Disrupted brain circuitry for pain-related reward/punishment in fibromyalgia.

[Ecoclimber]

Arthritis Rheumatol. 2014 Jan;66(1):203-12. doi: 10.1002/art.38191.
Disrupted brain circuitry for pain-related reward/punishment in fibromyalgia
Loggia ML, Berna C, Kim J, Cahalan CM, Gollub RL, Wasan AD, Harris RE, Edwards RR, Napadow V.
Author information
Abstract
OBJECTIVE:
While patients with fibromyalgia (FM) are known to exhibit hyperalgesia, the central mechanisms contributing to this altered pain processing are not fully understood. This study was undertaken to investigate potential dysregulation of the neural circuitry underlying cognitive and hedonic aspects of the subjective experience of pain, such as anticipation of pain and anticipation of pain relief.

METHODS:
Thirty-one FM patients and 14 controls underwent functional magnetic resonance imaging, while receiving cuff pressure pain stimuli on the leg calibrated to elicit a pain rating of ∼50 on a 100-point scale. During the scan, subjects also received visual cues informing them of the impending onset of pain (pain anticipation) and the impending offset of pain (relief anticipation).

RESULTS:
Patients exhibited less robust activation during both anticipation of pain and anticipation of relief within regions of the brain commonly thought to be involved in sensory, affective, cognitive, and pain-modulatory processes. In healthy controls, direct searches and region-of-interest analyses of the ventral tegmental area revealed a pattern of activity compatible with the encoding of punishment signals: activation during anticipation of pain and pain stimulation, but deactivation during anticipation of pain relief. In FM patients, however, activity in the ventral tegmental area during periods of pain and periods of anticipation (of both pain and relief) was dramatically reduced or abolished.

CONCLUSION:
FM patients exhibit disrupted brain responses to reward/punishment. The ventral tegmental area is a source of reward-linked dopaminergic/γ-aminobutyric acid-releasing (GABAergic) neurotransmission in the brain, and our observations are compatible with reports of altered dopaminergic/GABAergic neurotransmission in FM. Reduced reward/punishment signaling in FM may be related to the augmented central processing of pain and reduced efficacy of opioid treatments in these patients.

Copyright © 2014 by the American College of Rheumatology.

Note: Since this study is published in a top tier journal, it will have an impact in the field of Rheumatology and will add to the other published research articles regarding neuropathic pain and Fibromyalgia.

 

[Snow Leopard]

This is interesting, but I suspect such findings are not specific to FM, but could be observed in any patient with some sort of chronic pain (regardless of cause) that have had a similar pattern in medication use (eg similar prior use of opiods and the like).

 

[barbc56]

Interesting

I would not be surprised if someday FM will be seen by all in the medical community as a separate or subset of ME/CFS.

I noticed when I changed insurance companies there was only a diagnostic code for FM so don't know if it was lost during the transition nor do I remember the original diagnostic code but was told cfs.

When I was referred to a neurologist who specializes in sleep disorders, I found him more knowledable so he now handles my FM/ME/CFS. When I asked him if FM is neurological, immunological, or both he said it's still being debated.


I find the subject of brain images fascinating and hopefully someday doctors will be able to go beyond seeing abnormalities and actually be able to diagnosed.by just looking at a scan.

Some days I feel that if I had a brain scan all you would see is a vast emptiness.