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Fear of pain, not pain catastrophizing, predicts acute pain intensity, but neither factor predicts tolerance or blood pressure reactivity: An experimental investigation in pain-free individuals
European Journal of Pain 10 (2006) 457–465 www.EuropeanJournalPain.com
Fear of pain, not pain catastrophizing, predicts acute pain intensity, but neither factor predicts tolerance or blood pressure reactivity: An experimental investigation in pain-free individuals Steven Z. George
a,*
, Erin A. Dannecker b, Michael E. Robinson
c
a
c
Department of Physical Therapy, Brooks Center for Rehabilitation Studies, University of Florida, United States b Department of Physical Therapy, University of Missouri, United States Department of Clinical and Health Psychology, Center for Pain Research and Behavioral Health, University of Florida, P.O. Box 100154, Gainesville, FL 32610-0154, United States Received 22 November 2004; accepted 28 June 2005 Available online 10 August 2005
Abstract Previous studies of the Fear-Avoidance Model of Exaggerated Pain Perception have commonly included patients with chronic low back pain, making it difficult to determine which psychological factors led to the development of an ‘‘exaggerated pain perception’’. This study investigated the validity of the Fear-Avoidance Model of Exaggerated Pain Perception by considering the influence of fear of pain and pain catastrophizing on acute pain perception, after considering sex and anxiety. Thirty-two males and 34 females completed the State-Trait Anxiety Inventory, the Fear of Pain Questionnaire, and the Coping Strategies Questionnaire. Subjects underwent a cold pressor procedure and tolerance, pain intensity, and blood pressure reactivity were measured. Sex, anxiety, fear of pain, and pain catastrophizing were simultaneously entered into separate multiple regression models to predict different components of pain perception. Tolerance was not predicted by fear of pain, pain catastrophizing, or anxiety. Pain intensity at threshold and tolerance were significantly predicted by fear of pain, only. Blood pressure reactivity to pain was significantly predicted by anxiety, only. These results suggest that fear of pain may have a stronger influence on acute pain intensity when compared to pain catastrophizing, while neither of the factors predicted tolerance or blood pressure reactivity. Ó 2005 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. Keywords: Fear-avoidance; Pain sensitivity; Quantitative sensory testing; Cold pressor; Experimental pain; Threshold; Tolerance; Anxiety
1. Introduction The Fear-Avoidance Model of Exaggerated Pain Perception (FAMEPP) describes one way chronic sympAbbreviations: FAMEPP, Fear-Avoidance Model of Exaggerated Pain Perception; LBP, low back pain; STAI, State-Trait Anxiety Questionnaire; FPQ-III, Fear of Pain Questionnaire; CSQ, Coping Strategies Questionnaire; NRS, numerical rating scale; SBP, systolic blood pressure. * Corresponding author. Tel.: +1 352 273 6432. E-mail address: [email protected]fl.edu (S.Z. George).
toms develop following an acute injury (Lethem et al., 1983; Slade et al., 1983). In this model, elevated fear of pain is hypothesized to induce avoidance behavior, which in turn leads to a disuse syndrome, chronic disability, and an exaggerated pain perception. The definition of exaggerated pain perception used for this study was proposed as (Lethem et al., 1983), ‘‘pain experience and/or behavior (and/or physiological responses to pain stimulation), which are (is) out of all proportion to demonstrable organic pathology or current levels of nociceptive stimulation (page 402).’’ In 1995 and 2000,
1090-3801/$32 Ó 2005 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ejpain.2005.06.007
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Vlaeyen et al. modified the FAMEPP by stressing the importance of pain catastrophizing (Vlaeyen et al., 1995a,b; Vlaeyen and Linton, 2000). Pain catastrophizing is conceptualized by cognitions of the inability to tolerate painful situations, thinking pain is unbearable, or ruminating on the worst possible outcome from the experienced pain (Sullivan et al., 2001). Thus, in the modified model, frequent pain catastrophizing and elevated fear of pain led to chronic disability and an exaggerated pain perception (Vlaeyen et al., 1995a,b; Vlaeyen and Linton, 2000). The literature on the FAMEPP has primarily sampled patients with low back pain (LBP) and prospective studies have demonstrated that fear of pain and pain catastrophizing are involved in the development of chronic disability. For example, during acute LBP, elevated fear of pain has been predictive of self-report of disability 4 weeks later (Fritz et al., 2001), 8 weeks later (Klenerman et al., 1995), and 12 months later (Sieben et al., 2002). In addition, frequent pain catastrophizing during acute LBP was predictive of self-reported disability 6 months (Picavet et al., 2002) and 1 year later (Burton et al., 1995), even after considering select historical and clinical predictors. Together, these studies provide strong evidence that fear of pain and pain catastrophizing are precursors to chronic disability, not the result of experiencing chronic symptoms (Linton, 2000; Pincus et al., 2002). Other studies have also shown that fear of pain and pain catastrophizing are associated with an exaggerated pain perception (Crombez et al., 1999; Severeijns et al., 2001; van den Hout et al., 2001; Vlaeyen et al., 1995b). However, cross-sectional studies involving patients with chronic symptoms do not directly address whether fear of pain and pain catastrophizing are involved in the development of an exaggerated pain perception. Some evidence exists in the literature, as increasing fear of pain during the first 2 weeks of acute LBP was reported to have a trend relationship (p = 0.08) with increasing pain intensity (Sieben et al., 2002) and pain catastrophizingÕs association with acute pain perception has been observed in experimental settings (Geisser et al., 1992; Sullivan et al., 1995, 2000). Studies investigating fear of pain and pain catastrophizingÕs influence on acute pain perception are another method of examining this topic, but such studies are uncommon in the literature. The FAMEPP makes a theoretical distinction between the concepts of fear of pain and pain catastrophizing. Simultaneous use of these measures is infrequently reported in the literature and each measureÕs unique contribution to acute pain perception beyond pain intensity has not been previously reported to the best of our knowledge. Another study investigating fear of pain and pain catastrophizing studied their association with pain intensity, but pain sensitivity and physiologi-
cal response measures were not utilized (Sullivan et al., 1995). Clinical studies of the FAMEPP can be difficult to interpret because of variability from several sources (e.g., mechanisms, onset, and severity of the low back injury, experience with previous episodes of LBP onset, and delay from LBP onset to seeking treatment). There is also the question of whether fear of pain and pain catastrophizing precede or are a result of long standing LBP (Hadjistavropoulos and Craig, 1994; Mannion et al., 1996). Given these considerations, we believe a laboratory investigation using a controlled stimulus to induce pain that mimics musculoskeletal pain is warranted to investigate the FAMEPP. The purpose of this study was to determine whether the FAMEPP components of fear of pain and pain catastrophizing significantly contribute to the subsequent perception of pain. A standardized stimulus (cold pressor) was used to induce pain and measures of pain tolerance, pain intensity, and systolic blood pressure (SBP) reactivity were assessed. Our hypothesis was that fear of pain and pain catastrophizing would significantly contribute to tolerance, pain intensity, and SBP reactivity related to the induced pain.
