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Connections: the Pain and Distress Circuit in Fibromyalgia Identified

Ecoclimber

Senior Member
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Arthritis Rheumatol. 2015 Jan 26. doi: 10.1002/art.39043. [Epub ahead of print]
The somatosensory link: S1 functional connectivity is altered by sustained pain and associated with clinical/autonomic dysfunction in fibromyalgia.
Kim J1, Loggia ML, Cahalan CM, Harris RE, Beissner F, Garcia RG, Kim H, Wasan AD, Edwards RR, Napadow V.

Abstract:
Objective: Fibromyalgia (FM) is a chronic functional pain syndrome characterized by widespread pain, significant pain catastrophizing,sympathovagal dysfunction, and amplified temporal summation for evoked pain. While several studies have found altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system, and its role in both somatic and non-somatic FM symptomatology.

Our objective was to evaluate resting primary somatosensory cortex (S1) connectivity, and explore how sustained, evoked deep-tissue pain modulates this connectivity.

Methods:
We acquired fMRI and electrocardiography data from FM patients and healthy controls (HC) during rest (REST) and sustained mechanical pressure pain (PAIN) over the lower leg.Functional connectivity associated withdifferent S1 subregions was calculated, while S1leg (leg representation) connectivity was contrast between REST and PAIN, and correlated with clinically-relevant measures in FM.

Results:
At REST, FM showed decreased connectivity between multiple ipsilateral and cross-hemispheric S1 subregions, which was correlated with clinical pain severity. PAIN, compared to REST, produced increased S1leg connectivity to bilateral anterior insula in FM, but not in HC. Moreover, in FM, sustained pain-altered S1leg connectivity to anterior insula was correlated with clinical/behavioral pain measures and autonomic responses.

Conclusion:

Our study demonstrates that both somatic and non-somatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are all closely linked with the degree to which evoked deep-tissue pain alters S1 connectivity to salience/affective pain processing regions. Additionally, diminished connectivity between S1 subregions at REST in FM may result from ongoing widespread clinical pain.

This article is protected by copyright. All rights reserved. Copyright © 2015 American College of Rheumatology.



Along with other research papers, analysis could shed further light on the biomedical (organic) cause of the reported symptoms in Fibromyalgia and ME/CFS such as brain fog, pain, light-sound-noise-sensitivities, MCS, pain, exhaustion etc. impacting the amydala and insular cortex via ANS caused by pathogens or autoimmunity.


For a more in depth analysis click below:
Connections: the Pain and Distress Circuit in Fibromyalgia Identified

Fibromyalgia (FM), of course, is much more than about pain. Called the “prototypical functional pain syndrome,” people with fibromyalgia often experience problems thinking (fibro-fog), sleep and autonomic nervous system problems, depression and catastrophizing. The multidimensional aspects of fibromyalgia suggest that more than one part of the brain must be involved.

There’s also more to pain that just pain. Pain can be accompanied by catastrophizing thoughts and feelings of unpleasantness that are separate from the pain itself. These “pain plus” symptoms are common in fibromyalgia, and they imply different areas of the brain are affected as well.

http://www.cortjohnson.org/blog/2015/02/06/connections-pain-distress-circuit-fibromyalgia/
 
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