有症状的发作性运动诱发性运动障碍的皮肤和混合神经静息期记录
Cutaneous and Mixed Nerve Silent Period Recordings in Symptomatic Paroxysmal Kinesigenic Dyskinesia.
作者信息
Cogez Julien, Etard Olivier, Derache Nathalie, Defer Gilles
机构信息
CHU de Caen, Service de Neurologie, CHU de Caen, Caen, F-14000, France.
CHU de Caen, Service D'explorations Fonctionnelles du Systeme Nerveux, Caen, F-14000, France; Université de Caen Basse-Normandie, UFR de Médecine, Caen, F-14000, France.
出版信息
Open Neurol J. 2016 May 26;10:9-14. doi: 10.2174/1874205X01610010009. eCollection 2016.
OBJECTIVE
The underlying neurophysiologic mechanism responsible for secondary paroxysmal kinesigenic dyskinesia (PKD) is still unclear. Here, we study the pathogenesis of PKD in two patients with a demyelinating lesion in the spinal cord.
METHODS
Electromyogram recordings from affected arms of two patients with spinal cord lesions presenting PKD were compared with our laboratory standards. The cutaneous silent period (CuSP), mixed nerve silent period (MnSP) and coincidence period (CiP), defined as the common period between the CuSP and MnSP, were recorded.
RESULTS
A large decrease in the MnSP and disappearance of the CiP were observed in our patients, which was secondary to simultaneous extinction of the third portion of the MnSP, while the CuSP was normal. The MnSP and CiP were normal after recovery.
CONCLUSIONS
Our results demonstrate that the third portion of the MnSP and the CuSP do not correspond to the same physiologic process. These findings suggest that PKD patients have abnormal spinal interneuron integration.
目的
继发性阵发性运动诱发性运动障碍（PKD）的潜在神经生理机制仍不清楚。在此，我们研究了两名脊髓存在脱髓鞘病变患者的PKD发病机制。
方法
将两名表现为PKD的脊髓病变患者患侧手臂的肌电图记录与我们实验室的标准进行比较。记录皮肤静息期（CuSP）、混合神经静息期（MnSP）以及定义为CuSP和MnSP共同时间段的重合期（CiP）。
结果
我们的患者中观察到MnSP大幅缩短以及CiP消失，这继发于MnSP第三部分的同时消失，而CuSP正常。恢复后MnSP和CiP正常。
结论
我们的结果表明，MnSP的第三部分和CuSP并不对应相同的生理过程。这些发现提示PKD患者存在异常的脊髓中间神经元整合。
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