Department of Psychosomatic Medicine and Psychotherapy, LWL University Hospital, Ruhr University Bochum, Bochum 44791, Germany.
Computer Assisted Clinical Medicine, Medical Faculty Mannheim, Heidelberg University, Mannheim 68167, Germany; Mannheim Institute for Intelligent Systems in Medicine, Heidelberg University, Mannheim 68167, Germany.
Neuroimage Clin. 2023;37:103355. doi: 10.1016/j.nicl.2023.103355. Epub 2023 Feb 21.
The perceived lack of control over the experience of pain is arguably-one major cause of agony and impaired life quality in patients with chronic pain disorders as fibromyalgia (FM). The way perceived control affects subjective pain as well as the underlying neural mechanisms have so far not been investigated in chronic pain. We used functional magnetic resonance imaging (fMRI) to examine the neural correlates of self-controlled compared to computer-controlled heat pain in healthy controls (HC, n = 21) and FM patients (n = 23). Contrary to HC, FM failed to activate brain areas usually involved in pain modulation as well as reappraisal processes (right ventrolateral (VLPFC), dorsolateral prefrontal cortex (DLPFC) and dorsal anterior cingulate cortex (dACC)). Computer-controlled (compared to self-controlled) heat revealed significant activations of the orbitofrontal cortex (OFC) in HC, whereas FM activated structures that are typically involved in neural emotion processing (amygdala, parahippocampal gyrus). Additionally, FM displayed disrupted functional connectivity (FC) of the VLPFC, DLPFC and dACC with somatosensory and pain (inhibition)-related areas during self-controlled heat stimulation as well as significantly decreased gray matter (GM) volumes compared to HC in DLPFC and dACC. The described functional and structural changes provide evidence for far-reaching impairments concerning pain-modulatory processes in FM. Our investigation represents a first demonstration of dysfunctional neural pain modulation through experienced control in FM according to the extensive functional and structural changes in relevant sensory, limbic and associative brain areas. These areas may be targeted in clinical pain therapeutic methods involving TMS, neurofeedback or cognitive behavioral trainings.
患者对疼痛体验的控制感缺失，可能是纤维肌痛症（FM）等慢性疼痛障碍患者感到痛苦和生活质量受损的一个主要原因。在慢性疼痛中，目前还没有研究感知控制对主观疼痛的影响以及潜在的神经机制。我们使用功能磁共振成像（fMRI）来研究健康对照组（HC，n=21）和 FM 患者（n=23）中自我控制与计算机控制热痛之间的神经相关性。与 HC 相反，FM 未能激活通常参与疼痛调节和重新评估过程的大脑区域（右侧腹外侧（VLPFC）、背外侧前额叶皮层（DLPFC）和背侧前扣带皮层（dACC））。与自我控制（相比）相比，计算机控制（的热痛）在 HC 中会显著激活眶额皮层（OFC），而 FM 则会激活通常参与神经情绪处理的结构（杏仁核、海马旁回）。此外，FM 在自我控制热刺激期间还表现出 VLPFC、DLPFC 和 dACC 与体感和疼痛（抑制）相关区域的功能连接（FC）中断，并且与 HC 相比，DLPFC 和 dACC 的灰质（GM）体积明显减少。这些描述的功能和结构变化为 FM 中与疼痛调节过程相关的广泛损伤提供了证据。我们的研究根据相关感觉、边缘和联想大脑区域的广泛功能和结构变化，首次证明了 FM 中通过经验控制出现的神经疼痛调节功能障碍。这些区域可能是涉及 TMS、神经反馈或认知行为训练的临床疼痛治疗方法的目标。
