Castillo Saavedra Laura, Mendonca Mariana, Fregni Felipe
Spaulding Neuromodulation Center, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA, USA.
Nucleo de Neurociencias e Comportamento (NEC), Institute of Psychology, University of Sao Paulo, Sao Paulo, Brazil.
Med Hypotheses. 2014 Sep;83(3):332-6. doi: 10.1016/j.mehy.2014.06.007. Epub 2014 Jun 17.
Fibromyalgia is a highly prevalent, debilitating disease, characterized by chronic widespread pain. The mechanisms underlying pain are not completely understood, but it is believed to be associated with important neuroplastic changes in pain-related neural circuits. Although the involvement of the pain matrix in fibromyalgia is well established, another area that has been found to play a role in the maintenance and treatment of chronic pain is the primary motor cortex (M1). Maladaptive plasticity of M1 is a common finding in patients with chronic pain and many studies in animal models and in human subjects have shown that modulation of the activity of this cortical area induces significant analgesic effects. Furthermore, studies in other chronic pain syndromes have found alterations in baseline characteristics of M1, including an increase in cortical excitability and an abnormally enhanced response to incoming sensory stimuli. Given these findings, we hypothesize that M1 is a major modulator of pain in fibromyalgia and therefore its baseline activity reflects this strong feedback between M1 and pain-related neural areas. However, the feedback loop between M1 and the pain matrix is not enough to decrease pain in fibromyalgia per se, thus increasing its modulatory effect by engaging this network through different behavioral and modulatory techniques is a potentially beneficial treatment for pain in fibromyalgia.
纤维肌痛是一种高度流行的、使人衰弱的疾病，其特征为慢性广泛性疼痛。疼痛背后的机制尚未完全明确，但据信与疼痛相关神经回路中的重要神经可塑性变化有关。尽管疼痛矩阵在纤维肌痛中的作用已得到充分证实，但另一个被发现与慢性疼痛的维持和治疗相关的区域是初级运动皮层（M1）。M1的适应性不良可塑性在慢性疼痛患者中很常见，许多动物模型和人体研究表明，调节该皮层区域的活动可产生显著的镇痛效果。此外，对其他慢性疼痛综合征的研究发现，M1的基线特征存在改变，包括皮层兴奋性增加以及对传入感觉刺激的反应异常增强。基于这些发现，我们推测M1是纤维肌痛疼痛的主要调节因子，因此其基线活动反映了M1与疼痛相关神经区域之间的这种强烈反馈。然而，M1与疼痛矩阵之间的反馈回路本身不足以减轻纤维肌痛中的疼痛，因此通过不同的行为和调节技术激活该网络来增强其调节作用，可能是治疗纤维肌痛疼痛的有益方法。
