Fibromyalgia syndrome (FM) is a chronic pain disorder characterized by widespread pain, sleep disturbance, fatigue and cognitive/affective symptoms. Functional imaging studies have revealed that FM and other chronic pain syndromes can affect resting brain activity. This study utilized electroencephalographic (EEG) recordings to investigate the relative power of ongoing oscillatory activity in the resting brain.
A 64-channel EEG was recorded at rest in 19 female FM patients and 18 healthy, age-matched, control subjects. The Manual Tender Point Scale (MTPS) examination was performed to quantify tonic pain and tenderness on the day of testing along with measures of mood, arousal and fatigue. Oscillations in delta, theta, alpha, beta and gamma frequency bands were analysed using Standardised Low-Resolution Brain Electromagnetic Tomography to evaluate sources of spectral activity throughout the whole brain.
FM patients exhibited greater pain, tiredness and tension on the day of testing relative to healthy control participants and augmented theta activity in prefrontal and anterior cingulate cortices. No significant differences were seen in other frequency bands. Augmented frontal theta activity in FM patients significantly correlated with measures of tenderness and mean tiredness scores.
Increased prefrontal theta activity may contribute to persistent pain in fibromyalgia or represent the outcome of prolonged symptoms. The findings point to the potential for therapeutic interventions aimed at normalizing neural oscillations, while further research utilizing quantitative analysis of resting EEG could benefit our understanding of fibromyalgia pathophysiology.
The findings indicate that alterations to resting-state oscillatory activity may relate to ongoing tonic pain and fatigue in FM, and manifest in brain regions relevant for cognitive-attentional aspects of pain processing and endogenous pain inhibition. Enhanced low-frequency oscillations were previously seen in FM and other chronic pain syndromes, and may relate to pathophysiological mechanisms for ongoing pain such as thalamocortical dysrhythmia.