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Somatosensory Cortex Linked to Increased Sensitivity to Touch in Fibromyalgia

  [ 18 votes ]   [ 2 Comments ]
By Manyoel Lim, PhD et al. • www.ProHealth.com • February 2, 2015


Editor's comment: The somatosensory cortex is the part of the brain that processes input from areas of the body that are sensitive to touch. This study found that rather than inhibiting or reducing the sensation of pain experienced by touch, the somatosensory cortex of people with fibromyalgia is more excitable and thus more likely to interpret touch as painful.

Disinhibition of the primary somatosensory cortex in patients with fibromyalgia.

Abstract:

Fibromyalgia (FM) is a chronic widespread pain condition linked to central sensitization. Altered excitability of sensorimotor cortex has been proposed as an underlying pathology of FM. This study aimed to investigate intracortical excitability of the primary somatosensory cortex (S1) and its potential role in clinical pain in patients with FM.

Somatosensory evoked magnetic fields were recorded in 17 right-handed females with FM and 21 age-, sex- and handedness-matched healthy control subjects. Paired-pulse median nerve stimulation was delivered to the left and right wrist. We assessed the peak-to-peak amplitudes of the N20m-P35m and peak amplitude of each N20m and P35m component. Paired-pulse suppression (PPS) of the second response was quantified as the ratio of the amplitudes of the second to the first response.

Patients with FM displayed significantly higher PPS ratio for the N20m-P35m in both hemispheres, indicating reduced intracortical inhibition in the S1. Notably, PPS ratio for the P35m was higher in patients with FM than in healthy controls, while no differences were apparent in PPS ratio for the N20m in both hemispheres. PPS ratios for both the N20m-P35m and the P35m in the left hemisphere were positively associated with the sensory pain on the short-form McGill Pain Questionnaire.

The present study demonstrated that intracortical inhibition in the S1 is compromised bilaterally in patients with FM, and the extent of disinhibition can be closely associated with increased clinical pain. Our results suggest that changes of intracortical inhibition of the S1 may contribute to the pathophysiology of FM pain.

Source: Pain, January 27, 2015. By Lim, Manyoel PhD; Roosink, Meyke PhD; Kim, June Sic PhD; Kim, Dajung J. PhD; Kim, Hye Won MD; Lee, Eun Bong MD, PhD; Kim, Hyun Ah MD, PhD; Chung, Chun Kee MD, PhD. Seoul National University Hospital, Seoul, South Korea.




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Article Comments Post a Comment

Thank You
Posted by: IanH
Feb 2, 2015
for bringing this study to a our attention.
Disinhibition is now becoming a significant factor in both FM and ME.
Reply Reply

 
Sensitivity possibly explained
Posted by: SiSiRN
Feb 3, 2015
This is an important piece of information and I hope to see the study repeated. For the patient community, it explains that we do experience pain others would find innocuous. It is difficult for us and those around us to understand, now we may know why. Knowing won't change it, but it does give us ammunition for improving the neuroplasticity we experience through creative visualization. To do be able to do something, is better than to do nothing.

 

 
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