Buspirone, a 5-hydroxytryptamine1A agonist, is active in cerebellar ataxia. Results of a double-blind drug placebo study in patients with cerebellar cortical atrophy.
Buspirone, a 5-hydroxytryptamine1A agonist, is active in cerebellar ataxia. Results of a double-blind drug placebo study in patients with cerebellar cortical atrophy.
复制标题
Buspirone 是一种 5-羟色胺 1A 激动剂，对小脑性共济失调具有活性。
DOI：
10.1001/archneur.1997.00550180059013
复制
发表时间：
1997
影响因子：
--
通讯作者：
B. Laurent
中科院分区：
文献类型：
--
作者：
P. Trouillas;J. Xie;P. Adeleine;D. Michel;A. Vighetto;J. Honnorat;R. Dumas;N. Nighoghossian;B. Laurent
客观化
为了建立盐酸丁螺环酮的抗共济失调作用，丁螺环酮是一种5-羟色胺1A(5-HT1A)激动剂，在具有相同明确单一疾病特征的同质患者组中，小脑皮质萎缩。
设置
大学共济失调研究中心。
方法
丁螺环酮与安慰剂在4个月期间的双盲随机研究。
病人
19名患者符合纳入标准；所有患者都完成了研究。在这19名患者中，9名接受了安慰剂治疗，10名接受了药物治疗。
主要结果衡量标准
用于动态和静态(“姿势”)小脑功能的半定量标尺；用于评估站姿、说话、书写和画图的标准测试中测量时间的定量临床测量；以及脚部中心压力的摆动路径和摆动区域的姿势图分析。主要终点是改善治疗后其中一个半定量共济失调评分的变化。次要终点是修改定量测量的变化--临床或体位描记。
结果
在意向处理分析中，主要终点，即治疗后共济失调运动评分的变化，显示出显著的改善。在次要终点中，双脚同时站立的最大时间也有显著改善。
结论
丁螺环酮对小脑萎缩患者的小脑性共济失调有积极作用。这些结果证实了丁螺环酮开放标签研究提出的数据。然而，这种影响是部分的，在临床上并不是主要的。这些药理学结果可能是由于5-羟色胺能机制，并证实了小脑性共济失调与5-羟色胺代谢之间的可能联系。
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.