Dr. Lee owns stock or stock options in Merck, Novartis, and Elan and has received research grants from Forest Research Institute.
The role of sleep problems in central pain processing in rheumatoid arthritis†
Article first published online: 27 DEC 2012
Copyright © 2013 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 65, Issue 1, pages 59–68, January 2013
How to Cite
Lee, Y. C., Lu, B., Edwards, R. R., Wasan, A. D., Nassikas, N. J., Clauw, D. J., Solomon, D. H. and Karlson, E. W. (2013), The role of sleep problems in central pain processing in rheumatoid arthritis. Arthritis & Rheumatism, 65: 59–68. doi: 10.1002/art.37733
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.
- Issue published online: 27 DEC 2012
- Article first published online: 27 DEC 2012
- Accepted manuscript online: 1 NOV 2012 12:38PM EST
- Manuscript Accepted: 27 SEP 2012
- Manuscript Received: 26 MAR 2012
- Harvard Catalyst | The Harvard Clinical and Translational Science Center
- National Center for Research Resources
- National Center for Advancing Translational Sciences
- NIH. Grant Numbers: UL1-RR-025758, AR-057578, AG-034982, AR-057920, AR-055989, AR-49880, AR-047782, AR-052403
- Harvard University
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.
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.
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).
RA patients have impaired CPM when compared to pain-free control subjects. Sleep problems may mediate the association between RA and attenuated CPM.