A Framework for Understanding the Relationship between Descending Pain Modulation, Motor Corticospinal, and Neuroplasticity Regulation Systems in Chronic Myofascial Pain
A Framework for Understanding the Relationship between Descending Pain Modulation, Motor Corticospinal, and Neuroplasticity Regulation Systems in Chronic Myofascial Pain
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DOI：
10.3389/fnhum.2016.00308
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发表时间：
2016-06-27
影响因子：
2.9
通讯作者：
Caumo, Wolnei
中科院分区：
文献类型：
--
作者：
Botelho, Leonardo M.;Morales-Quezada, Leon;Caumo, Wolnei
肌筋膜疼痛综合征（MPS）是慢性肌肉骨骼疼痛的主要原因。然而，其神经生物学机制尚未完全阐明。由于疼痛过程中涉及的网络之间的复杂相互作用，我们的方法，提供洞察疼痛的神经机制，是调查神经生理学，神经化学和临床结果之间的关系，如皮质脊髓兴奋性。近年来的研究表明，慢性疼痛涉及三个神经系统：（i）运动皮质脊髓系统;（ii）内部下行疼痛调制系统;（iii）神经可塑性调节系统。在这项横断面研究中，我们的目的是检查这三个中央系统之间的关系，慢性MPS患者的条件性疼痛调制任务（CPM任务）做/不响应。CPM任务是将她的非优势手浸入冷水（0-1摄氏度）中以产生异位伤害性刺激。皮质脊髓兴奋性是主要结果;具体而言，通过经颅磁刺激（TMS）评估运动诱发电位（MEP）和皮质内易化（ICF）。次要结局为皮质兴奋性参数[当前静默期（CSP）和短皮质内抑制（SIGN）、血清脑源性神经营养因子（BDNF）、热痛阈值（HPT）和疼痛相关残疾（DRP）。我们纳入了33名女性（18-65岁）。使用Bonferroni多重比较检验的MANCOVA模型显示，与反应者（n = 23）相比，无反应者（n = 10）表现出增加的皮质内易化（ICF;平均值+/- SD）1.43（0.3）vs. 1.11（0.12），较大运动诱发电位振幅（μ V）1.93（0.54）vs.1.40（0.27），以及更高的血清BDNF（pg/MI）32.56（9.95）vs.25.59（10.24），（均P < 0.05）。无应答者的DRP水平高于无应答者，HPT水平低于无应答者（P均< 0.05）。这些发现表明，净下行疼痛抑制的丧失与ICF、血清BDNF水平和DRP的增加有关。我们提出了一个框架来解释这些因素的关系和潜在的方向性。在这个框架中，我们假设，增加中枢致敏导致下行疼痛抑制的损失，触发代偿机制，如运动皮层兴奋性增加所示。
Myofascial pain syndrome (MPS) is a leading cause of chronic musculoskeletal pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in pain process, our approach, to providing insights into the neural mechanisms of pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic pain: (i) motor corticospinal system; (ii) internal descending pain modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0-1 degrees C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SIGN, serum brain-derived neurotrophic factor (BDNF), heat pain threshold (HPT), and the disability related to pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean +/- SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (mu V) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/MI) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.