Abstract
The aim of this study was to investigate augmented pain processing in the cortical somatosensory system in patients with fibromyalgia (FM). Cortical evoked responses were recorded in FM (n = 19) and healthy subjects (n = 21) using magnetoencephalography after noxious intra-epidermal electrical stimulation (IES) of the hand dorsum (pain rating 6 on a numeric rating scale, perceptually-equivalent). In addition, healthy subjects were stimulated using the amplitude corresponding to the average stimulus intensity rated 6 in patients with FM (intensity-equivalent). Quantitative sensory testing was performed on the hand dorsum or thenar muscle (neutral site) and over the trapezius muscle (tender point), using IES (thresholds, ratings, temporal summation of pain, stimulus-response curve) and mechanical stimuli (threshold, ratings). Increased amplitude of cortical responses was found in patients with FM as compared to healthy subjects. These included the contralateral primary (S1) and bilateral secondary somatosensory cortices (S2) in response to intensity-equivalent stimuli and the contralateral S1 and S2 in response to perceptually-equivalent stimuli. The amplitude of the contralateral S2 response in patients with FM was positively correlated with average pain intensity over the last week. Quantitative sensory testing results showed that patients with FM were more sensitive to painful IES as well as to mechanical stimulation, regardless of whether the stimulation site was the hand or the trapezius muscle. Interestingly, the slope of the stimulus-response relationship as well as temporal summation of pain in response to IES was not different between groups. Together, these results suggest that the observed pain augmentation in response to IES in patients with FM could be due to sensitization or disinhibition of the cortical somatosensory system. Since the S2 has been shown to play a role in higher-order functions, further studies are needed to clarify the role of augmented S2 response in clinical characteristics of FM.
Highlights
Fibromyalgia (FM) is commonly associated with chronic wide-spread pain, but is notorious for its multi-modal symptoms such as anxiety and depression, sleep disturbances, fatigue and cognitive symptoms [1]
Patients were eligible for participation if they were clinically diagnosed as having primary FM, their disease duration was at least 3 months, they reported an average pain intensity of at least 40 on a 0−100 mm visual analogue scale (VAS; 0 mm = no pain, 100 mm = worst pain imaginable) during the past week, and they were willing to stop taking medications known to influence the somatosensory system at least 3 days prior to assessments
FM: fibromyalgia, HC: healthy controls, NSAIDs: nonsteroidal anti-inflammatory drugs, Beck’s Anxiety Inventory (BAI): Beck’s anxiety inventory, Beck’s Depression Inventory (BDI): Beck’s depression inventory, Pittsburgh Sleep Quality Index (PSQI): Pittsburgh sleep quality index, TP: tender points, FIQ: fibromyalgia impact questionnaire, SF-MPQ: short-form McGill pain questionnaire. p-values are based on independent t-tests and X2-tests with factor [Group]
Summary
Fibromyalgia (FM) is commonly associated with chronic wide-spread pain, but is notorious for its multi-modal symptoms such as anxiety and depression, sleep disturbances, fatigue and cognitive symptoms [1]. Patients with FM may show reduced endogenous pain inhibitory functions [5, 6, 19,20,21] and abnormal responses to innocuous somatosensory [5, 22,23,24], auditory [25,26,27], and olfactory stimuli [28] Together, these findings suggest that sensory augmentation could be “generalized”, i.e. occurring at the central level and not being specific for pain, some inconsistencies remain [4, 29,30,31]. What remains largely unclear from studies assessing sensory symptoms and signs in patients with FM is how different outcome measures relate to each other This is important since patients with FM are notorious for their heterogeneity, and symptoms tend to evolve over time. A better understanding of the mechanisms underlying pain augmentation may help to develop pathophysiological models of FM and may contribute to improved diagnosis and treatment
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