Meniere's disease were compared with those of betahistine (36 mg daily) during a double-blind study spanning two months. Enrolled in the study were 45 patients (33 treated with trimetazidine, 23 with betahistine) presenting cochlear symptoms (vertigo, tinnitus, hearing loss) compatible with a diagnosis of Meniere's disease. Five patients dropped out of the study (3 in the trimetazidine group did not comply with the therapy and 2 in the betahistine group complained of poor response to the treatment) and were not taken into account in the final analysis, which therefore bore on 40 patients (19 receiving trimetazidine and 21 receiving betahistine). Trimetazidine was found to be significantly more effective than betahistine as far as the overall evolution of the ENT disease was concerned, yielding 79% and 57% improvement rates in each group, respectively (p = 0.027). Complete disappearance of the dizziness attacks was noted in 10 patients out of 19 in the trimetazidine group, versus 5/21 patients in the betahistine group (p = 0.06). There was no statistically significant difference between both treatments, as assessed from other clinical or audiometric criteria. Clinical acceptability was equally excellent in both treatment groups.

Adolescent↗
PubMed1978

Reduction of experimental myocardial infarct size by combined treatment with methylprednisolone sodium succinate and betahistine hydrochloride.

This laboratory and others have shown that methylprednisolone sodium succinate and betahistine hydrochloride can each reduce the size of experimental myocardial infarct in dogs at six hours. In light of the fact that these two agents probably act via different mechanisms, a study was carried out to determine if there would be cumulative effects of using these two agents together. Using a left anterior descending coronary artery ligation model to create an experimental myocardial infarction and an intracellular lactic dehydrogenase (LDH) stain to measure the infarct size, 66 dogs were studied. Nineteen dogs served as controls with no therapy; 20 received a continuous intravenous infusion of betahistine hydrochloride (0.24 mg/kg/min) for six hours following ligation; 10 dogs received methylprednisolone sodium succinate intravenously 30 mg/kg at one hour postligation; and 17 other dogs received betahistine hydrochloride intravenously (0.24 mg/kg/min) over six hours following ligation, plus methylprednisolone sodium succinate intravenously (30 mg/kg) at one hour postligation. At six hours, the combined treatment demonstrated no significant improvement over betahistine HCl alone (control, 16.0%; betahistine HCl, 11.4%; combined, 11.2% P less than 0.05). At 24 hours, only the combined treatment group demonstrated a significant infarct size reduction (control, 15.5%; methylprednisolone, 13.1%; betahistine--HCl, 14.2%; combined, 9.7%; P less than 0.0025). Other parameters that were evaluated and analyzed include mean aortic pressure, left atrial pressure, cardiac index, total peripheral resistance, arterial and coronary sinus pH, pCO2, pO2, hematocrit, O2 consumption, O2 content difference, and coronary sinus lactate and creatine phosphokinase (CPK). These results suggest a significant cumulative effect in reducing infarct size over that achieved with one agent alone; however, further studies are needed to determine the appropriate dosage and temporal factors.

Animals↗
PubMed2005

Effects of betahistine on the spatiotemporal response properties of vestibulospinal neurons to labyrinthine volleys.

Betahistine, a drug used in the treatment of vestibular disorders, speeds-up the recovery from hemilabyrinthectomy in experimental animals, likely through the activation of histamine receptors. In order to better understand the mechanism of action of this drug we investigated, in adult, urethane anesthetized rats, whether betahistine modifies the spatial (directional) and temporal response properties of vestibular nuclear neurons to the labyrinthine input, as well as the convergence of different labyrinthine signals on single units. Extracellular single-unit activity was recorded from the caudal, spinal-projecting region of the vestibular nuclei during tilt of the animal, before and after i.p. injection of betahistine. The two orthogonal directions of maximal and minimal response to tilt, as well as the corresponding gains were determined for each neuron. Betahistine reduced the maximal response gain of units showing larger basal values of this parameter and increased it in neurons with smaller basal values, while the minimal response gain was on the average raised. These changes led to a significant decrease in the spatial specificity of the neurons, suggesting that betahistine affects the process of spatiotemporal convergence on vestibular units, likely through a rearrangement of the various inputs. This could be related to the effect of the drug on vestibular compensation.

Acoustic Stimulation↗
PubMed2005

Dose- and duration-dependent effects of betahistine dihydrochloride treatment on histamine turnover in the cat.

Drugs interacting with the histaminergic system are currently used for vertigo treatment and it was shown in animal models that structural analogues of histamine like betahistine improved the recovery process after vestibular lesion. This study was aimed at determining the possible dose and duration effects of betahistine treatment on histamine turnover in normal adult cats, as judged by the level of messenger RNA for histidine decarboxylase (enzyme synthesizing histamine) in the tuberomammillary nuclei. Experiments were conducted on betahistine-treated cats receiving daily doses of 2, 5, 10, or 50 mg/kg during 1 week, 3 weeks, 2 months, or 3 months. The 1-week, 3-week, and 2- and 3-month treatments correspond to the acute, compensatory, and sustained compensatory stages of vestibular compensation, respectively. The lowest dose (2 mg/kg) given the longest time (3 months) was close to the dosage for vestibular defective patients. Data from the experimental groups were compared to control, untreated cats and to placebo-treated animals. The results clearly show that betahistine dihydrochloride administered orally in the normal cat interferes with histamine turnover by increasing the basal expression level of histidine decarboxylase mRNA of neurons located in the tuberomammillary nuclei of the posterior hypothalamus. The effects were both dose- and time-dependent. In conclusion, compensation of both static and dynamic deficits is subtended by long-term adaptive mechanisms that could be facilitated pharmacologically using betahistine dihydrochloride.