2. Methods 2.1. Subjects Subjects were recruited from undergraduate and graduate psychology, business management, and exercise science courses at the University and received extra credit for their research participation. Exclusion criteria for the study were a history of any one of the following: prior experience with the cold pressor stimulus, RaynaudÕs phenomenon or disease, diabetes, high blood pressure, vascular insufficiency, or a chronic pain condition. The sample consisted of 66 subjects, 32 (49%) males, mean age of 21.8 years (SD = 3.4 years), and 15.1 (SD = 1.6) years of formal education. The sample was 74% (49/66) Caucasian, 9% (6/66) Hispanic, 6% (4/66) Asian, 6% (4/66) African American, 3% (2/66) Native American, and 1% (1/66) other. 2.2. Fear-Avoidance Model The current version of the FAMEPP proposes that negative affect (anxiety), pain catastrophizing, and pain-related fear are relevant psychological components leading to the development of an exaggerated pain perception (Vlaeyen and Linton, 2000). Therefore, subjects completed the following psychological questionnaires: The State-Trait Anxiety Questionnaire (STAI) measured negative affect from anxiety. The STAI is a 40-item, 4-point rating scale that is commonly used to assess dispositional (trait) and situational (state)
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anxiety symptoms (Spielberger et al., 1983). We administered and reported the state portion of the STAI as it best matched the FAMEPP and our proposed hypotheses. The Fear of Pain Questionnaire (FPQ-III) measured fear of pain. The FPQ-III is a 30-item, 5-point rating scale that measures fear about specific situations that would normally produce pain (McNeil and Rainwater, 1998). The FPQ-III is a commonly used and wellvalidated instrument that is appropriate for use in non-clinical and clinical populations (Albaret et al., 2004; McNeil and Rainwater, 1998; Osman et al., 2002). We administered and reported the total score of the FPQ-III as it best matched the FAMEPP and our proposed hypotheses. The Coping Strategies Questionnaire (CSQ) measured pain catastrophizing. The CSQ is a 27-item, 7-point rating scale that measures the frequency of use for common pain coping strategies (Rosenstiel and Keefe, 1983). The CSQ contains a catastrophizing subscale that measures helplessness and pessimistic cognitions related to pain perception. The validity of this particular subscale has been supported (Keefe et al., 1989; Robinson et al., 1997; Rosenstiel and Keefe, 1983; Stewart et al., 2001) and the currently recommended scoring system was used in this study (Robinson et al., 1997).
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2.5. Measures of pain perception Measures of tolerance, pain intensity, and SBP reactivity were assessed in this study. Tolerance was noted when subjects removed their hand from the cold pressor because they could no longer withstand the cold water due to pain and it was measured by time. Subjects were also asked to provide pain intensity ratings at threshold (when pain was first noted by the subject) and at tolerance. A numerical rating scale (NRS) with zero corresponding to ‘‘no pain sensation’’ and 100 corresponding to ‘‘most intense pain sensation imagined’’ was used. SBP reactivity was selected as the physiological measure of pain response for this study because previous studies have demonstrated significant associations between experimental pain stimuli, resting SBP (Bruehl et al., 1992; Lowery et al., 2003; Myers et al., 2001), and SBP reactivity (Lowery et al., 2003; Maixner and Humphrey, 1993; Peckerman et al., 1991). SBP was monitored on the subjectÕs right arm throughout the study procedures using a Dinamap Critikon automatic monitor. Mean baseline SBP was calculated from three resting systolic BP measures taken 1-minute apart. Then, SBP readings taken at pain tolerance were subtracted from the baseline SBP to determine SBP reactivity. 2.6. Procedures
2.3. Experimental pain procedure Pain was induced in the left hand using a cold pressor (NesLab Instruments, Portsmouth, NH) that maintained temperature at 2.0 °C (±0.2 °C). The cold pressor continuously circulated cold water to prevent local warming around the hand. There were two reasons the cold pressor was selected for this study: (1) A previous study (Rainville et al., 1992) has suggested that the pain quality of this procedure is similar to that of musculoskeletal pain, since ratings of pain unpleasantness typically exceed those of pain intensity (Price et al., 1987). (2) It is a tonic nociceptive stimulus with a long enough stimulus duration to elicit pain responses related to the psychological components measured in this study (Geisser et al., 1992; Sullivan et al., 1995, 2000). 2.4. Assessment of threat from pain stimulus After a description of the cold pressor procedure was provided, the subjectsÕ perception of threat from the stimulus was measured. The definition of threat used for this study was ‘‘anticipated or actual physical or psychological harm, loss, injury or damage’’ the subject expected while performing the cold pressor task. Subjects were provided this written definition while rating their ‘‘threat’’ using a 10-cm VAS with endpoints of ‘‘none’’ and ‘‘most severe threat imaginable’’.
