Altered brain activity during pain processing in fibromyalgia
Department of Psychosomatics and Psychotherapy, University Hospital Münster, Münster, Germany. NeuroImage
(Impact Factor: 6.36).
10/2008; 44(2):502-8. DOI: 10.1016/j.neuroimage.2008.09.008
Fibromyalgia syndrome (FMS) is characterized by widespread pain. Studies with functional neuroimaging support the hypothesis of central pain augmentation in FMS. We tested this in our study with a novel paradigm of tonic pain induced by a single stimulus. Tonic pain, in contrast to phasic pain, seems to be a more appropriate experimental approach to study adaptive mechanisms of pain processing in FMS. We hypothesized that brain areas related to the "medial" pain system and the amygdalae will present different activation in patients compared to healthy subjects. An fMRI-block design before, during and after an incision was made in patients with FMS and in healthy controls. Acute pain caused by the incision was measured during the course of the experiment. A 2 factorial model of BOLD-signal changes was designed to explore significant differences of brain activation between both groups during the pain stimulus. Additionally the first Eigenvariates in those areas which show an interaction between both factors were determined over the time course of pain stimulation. Differences of activation in the fronto-cingulate cortex, the supplemental motor areas, and the thalamus were found between both groups with distinct differences in BOLD-signals changes over the time course of pain stimulation, even during anticipation of pain. Our results support the hypothesis that central mechanisms of pain processing in the medial pain system, favourable cognitive/affective factors even during the anticipation of pain, may play an important role for pain processing in patients with FMS.
Available from: Jean Decety
- "Secondly, we hypothesized that FM patients would activate pain ROIs more than HC—particularly at low pain levels. By using visual stimuli, such results would support that higher painrelated cerebral activity does not rely on peripheral pain stimulation (as in previous studies   )—but instead results from the sensitization of central processing. In addition and importantly, we studied interactions of the relevant factors, i.e. group, perspective and pain. "
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ABSTRACT: Dysfunction of central nervous pain processing is assumed to play a key role in primary fibromyalgia (FM) syndrome. This pilot study examined differences of pain processing associated with adopting different interpersonal perspectives.
Eleven FM patients and 11 healthy controls (HC) were scanned with functional magnetic resonance imaging. Participants were trained to take either a self-perspective or another person's perspective when viewing the visual stimuli. Stimuli showed body parts in painful situations of varying intensity (low, medium, and high) and visually similar but neutral situations.
Patients with FM showed a higher increase in blood oxygen level dependent (BOLD) response, particularly in the supplementary motor area (SMA). All pain-related regions of interest (anterior insula, somatosensory cortices, anterior cingulate cortex, and SMA) showed stronger modulation of BOLD responses in FM patients in the self-perspective. In contrast to pain processing regions, perspective-related regions (e.g. temporoparietal junction) did not differ between FM and HC.
The stronger response of all four pain processing cerebral regions during self-perspective is discussed in the light of disturbed bottom-up processing. Furthermore, the results confirm earlier reports of augmented pain processing in FM, and provide evidence for sensitization of central nervous pain processing.
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Available from: Mira Meeus
- "Burgmer et al.   "
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The aim of the present study was to systematically review the literature addressing pain induced changes in the brain related to central sensitization in patients with fibromyalgia (FM) using specific functional (rs-fMRI and fMRI) and structural (Voxel-Based Morphometry - VBM) brain MRI techniques.
Pubmed and Web of Science were searched for relevant literature using different key word combinations related to FM, brain MRI and central sensitization. Full text reports fulfilling the inclusion criteria were assessed on risk of bias and reviewed by two independent reviewers.
From the 61 articles that were identified, 22 met the inclusion criteria and achieved sufficient methodological quality. Eight articles examined structural brain (VBM) changes in patients with FM, showing moderate evidence that central sensitization is correlated with gray matter volume decrease in specific brain regions (mainly anterior cingulate cortex and prefrontal cortex). Global gray matter volume however remains unchanged. Thirteen articles evaluated brain activity (fMRI) in response to a nociceptive stimulus. Findings suggest a higher but similar pattern of activation of the pain matrix in FM patients compared to controls. There is also evidence of decreased functional connectivity in the descending pain modulating system in FM patients. Two articles examined intrinsic brain connectivity in FM patients with rs-fMRI. In conclusion, there is moderate evidence for a significant imbalance of the connectivity within the pain network during rest in patients with FM.
The included studies showed a moderate evidence for region-specific changes in gray matter volume, a decreased functional connectivity in the descending pain modulating system and an increased activity in the pain matrix related to central sensitization. More research is needed to evaluate the cause-effect relationship.
Available from: Indre Bileviciute-Ljungar
- "In a recent review, Cagnie and colleagues (2014) points out several reoccurring findings of central sensitization in FM as revealed by brain imaging: There is moderate evidence for gray matter reductions in anterior cingulate cortex (ACC) and prefrontal regions (reported by, e.g., Burgmer et al., 2009; Jensen et al., 2013), while overall gray matter volume is unaffected. There also exists moderate evidence for spatially similar but stronger response in pain-related regions (including primary (S1) and secondary (S2) somatosensory cortex, cerebellum, insula, posterior cingulate cortex (PCC), and ACC to experimentally induced pain in patients diagnosed with FM relative to controls. "
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ABSTRACT: Fibromyalgia (FM) is a syndrome characterized by chronic pain without known peripheral causes. Previously we have reported dysfunctional pain inhibitory mechanisms for FM patients during pain administration. In the current study we employed a seed correlation analysis (SCA), independent component analysis (ICA), and an analysis of fractional amplitude of low frequency fluctuations (fALFF) to study differences between a cohort of female fibromyalgia patients and an age- and sex matched healthy control group during a resting state condition. FM patients showed decreased connectivity between thalamus and premotor areas, between the right insula and primary sensorimotor areas, as well as between supramarginal and prefrontal areas. Individual sensitivity to painful pressure was associated with increased connectivity between pain related regions (e.g. insula and thalamus) and midline regions of the default mode network (including posterior cingulate cortex and medial prefrontal cortex) among patients and controls. However, neither ICA nor fALFF revealed any group differences. Our findings suggest that abnormal connectivity patterns between pain related regions and the remaining brain during rest reflect an impaired central mechanism of pain modulation in FM. Weaker coupling between pain regions and prefrontal- and sensorimotor areas might indicate a less efficient system level control of pain circuits. Moreover, our results show that multiple, complementary analytical approaches are valuable for obtaining a more comprehensive characterization of deviant resting state activity. In conclusion, our findings show that FM primarily is associated with decreased connectivity, e.g. between several pain related areas and sensorimotor regions, which could reflect a deficiency in pain regulation.
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