Differential pain modulation properties in central neuropathic pain after spinal cord injury
Differential pain modulation properties in central neuropathic pain after spinal cord injury
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DOI：
10.1097/j.pain.0000000000000532
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发表时间：
2016-07-01
期刊：
影响因子：
7.4
通讯作者：
Defrin, Ruth
中科院分区：
文献类型：
--
作者：
Gruener, Hila;Zeilig, Gabi;Defrin, Ruth
中枢神经性疼痛（CNP）似乎与调节疼痛的能力改变有关;而下行疼痛抑制功能障碍与慢性疼痛分布的程度有关，增强的疼痛兴奋与慢性疼痛的强度有关。我们研究了以下假设：CNP与下行性疼痛抑制降低沿着神经元兴奋性增加相关，并且这两种特征均与脊髓丘脑束（STT）损伤相关。慢性脊髓损伤受试者（27例）和无CNP（23例）和健康对照组（20例）进行了疼痛适应，条件性疼痛调制（CPM），强直性阈上疼痛（TSP）和损伤水平以上的疼痛空间总和的测量。中枢神经性疼痛受试者还接受了病灶处和病灶下STT评估并完成了问卷调查。与对照组相比，中枢神经性疼痛受试者CPM降低，TSP增强。在CNP受试者中，CPM和疼痛适应功能障碍与疼痛部位的数量呈正相关。TSP的大小和疼痛的空间总和与CNP强度呈正相关。STT评分与CNP强度和TSP相关，因此损伤水平以下STT受影响越大，CNP和TSP的幅度越大。CNP似乎与调节疼痛的能力改变相关，而下行疼痛抑制功能障碍与慢性疼痛分布程度相关，疼痛兴奋增强与慢性疼痛强度相关。因此，自上而下的过程可以确定CNP的扩散，而自下而上的过程可以确定CNP强度。CNP的作用机制可能与STT诱导的兴奋过度有关。未来的纵向研究可能会调查这种情况的时间轴。
It seems that central neuropathic pain (CNP) is associated with altered abilities to modulate pain; whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution, enhanced pain excitation is associated with the intensity of chronic pain. We investigated the hypothesis that CNP is associated with decreased descending pain inhibition along with increased neuronal excitability and that both traits are associated with spinothalamic tract (STT) damage. Chronic spinal cord injury subjects with CNP (n = 27) and without CNP (n = 23) and healthy controls (n = 20) underwent the measurement of pain adaptation, conditioned pain modulation (CPM), tonic suprathreshold pain (TSP), and spatial summation of pain above injury level. Central neuropathic pain subjects also underwent at and below-lesion STT evaluation and completed the questionnaires. Central neuropathic pain subjects showed decreased CPM and increased enhancement of TSP compared with controls. Among CNP subjects, the dysfunction of CPM and pain adaptation correlated positively with the number of painful body regions. The magnitude of TSP and spatial summation of pain correlated positively with CNP intensity. STT scores correlated with CNP intensity and with TSP, so that the more affected the STT below injury level, the greater the CNP and TSP magnitude. It seems that CNP is associated with altered abilities to modulate pain, whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution and enhanced pain excitation is associated with the intensity of chronic pain. Thus, top-down processes may determine the spread of CNP, whereas bottom-up processes may determine CNP intensity. It also seems that the mechanisms of CNP may involve STT-induced hyperexcitability. Future, longitudinal studies may investigate the timeline of this scenario.