European journal of pain : EJP
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Habituation refers to the brain's inhibitory mechanism against sensory overload and its brain correlate has been investigated in the form of a well-defined event-related potential, N100 (N1). Fibromyalgia is an extensively described chronic pain syndrome with concurrent manifestations of reduced tolerance and enhanced sensation of painful and non-painful stimulation, suggesting an association with central amplification of all sensory domains. Among diverse sensory modalities, we utilized repetitive auditory stimulation to explore the anomalous sensory information processing in fibromyalgia as evidenced by N1 habituation. ⋯ Fibromyalgia patients failed to demonstrate auditory N1 habituation to repetitively presenting stimuli, which indicates their compromised early auditory information processing. Our findings provide neurophysiological evidence of inhibitory failure and cortical augmentation in fibromyalgia. WHAT'S ALREADY KNOWN ABOUT THIS TOPIC?: Fibromyalgia has been associated with altered filtering of irrelevant somatosensory input. However, whether this abnormality can extend to the auditory sensory system remains controversial. N!00, an event-related potential, has been widely utilized to assess the brain's habituation capacity against sensory overload. WHAT DOES THIS STUDY ADD?: Fibromyalgia patients showed defect in N100 habituation to repetitive auditory stimuli, indicating compromised early auditory functioning. This study identified deficient inhibitory control over irrelevant auditory stimuli in fibromyalgia.
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It is still unclear to what extent the most common animal models of pain and analgesia, based on indirect measures such as nocifensive behaviours, provide valid measures of pain perception. ⋯ The present findings provide direct evidence that chronic recordings in S1 in awake animals can offer a powerful, and much sought for, translational model of the perception of pain magnitude during hyperalgesia. WHAT DOES THIS STUDY ADD?: In a novel animal model, chronic recordings of nociceptive activity in primary somatosensory cortex (S1) in awake freely moving rats are compared to behavioural readouts during UVB-induced hyperalgesia. Evoked activity in rat S1 replicates altered pain perception in humans during development of hyperalgesia, but withdrawal reflexes do not.
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Amylin is a peptide from the calcitonin gene-related peptides (CGRP) family that is expressed by nociceptors. Amylin may modulate pain via a spinal action. ⋯ Overall, data suggested that amylin modulates pain with an inflammatory component and the autoanalgesic/inhibitory mechanisms occurring in the interphase of the formalin test. Amylin might have affected the nociceptive system at different levels (spinal cord and brain), explaining the different effects observed according to the time of amylin injection. WHAT DOES THIS STUDY ADD?: Amylin modulated formalin interphase and tonic pain behaviours probably by targeting spinal neurons and affecting supraspinal areas involved in affective and modulatory components of pain. Activation of spinal amylin-receptors may contribute to the initiation of inflammatory pain mechanisms.