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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.