Brain Advance Access originally published online on February 11, 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Brain, Vol. 127, No. 4, 835-843, 2004
© 2004 Guarantors of Brain
doi: 10.1093/brain/awh098
Pain catastrophizing and neural responses to pain among persons with fibromyalgia
1 Chronic Pain and Fatigue Research Center, Department of Internal Medicine, Division of Rheumatology, 2 Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA and 3 Department of Anesthesiology and Intensive Care, University of Cologne, Cologne, Germany
Correspondence to: Daniel J. Clauw, MD, University of Michigan Health System, Department of Internal Medicine, Division of Rheumatology, Chronic Pain and Fatigue Research Center, 24 Frank Lloyd Wright Drive, PO Box 385, Ann Arbor, MI 48106, USA E-mail: dclauw{at}med.umich.edu
Pain catastrophizing, or characterizations of pain as awful, horrible and unbearable, is increasingly being recognized as an important factor in the experience of pain. The purpose of this investigation was to examine the association between catastrophizing, as measured by the Coping Strategies Questionnaire Catastrophizing Subscale, and brain responses to blunt pressure assessed by functional MRI among 29 subjects with fibromyalgia. Since catastrophizing has been suggested to augment pain perception through enhanced attention to painful stimuli, and heightened emotional responses to pain, we hypothesized that catastrophizing would be positively associated with activation in structures believed to be involved in these aspects of pain processing. As catastrophizing is also strongly associated with depression, the influence of depressive symptomatology was statistically removed. Residual scores of catastrophizing controlling for depressive symptomatology were significantly associated with increased activity in the ipsilateral claustrum (r = 0.51, P < 0.05), cerebellum (r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.47, P < 0.05), and parietal cortex (r = 0.41, P < 0.05), and in the contralateral dorsal anterior cingulate gyrus (ACC; r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.41, P < 0.05), medial frontal cortex (r = 0.40, P < 0.05) and lentiform nuclei (r = 0.40, P < 0.05). Analysis of subjects classified as high or low catastrophizers, based on a median split of residual catastrophizing scores, showed that both groups displayed significant increases in ipsilateral secondary somatosensory cortex (SII), although the magnitude of activation was twice as large among high catastrophizers. Both groups also had significant activations in contralateral insula, SII, primary somatosensory cortex (SI), inferior parietal lobule and thalamus. High catastrophizers displayed unique activation in the contralateral anterior ACC, and the contralateral and ipsilateral lentiform. Both groups also displayed significant ipsilateral activation in SI, anterior and posterior cerebellum, posterior cingulate gyrus, and superior and inferior frontal gyrus. These findings suggest that pain catastrophizing, independent of the influence of depression, is significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala) and motor control. These results support the hypothesis that catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain. Activation associated with catastrophizing in motor areas of the brain may reflect expressive responses to pain that are associated with greater pain catastrophizing.
Key Words: catastrophizing; functional neuroimaging; fibromyalgia; pain modulation
Abbreviations: ACC= anterior cingulate cortex; BA = Brodmann area; fMRI = funtional MRI; IPL = inferior parietal lobule; MPQ = McGill Pain Questionnaire; SI = primary somatosensory cortex; SII = secondary somatosensory cortex; VAS = visual analogue scale
Received August 18, 2003. Revised November 25, 2003. Accepted December 9, 2003.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  M. Burgmer, M. Gaubitz, C. Konrad, M. Wrenger, S. Hilgart, G. Heuft, and B. Pfleiderer Decreased Gray Matter Volumes in the Cingulo-Frontal Cortex and the Amygdala in Patients With Fibromyalgia Psychosom Med, June 1, 2009; 71(5): 566 - 573. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Seifert, G. Kiefer, R. DeCol, M. Schmelz, and C. Maihofner Differential endogenous pain modulation in complex-regional pain syndrome Brain, March 1, 2009; 132(3): 788 - 800. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Lane, S. R. Waldstein, H. D. Critchley, S. W. G. Derbyshire, D. A. Drossman, T. D. Wager, N. Schneiderman, M. A. Chesney, J. R. Jennings, W. R. Lovallo, et al. The Rebirth of Neuroscience in Psychosomatic Medicine, Part II: Clinical Applications and Implications for Research Psychosom Med, February 1, 2009; 71(2): 135 - 151. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. A. Strigo, A. N. Simmons, S. C. Matthews, A. D. Craig, and M. P. Paulus Association of Major Depressive Disorder With Altered Functional Brain Response During Anticipation and Processing of Heat Pain Arch Gen Psychiatry, November 1, 2008; 65(11): 1275 - 1284. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. G. Astrakas, S. Konitsiotis, P. Margariti, S. Tsouli, L. Tzarouhi, and M. I. Argyropoulou T2 relaxometry and fMRI of the brain in late-onset restless legs syndrome Neurology, September 16, 2008; 71(12): 911 - 916. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Tracey Imaging pain Br. J. Anaesth., July 1, 2008; 101(1): 32 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Berman, B. D. Naliboff, B. Suyenobu, J. S. Labus, J. Stains, G. Ohning, L. Kilpatrick, J. A. Bueller, K. Ruby, J. Jarcho, et al. Reduced Brainstem Inhibition during Anticipated Pelvic Visceral Pain Correlates with Enhanced Brain Response to the Visceral Stimulus in Women with Irritable Bowel Syndrome J. Neurosci., January 9, 2008; 28(2): 349 - 359. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Passard, N. Attal, R. Benadhira, L. Brasseur, G. Saba, P. Sichere, S. Perrot, D. Januel, and D. Bouhassira Effects of unilateral repetitive transcranial magnetic stimulation of the motor cortex on chronic widespread pain in fibromyalgia Brain, October 1, 2007; 130(10): 2661 - 2670. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Cole, M. J. Farrell, E. P. Duff, J. B. Barber, G. F. Egan, and S. J. Gibson Pain sensitivity and fMRI pain-related brain activity in Alzheimer's disease Brain, November 1, 2006; 129(11): 2957 - 2965. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Montoya, C. Sitges, M. Garcia-Herrera, R. Izquierdo, M. Truyols, N. Blay, and D. Collado Abnormal Affective Modulation of Somatosensory Brain Processing Among Patients With Fibromyalgia Psychosom Med, November 1, 2005; 67(6): 957 - 963. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. McLean, D. J. Clauw, J. L. Abelson, and I. Liberzon The Development of Persistent Pain and Psychological Morbidity After Motor Vehicle Collision: Integrating the Potential Role of Stress Response Systems Into a Biopsychosocial Model Psychosom Med, September 1, 2005; 67(5): 783 - 790. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. R. Edwards Individual differences in endogenous pain modulation as a risk factor for chronic pain Neurology, August 9, 2005; 65(3): 437 - 443. [Abstract] [Full Text] [PDF]
|
|