Niddam David M, Chan Rai-Chi, Lee Si-Huei, Yeh Tzu-Chen, Hsieh Jen-Chuen
Laboratory of Integrated Brain Research, Department of Medical Research and Education, Taipei Veterans General Hospital, No. 201 Section 2 Shih-Pai Road, Taipei 112, Taiwan.
Clin J Pain. 2007 Jun;23(5):440-8. doi: 10.1097/AJP.0b013e318058accb.
Low-intensity low-frequency electrostimulation delivered within a myofascial trigger point (MTP) has been used as intervention to deactivate MTPs. The therapeutic effect has been suggested to be due to peripheral mechanisms. However, nonpainful stimuli are also known to reduce simultaneous pain through central effects. The primary objective of the present study was to assess if central pain modulation occurs after intervention with low-intensity electrostimulation within an MTP. We hypothesized that intervention induces pain inhibition via the periaqueductal gray (PAG).
Twenty-four patients with myofascial pain syndrome participated in the study. During functional magnetic resonance scanning, painful (high-intensity) intramuscular electrostimulation was delivered at random intervals (mean interstimulus interval=10.2 s) within an MTP of the upper left trapezius muscle. In-between scanning sessions, intervention (intramuscular electrostimulation, low-intensity, interstimulus interval=0.5 s) was applied to the same area. Patients were divided into responders and nonresponders according to their change in pressure pain thresholds relative to intervention. In addition to a whole brain search, a region of interest approach was also implemented to test the effect of intervention on PAG signal change.
The main findings were: (1) intervention modulated PAG activity to painful stimuli more in responders than in nonresponders, (2) change in PAG activity from the whole patient population correlated with change in pressure pain threshold, and (3) a network known to regulate affective qualities of the pain experience was (subsignificantly) engaged more in responders than in nonresponders.
The applied intervention most likely involves supraspinal pain control mechanisms related to both antinociception and regulation of pain affect.
在肌筋膜触发点（MTP）内进行的低强度低频电刺激已被用作使MTP失活的干预措施。其治疗效果被认为是由于外周机制。然而，已知非疼痛性刺激也可通过中枢效应减轻同时存在的疼痛。本研究的主要目的是评估在MTP内进行低强度电刺激干预后是否会发生中枢性疼痛调制。我们假设干预通过中脑导水管周围灰质（PAG）诱导疼痛抑制。
24名肌筋膜疼痛综合征患者参与了本研究。在功能磁共振扫描期间，在左斜方肌上部的一个MTP内以随机间隔（平均刺激间隔 = 10.2秒）进行疼痛性（高强度）肌内电刺激。在扫描 session 之间，对同一区域施加干预（肌内电刺激，低强度，刺激间隔 = 0.5秒）。根据患者相对于干预的压力疼痛阈值变化将其分为反应者和无反应者。除了全脑搜索外，还采用了感兴趣区域方法来测试干预对PAG信号变化的影响。
主要发现为：（1）干预对反应者的PAG对疼痛刺激的活动调制比对无反应者更多；（2）整个患者群体的PAG活动变化与压力疼痛阈值变化相关；（3）一个已知调节疼痛体验情感特质的网络在反应者中比在无反应者中（次要显著地）更多地被激活。
所应用的干预最有可能涉及与抗伤害感受和疼痛情感调节相关的脊髓上疼痛控制机制。
