Catastrophizing about pain is related to elevated pain severity and poor adjustment among chronic pain patients, but few physiological mechanisms by which pain catastrophizing maintains and exacerbates pain have been explored. We hypothesized that resting levels of lower paraspinal muscle tension and/or lower paraspinal and cardiovascular reactivity to emotional arousal may: (a) mediate links between pain catastrophizing and chronic pain intensity; (b) moderate these links such that only patients described by certain combinations of pain catastrophizing and physiological indexes would report pronounced chronic pain. Chronic low back pain patients (N = 97) participated in anger recall and sadness recall interviews while lower paraspinal and trapezius EMG and systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded. Mediation models were not supported. However, pain catastrophizing significantly interacted with resting lower paraspinal muscle tension to predict pain severity such that high catastrophizers with high resting lower paraspinal tension reported the greatest pain. Pain catastrophizing also interacted with SBP, DBP and HR reactivity to affect pain such that high catastrophizers who showed low cardiovascular reactivity to the interviews reported the greatest pain. Results support a multi-variable profile approach to identifying pain catastrophizers at © Springer Science+Business Media, LLC 2007 john.burns@rosalindfranklin.edu.
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KeywordsPain catastrophizing; Chronic pain severity; Lower paraspinal muscle tension; Cardiovascular reactivity; Profile approachCatastrophizing about pain is linked to elevated pain severity and poor adjustment among chronic pain patients (Sullivan et al. 1995). It is defined as a tendency to rumi-nate, magnify and feel helpless about pain (Sullivan et al. 1995), and as a negative automatic appraisal of painful stimuli rooted in activation of maladaptive beliefs or pain schemas (Michael and Burns 2004;Spanos et al. 1979;Sullivan et al. 2001). Irrespective of theoretical conceptualization, only a few physiological mechanisms by which pain catastrophizing maintains and exacerbates chronic pain intensity have been explored (e.g., Edwards and Fillingim 2005).Physical and psychological stress may lead to frequent and intense, or low level but sustained muscular contractions (Sjegaard et al. 2000). This muscle activity can increase pain through ischemia and hypoxia (Fields 1987), and through changes in mechanoreceptor sensitivity (Mense 1993). Flor and colleagues (Flor et al. 1985(Flor et al. , 1991(Flor et al. , 1992 proposed a "symptom-specificity" model of chronic pain, which proposes that patients with certain kinds of musculoskeletal disorders can be distinguished from patients with other kinds of musculoskeletal disorders by substantial stres...