Volume 65, Issue 1 pp. 59-68
Rheumatoid Arthritis

The role of sleep problems in central pain processing in rheumatoid arthritis

Yvonne C. Lee

Corresponding Author

Yvonne C. Lee

Brigham and Women's Hospital, Boston, Massachusetts

Dr. Lee owns stock or stock options in Merck, Novartis, and Elan and has received research grants from Forest Research Institute.

Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, 75 Francis Street, PBB-B3, Boston, MA 02115Search for more papers by this author
Bing Lu

Bing Lu

Brigham and Women's Hospital, Boston, Massachusetts

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Robert R. Edwards

Robert R. Edwards

Brigham and Women's Hospital, Boston, Massachusetts

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Ajay D. Wasan

Ajay D. Wasan

Brigham and Women's Hospital, Boston, Massachusetts

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Nicholas J. Nassikas

Nicholas J. Nassikas

Brigham and Women's Hospital, Boston, Massachusetts

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Daniel J. Clauw

Daniel J. Clauw

University of Michigan, Ann Arbor

Dr. Clauw has received consulting fees from Jazz Pharmaceuticals, Pfizer, Eli Lilly, Forest Laboratories, Pierre Fabre Pharmaceuticals, UCB, Nuvo Research, and Merck & Company (less than $10,000 each) and has received research grants from Pfizer, Nuvo Research, and Forest Laboratories.

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Daniel H. Solomon

Daniel H. Solomon

Brigham and Women's Hospital, Boston, Massachusetts

Dr. Solomon has received research grants from Amgen, Abbott, and Eli Lilly and has served as an uncompensated member of committees overseeing pain medication clinical trials sponsored by Pfizer.

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Elizabeth W. Karlson

Elizabeth W. Karlson

Brigham and Women's Hospital, Boston, Massachusetts

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First published: 01 November 2012
Citations: 109

The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University and its affiliated academic health care centers, or the NIH.

Abstract

Objective

Among rheumatoid arthritis (RA) patients, the intensity of pain may be out of proportion to the severity of peripheral inflammation. This observation suggests that mechanisms of central nervous system pain amplification, such as diminished conditioned pain modulation (CPM), may play a role in enhancing pain perception among some RA patients. This study was undertaken to examine the level of CPM, pressure–pain threshold, and pressure–pain tolerance among RA patients compared to healthy controls.

Methods

Fifty-eight female RA patients and 54 age-matched female control subjects without chronic pain underwent quantitative sensory testing (QST) to assess CPM levels, pressure–pain thresholds, and pressure–pain tolerance levels. CPM was induced using a cold water bath, and the pain threshold (when patients first felt pain) and pain tolerance (when pain was too much to bear) were assessed with an algometer. Associations between RA and each QST outcome were analyzed using linear regression. Sleep problems, mental health, and inflammation were assessed as mediators of the relationship between RA and QST outcomes.

Results

The median CPM level was 0.5 kg/cm2 (interquartile range [IQR] −0.1, 1.6) among RA patients, compared to a median of 1.5 kg/cm2 (IQR −0.1, 2.5) among controls (P = 0.04). RA patients, compared to controls, had a lower pain threshold and lower pain tolerance at the wrists (each P ≤ 0.05). In addition, RA patients had greater problems with sleep, pain catastrophizing, depression, and anxiety (P < 0.0001 versus controls). Results of mediation analyses suggested that low CPM levels might be attributed, in part, to sleep disturbance (P = 0.04).

Conclusion

RA patients have impaired CPM when compared to pain-free control subjects. Sleep problems may mediate the association between RA and attenuated CPM.

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