盐酸金刚烷胺治疗遗传性共济失调：一项双盲研究。
Amantadine hydrochloride treatment in heredodegenerative ataxias: a double blind study.
作者信息
Botez M I, Botez-Marquard T, Elie R, Pedraza O L, Goyette K, Lalonde R
机构信息
Neurology Service, Hôtel-Dieu de Montréal, Québec, Canada.
出版信息
J Neurol Neurosurg Psychiatry. 1996 Sep;61(3):259-64. doi: 10.1136/jnnp.61.3.259.
OBJECTIVE
A group of 27 patients with Friedreich's ataxia and another group of 30 patients with olivopontocerebellar atrophies were each randomly divided into two subgroups, one receiving placebo and the other amantadine hydrochloride (AH; 200 mg daily) for three to four months.
METHODS
The effect of double blind treatment was evaluated by simple visual and auditory reaction time (RT) and movement time (MT) for both right and left hands.
RESULTS
The subgroup with olivopontocerebellar atrophies receiving AH showed significant improvement on seven out of eight variables studied by analysis of covariance. In patients with Friedreich's ataxia, improvement was definitely less. Treatment remained contraindicated for those with cardiomyopathies or drug intolerance.
CONCLUSION
The rationale of AH use in heredodegenerative ataxias can be explained by its replacement effect (dopamine release) and by direct involvement of N-methyl-D-aspartate (NMDA) in glutamate mediated neurotoxicity in cerebellar granular cells; memantine, an AH analogue, is a potent blocker of NMDA receptors.
目的
将27例弗里德赖希共济失调患者和另一组30例橄榄体脑桥小脑萎缩患者分别随机分为两个亚组，一组接受安慰剂，另一组接受盐酸金刚烷胺（AH；每日200毫克）治疗三至四个月。
方法
通过简单的视觉和听觉反应时间（RT）以及左右手的运动时间（MT）来评估双盲治疗的效果。
结果
接受AH治疗的橄榄体脑桥小脑萎缩亚组在通过协方差分析研究的八个变量中的七个上显示出显著改善。在弗里德赖希共济失调患者中，改善明显较少。对于患有心肌病或药物不耐受的患者，治疗仍然是禁忌的。
结论
AH用于遗传性共济失调的原理可以通过其替代作用（多巴胺释放）以及N-甲基-D-天冬氨酸（NMDA）直接参与小脑颗粒细胞中谷氨酸介导的神经毒性来解释；美金刚，一种AH类似物，是NMDA受体的有效阻滞剂。
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