Analysis of Variance↗
PubMed2002

Betahistine dihydrochloride interaction with the histaminergic system in the cat: neurochemical and molecular mechanisms.

Drugs interfering with the histaminergic system facilitate behavioral recovery after vestibular lesion, likely by increasing histamine turnover and release. The effects of betahistine (structural analogue of histamine) on the histaminergic system were tested by quantifying messenger RNA for histidine decarboxylase (enzyme synthesizing histamine) by in situ hybridization and binding to histamine H(3) receptors (mediating, namely, histamine autoinhibition) using a histamine H(3) receptor agonist ([(3)H]N-alpha-methylhistamine) and radioautography methods. Experiments were done in brain sections of control cats (N=6) and cats treated with betahistine for 1 (N=6) or 3 (N=6) weeks. Betahistine treatment induced symmetrical changes with up-regulation of histidine decarboxylase mRNA in the tuberomammillary nucleus and reduction of [(3)H]N-alpha-methylhistamine labeling in both the tuberomammillary nucleus, the vestibular nuclei complex and nuclei of the inferior olive. These findings suggest that betahistine upregulates histamine turnover and release, very likely by blocking presynaptic histamine H(3) receptors, and induces histamine H(3) receptor downregulation. This action on the histaminergic system could explain the effectiveness of betahistine in the treatment of vertigo and vestibular disease.

Administration, Oral↗
PubMed2000

Effects of betahistine metabolites on frog ampullar receptors.

Previous studies have demonstrated that betahistine, an histamine-like substance used widely as an anti-vertigo drug, can decrease ampullar receptor resting discharge without affecting their mechanically evoked responses. Pharmacokinetic studies have shown that this drug is transformed, mainly at the hepatic level, into aminoethylpyridine (M1), hydroxyethylpyridine (M2), then excreted with the urine as pyridylacetic acid (M3). The goal of the present study was to investigate whether betahistine metabolites are also able to affect vestibular receptor activity. Results demonstrated that, in the range tested (10(-7)-10(-2) M), M2 and M3 exerted no effect, whereas M1, at concentrations higher than 10(-6) M, was able to reduce the resting discharge of ampullar receptors without affecting the evoked responses. M1 therefore exerts effects similar to those of betahistine on ampullar receptors. This might be of some clinical interest. On the basis of our data, the hypothesis may be put forward that the anti-vertigo action of betahistine is at first achieved by betahistine itself and then sustained by M1.

Animals↗
PubMed1998

Effects of betahistine on vestibular receptors of the frog.

Betahistine is widely used in the symptomatic treatment of peripheral and central vestibular disorders. However, its remains unknown whether the drug can act directly on inner ear sensory organs. To this end, the effects of betahistine (10(-7)-10(-2) M) were examined on isolated preparations of frog semicircular canal mounted in a double-celled bath which allowed drug administration both in the endolymphatic and in the perilymphatic fluid. The effects of betahistine were evaluated by recording ampullar receptor potentials and nerve firing rate both at rest and during mechanical stimulation of the isolated preparation. The results demonstrated that endolymphatic administration of betahistine had no effect, whereas its perilymphatic administration could reduce greatly ampullar receptor resting discharge but had little effect on mechanically evoked responses. This observation may explain the anti-vertigo effects of betahistine. Vertigo is normally due to uncontrolled changes in vestibular receptor resting discharge. It is therefore probable that any factor able to reduce the resting firing rate of vestibular receptors and, in consequence, its variations, may have an anti-vertigo action.

Animals↗
PubMed2006

[Efficacy of Betahistine Mesilate combined with Flunarizine Hydrochloride for treating tinnitus].

OBJECTIVE: To determine whether Betahistine mesilate is effective in treating tinnitus. METHODS: Randomized, prospective, double-blind, controlled trial was used in our study. The study group consisted of 60 adult patients who consulted our outpatient clinic complaining of subjective tinnitus, excluded objective tinnitus and the patients who had tinnitus caused by obvious diseases, such as outer and middle ear diseases. Thirty patients were given Betahistine mesilate and Flunarizine Hydrochloride as an experimental group, 30 patients were given Vitamin B6 and Flunarizine Hydrochloride as a control group. After a week of treatment the efficacy of the medicines in two groups was observed. Tinnitus questionnaire was performed before the treatment, and pure tone audiogram, tinnitus pitch and loudness matching were performed both in the beginning and at the end of the treatment. RESULTS: Completion of treatment, tinnitus loudness matching assessment showed that the efficacy of the Betahistine mesilate group was better then the control group. The efficacy of treatment was respectively 65.5% by per protocol (PP) and 63.3% by intend to treat (ITT) in the Betahistine mesilate group and 39.3% by PP and 36.7% by ITT in the control group. The difference of tinnitus loudness improvement rate between the experimental group and control group was statistically significant. But the subjective tinnitus improvement rate showed no difference between two groups. There were not serious side effects in the two groups. CONCLUSIONS: Betahistine mesilate can be a choice for tinnitus treatment clinically. Further studies of larger series and placebo-controlled trial are needed.