This protocol was approved by the UniversityÕs Institutional Review Board and subjects read and signed a consent form that had also been approved by the UniversityÕs Institutional Review Board before participating in any study-related procedures. Subjects were screened by self-report for tobacco use or caffeine ingestion in the last 3 h and/or the use of pain relievers in the last 12 h because of potential effects on physiological and pain measures. Then, demographic and psychological questionnaires were completed. Resting blood pressure measures were completed after a 20-min seated, quiet rest period. Then, subjects remained seated and the investigator provided the following instructions: ‘‘I will ask you to submerge your left hand up to your wrist, into this container of water. Keep your fingers spread apart under the water, but do not move your fingers. Please say ‘‘pain’’ at the point the cold sensation first begins to feel painful. This is very important, as I cannot tell when you feel pain unless you tell me. You may remove your hand from the water when you can no longer tolerate the pain, but it is important that you leave your hand in the water as long as you possibly can.’’ The investigator recorded the subjectsÕ responses to the cold pressor at threshold (time and intensity rating) and at tolerance (time, intensity rating, and SBP). Subjects were not informed of the amount of time that
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sex, anxiety, and time to stimulus tolerance (to account for any time-related differences in reaching tolerance) in the first block and fear of pain and pain catastrophizing in the second block. An alpha level of 0.05 was used to test our hypotheses.
passed while their hand was immersed in the cold pressor, but they were instructed to remove their hand if more than 4 min elapsed for safety purposes.
3. Data analysis Descriptive statistics were generated for all the measures and effect sizes (CohenÕs d) were calculated to assess the magnitude of sex differences in threshold and tolerance. Correlation coefficients were reported between the psychological and pain perception measures to assess univariate associations before variables were entered into multivariate models. Then, four separate hierarchical regression analyses were constructed. All regression models included sex to account for previous reports describing significant sex differences in response to experimental pain stimuli (Edwards et al., 2000; Fillingim et al., 1998; Frot et al., 2004; Maixner and Humphrey, 1993; Riley et al., 1998; Robinson et al., 2004; Sarlani et al., 2004; Sarlani and Greenspan, 2002). All regression models also included anxiety to account for negative affect as per the modified FAMEPP utilized in this study (Vlaeyen and Linton, 2000). Variance inflation factor (VIF) was reported for all regression models to investigate the potential of collinearity among independent variables.(Kleinbaum et al., 1998) The first regression model predicted tolerance with sex and anxiety in the first block and fear of pain and pain catastrophizing in the second block. The second regression model predicted pain intensity at threshold with sex, anxiety, and time to threshold (to account for any time-related differences in reaching threshold) in the first block and fear of pain and pain catastrophizing in the second block. The third regression model predicted pain intensity at tolerance with sex, anxiety, and time to symptom tolerance (to account for any time-related differences in reaching tolerance) in the first block and fear of pain and pain catastrophizing in the second block. The fourth model predicted SBP reactivity with
4. Results Descriptive statistics for the measures are included within Table 1. The mean threat level from the cold pressor was 1.9 cm (SD = 1.6 cm) for these subjects. The effect sizes observed in this study for sex differences were d = 0.42 for threshold and d = 0.36 for stimulus tolerance with higher ratings in women than men, which are consistent with previous reports in the literature involving experimental pain stimuli (Riley et al., 1998). Correlation coefficients for the relationships between all measures are provided within Table 2. Among the independent variables (i.e., psychological measures), the strongest univariate association was between fear of pain and pain catastrophizing (r = 0.453, p < 0.01) and the VIFÕs for the multiple regression models were low (Tables 3–6). These results provided a strong indication that excessive collinearity among independent variables was not a major concern in this study (KleinTable 1 Summary of pain perception and fear-avoidance measures Measure (n = 66)
Observed range
Mean (SD)
Pain perception Threshold intensity (NRS rating) Threshold time (s) Tolerance intensity (NRS rating) Tolerance time (s) Change in SBP (mm/Hg)
10–100 1–33 50–100 7–213 11–53
48.8 11.5 82.3 78.9 15.4
21–58 46–122
46.4 (9.8) 78.8 (17.5)
Fear-avoidance model State-trait anxiety index Fear of pain questionnaire Coping strategies questionnaire Catastrophizing scale
0–14
(21.9) (7.8) (15.6) (61.0) (12.7)
6.2 (4.0)
Table 2 Associations between pain perception and fear-avoidance measures Measures Threshold intensity (1) Threshold time (2) Tolerance intensity (3) Tolerance time (4) Change in systolic BP (5) Fear of pain questionnaire (6) Coping strategies questionnaire Catastrophizing scale (7) State-trait anxiety index (8) * **
p < 0.05 (2-tailed). p < 0.01 (2-tailed).
2
3 0.156
0.351** 0.164
4
5 0.273* 0.407** 0.221
6 0.104 0.099 0.044 0.174
7 0.355** 0.020 0.327** 0.113 0.188
8 0.254* 0.148 0.036 0.200 0.044 0.453**
0.053 0.015 0.032 0.042 0.283* 0.173 0.070
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Table 3 Hierarchical regression model for tolerance Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI)
0.06
0.161
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.09
Ba (95% CI)
Betaa
p-Valuea
VIF
26.0 ( 55.8, 3.8) 0.1 ( 1.7, 1.4)
0.23 0.02
0.086 0.857
1.01 1.03
2.6 ( 6.8, 1.7) 0.1 ( 1.0, 0.9)
0.17 0.02
0.228 0.897
1.27 1.29
p-Valuea
VIF
0.366
VIF – variance inflation factor. a Reported coefficients are for final models.
