Kleine B U, Praamstra P, Stegeman D F, Zwarts M J
Department of Clinical Neurophysiology, Institute of Neurology, University Medical Centre Nijmegen, The Netherlands.
Exp Brain Res. 2001 Jun;138(4):477-83. doi: 10.1007/s002210100731.
Transcranial magnetic stimulation (TMS)-induced corticospinal volleys can be investigated in detail by analysing the firing pattern modulation of active motor units (MUs) at close to threshold stimulation strengths. In amyotropic lateral sclerosis (ALS) these volleys are dispersed and prolonged, attributed to altered motor cortical excitability. Impaired intracortical inhibition, as found in ALS, is not unique to this disease, but is also a well-established finding in Parkinson's disease (PD). The present study explored whether reduced inhibition in the motor cortex in PD is accompanied by similar changes in motor unit firing modulation by TMS as are found in ALS. TMS was applied to the contralateral motor cortex during a low-force voluntary elbow flexion while 126-channel surface electromyography (SEMG) was recorded from the brachial biceps muscle. A recently developed method for SEMG decomposition was used to extract the firing pattern of up to five simultaneously active MUs. Sixteen MUs in 7 PD patients and 17 MUs in 5 healthy control subjects were analysed and peristimulus time histograms (PSTHs) and interspike interval change functions (IICFs) were calculated. The IICF provides an estimate of the modulation of the postsynaptic membrane potential at the spinal motoneuron, evoked by the stimulus. In PD the duration of the PSTH peak was significantly increased and the synchrony was decreased. The excitatory phase at 20-50 ms of the IICF was broader in PD, reflecting a longer duration of the TMS-evoked excitatory postsynaptic potential. It is proposed that these results are due to prolonged corticospinal volleys resulting from impaired intracortical inhibition.
通过分析接近阈值刺激强度下主动运动单位（MUs）的放电模式调制，可对经颅磁刺激（TMS）诱发的皮质脊髓冲动进行详细研究。在肌萎缩侧索硬化症（ALS）中，这些冲动会分散且延长，这归因于运动皮质兴奋性的改变。ALS中发现的皮质内抑制受损并非该疾病所特有，在帕金森病（PD）中也是一个公认的现象。本研究探讨了PD患者运动皮质抑制减少是否伴随着与ALS中类似的TMS对运动单位放电调制的变化。在低强度自愿性肘部屈曲过程中，将TMS应用于对侧运动皮质，同时从肱二头肌记录126通道表面肌电图（SEMG）。使用一种最近开发的SEMG分解方法来提取多达五个同时活跃的运动单位的放电模式。分析了7例PD患者的16个运动单位和5例健康对照者的17个运动单位，并计算了刺激后时间直方图（PSTHs）和峰间期变化函数（IICFs）。IICF可估计刺激诱发的脊髓运动神经元突触后膜电位的调制情况。在PD中，PSTH峰值的持续时间显著增加，同步性降低。PD患者IICF在20 - 50毫秒的兴奋期更宽，这反映了TMS诱发的兴奋性突触后电位持续时间更长。有人认为，这些结果是由于皮质内抑制受损导致皮质脊髓冲动延长所致。
