Associations Between Catastrophizing and Endogenous Pain-Inhibitory Processes: Sex Differences |
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| Authors: | Burel R. Goodin Lynanne McGuire Mark Allshouse Laura Stapleton Jennifer A. Haythornthwaite Noel Burns Lacy A. Mayes Robert R. Edwards |
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| Affiliation: | 2. Department of Psychology, Pennsylvania State University, York Campus, York, Pennsylvania;3. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland;1. Pain Research and Intervention Center of Excellence, Gainesville, Florida;2. Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, Tennessee;3. Department of Neurology in the Center for Human Experimental Therapeutics; and Director, Analgesic, Anesthetic, and Addiction Clinical Trial Translations, Innovations, Opportunities, and Networks (ACTTION), University of Rochester School of Medicine and Dentistry, Rochester, New York;4. Department of Psychiatry and Behavioral Sciences, School of Medicine, Department of Oral Medicine, School of Dentistry, University of Washington, Seattle, Washington;5. Department of Neurological Surgery, University of Washington, Seattle, Washington;1212. Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington;7. Department of Psychiatry and Behavioral Neuroscience, and Director, Women''s Health Research Program, University of Cincinnati College of Medicine, Cincinnati, Ohio;11. Fibromyalgia Research Unit, Oregon Health & Science University, Portland, Oregon;12. Brigham & Women''s Hospital, Chestnut Hill, Massachusetts;8. Department of Neurology, Harvard Medical School, Cambridge, Massachusetts;9. Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York;12121212. Food and Drug Administration, Center for Drug Evaluation and Research, Silver Spring, Maryland;71. Departments of Anesthesiology, Perioperative, and Pain Medicine, Pediatrics, Stanford University School of Medicine, Stanford, California;112. Department of Pharmacology, University of Arizona, Tucson, Arizona;123. University of Rochester Medical Center, School of Medicine and Dentistry, Rochester, New York;84. Clinical Epidemiology Unit, Boston, Massachusetts;95. Department of Oral Diagnostic Sciences, University at Buffalo, Buffalo, New York;121212121212. Director, Cancer Pain Program, Division of Hematology-Oncology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois;77. Food and Drug Administration, Center for Drug Evaluation and Research, Silver Spring, Maryland;1111. Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York;1212. Department of Oncology, Harry J. Duffey Family Professor of Palliative Medicine, and Director of Palliative Medicine, Johns Hopkins Medical Institutions, The Johns Hopkins Hospital, Baltimore, Maryland;88. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington;99. Department of Medicine, University of Texas Medical Branch, Galveston, Texas;1212121212121212. Department of Anesthesiology and Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania;1. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland;2. Department of Psychology, University of Alabama-Birmingham, Birmingham, Alabama;3. Department of Anesthesiology, University of Alabama-Birmingham, Birmingham, Alabama;1. Pain Center South, University Hospital Odense, Odense, Denmark;2. Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark;1. Department of Neurology, University of Wisconsin-Madison, Madison, WI, USA;2. CRI Lifetree Research, Salt Lake City, UT, USA;3. INSERM U-987, Centre d’Evaluation et de Traitement de la Douleur, Hôpital Ambroise Paré, APHP, Boulogne-Billancourt, France;4. Université Versailles Saint-Quentin, France;5. Division of Neurological Pain Research and Therapy, Department of Neurology, Universitatsklinikum Schleswig-Holstein, Kiel, Germany;6. Dental Public Health Sciences, University of Washington, Seattle, WA, USA;7. Mayo Clinic, 200 First Street SW, Rochester, MN, USA;8. Department of Anesthesiology, Harvard Medical School, Brigham & Women’s Hospital, Chestnut Hill, MA, USA;9. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA;10. Center for Neurosensory Disorders, University of North Carolina, CB No. 7280, 3330 Thurston Bldg, Chapel Hill, NC, USA;11. Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland;12. Clinical Pain Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, 17176 Stockholm, Sweden;13. Clinic of Physical and Rehabilitation Medicine, Brugmann University Hospital, 4 place Van Gehuchten, B-1020 Brussels, Belgium;14. Institute of Neuroscience, 52, Avenue E. Mounier, B-1200 Brussels, Belgium;15. Université Catholique de Louvain, Leuven, Belgium;p. Department of Neurology, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbH, Ruhr-University Bochum, Germany;q. Danish Pain Research Center and Department of Neurology, Aarhus University Hospital, Aarhus, Denmark;r. Department of Pain Medicine, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbH Bochum, Ruhr University Bochum, Germany;s. Center for Pain Evaluation and Treatment, University Neurological Hospital, Lyon, France;t. Imperial College London, UK;u. Chelsea and Westminster Hospital London, UK;v. Department of Palliative Medicine, Rheinische Friedrich-Wilhelms University, Bonn, Germany;w. Department of Neurology, MC Mutual, Barcelona, Spain;x. Neuroscience Technologies, Barcelona, Spain;y. Neuroscience Technologies, London, UK;z. Department of Neurology, Technische Universität München, Munich, Germany;11. Chair of Neurophysiology, Center for Biomedicine and Medical Technology Mannheim, Heidelberg University, Heidelberg, Germany;12. Department of Neuroscience and Rehabilitation, S. Anna University Hospital of Ferrara, Ferrara, Italy;13. University of Minnesota, 425 Delaware St SE, MMC 295, Minneapolis, MN, USA;14. Department of Anesthesiology, University of California-San Diego, La Jolla, CA, USA;15. Department of Family Medicine and Department of Anesthesia, McGill University, Montreal, Quebec, Canada;16. Department of Neurology, Rambam Health Care Campus, Haifa, Israel;17. Institute for Clinical Diabetology, German Diabetes Center at Heinrich Heine University, Leibniz Center for Diabetes Research and Department of Metabolic Diseases, University Hospital, Düsseldorf, Germany |
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| Abstract: | Pain catastrophizing is among the most robust predictors of pain outcomes, and a disruption in endogenous pain-inhibitory systems is 1 potential mechanism that may account for increased pain among individuals who report higher pain catastrophizing. Pain catastrophizing may negatively influence diffuse noxious inhibitory controls (DNIC), a measure of endogenous pain inhibition, through complex anatomical circuitry linking cortical responses to pain with processes that modulate pain. The current study examined whether DNIC mediated the relationship between catastrophizing and pain among 35 healthy young adults and examined the moderating effects of sex to determine whether the magnitude or direction of associations differed among men and women. DNIC was assessed using pressure pain thresholds on the forearm before and during a cold pressor task. Using bias-corrected bootstrapped confidence intervals, results showed that diminished DNIC was a significant partial mediator of the relation between greater pain-related catastrophizing and more severe pain ratings. Participant sex moderated these associations; higher catastrophizing predicted lower DNIC for men and women, however, the effect of catastrophizing on pain ratings was partially mediated by DNIC for women only. These findings further support the primary role of pain catastrophizing in modulation of pain outcomes.PerspectiveThese findings support the hypothesis that the heightened pain reported by individuals higher in pain catastrophizing may be related to a disruption in the endogenous modulation of pain, operationalized by assessing DNIC. Whether interventions that reduce pain catastrophizing affect pain outcomes via effects on DNIC is in need of investigation. |
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