From the Psychophysiology Lab (González-Villar, Carrillo-de-la-Peña), Faculty of Psychology, Universidade de Santiago de Compostela, Santiago, Spain; Psychological Neuroscience Lab (González-Villar), Research Center in Psychology, School of Psychology, Universidade do Minho, Braga, Portugal; Departamento de Neuroloxía (Arias), Complexo Hospitalario Universitario de Santiago, Santiago de Compostela, Spain.
Psychosom Med. 2019 May;81(4):380-388. doi: 10.1097/PSY.0000000000000677.
Fibromyalgia (FM) is a generalized chronic pain condition associated with multiple cognitive impairments, including altered inhibitory processes. Inhibition is a key component of human executive functions and shares neural substrate with pain processing, which may explain the inhibitory deficits in FM. Here, we investigated the integrity of brain inhibitory mechanisms in these patients.
We recorded the electroencephalographic activity of 27 patients with FM and 27 healthy controls (HCs) (all women) while they performed a reactive motor inhibition task (the stop-signal paradigm). We analyzed task-induced modulations in electrophysiological markers related to inhibition (N2, P3, and midfrontal theta oscillations) and visual attention (posterior alpha oscillations).
The FM group performed the task correctly, with no differences relative to HCs at the behavioral level. We did not find any between-group differences in N2 amplitude (F(1,52) = 0.01, p = .93), P3 amplitude (F(1,52) = 3.46; p = .068), or theta power (F(1,52) = 0.05; p = .82). However, modulation of posterior alpha power after presentation of either the go or stop stimuli was lower in patients than in HCs (F(1,52) = 7.98; p = .007).
N2, P3, theta power, and behavioral results indicate that the mechanisms of motor inhibition are sufficiently preserved to enable correct performance of the stop-signal task in patients with FM. Nevertheless, the lower modulation of alpha suggests greater difficulty in mobilizing and maintaining visual attentional resources, a result that may explain the cognitive dysfunction observed in FM.
纤维肌痛（FM）是一种全身性慢性疼痛疾病，与多种认知障碍有关，包括抑制过程改变。抑制是人类执行功能的关键组成部分，与疼痛处理共享神经基础，这可能解释了 FM 中的抑制缺陷。在这里，我们研究了这些患者大脑抑制机制的完整性。
我们记录了 27 名纤维肌痛患者和 27 名健康对照者（均为女性）在执行反应性运动抑制任务（停止信号范式）时的脑电图活动。我们分析了与抑制（N2、P3 和中额theta 振荡）和视觉注意（后alpha 振荡）相关的电生理标记物的任务诱导调制。
FM 组在行为水平上与 HC 组相比，任务完成正确，无差异。我们没有发现 N2 振幅（F（1,52）= 0.01，p =.93）、P3 振幅（F（1,52）= 3.46；p =.068）或 theta 功率（F（1,52）= 0.05；p =.82）之间的组间差异。然而，与 HC 相比，患者在呈现 Go 或停止刺激后，后 alpha 功率的调制较低（F（1,52）= 7.98；p =.007）。
N2、P3、theta 功率和行为结果表明，运动抑制机制足以保持，以使 FM 患者能够正确执行停止信号任务。然而，alpha 的调制较低表明动员和维持视觉注意力资源的难度更大，这一结果可能解释了在 FM 中观察到的认知功能障碍。
