Tsao H, Galea M P, Hodges P W
NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Qld 4072, Australia.
Brain. 2008 Aug;131(Pt 8):2161-71. doi: 10.1093/brain/awn154. Epub 2008 Jul 18.
Many people with recurrent low back pain (LBP) have deficits in postural control of the trunk muscles and this may contribute to the recurrence of pain episodes. However, the neural changes that underlie these motor deficits remain unclear. As the motor cortex contributes to control of postural adjustments, the current study investigated the excitability and organization of the motor cortical inputs to the trunk muscles in 11 individuals with and without recurrent LBP. EMG activity of the deep abdominal muscle, transversus abdominis (TrA), was recorded bilaterally using intramuscular fine-wire electrodes. Postural control was assessed as onset of TrA EMG during single rapid arm flexion and extension tasks. Motor thresholds (MTs) for transcranial magnetic stimulation (TMS) were determined for responses contralateral and ipsilateral to the stimulated cortex. In addition, responses of TrA to TMS over the contralateral cortex were mapped during voluntary contractions at 10% of maximum. MTs and map parameters [centre of gravity (CoG) and volume] were compared between healthy and LBP groups. The CoG of the motor cortical map of TrA in the healthy group was approximately 2 cm anterior and lateral to the vertex, but was more posterior and lateral in the LBP group. The location of the CoG and the map volume were correlated with onset of TrA EMG during rapid arm movements. Furthermore, the MT needed to evoke ipsilateral responses was lower in the LBP group, but only on the less excitable hemisphere. These findings provide preliminary evidence of reorganization of trunk muscle representation at the motor cortex in individuals with recurrent LBP, and suggest this reorganization is associated with deficits in postural control.
许多复发性下背痛（LBP）患者存在躯干肌肉姿势控制缺陷，这可能导致疼痛发作复发。然而，这些运动缺陷背后的神经变化仍不清楚。由于运动皮层有助于控制姿势调整，本研究调查了11名有和没有复发性LBP的个体中，运动皮层输入到躯干肌肉的兴奋性和组织情况。使用肌内细线电极双侧记录腹横肌（TrA）这一深部腹肌的肌电图活动。姿势控制通过在单次快速手臂屈伸任务中TrA肌电图的起始情况进行评估。确定经颅磁刺激（TMS）对受刺激皮层对侧和同侧反应的运动阈值（MTs）。此外，在最大收缩力的10%的自主收缩过程中，绘制对侧皮层TMS刺激下TrA的反应图。比较健康组和LBP组的MTs和图谱参数[重心（CoG）和体积]。健康组中TrA运动皮层图谱的CoG大约在头顶前外侧2厘米处，但在LBP组中更靠后外侧。CoG的位置和图谱体积与快速手臂运动期间TrA肌电图的起始相关。此外，LBP组中诱发同侧反应所需的MT较低，但仅在兴奋性较低的半球。这些发现为复发性LBP个体运动皮层处躯干肌肉表征的重组提供了初步证据，并表明这种重组与姿势控制缺陷有关。
