Homeostatic-like plasticity of the primary motor hand area is impaired in focal hand dystonia
Homeostatic-like plasticity of the primary motor hand area is impaired in focal hand dystonia
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DOI：
10.1093/brain/awh527
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发表时间：
2005-08-01
期刊：
影响因子：
14.5
通讯作者：
Siebner, HR
中科院分区：
文献类型：
--
作者：
Quartarone, A;Rizzo, V;Siebner, HR
书写痉挛患者的感觉运动系统内的多个水平的抑制回路的兴奋性均降低，包括初级运动手区（M1）。尽管这可能在书写痉挛的病理生理学中发挥重要作用，但仍不清楚哪些因素可能导致抑制和兴奋之间出现不平衡。一种可能性是，将皮质兴奋性保持在正常生理范围内的稳态机制受到损害。在 8 名书写痉挛患者和 8 名年龄匹配的健康对照中，我们将低频重复经颅磁刺激 (rTMS) 与经颅直流电刺激 (TDCS) 结合起来，以探测左侧 M1 的区域稳态可塑性。证实了我们之前的研究（Siebner 等人，J Neurosci 2004；24：3379-85），用阳极 TDCS 对 M1 进行“促进”预处理增强了随后 1 Hz rTMS 对皮质脊髓兴奋性的抑制作用。相反，阴极 TDCS 的“抑制性”预处理逆转了 1 Hz rTMS 的后效应，导致皮质脊髓兴奋性增加。对于书写痉挛患者来说，结果却大不相同。用 TDCS 预处理后，1 Hz rTMS 并未引起皮质脊髓兴奋性的一致变化，表明正常“稳态”反应模式的丧失。此外，阴极 TDCS 预处理的正常抑制作用也不存在。目前的数据表明，在书写痉挛患者中，将兴奋性水平稳定在有用的动态范围内的稳态机制受到损害。我们认为，对皮质脊髓兴奋性急剧增加的错误稳态反应有利于适应不良的运动可塑性。类稳态可塑性在任务特异性肌张力障碍病理生理学中的作用值得进一步研究。
The excitability of inhibitory circuits in patients with writer's cramp is reduced at multiple levels within the sensorimotor system, including the primary motor hand area (M1). Although this may play a major role in the pathophysiology of writer's cramp, it is still unclear what factors may cause the imbalance between inhibition and excitation to arise. One possibility is that homeostatic mechanisms that keep cortical excitability within a normal physiological range are impaired. In eight patients with writer's cramp and eight healthy age-matched controls, we combined low-frequency repetitive transcranial magnetic stimulation (rTMS) with transcranial direct current stimulation (TDCS) to probe regional homeostatic plasticity of the left M1. Confirming our previous study (Siebner et al., J Neurosci 2004; 24: 3379-85), 'facilitatory' preconditioning of the M1 with anodal TDCS enhanced the inhibitory effect of subsequent 1 Hz rTMS on corticospinal excitability. Conversely, 'inhibitory' preconditioning with cathodal TDCS reversed the after effect of 1 Hz rTMS, producing an increase in corticospinal excitability. The results were quite different in patients with writer's cramp. Following preconditioning with TDCS, 1 Hz rTMS induced no consistent changes in corticospinal excitability, indicating a loss of the normal 'homeostatic' response pattern. In addition, the normal inhibitory effect of preconditioning with cathodal TDCS was absent. The present data suggest that homeostatic mechanisms that stabilize excitability levels within a useful dynamic range are impaired in patients with writer's cramp. We propose that a faulty homeostatic response to acute increases in corticospinal excitability favours maladaptive motor plasticity. The role of homeostatic-like plasticity in the pathophysiology of task-specific dystonias warrants further study.