Svetel M, Vojvodić N, Filipović S R, Dragasević N, Sternić N, Kostić V S
Institute of Neurology, Clinical Centre of Serbia, Belgrade.
Srp Arh Celok Lek. 1999 Sep-Oct;127(9-10):312-5.
Ataxia is defined as a disturbance which, quite independent of any motor weakness, alters direction and extent of voluntary movement and impairs the sustained voluntary of reflex muscle contraction necessary for maintaining postiue and equilibrium [1]. Since pathophysiological basis of cerebeller ataxia is still not completely clear, the current therapeutic attempts are mainly symptom-oriented [3]. One possible approach could be a modification of potentially involved neurotransmitter systems of the cerebellum, where particularly interesting is the serotonergic system. However, attempts with levorotatory form of tryptophan (5-HT precursors) proved to be ineffective [4, 5]. Since receptors in the cerebellum are mainly of 5-HTIA subtype, the use of specific agonists might be a more reasonable therapy [6]. The study initially involved 11 patients, but only 9 completed the protocol due to unfavorable side effects. Our open label prospective study lasted for 15 weeks. The patients were tested before the beginning of the treatment (initial visit), at 7th (first visit) and 11th week (second visit) of continuous therapy, and eventually at 15th week (final visit). The daily dose was 40 mg at the first and 60 mg at the second visit. We used the evaluation scale gurposed for cerebellar functions testing (speech, gait, coordination and ocular movements). Significant improvement of cerebellar ataxia in patients under buspiron therapy has been noted. We analyzed the results obtained from our 9 patients (4 females and 5 males), of which 6 patients suffered from cerebellar degeneration, one from multiple sclerosis, one from Ramsey-Hunt syndrome, and one from pontine myelinolysis. At the initial visit the patient score was 18.9 (SD = 7.3), subsequently, at the iirst visit the score was 15.4 (SD = 8), while the second visit yielded the score of 12.9 (SD = 8.2), and finally, after a two-weeks lasting wash-out period, it was 17.7 (SD = 7.1) (Table 1). It was found that patients exhibiting mild ataxia showed a better improvement in comparison to the patients who had marked cerebellar symptoms at the beginning of the treatment (Table 2). In conclusion, our prospective study shows that buspiron treatment improves cerebellar symptoms.
共济失调被定义为一种紊乱，它完全独立于任何运动无力，改变自主运动的方向和幅度，并损害维持姿势和平衡所需的反射性肌肉持续自主收缩[1]。由于小脑共济失调的病理生理基础仍不完全清楚，目前的治疗尝试主要以症状为导向[3]。一种可能的方法可能是对小脑潜在涉及的神经递质系统进行调节，其中特别有趣的是血清素能系统。然而，左旋色氨酸（5-羟色胺前体）的尝试被证明是无效的[4,5]。由于小脑中的受体主要是5-HTIA亚型，使用特异性激动剂可能是一种更合理的治疗方法[6]。该研究最初涉及11名患者，但由于不良副作用，只有9名患者完成了方案。我们的开放标签前瞻性研究持续了15周。在治疗开始前（初次就诊）、持续治疗的第7周（第一次就诊）和第11周（第二次就诊）以及最终在第15周（末次就诊）对患者进行测试。第一次就诊时的每日剂量为40毫克，第二次就诊时为60毫克。我们使用了专门用于小脑功能测试（言语、步态、协调和眼球运动）的评估量表。已注意到接受丁螺环酮治疗的患者小脑共济失调有显著改善。我们分析了从9名患者（4名女性和5名男性）获得的结果，其中6名患者患有小脑变性，1名患有多发性硬化症，1名患有拉姆齐-亨特综合征，1名患有脑桥髓鞘溶解症。初次就诊时患者评分为18.9（标准差=7.3），随后，第一次就诊时评分为15.4（标准差=8），第二次就诊时评分为12.9（标准差=8.2），最后，在为期两周的洗脱期后，评分为17.7（标准差=7.1）（表1）。发现与治疗开始时患有明显小脑症状的患者相比，表现为轻度共济失调的患者改善更好（表2）。总之，我们的前瞻性研究表明丁螺环酮治疗可改善小脑症状。
