Ratings of experimental pain and pain-related negative affect predict clinical pain in patients with fibromyalgia syndrome Roland Staud a, * , Michael E. Robinson b , Charles J. Vierck Jr. c , Richard C. Cannon c , Andre P. Mauderli c , Donald D. Price d a Department of Medicine, McKnight Brain Institute, University of Florida College of Medicine, SW Archer Road, P.O. Box 100221, Gainesville, FL 32610-0221, USA b Department of Clinical and Health Psychology, McKnight Brain Institute, University of Florida College of Medicine, SW Archer Road, P.O. Box 100221, Gainesville, FL 32610-0221, USA c Department of Neuroscience, McKnight Brain Institute, University of Florida College of Medicine, SW Archer Road, P.O. Box 100221, Gainesville, FL 32610-0221, USA d Department of Prosthodontics, McKnight Brain Institute, University of Florida College of Medicine, SW Archer Road, P.O. Box 100221, Gainesville, FL 32610-0221, USA Received 3 February 2003; received in revised form 23 April 2003; accepted 6 May 2003 Abstract Patients with fibromyalgia syndrome (FMS) report chronic pain related to abnormal sensitivity of muscles that is reflected by so-called tender points (TP). TP represent areas of abnormal mechanical pain thresholds that have only shown a minor correlation with clinical pain of FMS patients and seem to be better suited for predicting distress. Pain-related negative affect (PRNA), abnormal temporal summation of second pain (termed wind-up or WU), and abnormal WU decay are frequently present in FMS patients. WU and WU decay can provide measures of central sensitization, which may contribute to clinical FMS pain. We therefore investigated the role of WU, WU decay, TP count, and PRNA as predictors of clinical pain in FMS subjects. Fifty-five FMS subjects rated their clinical pain at entry into the study using a visual analogue scale (VAS). After a TP evaluation, all subjects received two trials of thermal WU and WU decay testing. Hierarchical regression analysis demonstrated that the combination of PRNA ratings, TP count, and WU decay ratings predicted 49.7% of the variance of clinical pain in FMS. This model demonstrates independent relationships of biological and psychological factors to clinical pain and underscores the important role of abnormal peripheral and central pain mechanisms for FMS. Therefore, the combination of PRNA, TP count, and WU decay may provide an excellent measure for future clinical studies of FMS patients. q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Keywords: Fibromyalgia; Muscle; Predictor; Chronic pain intensity; Temporal summation 1. Introduction Widespread musculoskeletal pain is required for the diagnosis of fibromyalgia syndrome (FMS). The pain is most consistently described as dull and aching and appears to be related to deep tissue structures. Accordingly, FMS patients will present with widespread tenderness to mechan- ical stimulation of deep tissues (Simms et al., 1988; Arroyo and Cohen, 1993; Berglund et al., 2002). Tenderness in FMS is usually assessed by pressure algometry, the reliability of which has been reported previously (Jensen et al., 1986; Ohrbach and Gale, 1989a; Ohrbach and Gale, 1989b; Kosek et al., 1993). There is convincing evidence of generalized lower pressure pain thresholds in FMS patients compared to normal controls (NC) (Lautenschlager et al., 1988; Quimby et al., 1988; Tunks et al., 1988; Wolfe et al., 1990; Mikkelsson et al., 1992; Granges and Littlejohn, 1993; Kosek et al., 1995). The muscle tenderness of FMS patients is reflected by the allodynia of tender point (TP) which have been defined for 18 areas of the body by the American College of Rheumatology (ACR) (Wolfe et al., 1990). In contrast to NC, FMS patients report pain at TP sites when stimulated with pressures of # 4 kg (Wolfe et al., 1990). TP counts of FMS patients have shown a disappoint- ing lack of predictability for clinical pain in most studies 0304-3959/03/$20.00 q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. doi:10.1016/S0304-3959(03)00208-2 Pain 105 (2003) 215–222 www.elsevier.com/locate/pain * Corresponding author. Tel.: þ 1-352-392-4681; fax: þ1-352-392-8483. E-mail address: staudr@ufl.edu (R. Staud).