Chiou S Y, Shih Y F, Chou L W, McGregor A H, Strutton P H
Department of Physical Therapy and Assistive Technology, National Yang-Ming University, Taiwan; The Nick Davey Laboratory, Human Performance Group, Division of Surgery, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, UK.
Eur J Pain. 2014 Jul;18(6):794-802. doi: 10.1002/j.1532-2149.2013.00428.x. Epub 2013 Nov 27.
Control of trunk movement relies on the integration between central neuronal circuits and peripheral skeletomuscular activities and it can be altered by pain. There is increasing evidence that there are deficits within the central nervous system controlling the trunk muscles in people with low back pain (LBP). However, it is unclear how LBP impacts upon neural drive to back muscles at different levels of voluntary contraction. Therefore, the purpose of this study was to investigate if neural drive is impaired in these patients.
Seventeen patients with LBP and 11 healthy controls were recruited. Bilateral electromyographic (EMG) recordings were obtained from the erector spinae (ES) muscles at two vertebral levels (T12 and L4). Participants performed a series of brief isometric back extensions (50-100% maximum voluntary contraction - MVC), during which transcranial magnetic stimulation was delivered. The size of the evoked (superimposed) twitch was measured using dynamometry.
The size of the superimposed twitch decreased linearly with increasing contraction strength in the controls; however, this linear relationship was not observed in the patients. Additionally, patients had larger superimposed twitches and longer time-to-peak amplitudes during MVCs than those observed in controls. Furthermore, patients had lower MVC and root-mean-square EMG activity of ES muscles during MVCs.
A decline of central neural drive to the back muscles at high level of voluntary contraction was observed in patients with LBP. These results suggest that it might be pertinent to include neuromuscular facilitation programmes and therapeutic exercise utilizing high voluntary contractions for patients with LBP.
躯干运动的控制依赖于中枢神经回路与外周骨骼肌肉活动之间的整合，并且会因疼痛而改变。越来越多的证据表明，下背痛（LBP）患者的中枢神经系统在控制躯干肌肉方面存在缺陷。然而，尚不清楚LBP如何在不同程度的自主收缩时影响背部肌肉的神经驱动。因此，本研究的目的是调查这些患者的神经驱动是否受损。
招募了17名LBP患者和11名健康对照者。在两个椎体水平（T12和L4）从竖脊肌（ES）获取双侧肌电图（EMG）记录。参与者进行了一系列短暂的等长背部伸展运动（最大自主收缩的50 - 100% - MVC），在此期间进行经颅磁刺激。使用测力计测量诱发（叠加）抽搐的大小。
在对照组中，叠加抽搐的大小随收缩强度增加呈线性下降；然而，在患者中未观察到这种线性关系。此外，患者在MVC期间的叠加抽搐更大，达到峰值幅度的时间更长。此外，患者在MVC期间的MVC和ES肌肉的均方根EMG活动较低。
在LBP患者中观察到在高水平自主收缩时，背部肌肉的中枢神经驱动下降。这些结果表明，对于LBP患者，纳入神经肌肉促进计划和利用高自主收缩的治疗性运动可能是恰当的。
