cinnarizine and Body-Weight

Topics: Adult; Body Weight; Calcium Channel Blockers; Cinnarizine; Clinical Trials as Topic; Double-Blind Method; Female; Flunarizine; Humans; Male; Middle Aged; Migraine Disorders; Pizotyline; Random Allocation; Thiophenes

In order to assess the effects of flunarizine in long-term prophylaxis of common migraine, 120 subjects (90 female and 30 male) were treated with 10 mg at bedtime and followed-up for two years. The effectiveness of the drug was assessed by investigating the variations of the Headache Index (HI) and of the intake of analgesics. The patients considered responders were those with an at least 60% reduction of the HI compared with the baseline value. To assess side effects, on each follow-up examination the patients were weighed and submitted to the Hamilton Rating Scale for Depression, Toulouse-Pieron test for attention, and arousal test. By the third month of therapy, the average monthly HI had decreased from a baseline value of 16.5 +/- 7.0 to 7.5 +/- 4.2. Also by the third month, 60 subjects had proved responders and 50 non-responders; 10 had dropped out of the study because of side effects or for other reasons. The only statistically significant differences between responders and non-responders were in the baseline HI, which was higher among responders, and in the baseline intake of analgesics, which was higher in non-responders.

Topics: Adolescent; Adult; Body Weight; Calcium Channel Blockers; Cinnarizine; Clinical Trials as Topic; Female; Flunarizine; Follow-Up Studies; Humans; Male; Middle Aged; Migraine Disorders; Patient Compliance; Piperazines

The effects of flunarizine administration (10 mg/day, at bed time) were studied in 120 common migraine patients who were followed for 24 months with quarterly controls. Besides headache index (HI) and analgesic use, other variables were monitored, such as arousal (Tolouse Pieron test), mood (Hamilton rating scale for depression), sleep/wake (hrs) and body weight. The study was open-type and after the 6th month control some responder (R) cases (HI reduction greater than or equal to 60%) presenting HI scores less than or equal to 4 could continue the survey off-treatment. The percentage of R cases was 54.5% at the 3rd month, a figure that further increased up to 72% by the 9th month; relapses on treatment were not observed and rebound-headache occurred in 1/4 of R cases let off-treatment. Lower (p less than 0.05) baseline HI values characterized non-responders. Side-effects not requiring withdrawal were drowsiness (42% within the 1st month) and weight gain (mean 7.9 +/- 6.9 kg) in 54% of the cases, while a retarded type depression was the most frequent cause of drop-out from trial (7.5%). The results, while confirming the high prophylactic activity of flunarizine in common migraine, stress the importance of clinical long-term survey of side-effects using antimigraine drugs and suggest the need for further investigations about flunarizine effects on CNS.

Topics: Adolescent; Adult; Body Weight; Calcium Channel Blockers; Cinnarizine; Clinical Trials as Topic; Depression; Female; Flunarizine; Follow-Up Studies; Humans; Male; Middle Aged; Migraine Disorders; Piperazines; Sleep Stages

Seventeen patients with common or classical migraine were prophylactically treated with 10 mg flunarizine daily whereas 18 patients received a placebo during a 3-month randomized double-blind study. Globally, flunarizine was significantly superior to the placebo. Only three patients felt that flunarizine had been useless and the investigator also guessed the medication code correctly in all but these three cases. Beyond a 1-month starting period the frequency of the migraine attacks became significantly lower with flunarizine than with the placebo. The mean monthly number of attacks was respectively 3.3 and 3.8 before the study and 1.4 and 3.2 during the study. The limited scale of the trial precludes a judgment as to whether one type of migraine would respond better to flunarizine than the other. Side-effects were negligible, weight gain being considered rather a secondary gain than an untoward consequence of treatment.

Topics: Body Weight; Calcium Channel Blockers; Cinnarizine; Clinical Trials as Topic; Double-Blind Method; Flunarizine; Humans; Migraine Disorders; Piperazines; Vasodilator Agents

Cinnarizine, a calcium antagonist that produces parkinsonism in humans, induces behavioural changes such as alopecia, buco-lingual dyskinesia and reduction of motor activity in female parkin knock out (PK-KO) mice but not in wild-type (WT) controls. PK-KO mice have high striatal dopamine levels and increased dopamine metabolism in spite of low reduced tyrosine hydroxylase protein. Cinnarizine, which blocks dopamine receptors and increases dopamine release, further increased dopamine metabolism. PK-KO mice increased GSH levels as a compensatory mechanism against enhanced free radical production related to acceleration of dopamine turnover. Neuronal markers, such as beta-tubulin slightly increased in PK-KO and furthermore with cinnarizine. Astroglial markers were decreased in PK-KO mice, and this effect was potentiated by cinnarizine, suggesting abnormal glia in these animals. Microglia was hyperactivated in PK-KO midbrain, suggesting inflammation in these animals. Proapoptotic proteins were increased by cinnarizine and, to a lesser extent, in PK-KO mice. Our data indicate that mutation of parkin is a risk factor for drug-induced parkinsonism.

Topics: Analysis of Variance; Animals; Antigens, Differentiation; bcl-2-Associated X Protein; bcl-X Protein; Behavior, Animal; Biogenic Monoamines; Blotting, Western; Body Weight; Brain Chemistry; Calcium Channel Blockers; Chromatography; Cinnarizine; Drinking; Eating; Gene Expression Regulation; Glial Fibrillary Acidic Protein; Glutathione; Humans; Mice; Mice, Inbred C57BL; Mice, Knockout; Motor Activity; Parkinsonian Disorders; Proto-Oncogene Proteins c-bcl-2; Tyrosine 3-Monooxygenase; Ubiquitin-Protein Ligases

Verapamil, Prenylamine and, to a lesser extent, Cinnarizine were highly efficient in preventing the development or reducing the severity of heart lesions in cardiomyopathic hamster of the UM-X7.1 line. The calcium antagonistic compounds did not protect against the skeletal muscle changes already present at the time when treatment was initiated. The cardiac lesions were also significantly diminished in frequency and severity by a low calcium diet and in apparent contradiction, by parenteral administration of calcium gluconate. The relation of these electrolytes and creatine phosphokinase is not yet fully understood but suggests that a primary defect in muscles cell membranes may be responsible for hereditary cardiomyopathy in hamsters.

Topics: Animals; Body Weight; Calcium; Cardiomyopathies; Cell Membrane; Cinnarizine; Creatine Kinase; Cricetinae; Electrolytes; Female; Gluconates; Male; Muscles; Myocardium; Prenylamine; Verapamil