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
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
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
.