The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort
Version of Record online: 5 MAY 2005
Copyright © 2005 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 52, Issue 5, pages 1577–1584, May 2005
How to Cite
Giesecke, T., Gracely, R. H., Williams, D. A., Geisser, M. E., Petzke, F. W. and Clauw, D. J. (2005), The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort. Arthritis & Rheumatism, 52: 1577–1584. doi: 10.1002/art.21008
- Issue online: 5 MAY 2005
- Version of Record online: 5 MAY 2005
- Manuscript Accepted: 20 JAN 2005
- Manuscript Received: 25 OCT 2004
- Department of the Army. Grant Number: DAMD 17-00-2-0018
- NIH (grant from the General Clinical Research Center Program of the National Center for Research Resources). Grant Numbers: 5-R01-AT000004-02, 5-M01-RR13297
Individuals with chronic pain frequently display comorbid depression, but the impact of symptoms of depression on pain processing is not completely understood. This study evaluated the effect of symptoms of depression and/or clinically diagnosed major depressive disorder (MDD) on pain processing in patients with fibromyalgia (FM).
Results of quantitative sensory testing and neural responses to equally painful pressure stimuli (measured by functional magnetic resonance imaging [fMRI]) were compared with the levels of symptoms of depression and comorbid MDD among patients with FM.
Neither the level of symptoms of depression nor the presence of comorbid MDD was associated with the results of sensory testing or the magnitude of neuronal activation in brain areas associated with the sensory dimension of pain (primary and secondary somatosensory cortices). However, symptoms of depression and the presence of MDD were associated with the magnitude of pain-evoked neuronal activations in brain regions associated with affective pain processing (the amygdalae and contralateral anterior insula). Clinical pain intensity was associated with measures of both the sensory dimension of pain (results of sensory testing) and the affective dimension of pain (activations in the insula bilaterally, contralateral anterior cingulate cortex, and prefrontal cortex).
In patients with FM, neither the extent of depression nor the presence of comorbid major depression modulates the sensory-discriminative aspects of pain processing (i.e., localizing pain and reporting its level of intensity), as measured by sensory testing or fMRI. However, depression is associated with the magnitude of neuronal activation in brain regions that process the affective-motivational dimension of pain. These data suggest that there are parallel, somewhat independent neural pain-processing networks for sensory and affective pain elements. The implication for treatment is that addressing an individual's depression (e.g., by prescribing an antidepressant medication that has no analgesic properties) will not necessarily have an impact on the sensory dimension of pain.