Table 4 Hierarchical regression model for pain intensity at threshold Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to intensity (s)
0.03
0.619
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.19
Ba (95% CI)
Betaa
3.1 ( 13.6, 7.3) 0.3 ( 0.8, 0.3) 0.6 ( 1.2, 0.1)
0.07 0.12 0.20
0.550 0.317 0.099
1.07 1.03 1.08
0.9 ( 0.6, 2.3) 0.4 (0.1, 0.7)
0.176 0.31
0.240 0.021
1.31 1.29
Ba (95% CI)
Betaa
p-Valuea
VIF
0.004
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
Table 5 Hierarchical regression model for pain intensity at tolerance Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to symptom tolerance (s)
0.05
0.354
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.18
0.9 ( 8.3, 6.4) 0.1 ( 0.4, 0.3) 0.1 ( 0.1, 0.1)
0.03 0.02 0.24
0.802 0.868 0.054
1.06 1.03 1.10
0.4 ( 1.4, 0.7) 0.4 (0.1, 0.6)
0.09 0.40
0.482 0.004
1.30 1.29
p-Valuea
VIF
0.011
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
Table 6 Hierarchical regression model for SBP reactivity Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to symptom tolerance (s)
0.11
0.074
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.13
Ba (95% CI)
Betaa
0.2 ( 6.2, 6.4) 0.3 (0.1, 0.6) 0.1 ( 0.1, 0.1)
0.01 0.25 0.16
0.962 0.044 0.214
1.06 1.03 1.09
0.3 ( 1.1, 0.6) 0.1 ( 0.1, 0.3)
0.08 0.16
0.567 0.253
1.29 1.29
0.516
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
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baum et al., 1998). Among the dependent variables (i.e., pain perception measures), there were statistically significant associations between threshold and tolerance time (r = 0.407, p < 0.01), pain intensity at threshold and at tolerance (r = 0.351, p < 0.01), and pain intensity at threshold and the tolerance time (r = 0.273, p < 0.05). These results indicated that the pain perception measures shared a maximum of 16% variance and were appropriate for use as separate dependent variables in our subsequent regression models. 4.1. Regression analyses for tolerance The regression model for tolerance time is summarized in Table 3. Sex and anxiety were not significant predictors of pain behavior, explaining only 6% variance (p = 0.161). The addition of fear of pain and pain catastrophizing explained an additional 3% variance in pain behavior, but this addition was not statistically significant (p = 0.366). These results suggest that the specific psychological components of the FAMEPP did not improve prediction of tolerance. 4.2. Regression analyses for pain intensity The regression models for pain intensity at threshold and tolerance are summarized in Tables 4 and 5, respectively. Sex and anxiety were not significant predictors of pain intensity explaining only 3% variance (p = 0.619) at threshold and 5% variance (p = 0.354) at tolerance. The addition of fear of pain and pain catastrophizing significantly improved (p < 0.05) the prediction of pain intensity for both models, explaining an additional 16% variance at threshold and 13% variance at tolerance. In the final model, fear of pain was the only statistically significant predictor for pain intensity at threshold (b = 0.31, p = 0.021) and tolerance (b = 0.40, p = 0.004). These results suggest that the specific psychological components of the FAMEPP improve the prediction of pain intensity at threshold and tolerance, after considering sex and anxiety. In addition, these results suggest that fear of pain was the only significant individual predictor of pain intensity. 4.3. Regression analyses for SBP reactivity to pain The regression model for SBP reactivity to pain is summarized in Table 6. Sex and anxiety were not significant predictors of SBP reactivity to pain, explaining 11% variance (p = 0.074). The addition of fear of pain and pain catastrophizing explained an additional 2% variance in SBP reactivity to pain (p = 0.516). These results suggest that the specific psychological components of the FAMEPP were not significant predictors of change in SBP. While the final model was not predictive of SBP reactivity to pain, anxiety was a significant indi-
vidual predictor (b = 0.25, p = 0.044) suggesting it alone influenced SBP reactivity to pain.
5. Discussion This study investigated specific psychological components of the FAMEPP for their influence on acute pain perception during application of a standardized pain stimulus. This stimulus produced a tonic experimental pain, which we believed to be of sufficient duration to allow psychological and coping parameters to operate (Geisser et al., 1992; Sullivan et al., 1995, 2000). In addition, the use of such a laboratory setting allowed subjects to complete psychological questionnaires prior to pain onset, which allowed for variation in pain perception to be attributed to psychological factors of interest. This methodology also allowed for a multidimensional definition of pain perception to be studied including the measurement of tolerance, pain intensity, and SBP reactivity. Neither fear of pain nor pain catastrophizing improved the prediction of tolerance during the cold pressor task. This unexpected finding contrasts with the majority of clinical studies linking these factors with avoidance behavior (Al Obaidi et al., 2000, 2003; Crombez et al., 1999; Geisser et al., 1992; McNeil and Rainwater, 1998; Sullivan et al., 2002; Vlaeyen et al., 1995a). However, previous studies involving patients with chronic LBP were primarily cross-sectional, unable to distinguish if fear of pain or pain catastrophizing preceded or followed avoidance behavior (Al Obaidi et al., 2000, 2003; Crombez et al., 1999; Sullivan et al., 2002; Vlaeyen et al., 1995a). The previous studies involving tolerance in pain free individuals did not include both fear of pain and pain catastrophizing measures (Geisser et al., 1992; McNeil and Rainwater, 1998) and one of these studies examined observation of a painful procedure instead of administration of controlled pain stimulus (McNeil and Rainwater, 1998). The poor prediction by fear of pain and pain catastrophizing in this study suggests that other factors may influence tolerance during the acute stage of pain. Future studies should consider alternative factors that have recently been highlighted in the experimental pain literature, for example, gender role expectations of pain (Robinson et al., 2003, 2004; Wise et al., 2002). A competing explanation for not predicting tolerance is that the pain stimulus was not threatening enough to elicit avoidance behavior from fear of pain or pain catastrophizing, despite the fact that the cold pressor is believed to be an acceptable model for musculoskeletal pain (Price et al., 1987; Rainville et al., 1992). There is support for this contention in the literature as Gracely et al. (2004) have hypothesized that the influence of pain catastrophizing on pain perception may be weakened
