Quartarone Angelo, Rizzo Vincenzo, Bagnato Sergio, Morgante Francesca, Sant'Angelo Antonino, Romano Marcello, Crupi Domenica, Girlanda Paolo, Rothwell John C, Siebner Hartwig R
Department of Neuroscience, Psychiatric and Anaethesiological Sciences, University of Messina, Italy.
Brain. 2005 Aug;128(Pt 8):1943-50. doi: 10.1093/brain/awh527. Epub 2005 May 4.
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.
书写痉挛患者抑制性回路的兴奋性在感觉运动系统的多个层面降低，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起主要作用，但仍不清楚哪些因素可能导致抑制和兴奋之间的失衡。一种可能性是，将皮质兴奋性维持在正常生理范围内的稳态机制受损。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）相结合，以探究左侧M1区的局部稳态可塑性。正如我们之前的研究（西布纳等人，《神经科学杂志》2004年；24: 3379 - 85）所证实的，用阳极TDCS对M1进行“易化性”预处理增强了随后1Hz rTMS对皮质脊髓兴奋性的抑制作用。相反，用阴极TDCS进行“抑制性”预处理则逆转了1Hz rTMS的后效应，使皮质脊髓兴奋性增加。书写痉挛患者的结果则大不相同。在TDCS预处理后，1Hz rTMS并未引起皮质脊髓兴奋性的一致变化，这表明正常的“稳态”反应模式丧失。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效动态范围内的稳态机制受损。我们提出，对皮质脊髓兴奋性急性增加的错误稳态反应有利于适应不良的运动可塑性。类稳态可塑性在特定任务性肌张力障碍病理生理学中的作用值得进一步研究。
