Obeso J A, Artieda J, Quinn N, Rothwell J C, Luquin M R, Vaamonde J, Marsden C D
Department of Neurology, Clinica Universitaria, Pamplona, Spain.
Clin Neuropharmacol. 1988 Dec;11(6):529-36. doi: 10.1097/00002826-198812000-00006.
Forty patients with different clinical and electrophysiological types of myoclonus were treated with piracetam (18-24 g per day, p.o.) alone, or with other drugs (clonazepam, sodium valproate, and primidone) in different combinations. Piracetam in monotherapy improved the electrophysiological abnormalities in patients with cortical reflex myoclonus, but had no useful clinical effect. Sixteen patients obtained benefit from piracetam when given in combination with other antimyoclonic drugs; improvement was dramatic in two patients, moderate in seven and mild in seven. All patients showing some response to piracetam had myoclonus of cortical origin; however, five other patients with similar cortical myoclonus failed to improve when piracetam was added. Tolerance was excellent and side effects were minimal and transient. It is concluded that piracetam probably has an antimyoclonic action, but its potential value as a therapeutic tool for disabling myoclonus requires further study.
40例患有不同临床和电生理类型肌阵挛的患者，单独使用吡拉西坦（每天口服18 - 24克）治疗，或与其他药物（氯硝西泮、丙戊酸钠和扑米酮）以不同组合治疗。吡拉西坦单一疗法改善了皮质反射性肌阵挛患者的电生理异常，但无明显临床效果。16例患者在与其他抗肌阵挛药物联合使用吡拉西坦时获益；2例患者改善显著，7例中度改善，7例轻度改善。所有对吡拉西坦有反应的患者均有皮质源性肌阵挛；然而，另外5例患有类似皮质肌阵挛的患者在加用吡拉西坦后未改善。耐受性良好，副作用轻微且短暂。结论是吡拉西坦可能具有抗肌阵挛作用，但其作为致残性肌阵挛治疗工具的潜在价值需要进一步研究。