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with the use of low threat stimuli commonly used in experimental studies. In the present study, subjects spent a relatively short time (mean = 78.9 s) experiencing pain in a low threat condition (their mean threat levels = 1.9 cm on a 10-cm VAS) with little variation (SD = 1.6 cm) in these ratings. Therefore, this study provides circumstantial evidence that the cold pressor stimuli may actually have not elicited cognitions related to fear of pain and pain catastrophizing that influenced pain behavior. However, further study directly testing this assertion is warranted. Previous studies of the FAMEPP have not considered the role of threat despite the fact that, ‘‘threatening illness information’’ is hypothesized to be involved with the development of an exaggerated pain perception (Vlaeyen and Linton, 2000). Future clinical and experimental FAMEPP studies should measure perceived clinical threat and the threat of other experimental models (e.g., intra-muscular saline injections (Arendt-Nielsen et al., 1996; Moseley et al., 2004), delayed onset muscle soreness (Dannecker et al., 2002, 2003), capsaicin (Frot et al., 2004)), or ischemia should be assessed. Perhaps experimental studies could ethically manipulate the level of threat (i.e., through instructional set) by including a debriefing session that offset any deleterious effects of the instructional set. This methodology would also allow for the interaction of threat with fear of pain and pain catastrophizing to be empirically investigated. Elevated fear of pain before the onset of pain was predictive of elevated pain intensity ratings during acute pain perception, which is consistent with a clinical report indicating fear of pain was likely to have an early influence on pain intensity (Sieben et al., 2002). Pain catastrophizing is also known to predict acute pain perception from experimental stimuli (Geisser et al., 1992; Sullivan et al., 1995, 2000), but this study suggests it does not influence pain intensity when fear of pain is considered. This issue is relevant to the validity of the FAMEPP and has not been previously reported for acute pain perception. It is also noteworthy that these results converge with those from a study involving patients with chronic LBP, demonstrating that pain related fear was the only significant predictor of pain related disability when pain related fear, catastrophizing, and appraisal of control were considered (Woby et al., 2004). While this study suggests that acute pain intensity was only predicted by fear of pain, the literature linking pain catastrophizing with clinical and experimental pain perception should not be ignored (Geisser et al., 1994; Gracely et al., 2004; Severeijns et al., 2001, 2002; Sullivan et al., 1995, 2000, 2002). The current study considered pain catastrophizingÕs influence on pain intensity before pain was experienced, not while subjects were actually experiencing pain. This methodological approach may have limited pain catastrophizingÕs influence on pain intensity as a recent study involving acute dental pain
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suggested that pain catastrophizing promotes sensitization processes that result in enhanced pain sensitivity or reduced pain tolerance (Edwards et al., 2004). Other recent reports suggest that ‘‘in vivo’’ (i.e., while experiencing pain) catastrophizing was correlated with pain intensity ratings and tolerance, while catastrophizing measures were not associated with pain sensitivity when taken before pain was experienced (Dixon et al., 2004; Edwards et al., 2005). Future experimental studies that consider pain catastrophizingÕs influence before and during application of noxious stimuli are necessary to help clarify this potentially important issue. The use of the CSQ could have also limited pain castastrophizingÕs influence on pain intensity, although the CSQ has discriminated between subjects that were pain sensitive or tolerant to the cold pressor stimuli in a previous study (Geisser et al., 1992). The CSQ could have limited the predictive ability of pain catastrophizing in the current study because it is comprised of cognitions (i.e., pessimism and helplessness) that might not be expected to assert much influence on responses to nonthreatening pain stimuli. Therefore, the CSQ may have lacked the necessary sensitivity to predict pain intensity in response to the cold pressor. Future studies of the FAMEPP in experimental settings should consider the Pain Catastrophizing Scale (PCS), which in addition to helplessness, assesses cognitions related to magnification and rumination. The PCS has been associated with pain intensity during a cold pressor task in previous studies (Sullivan et al., 1995, 2000), and it may potentially be a more appropriate measure than the CSQ to consider pain catastrophizingÕs influence on responses to standard noxious stimuli. The direct clinical implications of these results are limited, but this study provides circumstantial support in two areas. First, this study adds to the literature that suggests pre-morbid psychological factors, like fear of pain, have the potential to adversely influence the clinical presentation of musculoskeletal pain disorders (Carragee et al., 2000; Croft et al., 1995; Papageorgiou et al., 1997). Second, these results provide theoretical support for pain reducing cognitive/behavioral interventions applied during the acute stage of an injury. These results suggest that mitigating patientsÕ fear of pain should be the focus of such interventions, instead of emphasizing adaptive cognitive coping styles as an alternative to pain catastrophizing. Indeed, this study converges with recent clinical trials that have demonstrated the efficacy of fear-reduction interventions for patients with LBP (Burton et al., 1999; George et al., 2003; Klaber Moffett et al., 2004). However, as previously acknowledged, the direct application of the results of this study to clinical pain is limited. The FAMEPP hypothesizes that there are observable physiological consequences associated with fear of pain and avoidance behavior (Vlaeyen and Linton, 2000), but this topic has not been extensively reported in the
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literature. In the current study, fear of pain and pain catastrophizing did not predict SBP reactivity at tolerance. Anxiety was a significant individual predictor of SBP reactivity, but not enough variance was explained to support the significance of the entire regression model. This finding was despite a mean SBP increase of 15.4 mmHG from baseline, which is comparable to what has been previously reported in the literature when using the cold pressor (Lowery et al., 2003; Myers et al., 2001). Thus, preliminary evidence exists that the FAMEPP may not be associated with immediate blood pressure reactivity in response to acute pain. However, additional research in this area is needed to determine what role (if any) fear of pain and/or pain catastrophizing play in contributing to the physiological response to pain.
