Gernert M, Richter A, Rundfeldt C, Löscher W
Department of Pharmacology, Toxicology, and Pharmacy, School of Veterinary Medicine, Hannover, Germany.
Mov Disord. 1998 May;13(3):509-21. doi: 10.1002/mds.870130322.
Computerized EEG spectral analyses of depth electrode recordings from striatum (caudate/putamen; CPu), globus pallidus (GP), and parietal cortex (pCtx) were performed before and after dystonic attacks in freely moving mutant dt(sz) hamsters with paroxysmal dystonia. In these hamsters, sustained attacks of abnormal movements and postures can be reproducibly induced by stress, such as placing the animals in a new environment. Data recorded from mutant hamsters were compared with recordings from age-matched nondystonic control hamsters. The predominant EEG changes in CPu and GP of dystonic hamsters were significant decreases in the high-frequency beta2 range and there was a tendency to increase in delta and theta activities. These changes were seen both before and after onset of dystonic attacks, indicating a permanent disturbance of neural activities in the basal ganglia of dystonic animals. No such changes were seen in the pCtx. Furthermore, no epileptic or epileptiform activity was seen in any of the recordings, substantiating a previous notion from cortical and hippocampal recordings that paroxysmal dystonia in these mutant hamsters has no epileptogenic basis. The present finding of abnormal synchronization of neural activity in the CPu and GP of dystonic hamsters adds to the belief that the striatopallidal-thalamocortical circuit is the most likely site in which to search for the unknown defect in primary (idiopathic) dystonia. As suggested by this study, quantitative EEG analysis can increase the likelihood of detecting subtle EEG abnormalities in different types of idiopathic dystonia and thereby improves our understanding of the pathogenetic mechanisms of this movement disorder.
在自由活动的患有阵发性肌张力障碍的突变dt(sz)仓鼠发生肌张力障碍发作之前和之后,对来自纹状体(尾状核/壳核;CPu)、苍白球(GP)和顶叶皮质(pCtx)的深度电极记录进行了计算机化脑电图频谱分析。在这些仓鼠中,应激(如将动物置于新环境中)可重复性地诱发持续的异常运动和姿势发作。将突变仓鼠记录的数据与年龄匹配的非肌张力障碍对照仓鼠的记录进行比较。肌张力障碍仓鼠的CPu和GP中主要的脑电图变化是高频β2范围内显著降低,并且δ波和θ波活动有增加的趋势。这些变化在肌张力障碍发作之前和之后均可见,表明肌张力障碍动物基底神经节的神经活动存在永久性紊乱。在pCtx中未见此类变化。此外,在任何记录中均未观察到癫痫或癫痫样活动,这证实了之前从皮质和海马记录中得出的观点,即这些突变仓鼠的阵发性肌张力障碍没有致痫基础。目前关于肌张力障碍仓鼠CPu和GP中神经活动异常同步的发现进一步支持了这样一种观点,即纹状体苍白球 - 丘脑皮质回路是最有可能寻找原发性(特发性)肌张力障碍未知缺陷的部位。如本研究所示,定量脑电图分析可以增加在不同类型的特发性肌张力障碍中检测到细微脑电图异常的可能性,从而增进我们对这种运动障碍发病机制的理解。