Artieda J, Obeso J A
Department of Neurology, Clinica Universitaria, University of Navarra Medical School, Pamplona, Spain.
Ann Neurol. 1993 Aug;34(2):175-84. doi: 10.1002/ana.410340213.
We studied 6 patients with myoclonus elicited by flash stimulation (1-15 Hz). Multichannel electromyographic recording showed a rostrocaudal recruitment order for the generalized myoclonic jerk. In all patients, each flash induced a large (36.9 +/- 5.7 microV) frontal biphasic wave with an onset latency of 42 msec that preceded the earliest muscle response in the face by at least 4 msec (range, 4-7 msec), the activity in the biceps by 11 to 14 msec, and the activity in tibialis anterior by 26 to 34 msec. Occipital potentials evoked by the same flash stimulation had a latency of 33.7 msec and were of normal amplitude (2.1 +/- 1.2 microV). Brain-mapping analysis indicated that the frontal activity correlated with the myoclonus originated in the premotor and motor cortices. These findings provide evidence for a cortical origin of this form of stimulus-sensitive myoclonus in humans. Administration of apomorphine and lisuride (intravenously) and levodopa-carbidopa (orally) abolished the photic myoclonus. Intravenous 5-hydroxytryptophan plus carbidopa (orally) and piracetam (orally) were also effective against photic myoclonus. The wide range of drugs active against photic cortical myoclonus suggests the participation of several biochemical mechanisms in its origin.
我们研究了6例由闪光刺激（1-15赫兹）诱发肌阵挛的患者。多通道肌电图记录显示，全身性肌阵挛性抽搐呈头尾募集顺序。在所有患者中，每次闪光均诱发一个大的（36.9±5.7微伏）额部双相波，起始潜伏期为42毫秒，该波至少比面部最早的肌肉反应提前4毫秒（范围为4-7毫秒），比二头肌的活动提前11至14毫秒，比胫前肌的活动提前26至34毫秒。相同闪光刺激诱发的枕部电位潜伏期为33.7毫秒，振幅正常（2.1±1.2微伏）。脑图谱分析表明，与肌阵挛相关的额叶活动起源于运动前区和运动皮质。这些发现为人类这种形式的刺激敏感性肌阵挛的皮质起源提供了证据。静脉注射阿扑吗啡和利舒脲以及口服左旋多巴-卡比多巴可消除光性肌阵挛。静脉注射5-羟色氨酸加卡比多巴（口服）和吡拉西坦（口服）对光性肌阵挛也有效。多种对光性皮质肌阵挛有效的药物表明，其起源涉及多种生化机制。
