Abstract
Fibromyalgia (FM) has been associated to an increased processing of somatosensory stimuli, but its generalization to other sensory modalities is under discussion. To clarify this, we studied auditory event-related potentials (AEPs) to stimuli of different intensity in patients with FM and healthy controls (HCs), considering the effects of attention mechanisms and medication. We performed two experiments: In study 1 (n = 50 FM, 60 HCs), the stimuli were presented randomly within the sequence; in study 2 (n = 28 FM, 30 HCs), they were presented in blocks of the same intensity. We analyzed intensity and group effects on N1-P2 amplitude and, only for the FM group, the effect of medication and the correlation between AEPs and clinical variables. Contrary to the expectation, the patients showed a trend of reduced AEPs to the loudest tones (study 1) or no significant differences with the HCs (study 2). Medication with central effects significantly reduced AEPs, while no significant relationships between the N1-P2 amplitude/intensity function and patients’ symptoms were observed. The findings do not provide evidence of augmented auditory processing in FM. Nevertheless, given the observed effect of medication, the role of sensory amplification as an underlying pathophysiological mechanism in fibromyalgia cannot be discarded.
Highlights
Fibromyalgia (FM) has been associated to an increased processing of somatosensory stimuli, but its generalization to other sensory modalities is under discussion
The aim of the present paper was to analyze the brain electrical activity to auditory stimuli varying in intensity, and whether that response depend on the attentional mechanism involved, in a sample of patients with FM and healthy controls
All the patients were previously diagnosed according to the ACR recommendations[42], we found that 5 of them did not fulfill the criterion of having more than 11 tender points with values lower than 4 kg/cm[2]
Summary
Fibromyalgia (FM) has been associated to an increased processing of somatosensory stimuli, but its generalization to other sensory modalities is under discussion. Several studies postulate that the patients with FM present dysfunction of central nervous system mechanisms, affecting both nociceptive and non-nociceptive processing[2,3,4,5], and including alteration in the descending pain modulation mechanisms[3,6]. Based on those evidences, it has been proposed that central amplification of painful and non-painful sensory inputs may be at the basis of this syndrome, as well as of other chronic pain d iseases[7]. Goes against the hypothesis of a generalized hypervigilance in FM, which should be present to both nociceptive and harmless stimuli[26,27]
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