Department of Neural and Pain Sciences, University of Maryland School of Dentistry, Baltimore, Maryland; Center to Advance Chronic Pain Research, University of Maryland Baltimore, Baltimore, Maryland.
School of Science and Health, Western Sydney University, New South Wales, Australia.
J Pain. 2019 Dec;20(12):1498-1506. doi: 10.1016/j.jpain.2019.06.005. Epub 2019 Jun 13.
Aberrant motor cortex plasticity is hypothesized to contribute to chronic musculoskeletal pain, but evidence is limited. Critically, studies have not considered individual differences in motor plasticity or how this relates to pain susceptibility. Here we examined the relationship between corticomotor excitability and an individual's susceptibility to pain as pain developed, was sustained and resolved over 21 days. Nerve growth factor was injected into the right extensor carpi radialis brevis muscle of 20 healthy individuals on day 0, 2, and 4. Corticomotor excitability, pressure pain thresholds and performance on a cognitive conflict task were examined longitudinally (day 0, 2, 4, 6, and 14). Pain and disability were assessed on each alternate day (1,3…21). Two patterns of motor plasticity were observed in response to pain--corticomotor depression or corticomotor facilitation (P = .009). Individuals who displayed corticomotor depression experienced greater pain (P = .027), and had worse cognitive task performance (P = .038), than those who displayed facilitation. Pressure pain thresholds were reduced to a similar magnitude in both groups. Corticomotor depression in the early stage of pain could indicate a higher susceptibility to pain. Further work is required to determine whether corticomotor depression is a marker of pain susceptibility in musculoskeletal conditions. PERSPECTIVE: This article explores individual differences in motor plasticity in the transition to sustained pain. Individuals who developed corticomotor depression experienced higher pain and worse cognitive task performance than those who developed corticomotor facilitation. Corticomotor depression in the early stage of pain could indicate a higher susceptibility to pain.
异常的运动皮层可塑性被认为是导致慢性肌肉骨骼疼痛的原因之一，但证据有限。关键是，这些研究尚未考虑运动可塑性的个体差异，以及这种差异与疼痛易感性的关系。在这里，我们研究了皮质运动兴奋性与个体在疼痛发展、持续和缓解的 21 天过程中对疼痛的敏感性之间的关系。在第 0、2 和 4 天，将神经生长因子注入 20 名健康个体的右侧伸腕短肌。皮质运动兴奋性、压痛阈值和认知冲突任务的表现被纵向检查（第 0、2、4、6 和 14 天）。疼痛和残疾每隔一天评估一次（1、3…21）。在疼痛反应中观察到两种运动可塑性模式——皮质运动抑制或皮质运动易化（P=0.009）。表现出皮质运动抑制的个体经历了更大的疼痛（P=0.027），并且认知任务表现更差（P=0.038），而表现出易化的个体则没有。两组的压痛阈值都降低到相似的程度。疼痛早期的皮质运动抑制可能表明对疼痛的敏感性更高。需要进一步的工作来确定皮质运动抑制是否是肌肉骨骼疾病疼痛易感性的标志物。观点：本文探讨了向持续疼痛过渡过程中运动可塑性的个体差异。与出现皮质运动易化的个体相比，出现皮质运动抑制的个体经历了更高的疼痛和更差的认知任务表现。疼痛早期的皮质运动抑制可能表明对疼痛的敏感性更高。
