BUSPIRONE, A 5-HYDROXYTRYPTAMINE(1A) AGONIST, IS ACTIVE IN CEREBELLAR-ATAXIA - RESULTS OF A DOUBLE-BLIND DRUG PLACEBO STUDY IN PATIENTS WITH CEREBELLAR CORTICAL ATROPHY

Citation
P. Trouillas et al., BUSPIRONE, A 5-HYDROXYTRYPTAMINE(1A) AGONIST, IS ACTIVE IN CEREBELLAR-ATAXIA - RESULTS OF A DOUBLE-BLIND DRUG PLACEBO STUDY IN PATIENTS WITH CEREBELLAR CORTICAL ATROPHY, Archives of neurology, 54(6), 1997, pp. 749-752
Citations number
42
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
54
Issue
6
Year of publication
1997
Pages
749 - 752
Database
ISI
SICI code
0003-9942(1997)54:6<749:BA5AIA>2.0.ZU;2-U
Abstract
Objective: To establish the antiataxic effect of buspirone hydrochlori de, a serotonergic 5-hydroxytryptamine(1A) (5-HT1A) agonist, in a homo genous group of patients characterized by the same well-defined single condition, cerebellar cortical atrophy. Setting: University ataxia re search center. Methods: Double-blind randomized study of buspirone vs placebo during a dr-month period. Patients: Nineteen patients met the inclusion criteria; all completed the study. Of these 19 patients, 9 w ere treated with placebo and 10 were treated with the drug. Main Outco me Measurer: A semiquantitative scale for kinetic and static (''postur al'') cerebellar functions; quantitative clinical measurements measuri ng time in standard tests that evaluated stance, speech, writing, and drawing; and posturographic analysis of the sway path and sway area of the center-of-foot pressure. The primary end point was improvement of the posttherapeutic change of one of the semiquantitative ataxic scor es. The secondary end points were modification of the changes of quant itative measures-clinical or posturographic. Results: In intention-to- treat analysis, a significant improvement of the primary end point, ie , the posttherapeutic change of the ataxic kinetic score, was shown. A mong secondary end points, the maximum time of standing with feet toge ther also was significantly improved. Conclusions: Buspirone is active in cerebellar ataxia of patients with cerebellar atrophy. These resul ts confirm the data suggested by open-label studies with buspirone. Ho wever, the effect is partial and not clinically major. These pharmacol ogical results might be due to serotonergic mechanisms and confirm a p ossible link between cerebellar ataxia and the metabolism of serotonin .