Brown P, Day B L, Rothwell J C, Thompson P D, Marsden C D
MRC Human Movement and Balance Unit, Institute of Neurology, London, UK.
Brain. 1991 Oct;114 ( Pt 5):2333-51. doi: 10.1093/brain/114.5.2333.
Nine patients with cortical myoclonus (due to various pathologies), in whom movement of one limb induced bilateral limb jerks, were investigated. Three of these patients also had bilateral cortical reflex myoclonus when one limb was subjected to an electrical stimulus. The relative latencies to onset of electromyogram (EMG) activity in various ipsilateral and contralateral muscles in action and reflex jerks were studied. Bilateral reflex and action jerks induced by unilateral electrical stimuli or limb movement were not synchronous. EMG activity was usually recorded in the muscles of the stimulated or moved limb, before being recorded in the homologous muscles of the contralateral limb. It is proposed that this difference in relative latency between homologous muscles represents the interhemispheric delay due to the transcallosal spread of excitation from one sensorimotor cortex to the opposite cerebral cortex. The relative latencies of muscles on the same side of the body reflected not only the differences in efferent delays from the motor cortex via spinal cord and peripheral nerves, but also delays due to the spread of myoclonic activity within the sensorimotor cortex itself. This intrahemispheric spread followed a grossly somatotopic pattern. It is suggested that this spread involves cortico-cortical pathways. The additional delay due to spread of activity from hand to leg area of the sensorimotor cortex was about 10 ms in the first active hemisphere, in both generalized reflex and action jerks. The delays due to somatotopic spread of activity in the opposite later activated hemisphere were shorter. The tendency for spread of excitation through callosal and cortico-cortical pathways is an additional pathophysiological abnormality in some patients with cortical myoclonus, and may be important in the generalization of seizures seen in these patients.
对9例皮质肌阵挛患者（病因各异）进行了研究，这些患者一侧肢体的运动可诱发双侧肢体抽搐。其中3例患者在一侧肢体受到电刺激时还出现双侧皮质反射性肌阵挛。研究了在主动和反射性抽搐中，不同同侧和对侧肌肉肌电图（EMG）活动开始的相对潜伏期。由单侧电刺激或肢体运动诱发的双侧反射性和主动性抽搐不同步。EMG活动通常先在受刺激或运动肢体的肌肉中记录，然后才在对侧肢体的同源肌肉中记录。有人提出，同源肌肉之间这种相对潜伏期的差异代表了由于兴奋从一个感觉运动皮层经胼胝体扩散到对侧大脑皮层而导致的半球间延迟。身体同侧肌肉的相对潜伏期不仅反映了从运动皮层经脊髓和周围神经传出延迟的差异，还反映了感觉运动皮层本身内肌阵挛活动扩散导致的延迟。这种半球内扩散遵循大致的躯体定位模式。有人认为这种扩散涉及皮质 - 皮质通路。在第一个激活的半球中，无论是全身性反射性还是主动性抽搐，从感觉运动皮层的手部区域到腿部区域活动扩散导致的额外延迟约为10毫秒。在对侧后激活半球中，由于活动的躯体定位扩散导致的延迟较短。通过胼胝体和皮质 - 皮质通路的兴奋扩散趋势是一些皮质肌阵挛患者的另一种病理生理异常，可能对这些患者癫痫发作的泛化很重要。