6. Conclusion Our hypotheses that specific psychological components of the FAMEPP (fear of pain and pain catastrophizing) would predict tolerance, pain intensity, and SBP reactivity were partially supported by these results. The FAMEPP was a significant predictor for pain intensity, but not tolerance or SBP reactivity. These results suggest that fear of pain may have a stronger influence on acute pain intensity when compared to pain catastrophizing, while neither of the factors predicted tolerance or blood pressure reactivity to pain.
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Fear of pain, not pain catastrophizing, predicts acute pain intensity, but neither factor predicts tolerance or blood pressure reactivity: An experimental investigation in pain-free individuals Steven Z. George
a,*
, Erin A. Dannecker b, Michael E. Robinson
c
a
c
Department of Physical Therapy, Brooks Center for Rehabilitation Studies, University of Florida, United States b Department of Physical Therapy, University of Missouri, United States Department of Clinical and Health Psychology, Center for Pain Research and Behavioral Health, University of Florida, P.O. Box 100154, Gainesville, FL 32610-0154, United States Received 22 November 2004; accepted 28 June 2005 Available online 10 August 2005
Abstract Previous studies of the Fear-Avoidance Model of Exaggerated Pain Perception have commonly included patients with chronic low back pain, making it difficult to determine which psychological factors led to the development of an ‘‘exaggerated pain perception’’. This study investigated the validity of the Fear-Avoidance Model of Exaggerated Pain Perception by considering the influence of fear of pain and pain catastrophizing on acute pain perception, after considering sex and anxiety. Thirty-two males and 34 females completed the State-Trait Anxiety Inventory, the Fear of Pain Questionnaire, and the Coping Strategies Questionnaire. Subjects underwent a cold pressor procedure and tolerance, pain intensity, and blood pressure reactivity were measured. Sex, anxiety, fear of pain, and pain catastrophizing were simultaneously entered into separate multiple regression models to predict different components of pain perception. Tolerance was not predicted by fear of pain, pain catastrophizing, or anxiety. Pain intensity at threshold and tolerance were significantly predicted by fear of pain, only. Blood pressure reactivity to pain was significantly predicted by anxiety, only. These results suggest that fear of pain may have a stronger influence on acute pain intensity when compared to pain catastrophizing, while neither of the factors predicted tolerance or blood pressure reactivity. Ó 2005 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. Keywords: Fear-avoidance; Pain sensitivity; Quantitative sensory testing; Cold pressor; Experimental pain; Threshold; Tolerance; Anxiety
1. Introduction The Fear-Avoidance Model of Exaggerated Pain Perception (FAMEPP) describes one way chronic sympAbbreviations: FAMEPP, Fear-Avoidance Model of Exaggerated Pain Perception; LBP, low back pain; STAI, State-Trait Anxiety Questionnaire; FPQ-III, Fear of Pain Questionnaire; CSQ, Coping Strategies Questionnaire; NRS, numerical rating scale; SBP, systolic blood pressure. * Corresponding author. Tel.: +1 352 273 6432. E-mail address: [email protected]fl.edu (S.Z. George).
toms develop following an acute injury (Lethem et al., 1983; Slade et al., 1983). In this model, elevated fear of pain is hypothesized to induce avoidance behavior, which in turn leads to a disuse syndrome, chronic disability, and an exaggerated pain perception. The definition of exaggerated pain perception used for this study was proposed as (Lethem et al., 1983), ‘‘pain experience and/or behavior (and/or physiological responses to pain stimulation), which are (is) out of all proportion to demonstrable organic pathology or current levels of nociceptive stimulation (page 402).’’ In 1995 and 2000,
1090-3801/$32 Ó 2005 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ejpain.2005.06.007
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Vlaeyen et al. modified the FAMEPP by stressing the importance of pain catastrophizing (Vlaeyen et al., 1995a,b; Vlaeyen and Linton, 2000). Pain catastrophizing is conceptualized by cognitions of the inability to tolerate painful situations, thinking pain is unbearable, or ruminating on the worst possible outcome from the experienced pain (Sullivan et al., 2001). Thus, in the modified model, frequent pain catastrophizing and elevated fear of pain led to chronic disability and an exaggerated pain perception (Vlaeyen et al., 1995a,b; Vlaeyen and Linton, 2000). The literature on the FAMEPP has primarily sampled patients with low back pain (LBP) and prospective studies have demonstrated that fear of pain and pain catastrophizing are involved in the development of chronic disability. For example, during acute LBP, elevated fear of pain has been predictive of self-report of disability 4 weeks later (Fritz et al., 2001), 8 weeks later (Klenerman et al., 1995), and 12 months later (Sieben et al., 2002). In addition, frequent pain catastrophizing during acute LBP was predictive of self-reported disability 6 months (Picavet et al., 2002) and 1 year later (Burton et al., 1995), even after considering select historical and clinical predictors. Together, these studies provide strong evidence that fear of pain and pain catastrophizing are precursors to chronic disability, not the result of experiencing chronic symptoms (Linton, 2000; Pincus et al., 2002). Other studies have also shown that fear of pain and pain catastrophizing are associated with an exaggerated pain perception (Crombez et al., 1999; Severeijns et al., 2001; van den Hout et al., 2001; Vlaeyen et al., 1995b). However, cross-sectional studies involving patients with chronic symptoms do not directly address whether fear of pain and pain catastrophizing are involved in the development of an exaggerated pain perception. Some evidence exists in the literature, as increasing fear of pain during the first 2 weeks of acute LBP was reported to have a trend relationship (p = 0.08) with increasing pain intensity (Sieben et al., 2002) and pain catastrophizingÕs association with acute pain perception has been observed in experimental settings (Geisser et al., 1992; Sullivan et al., 1995, 2000). Studies investigating fear of pain and pain catastrophizingÕs influence on acute pain perception are another method of examining this topic, but such studies are uncommon in the literature. The FAMEPP makes a theoretical distinction between the concepts of fear of pain and pain catastrophizing. Simultaneous use of these measures is infrequently reported in the literature and each measureÕs unique contribution to acute pain perception beyond pain intensity has not been previously reported to the best of our knowledge. Another study investigating fear of pain and pain catastrophizing studied their association with pain intensity, but pain sensitivity and physiologi-
cal response measures were not utilized (Sullivan et al., 1995). Clinical studies of the FAMEPP can be difficult to interpret because of variability from several sources (e.g., mechanisms, onset, and severity of the low back injury, experience with previous episodes of LBP onset, and delay from LBP onset to seeking treatment). There is also the question of whether fear of pain and pain catastrophizing precede or are a result of long standing LBP (Hadjistavropoulos and Craig, 1994; Mannion et al., 1996). Given these considerations, we believe a laboratory investigation using a controlled stimulus to induce pain that mimics musculoskeletal pain is warranted to investigate the FAMEPP. The purpose of this study was to determine whether the FAMEPP components of fear of pain and pain catastrophizing significantly contribute to the subsequent perception of pain. A standardized stimulus (cold pressor) was used to induce pain and measures of pain tolerance, pain intensity, and systolic blood pressure (SBP) reactivity were assessed. Our hypothesis was that fear of pain and pain catastrophizing would significantly contribute to tolerance, pain intensity, and SBP reactivity related to the induced pain.
