Brain Stimulation and Rehabilitation (BrainStAR) Lab, School of Health Sciences, Western Sydney University, Sydney, New South Wales, Australia.
College of Nursing and Health Sciences, Flinders University, Adelaide, South Australia, Australia.
Pain Med. 2021 Jun 4;22(6):1312-1323. doi: 10.1093/pm/pnaa425.
Although acute pain has been shown to reduce corticomotor excitability, it remains unknown whether this response resolves over time or is related to symptom severity. Furthermore, acute pain research has relied upon data acquired from the cranial "hotspot," which do not provide valuable information regarding reorganization, such as changes to the distribution of a painful muscle's representation within M1. Using a novel, rapid transcranial magnetic stimulation (TMS) mapping method, this study aimed to 1) explore the temporal profile and variability of corticomotor reorganization in response to acute pain and 2) determine whether individual patterns of corticomotor reorganization are associated with differences in pain, sensitivity, and somatosensory organization.
Corticomotor (TMS maps), pain processing (pain intensity, pressure pain thresholds), and somatosensory (two-point discrimination, two-point estimation) outcomes were taken at baseline, immediately after injection (hypertonic [n = 20] or isotonic saline [n = 20]), and at pain resolution. Follow-up measures were recorded every 15 minutes until 90 minutes after injection.
Corticomotor reorganization persisted at least 90 minutes after pain resolution. Corticomotor depression was associated with lower pain intensity than was corticomotor facilitation (r = 0.47 [P = 0.04]). These effects were not related to somatosensory reorganization or peripheral sensitization mechanisms.
Individual patterns of corticomotor reorganization during acute pain appear to be related to symptom severity, with early corticomotor depression possibly reflecting a protective response. These findings hold important implications for the management and potential prevention of pain chronicity. However, further research is required to determine whether these adaptations relate to long-term outcomes in clinical populations.
尽管已经证实急性疼痛会降低皮质运动兴奋性，但目前尚不清楚这种反应是否会随着时间的推移而消失，或者是否与症状严重程度有关。此外，急性疼痛研究依赖于从颅部“热点”获得的数据，这些数据无法提供有关重组的有价值信息，例如疼痛肌肉在 M1 中的代表分布的变化。本研究采用一种新颖的快速经颅磁刺激（TMS）映射方法，旨在：1）探索急性疼痛反应中皮质运动重组的时间进程和可变性；2）确定皮质运动重组的个体模式是否与疼痛、敏感性和体感组织的差异相关。
在基线、注射后即刻（高渗[ n ＝20]或等渗盐水[ n ＝20]）和疼痛缓解时，分别测量皮质运动（TMS 图）、疼痛处理（疼痛强度、压痛阈值）和体感（两点辨别、两点估计）结果。在注射后 15 分钟直至 90 分钟进行随访测量。
皮质运动重组至少在疼痛缓解后 90 分钟内持续存在。皮质运动抑制与疼痛强度较低有关，而皮质运动兴奋与疼痛强度较高有关（ r ＝0.47 [ P ＝0.04]）。这些效应与体感组织变化或外周敏化机制无关。
急性疼痛期间皮质运动重组的个体模式似乎与症状严重程度相关，早期皮质运动抑制可能反映了一种保护反应。这些发现对疼痛慢性化的管理和潜在预防具有重要意义。然而，需要进一步的研究来确定这些适应性是否与临床人群的长期结果有关。
