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Widespread Pain Following Whiplash-Associated Disorders: Incidence, Course, and Risk Factors

LENA W. HOLM, LINDA J. CARROLL, J. DAVID CASSIDY, EVA SKILLGATE, and ANDERS AHLBOM

ABSTRACT.

Objective. To investigate the incidence and course of widespread pain (WP) subsequent to localized pain in subjects with whiplash-associated disorders (WAD); and to investigate the influence of depressive symptoms, neck pain intensity, number of whiplash-associated symptoms, and number of painful body areas on such conditions.

Methods. From a large prospective cohort of injury claimants who reported WAD after motor vehicle collision (MVC; n = 7462), we identified a subgroup with only localized head/neck/back pain, and who responded to one or more followup questionnaires mailed at 6 weeks and 4, 6, and 12 months after the MVC (n = 266). Pain drawings were distributed at the followup, and we defined WP as having 9 or more painful areas, including posterior neck, at any of these occasions. Depressive symptoms were assessed with the Center for Epidemiological Studies Depression Scale and pain intensity with a visual analog scale (VAS).

Results. The cumulative incidence of WP was 21%, and it occurred early after the injury. Continuous WP over the 12 months was rare. The odds for developing WP were greater in those with depressive symptoms (OR 3.2, 95% CI 1.6–6.3), VAS pain intensity 55–100 (OR 3.2, 95% CI 1.3–8.0), reporting ≥ 3 pain-associated symptoms (OR 1.9, 95% CI 0.9–3.8), and those reporting 4 or 5 painful body areas (OR 2.6, 95% CI 1.3–5.4).

Conclusion. WP occurred early in the course. Even though the cumulative incidence was 21%, continuous WP was rare. Subjects with WAD who report early depressive symptoms and more severe neck injury symptoms are at risk of developing WP after MVC. (First Release Dec 1 2006; J Rheumatol 2007;34:193–200)

Key Indexing Terms:

WHIPLASH
WIDESPREAD PAIN
NECK PAIN
DEPRESSIVE SYMPTOMS


From the Institute of Environmental Medicine, Division of Epidemiology, and Division of Cardiovascular Epidemiology, Karolinska Institutet; the Section of Personal Injury Prevention, Karolinska Institutet; and Stockholm Center for Public Health, Stockholm, Sweden; The Department of Public Health Sciences, Faculty of Medicine, and the Alberta Centre for Injury Control and Research, University of Alberta, Edmonton, Alberta, Canada; Rehabilitation Solutions, University Health Network; Division of Outcomes and Population Health, Toronto Western Research Institute; and Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

Supported by a grant from Saskatchewan Government Insurance. L.W. Holm is supported by a grant from the Swedish Council for Working Life and Social Research. L.J. Carroll is supported by a Health Scholar Award from the Alberta Heritage Foundation for Medical Research.

L.W. Holm, BSc, PhD candidate, Institute of Environmental Medicine, Division of Epidemiology, and the Section of Personal Injury Prevention, Karolinska Institutet; L.J. Carroll, PhD, Associate Professor, Department of Public Health Sciences, Faculty of Medicine, and Alberta Centre for Injury Control and Research; J.D. Cassidy, PhD, Professor, Rehabilitation Solutions, University Health Network; Division of Outcomes and Population Health, Toronto Western Research Institute, and Department of Public Health Sciences, Faculty of Medicine, University of Toronto; E. Skillgate, DN, PhD candidate, Institute of Environmental Medicine, Division of Cardiovascular Epidemiology, Karolinska Institutet; A. Ahlbom, PhD, Professor, Institute of Environmental Medicine, Division of Epidemiology, Karolinska Institutet, and Stockholm Center for Public Health.

Address reprint requests to L. Holm, Institute of Environmental Medicine, Division of Epidemiology, Karolinska Institutet, PO Box 210, SE-171 77 Stockholm, Sweden. E-mail: Lena.Holm@ki.se

Accepted for publication September 11, 2006.




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