The physiological effects of pallidal deep brain stimulation in dystonia
The physiological effects of pallidal deep brain stimulation in dystonia
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DOI：
10.1109/tnsre.2007.896994
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发表时间：
2007-06-01
影响因子：
4.9
通讯作者：
Corcos, Daniel M.
中科院分区：
文献类型：
--
作者：
Tisch, Stephen;Rothwell, John C.;Corcos, Daniel M.
肌张力障碍是一种不自主的运动障碍，其特征是肌肉收缩导致不正常的姿势和痉挛，影响身体的部分或全部。肌张力障碍可能是原发性的，可能是发现异常基因，最常见的是DYT1，或者继发于脑部结构性病变或遗传性退行性疾病。潜在的缺陷被认为是基底节对皮质运动通路的异常调节，已经证实了各种运动和感觉生理异常。许多患有更严重和更广泛形式的肌张力障碍的患者的药物治疗失败，重新引起了人们对神经外科治疗方法的兴趣。近年来，苍白球内脑深部电刺激(DBS)已成为治疗肌张力障碍的一种有效方法，尤其是原发性全身性肌张力障碍患者，可明显改善肌张力障碍。与帕金森氏症不同，DBS对肌张力障碍的益处不是立竿见影的，而是在几周到几个月的时间里逐渐产生。GPI DBS的肌张力障碍患者的生理和影像研究表明，GPI DBS对运动皮质和皮质下回路有短期和长期的影响，包括GPI DBS术后脊髓和脑干兴奋性的逐渐正常化，这与临床改善有关。根据现有的肌张力障碍的生理数据，这些效应提示GPI DBS的作用主要是通过改变脑干、丘脑和皮质的基底节输出而导致神经重组，这可能解释了GPI DBS术后肌张力障碍的特征进行性改善。
Dystonia is an involuntary movement disorder characterized by muscle contractions causing abnormal postures and spasms, affecting part or all of the body. Dystonia may be primary where an abnormal gene, most commonly DYT1, may be identified, or secondary to structural brain lesions or heredodegenerative disorders. The underlying defect is believed to be abnormal basal ganglia modulation of cortical motor pathways, and various motor and sensory physiological abnormalities have been demonstrated. The failure of medical treatment in many patients with the more severe and generalized forms of dystonia has led to renewed interest in neurosurgical treatment approaches. In recent years, deep brain stimulation (DBS) of globus pallidus internus (GPi) has emerged as an effective treatment for dystonia, particularly patients with primary generalized dystonia, where remarkable improvement may occur. In contrast to Parkinson's disease, the beneficial effects of DBS in dystonia are not immediate but progressive over weeks to months. Physiological and imaging studies in dystonia patients with GPi DBS have demonstrated both short and long-term effects of GPi DBS on motor cortex and subcortical circuits including progressive normalization of spinal and brainstem excitability after GPi DBS which correlate with clinical improvement. These effects, in light of existing physiological data in dystonia, suggest that GPi DBS acts primarily by major modification of basal ganglia output to brainstem, thalamus, and cortex resulting in neural reorganization, which may explain the characteristic progressive improvement in dystonia after GPi DBS.