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A study on pahtophysiology and non-invasive treatment of dystonia

肌张力障碍的病理生理学及无创治疗研究

基本信息

批准号：
15390274
负责人：
KAJI Ryuji
金额：
$ 9.6万
依托单位：
The University of Tokushima
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15390274/
关键词：
dystonia magnetic stimulation X-linked dystonia-parkinsonism persistent Na channel PSTH 前運動野補足運動野 silent period 皮質-皮質間制御 SPECT プライミング

项目摘要

Dystonia is a syndrome of sustained muscle contractions frequently causing repetitive or twisting movement or abnormal posture. It is a common disorder with its incidence being approximately one fifth of that of Parkinson's disease. Writer's cramp is a focal dystonia, affecting only writing in its onset. This task-specificity provides a unique opportunity of investigating the mechanism of normal motor control for performing a specific task. It is also known notorious because of the resistance to treatment. We tried to treat these patients with writer's cramp by decreasing the excitability of the premotor cortex, which is known to be hyperactive in previous PET studies. For this, we used subthreshold low-frequency repetitive transcranial magnetic stimulation (rTMS), which inhibits the cortex. Using a computerized system for evaluating handwriting, we demonstrated significant improvement in handwriting and normalization of the abnormal cortical silent periods. Therefore the premotor cortex, one of the major output receptive areas from the basal ganglia, was shown hyperactive in dystonia, and its correction by rTMS may provide a useful method for treating these patients.We on the other hand had a chance to examine the immunohistochemichal findings in 7 autopsied patients with X-linked recessive dystonia-parkinsonism. We found the early loss of striosomal neurons in the neostriatum is the pathological hallmark of the dystonic phase of this disease. Striosomal cells are inhibiting the nigrastriatal dopaminergic projections from substantia nigra pars compacta, and their loss should lead to uncontrolled release of dopamine. Dystonia may therefore be caused by excess dopamine, which disinhibits premotor and other cortical areas.

肌张力障碍是一种持续的肌肉收缩综合征，经常引起重复或扭转运动或异常姿势。它是一种常见的疾病，其发病率约为帕金森病的五分之一。书写痉挛是一种局灶性肌张力障碍，发作时只影响书写。这种任务特异性提供了一个独特的机会，调查机制正常的电机控制执行特定的任务。它也因为对治疗的抵抗而臭名昭著。我们试图通过降低运动前区皮层的兴奋性来治疗这些书写痉挛患者，在以前的PET研究中，运动前区皮层是过度活跃的。为此，我们使用了亚阈值低频重复经颅磁刺激（rTMS），它抑制了皮层。使用计算机系统评估笔迹，我们证明了显着改善笔迹和正常化的异常皮层沉默期。因此，前运动皮层，从基底神经节的主要输出接受区之一，表现出过度活跃的肌张力障碍，其校正rTMS可能提供了一个有用的方法来治疗这些patients.We另一方面有机会检查尸检7例X连锁隐性肌张力障碍-帕金森氏症的脑电化学研究结果。我们发现新纹状体中纹状体神经元的早期丢失是这种疾病张力障碍阶段的病理标志。纹状体细胞抑制黑质纹状体多巴胺能神经元从黑质的投射，它们的缺失会导致多巴胺的不受控制的释放。因此，肌张力障碍可能是由过量的多巴胺引起的，多巴胺会抑制运动前区和其他皮质区域。