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Central pain modulatory mechanisms of attentional analgesia are preserved in fibromyalgia.

ABSTRACT:

Abstract

Fibromyalgia is a prevalent pain condition that is associated with cognitive impairments including in attention, memory, and executive processing. It has been proposed that fibromyalgia may be caused by altered central pain processing characterised by a loss of endogenous pain modulation. We tested whether attentional analgesia, where cognitive engagement diminishes pain percept, was attenuated in patients with fibromyalgia (n = 20) compared with matched healthy controls (n = 20). An individually calibrated, attentional analgesia paradigm with a 2 × 2 factorial design was used with brain and brainstem-focussed functional magnetic resonance imaging. Patients with fibromyalgia had both lower heat pain thresholds and speeds in a visual attention task. When this was taken into account for both attentional task and thermal stimulation, both groups exhibited an equivalent degree of attentional analgesia. Functional magnetic resonance imaging analysis showed similar patterns of activation in the main effects of pain and attention in the brain and brainstem (with the sole exceptions of increased activation in the control group in the frontopolar cortex and the ipsilateral locus coeruleus). The attentional analgesic effect correlated with activity in the periaqueductal gray and rostral ventromedial medulla. These findings indicate that patients with fibromyalgia can engage the descending pain modulatory system if the attentional task and noxious stimulus intensity are appropriately titrated.

SUBMITTER: Oliva V

PROVIDER: S-EPMC8675057 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundExercise is one of the most recommended management strategies by treatment guidelines for fibromyalgia (FM); however, the mechanism through which exercise improves pain in FM is still unknown.ObjectiveWe aimed to summarize the hypothesized theoretical mechanisms for the pain-relieving effects of exercise in people with FM.Eligibility criteriaRandomized controlled trials (RCTs) in English reporting mechanisms for pain-relieving effects of exercise in the 'Introduction' and 'Discussion' sections and significant within- group or between-group effects of exercise interventions were included.Sources of evidenceWe searched the databases Ovid MEDLINE(R), EMBASE, CINAHL, COCHRANE, Sports Discuss, and AMED with the keywords: exercise and fibromyalgia until December 2021.Charting methodsTwo authors independently performed title/abstract, full-text review, and data abstraction using a data abstraction form. The hypothesized mechanisms from individual studies were grouped into three categories.ResultsThe literature search resulted in 2147 studies, out of which 220 studies were considered for full-text review. A total of 50 RCTs proposing 29 unique mechanisms for the pain-relieving effects of exercise were included. These mechanisms were divided into three categories: physical, neuro-physiological, and psychological. The neuro-physiological category was further subdivided into exercise-induced hypoalgesia (EIH), pain sensitization, the autonomic system, the immune system, the endocrine system, and miscellaneous categories. The most frequently hypothesized mechanisms were EIH (n = 15), autonomic modulation (n = 7), improved sleep (n = 6), muscle oxygenation (n = 6), self-efficacy (n = 5), mental health (n = 4), and benefits of the aquatic environment (n = 12). While all exercise interventions involved FM patients, most of the supporting evidence for these mechanisms was cited from previous studies conducted on healthy samples. No studies performed analyses to demonstrate causal associations between the mechanisms and outcomes.ConclusionMultiple mechanisms were hypothesized for the positive influence of exercise in people with FM. Future studies using causal analyses, such as mediation analysis, are recommended to validate these mechanisms.

Project description:Fibromyalgia is characterized by chronic pain and a striking discrepancy between objective signs of tissue damage and severity of pain. Function and structural alterations in brain areas involved in pain processing may explain this feature. Previous case-control studies in fibromyalgia focused on acute pain processing using experimentally-evoked pain paradigms. Yet, these studies do not allow conclusions about chronic, stimulus-independent pain. Resting-state cerebral blood flow (rsCBF) acquired by arterial spin labelling (ASL) may be a more accurate marker for chronic pain. The objective was to integrate four different functional and structural neuroimaging markers to evaluate the neural correlate of chronic, stimulus-independent pain using a resting-state paradigm. In line with the pathophysiological concept of enhanced central pain processing we hypothesized that rsCBF is increased in fibromyalgia in areas involved in processing of acute pain. We performed an age matched case-control study of 32 female fibromyalgia patients and 32 pain-free controls and calculated group differences in rsCBF, resting state functional connectivity, grey matter volume and cortical thickness using whole-brain and region of interest analyses. We adjusted all analyses for depression and anxiety. As centrally acting drugs are likely to interfere with neuroimaging markers, we performed a subgroup analysis limited to patients not taking such drugs. We found no differences between cases and controls in rsCBF of the thalamus, the basal ganglia, the insula, the somatosensory cortex, the prefrontal cortex, the anterior cingulum and supplementary motor area as brain areas previously identified to be involved in acute processing in fibromyalgia. The results remained robust across all neuroimaging markers and when limiting the study population to patients not taking centrally acting drugs and matched controls. In conclusion, we found no evidence for functional or structural alterations in brain areas involved in acute pain processing in fibromyalgia that could reflect neural correlates of chronic stimulus-independent pain.

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Central pain modulatory mechanisms of attentional analgesia are preserved in fibromyalgia.

Abstract

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