American Pain Society's 27th Annual Scientific Meeting (May 8 – 10, 2008): Biopsychosocial influence on induced shoulder pain

8089 Biopsychosocial influence on induced shoulder pain

May 9, 2008: May 9, 2008
East Hall (Tampa Convention Center)
Steven Z. George, PhD , Department of Physical Therapy, University of Florida, Gainesville, FL
Geoffrey Dover, PhD , Department of Applied Kinesiology, University of Florida, Gainesville, FL
Margaret R. Wallace, PhD , Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL
Brandon K. Sack, BS , Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL
Deborah M. Herbstman, BA , Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL
Ece Aydog , Department of Physical Therapy, University of Florida, Gainesville, FL
Jessica Neff , Department of Physical Therapy, University of Florida, Gainesville, FL
Michael Fleming , Department of Physical Therapy, University of Florida, Gainesville, FL
Roger B. Fillingim, PhD , Department of Community Dentistry and Behavioral Science, University of Florida, Gainesville, FL
A proposed model suggests that the experience of pain is influenced by psychological and genetic factors. Our previous study reported that pain catastrophizing and catechol-O-methyltransferase (COMT) genotype influenced clinical pain ratings for patients seeking operative treatment of shoulder pain. The current study investigated whether these same psychological and genetic factors predicted responses to induced shoulder pain. Our a priori hypothesis was that subjects with high pain catastrophizing and COMT genotype indicative of low COMT enzyme activity would have the highest induced shoulder pain ratings. Subjects (n = 63) completed the Pain Catastrophizing Scale (PCS) and had COMT genotype determined by PCR-based strategies. Subjects then completed a standardized fatigue protocol to induce delayed onset muscle soreness and underwent post-fatigue assessments at 24, 48, and 72 hours. The post-fatigue assessments included pain intensity (visual analog scale), evoked pressure pain (visual analog scale), muscle force production (maximum voluntary isometric contraction), and upper-extremity disability (Disability of Arm, Shoulder, and Hand Questionnaire). Hierarchical regression investigated the contributions of pain catastrophizing and previously described COMT diplotypes for shoulder pain intensity at 72 hours. A statistically significant interaction between pain catastrophizing and COMT diplotype was detected, and this interaction was the strongest unique predictor of 72 hour pain intensity ratings. This same interaction was statistically significant for prediction of evoked pressure pain at 72 hours, but not for muscle force production or upper-extremity disability. In conclusion, these findings converge with those from the surgical cohort and provide additional evidence that pain catastrophizing and COMT diplotype have the potential to increase the risk of developing chronic pain syndromes. This study was supported by a grant from the University of Florida.
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