Human Motor Control Section, National Institute of Neurological Disorders and Stroke, NIH, Building 10, Room 7D37, 10 Center Dr MSC 1428, Bethesda, MD 20892-1428, USA.
Neurobiol Dis. 2011 May;42(2):177-84. doi: 10.1016/j.nbd.2010.08.025. Epub 2010 Sep 15.
The pathophysiology of dystonia has been best studied in patients with focal hand dystonia. A loss of inhibitory function has been demonstrated at spinal, brainstem and cortical levels. Many cortical circuits seem to be involved. One consequence of the loss of inhibition is a failure of surround inhibition, and this appears to directly lead to overflow and unwanted muscle spasms. There are mild sensory abnormalities and deficits in sensorimotor integration; these also might be explained by a loss of inhibition. Increasing inhibition may be therapeutic. A possible hypothesis is that there is a genetic loss of inhibitory interneurons in dystonia and that this deficit is a substrate on which other factors can act to produce dystonia. This article is part of a Special Issue entitled "Advances in dystonia".
扭转痉挛的病理生理学在手部局部性肌张力障碍患者中得到了较好的研究。在脊髓、脑干和皮质水平都显示出抑制功能丧失。许多皮质回路似乎都参与其中。抑制丧失的一个后果是环绕抑制失败，这似乎直接导致了肌肉痉挛的溢出和不受控制。存在轻度感觉异常和感觉运动整合缺陷；这也可以通过抑制丧失来解释。增加抑制可能具有治疗作用。一个可能的假设是，在扭转痉挛中存在抑制性中间神经元的遗传缺失，而这种缺陷是其他因素作用产生扭转痉挛的基础。本文是特刊“扭转痉挛的研究进展”的一部分。
