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Central Sensitization in Fibromyalgia? A Systematic Review on Structural and Functional Brain MRI

  [ 3 votes ]   [ 1 Comment ]
By By Barbara Cagnie, PT, PhD, et al. • • February 14, 2014


OBJECTIVES: 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.

METHODS: 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.

RESULTS: From the 61 articles that were identified, 22 met the inclusion criteria and achieved sufficient methodological quality. Overall, 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). However, global gray matter volume remains unchanged. A total of 13 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. Overall, 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.

CONCLUSIONS: 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.

Source: Seminars in Arthritis and Rheumatism, January 8, 2014. By Barbara Cagnie, PT, PhD, Iris Coppieters, PT, Sien Denecker, PT, Jasmien Six, PT, Lieven Danneels, PT, PhD, Mira Meeus, PT, PhD.

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Pain Modulation and/or Central Sensitization
Posted by: IanH
Feb 15, 2014
Descending fibers also release substances such as norepinephrine (noradrenaline) and serotonin (endogenous opioids or endorphins) which have the capability of inhibiting the transmission of pain. This helps explain wide variations of pain among people and wide variations in pain in fibromyalgia.

Antidepressants interfere with the reuptake of serotonin and norepinephrine (noradrenaline)which increases their availability to inhibit pain.

However this rule does not apply completely in FM because pain modulation requires more energy than the generation of pain.

ATP and 5-HT (serotonin) are the principal neurotransmitters in the descending pain-modulating pathway. Because of this dependence of pain modulation on ATP and 5-HT (serotonin) and because both of these transmitters are depleted in FM, pain is not modulated effectively.

Hence in FM:
-depletion of ATP from neural mitochondrial dysfunction (especially those with ME/CFS) cause lowered ATP (causing both low energy and neurotransmitter) availability;
-depletion of 5-HT lowers inhibitory neurotransmitter for pain modulation.

-whereas people without FM can have normal ATP and 5-HT availability.

-however this does not explain why half of the people with ME/CFS do not have fibromyalgia. I am not sure what proportion of people with ME/CFS have widespread pain (not fitting criteria of FM). I would think it would be high. I don't know anyone with ME/CFS who does not have increased pain especially after exertion.
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