2. Methods 2.1. Subjects Subjects were recruited from undergraduate and graduate psychology, business management, and exercise science courses at the University and received extra credit for their research participation. Exclusion criteria for the study were a history of any one of the following: prior experience with the cold pressor stimulus, RaynaudÕs phenomenon or disease, diabetes, high blood pressure, vascular insufficiency, or a chronic pain condition. The sample consisted of 66 subjects, 32 (49%) males, mean age of 21.8 years (SD = 3.4 years), and 15.1 (SD = 1.6) years of formal education. The sample was 74% (49/66) Caucasian, 9% (6/66) Hispanic, 6% (4/66) Asian, 6% (4/66) African American, 3% (2/66) Native American, and 1% (1/66) other. 2.2. Fear-Avoidance Model The current version of the FAMEPP proposes that negative affect (anxiety), pain catastrophizing, and pain-related fear are relevant psychological components leading to the development of an exaggerated pain perception (Vlaeyen and Linton, 2000). Therefore, subjects completed the following psychological questionnaires: The State-Trait Anxiety Questionnaire (STAI) measured negative affect from anxiety. The STAI is a 40-item, 4-point rating scale that is commonly used to assess dispositional (trait) and situational (state)
S.Z. George et al. / European Journal of Pain 10 (2006) 457–465
anxiety symptoms (Spielberger et al., 1983). We administered and reported the state portion of the STAI as it best matched the FAMEPP and our proposed hypotheses. The Fear of Pain Questionnaire (FPQ-III) measured fear of pain. The FPQ-III is a 30-item, 5-point rating scale that measures fear about specific situations that would normally produce pain (McNeil and Rainwater, 1998). The FPQ-III is a commonly used and wellvalidated instrument that is appropriate for use in non-clinical and clinical populations (Albaret et al., 2004; McNeil and Rainwater, 1998; Osman et al., 2002). We administered and reported the total score of the FPQ-III as it best matched the FAMEPP and our proposed hypotheses. The Coping Strategies Questionnaire (CSQ) measured pain catastrophizing. The CSQ is a 27-item, 7-point rating scale that measures the frequency of use for common pain coping strategies (Rosenstiel and Keefe, 1983). The CSQ contains a catastrophizing subscale that measures helplessness and pessimistic cognitions related to pain perception. The validity of this particular subscale has been supported (Keefe et al., 1989; Robinson et al., 1997; Rosenstiel and Keefe, 1983; Stewart et al., 2001) and the currently recommended scoring system was used in this study (Robinson et al., 1997).
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2.5. Measures of pain perception Measures of tolerance, pain intensity, and SBP reactivity were assessed in this study. Tolerance was noted when subjects removed their hand from the cold pressor because they could no longer withstand the cold water due to pain and it was measured by time. Subjects were also asked to provide pain intensity ratings at threshold (when pain was first noted by the subject) and at tolerance. A numerical rating scale (NRS) with zero corresponding to ‘‘no pain sensation’’ and 100 corresponding to ‘‘most intense pain sensation imagined’’ was used. SBP reactivity was selected as the physiological measure of pain response for this study because previous studies have demonstrated significant associations between experimental pain stimuli, resting SBP (Bruehl et al., 1992; Lowery et al., 2003; Myers et al., 2001), and SBP reactivity (Lowery et al., 2003; Maixner and Humphrey, 1993; Peckerman et al., 1991). SBP was monitored on the subjectÕs right arm throughout the study procedures using a Dinamap Critikon automatic monitor. Mean baseline SBP was calculated from three resting systolic BP measures taken 1-minute apart. Then, SBP readings taken at pain tolerance were subtracted from the baseline SBP to determine SBP reactivity. 2.6. Procedures
2.3. Experimental pain procedure Pain was induced in the left hand using a cold pressor (NesLab Instruments, Portsmouth, NH) that maintained temperature at 2.0 °C (±0.2 °C). The cold pressor continuously circulated cold water to prevent local warming around the hand. There were two reasons the cold pressor was selected for this study: (1) A previous study (Rainville et al., 1992) has suggested that the pain quality of this procedure is similar to that of musculoskeletal pain, since ratings of pain unpleasantness typically exceed those of pain intensity (Price et al., 1987). (2) It is a tonic nociceptive stimulus with a long enough stimulus duration to elicit pain responses related to the psychological components measured in this study (Geisser et al., 1992; Sullivan et al., 1995, 2000). 2.4. Assessment of threat from pain stimulus After a description of the cold pressor procedure was provided, the subjectsÕ perception of threat from the stimulus was measured. The definition of threat used for this study was ‘‘anticipated or actual physical or psychological harm, loss, injury or damage’’ the subject expected while performing the cold pressor task. Subjects were provided this written definition while rating their ‘‘threat’’ using a 10-cm VAS with endpoints of ‘‘none’’ and ‘‘most severe threat imaginable’’.
