Motor Cortex Excitability and BDNF Levels in Chronic Musculoskeletal Pain According to Structural Pathology.
Motor Cortex Excitability and BDNF Levels in Chronic Musculoskeletal Pain According to Structural Pathology.
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DOI：
10.3389/fnhum.2016.00357
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发表时间：
2016
影响因子：
2.9
通讯作者：
Fregni F
中科院分区：
文献类型：
--
作者：
Caumo W;Deitos A;Carvalho S;Leite J;Carvalho F;Dussán-Sarria JA;Lopes Tarragó Mda G;Souza A;Torres IL;Fregni F
中枢致敏综合征（CSS）包括在结构病理学谱中具有重叠症状的病症，其范围从持续性伤害感受[例如，骨关节炎（OA）]到不存在组织损伤，例如纤维肌痛（FM）和肌筋膜疼痛综合征（MPS）中出现的组织损伤。首先，我们假设这些综合征在经颅磁刺激（TMS）评估的皮质兴奋性参数，即运动诱发电位（MEP），皮质沉默期（CSP），短皮质内抑制（SICI）和短皮质内易化（SICF）存在差异。其次，考虑到组织损伤的存在可以通过血清神经营养素检测，我们假设结构病理学的谱（即，从如OA中的持续性伤害感受到如FM和MPS中的组织损伤的不存在），可以通过它们的下行疼痛抑制系统的不同效率来检测，如通过条件性疼痛调制（CPM）范例所评估的。第三，我们探讨了脑源性神经营养因子（BDNF）是否对运动皮层兴奋性和结构病理之间的关系有影响。这项横断面研究汇总了三项随机临床试验的基线数据。我们纳入了女性（n = 114），年龄19-65岁，慢性疼痛综合征（CPS）残疾：FM（n = 19），MPS（n = 54），OA（n = 27）和健康受试者（n = 14）。我们评估了血清BDNF，运动皮层兴奋性的参数TMS测量和数字疼痛量表[<$（0-10）]的变化在CPM任务。在没有组织损伤的情况下观察到的SICI的校正平均值（SD）分别比持续伤害性输入低56.36%[0.31（0.18）vs. 0.55（0.32）]。脑源性神经营养因子与SICI和CPM任务中的波幅（0-10）变化呈负相关。这些发现表明，FM和MPS中运动皮层和下行疼痛抑制系统的去抑制作用大于OA和健康受试者。同样，与结构性损伤相比，在无组织损伤的慢性疼痛中，半球间去抑制以及下行疼痛调节系统的功能障碍更高。此外，他们认为更高水平的血清BDNF可能参与介导运动皮层兴奋性去抑制的过程，以及下行抑制性疼痛调制系统的功能，独立于肌肉骨骼疼痛综合征的生理病理学机制。
The central sensitization syndrome (CSS) encompasses disorders with overlapping symptoms in a structural pathology spectrum ranging from persistent nociception [e.g., osteoarthritis (OA)] to an absence of tissue injuries such as the one presented in fibromyalgia (FM) and myofascial pain syndrome (MPS). First, we hypothesized that these syndromes present differences in their cortical excitability parameters assessed by transcranial magnetic stimulation (TMS), namely motor evoked potential (MEP), cortical silent period (CSP), short intracortical inhibition (SICI) and short intracortical facilitation (SICF). Second, considering that the presence of tissue injury could be detected by serum neurotrophins, we hypothesized that the spectrum of structural pathology (i.e., from persistent nociception like in OA, to the absence of tissue injury like in FM and MPS), could be detected by differential efficiency of their descending pain inhibitory system, as assessed by the conditioned pain modulation (CPM) paradigm. Third, we explored whether brain-derived neurotrophic factor (BDNF) had an influence on the relationship between motor cortex excitability and structural pathology. This cross-sectional study pooled baseline data from three randomized clinical trials. We included females (n = 114), aged 19–65 years old with disability by chronic pain syndromes (CPS): FM (n = 19), MPS (n = 54), OA (n = 27) and healthy subjects (n = 14). We assessed the serum BDNF, the motor cortex excitability by parameters the TMS measures and the change on numerical pain scale [NPS (0–10)] during CPM-task. The adjusted mean (SD) on the SICI observed in the absence of tissue injury was 56.36% lower than with persistent nociceptive input [0.31(0.18) vs. 0.55 (0.32)], respectively. The BDNF was inversely correlated with the SICI and with the change on NPS (0–10)during CPM-task. These findings suggest greater disinhibition in the motor cortex and the descending pain inhibitory system in FM and MPS than in OA and healthy subjects. Likewise, the inter-hemispheric disinhibition as well as the dysfunction in the descending pain modulatory system is higher in chronic pain without tissue injury compared to a structural lesion. In addition, they suggest that a greater level of serum BDNF may be involved in the processes that mediate the disinhibition of motor cortex excitability, as well as the function of descending inhibitory pain modulation system, independently of the physiopathology mechanism of musculoskeletal pain syndromes.