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June 1997

Buspirone, a 5-Hydroxytryptamine1A Agonist, Is Active in Cerebellar Ataxia: Results of a Double-blind Drug Placebo Study in Patients With Cerebellar Cortical Atrophy

Author Affiliations

From the Ataxia Research Center and Cerebrovascular Unit (Drs Trouillas, Xie, Honnorat, and Nighoghossian), the Neuro-ophthalmology Service (Dr Vighetto), and the Biostatistical Unit (Dr Adeleine), Hôpital Neurologique and Alexis Carrel School of Medicine, Claude Bernard University, Lyon, France; the Neurology Service, Bellevue Hospital, Saint-Etienne, France (Drs Michel and Laurent); and the Neurology Service, Dijon Hospital, Dijon, France (Dr Dumas).

Arch Neurol. 1997;54(6):749-752. doi:10.1001/archneur.1997.00550180059013

Objective:  To establish the antiataxic effect of buspirone hydrochloride, a serotonergic 5-hydroxytryptamine1A (5-HT1A) agonist, in a homogenous group of patients characterized by the same well-defined single condition, cerebellar cortical atrophy.

Setting:  University ataxia research center. Methods: Double-blind randomized study of buspirone vs placebo during a 4-month period.

Patients:  Nineteen patients met the inclusion criteria; all completed the study. Of these 19 patients, 9 were treated with placebo and 10 were treated with the drug.

Main Outcome Measures:  A semiquantitative scale for kinetic and static ("postural") cerebellar functions; quantitative clinical measurements measuring 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 scores. The secondary end points were modification of the changes of quantitative 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. Among secondary end points, the maximum time of standing with feet together also was significantly improved.

Conclusions:  Buspirone is active in cerebellar ataxia of patients with cerebellar atrophy. These results confirm the data suggested by open-label studies with buspirone. However, the effect is partial and not clinically major. These pharmacological results might be due to serotonergic mechanisms and confirm a possible link between cerebellar ataxia and the metabolism of serotonin.

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