Adolescent↗
PubMed1990

[Trimetazidine versus betahistine in vestibular vertigo. A double blind study].

The efficacy of trimetazidine (60 mg/day) in vertigo was compared with that of betahistine (24 mg/day) in a three-month double-blind study. Included in the study were only patients with peripheral vertigo associated or not with tinnitus or hearing loss, and excluded were those presenting with symptoms related to retrocochlear or central disease. Out of the 40 patients enrolled, 20 suffered from Meniere's disease; 4 patients either dropped out of the study or were non-compliant to therapy and could not be taken into account in the final analysis, which bore on 36 patients (18 treated by trimetazidine and 18 with betahistine). There were no dropouts in the Meniere's disease subgroup (10 receiving trimetazidine and 10 receiving betahistine). Results revealed a better response to therapy with trimetazidine in patients suffering from vertigo, and this was particularly true of the Meniere's disease subgroup (p less than 0.025). Moreover, in the latter subgroup, all patients treated with trimetazidine fully recovered from vertigo spells, while these disappeared completely only in 4 of the patients administered betahistine (p less than 0.005). There was no noticeable difference between the two treatment groups as regards the evolution of the accompanying symptoms and the audiometric or vestibular test results. Clinical acceptability was equally excellent in both treatment groups. Overall, this study allowed to confirm the therapeutical efficacy of trimetazidine in the management of vertigo, as well as establishing the clinical advantage of trimetazidine over betahistine in patients suffering from Meniere's disease.

Adult↗
PubMed1982

[Long-term therapy of Ménière's disease. Comparison of the effects of betahistine dihydrochloride and hydrochlorothiazide].

During the last few years betahistine-dihydrochloride has been used extensively in the conservative treatment of M. Ménière. The question has arisen as to whether betahistine-dihydrochloride is more effective than diuretics. The effect of betahistine-dihydrochloride was compared to that of hydrochlorothiazide on 32 M. Ménière-patients. The patients were initially kept under observation for 3 months without medication apart from symptomatic anti-vertigo agents. The patients were then assigned to 2 groups each of 16 subjects and received either 3 X 8 mg betahistine-dihydrochloride or 3 X 25 mg hydrochlorothiazide for 6 months under double-blind conditions. Before and during treatment subjective symptoms such as vertigo, attacks of dizziness, tinnitus, sensation of blockage in the ear and general well-being were assessed at 4-weekly intervals. Apart from this the objective symptoms as measured by pure tone audiograms, Frenzel-test and electronystagmography were recorded. At the moment betahistine-dihydrochloride seems to be the drug of choice for Ménière-patients with a fluctuating auditory threshold. During the 6 months treatment period an impressive reduction in the frequency, severity and duration of the attacks of vertigo as well as an improvement in the general condition was found in all patients. In contrast the diuretic hydrochlorothiazide seemed to show a distinct therapeutic effect on vertigo and general well-being principally during the first few months of treatment in patients with a constant auditory threshold.

Audiometry, Pure-Tone↗
PubMedDate not supplied

Rheoencephalographic and other studies of betahistine in humans: I. The cerebral and peripheral circulatory effects of single doses in normal subjects.

Two groups of six young normal male subjects were studied by an improved form of rheoencephalography (intracranial rheoncephalography), by photoplethysmography, and by impedance plethysmography to investigate the possible effects of single doses of betahistine hydrochloride (SERC) and placebo on the normal human cranial, cerebral, scalp, and calf circulations. Two subjects participated in both groups. The results of the two studies were similar and were combined for this presentation. One subject reported slight transient faintness and visual blurring after 20 mg of the drug. No other adverse or side effects were encountered. The results show that the drug causes definite, strong, reproducible, and dose-related responses in the studied circulations, typically those of decreases in their waveform amplitudes and pulse propagation times. Betahistine hydrochloride thus acts as a potent cerebral and peripheral microcirculatory vasodilator in normal humans when given orally. Split-dose studies indicate that responses followed each dose and that the second response was superimposed on the first. The value of using betahistine hydrochloride in overlapping doses is suggested. Atypical cranial, cerebral, scalp, and calf amplitude increases were found in some high-dosage (16-mg) trials. These increases may indicate that betahistine hydrochloride can also act as an arterial vasodilator in sufficiently high dosage, but they equally may indicate that sufficiently profound microcirculatory vasodilatation can elicit secondary arterial circulatory increases.

Adult↗