The University of Queensland, School of Health & Rehabilitation Sciences, St Lucia, Queensland, Australia.
Centre Interdisciplinaire de Recherche en réadaptation et Integration Sociale (CIRRIS), Université Laval, Québec City, Québec, Canada.
Eur J Pain. 2024 Oct;28(9):1607-1626. doi: 10.1002/ejp.2313. Epub 2024 Jul 15.
Chronic pain involves communication between neural and immune systems. Recent data suggest localization of glial (brain immune cells) activation to the sensorimotor regions of the brain cortex (S1/M1) in chronic low back pain (LBP). As glia perform diverse functions that impact neural function, activation might contribute to sensorimotor changes, particularly in LBP maintained by increased nervous system sensitivity (i.e., nociplastic pain). This preliminary proof-of-concept study aimed to: (i) compare evidence of neuroinflammatory activation in S1/M1 between individuals with and without LBP (and between nociceptive and nociplastic LBP phenotypes), and (ii) evaluate relationships between neuroinflammatory activation and sensorimotor function.
Simultaneous PET-fMRI measured neuroinflammatory activation in functionally defined S1/M1 in pain-free individuals (n = 8) and individuals with chronic LBP (n = 9; nociceptive: n = 4, nociplastic: n = 5). Regions of S1/M1 related to the back were identified using fMRI during motor tasks and thermal stimuli. Sensorimotor measures included single and paired-pulse transcranial magnetic stimulation (TMS) and quantitative sensory testing (QST). Sleep, depression, disability and pain questionnaires were administered.
Neuroinflammatory activation was greater in the lower back cortical representation of S1/M1 of the nociplastic LBP group than both nociceptive LBP and pain-free groups. Neuroinflammatory activation in S1/M1 was positively correlated with sensitivity to hot (r = 0.52) and cold (r = 0.55) pain stimuli, poor sleep, depression, disability and BMI, and negatively correlated with intracortical facilitation (r = -0.41).
This preliminary proof-of-concept study suggests that neuroinflammation in back regions of S1/M1 in individuals with nociplastic LBP could plausibly explain some characteristic features of this LBP phenotype.
Neuroinflammatory activation localized to sensorimotor areas of the brain in individuals with nociplastic pain might contribute to changes in sensory and motor function and aspects of central sensitization. If cause-effect relationships are established in longitudinal studies, this may direct development of therapies that target neuroinflammatory activation.
慢性疼痛涉及神经和免疫系统之间的通讯。最近的数据表明，在慢性下背痛（LBP）中，胶质细胞（大脑免疫细胞）的激活定位于大脑皮层的感觉运动区域（S1/M1）。由于胶质细胞具有影响神经功能的多种功能，因此其激活可能导致感觉运动变化，特别是在神经系统敏感性增加维持的 LBP 中（即，伤害感受性疼痛）。这项初步的概念验证研究旨在：（i）比较有和没有 LBP 的个体之间以及伤害感受性和伤害感受性 LBP 表型之间 S1/M1 中的神经炎症激活证据，以及（ii）评估神经炎症激活与感觉运动功能之间的关系。
在无痛个体（n=8）和慢性 LBP 个体（n=9；伤害感受性：n=4，伤害感受性：n=5）中，同时使用 PET-fMRI 测量功能定义的 S1/M1 中的神经炎症激活。使用 fMRI 在运动任务和热刺激期间识别与背部相关的 S1/M1 区域。感觉运动测量包括单脉冲和双脉冲经颅磁刺激（TMS）和定量感觉测试（QST）。还进行了睡眠、抑郁、残疾和疼痛问卷评估。
伤害感受性 LBP 组 S1/M1 的下背部皮质代表区的神经炎症激活大于伤害感受性 LBP 组和无痛组。S1/M1 中的神经炎症激活与对热（r=0.52）和冷（r=0.55）疼痛刺激的敏感性、睡眠质量差、抑郁、残疾和 BMI 呈正相关，与皮质内易化呈负相关（r=-0.41）。
这项初步的概念验证研究表明，伤害感受性 LBP 个体的 S1/M1 背部区域的神经炎症可能可以解释这种 LBP 表型的一些特征。
伤害感受性疼痛个体的感觉运动脑区的神经炎症激活可能导致感觉和运动功能以及中央敏化的某些方面的变化。如果在纵向研究中建立了因果关系，这可能会指导针对神经炎症激活的治疗方法的开发。
