Osher Center for Integrative Medicine at Vanderbilt, Department of Physical Medicine & Rehabilitation, Vanderbilt University Medical Center, Suite 380, 3401 West End Avenue, Nashville, TN, 37203, USA.
Department of Clinical and Health Psychology, University of Florida, Gainesville, FL, USA.
Brain Imaging Behav. 2020 Jun;14(3):881-896. doi: 10.1007/s11682-018-0033-8.
Analgesic treatments that aim to eliminate pain display marginal success in relieving chronic pain and may increase pain vulnerability. Repeated exposure to pain may result in increased pain modulation via engagement of anti-nociceptive brain regions. It was hypothesized that repeated exposure to delayed onset muscle soreness (DOMS) would result in increased pain modulatory capacity (PMC) via functional neural adaptation. 23 healthy participants completed Baseline and Follow Up resting-state fMRI and quantitative sensory testing (QST) visits 40 days apart. Participants were randomized to two groups: A Repeated DOMS Group (RD Group) that received four, weekly DOMS inductions and a Control Group that received one baseline induction. Daily pain ratings were collected for seven days post-induction, as were quantitative sensory testing (QST) metrics at baseline and Follow Up. Regional functional connectivity (FC) was estimated among areas involved in pain modulation. Seed and network FC was estimated among areas involved in pain modulation and sensory processing. Changes in FC were compared between groups. The RD Group displayed significant reductions in post-DOMS pain ratings and significant changes in thermal QST measures. RD Group participants displayed greater adaptation in nucleus accumbens-medial prefrontal cortex (NAc-mPFC) FC and in sensorimotor network (SMN) connectivity with the dorsomedial, ventromedial, and rostromedial prefrontal cortices. Changes in SMN-PFC connectivity correlated with reductions in post-DOMS affective distress. Results suggest that repeated exposure to clinically-relevant pain results in adaptations among brain regions involved in pain modulation. Repeated exposure to clinically-relevant pain may serve as a mechanism to increase PMC via inhibition of emotional valuation of painful stimuli.
旨在消除疼痛的镇痛治疗在缓解慢性疼痛方面收效甚微，而且可能会增加疼痛易感性。反复暴露于疼痛之下可能会通过激活抗伤害性脑区而增加疼痛调制能力。我们假设，反复出现延迟性肌肉酸痛（DOMS）会通过功能性神经适应而增加疼痛调制能力（PMC）。23 名健康参与者在相隔 40 天的基础期和随访期接受了静息状态 fMRI 和定量感觉测试（QST）检查。参与者被随机分配到两组：重复 DOMS 组（RD 组）接受了 4 次每周的 DOMS 诱导，对照组接受了 1 次基线诱导。在诱导后 7 天内每天收集疼痛评分，并在基线和随访时收集定量感觉测试（QST）指标。估计了涉及疼痛调制的区域之间的区域功能连接（FC）。在涉及疼痛调制和感觉处理的区域之间估计了种子和网络 FC。比较了两组之间的 FC 变化。RD 组在 DOMS 后疼痛评分显著降低，热 QST 测量值显著变化。RD 组参与者在前扣带皮层-内侧前额叶皮质（NAc-mPFC）FC 和感觉运动网络（SMN）与背内侧、腹内侧和前脑回前额叶皮质的连接方面表现出更大的适应能力。SMN-PFC 连接的变化与 DOMS 后情感困扰的减少相关。结果表明，反复暴露于临床相关疼痛会导致参与疼痛调制的脑区发生适应性变化。反复暴露于临床相关疼痛可能通过抑制疼痛刺激的情感评价而增加 PMC 的机制。