This protocol was approved by the UniversityÕs Institutional Review Board and subjects read and signed a consent form that had also been approved by the UniversityÕs Institutional Review Board before participating in any study-related procedures. Subjects were screened by self-report for tobacco use or caffeine ingestion in the last 3 h and/or the use of pain relievers in the last 12 h because of potential effects on physiological and pain measures. Then, demographic and psychological questionnaires were completed. Resting blood pressure measures were completed after a 20-min seated, quiet rest period. Then, subjects remained seated and the investigator provided the following instructions: ‘‘I will ask you to submerge your left hand up to your wrist, into this container of water. Keep your fingers spread apart under the water, but do not move your fingers. Please say ‘‘pain’’ at the point the cold sensation first begins to feel painful. This is very important, as I cannot tell when you feel pain unless you tell me. You may remove your hand from the water when you can no longer tolerate the pain, but it is important that you leave your hand in the water as long as you possibly can.’’ The investigator recorded the subjectsÕ responses to the cold pressor at threshold (time and intensity rating) and at tolerance (time, intensity rating, and SBP). Subjects were not informed of the amount of time that
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sex, anxiety, and time to stimulus tolerance (to account for any time-related differences in reaching tolerance) in the first block and fear of pain and pain catastrophizing in the second block. An alpha level of 0.05 was used to test our hypotheses.
passed while their hand was immersed in the cold pressor, but they were instructed to remove their hand if more than 4 min elapsed for safety purposes.
3. Data analysis Descriptive statistics were generated for all the measures and effect sizes (CohenÕs d) were calculated to assess the magnitude of sex differences in threshold and tolerance. Correlation coefficients were reported between the psychological and pain perception measures to assess univariate associations before variables were entered into multivariate models. Then, four separate hierarchical regression analyses were constructed. All regression models included sex to account for previous reports describing significant sex differences in response to experimental pain stimuli (Edwards et al., 2000; Fillingim et al., 1998; Frot et al., 2004; Maixner and Humphrey, 1993; Riley et al., 1998; Robinson et al., 2004; Sarlani et al., 2004; Sarlani and Greenspan, 2002). All regression models also included anxiety to account for negative affect as per the modified FAMEPP utilized in this study (Vlaeyen and Linton, 2000). Variance inflation factor (VIF) was reported for all regression models to investigate the potential of collinearity among independent variables.(Kleinbaum et al., 1998) The first regression model predicted tolerance with sex and anxiety in the first block and fear of pain and pain catastrophizing in the second block. The second regression model predicted pain intensity at threshold with sex, anxiety, and time to threshold (to account for any time-related differences in reaching threshold) in the first block and fear of pain and pain catastrophizing in the second block. The third regression model predicted pain intensity at tolerance with sex, anxiety, and time to symptom tolerance (to account for any time-related differences in reaching tolerance) in the first block and fear of pain and pain catastrophizing in the second block. The fourth model predicted SBP reactivity with
4. Results Descriptive statistics for the measures are included within Table 1. The mean threat level from the cold pressor was 1.9 cm (SD = 1.6 cm) for these subjects. The effect sizes observed in this study for sex differences were d = 0.42 for threshold and d = 0.36 for stimulus tolerance with higher ratings in women than men, which are consistent with previous reports in the literature involving experimental pain stimuli (Riley et al., 1998). Correlation coefficients for the relationships between all measures are provided within Table 2. Among the independent variables (i.e., psychological measures), the strongest univariate association was between fear of pain and pain catastrophizing (r = 0.453, p < 0.01) and the VIFÕs for the multiple regression models were low (Tables 3–6). These results provided a strong indication that excessive collinearity among independent variables was not a major concern in this study (KleinTable 1 Summary of pain perception and fear-avoidance measures Measure (n = 66)
Observed range
Mean (SD)
Pain perception Threshold intensity (NRS rating) Threshold time (s) Tolerance intensity (NRS rating) Tolerance time (s) Change in SBP (mm/Hg)
10–100 1–33 50–100 7–213 11–53
48.8 11.5 82.3 78.9 15.4
21–58 46–122
46.4 (9.8) 78.8 (17.5)
Fear-avoidance model State-trait anxiety index Fear of pain questionnaire Coping strategies questionnaire Catastrophizing scale
0–14
(21.9) (7.8) (15.6) (61.0) (12.7)
6.2 (4.0)
Table 2 Associations between pain perception and fear-avoidance measures Measures Threshold intensity (1) Threshold time (2) Tolerance intensity (3) Tolerance time (4) Change in systolic BP (5) Fear of pain questionnaire (6) Coping strategies questionnaire Catastrophizing scale (7) State-trait anxiety index (8) * **
p < 0.05 (2-tailed). p < 0.01 (2-tailed).
2
3 0.156
0.351** 0.164
4
5 0.273* 0.407** 0.221
6 0.104 0.099 0.044 0.174
7 0.355** 0.020 0.327** 0.113 0.188
8 0.254* 0.148 0.036 0.200 0.044 0.453**
0.053 0.015 0.032 0.042 0.283* 0.173 0.070
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Table 3 Hierarchical regression model for tolerance Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI)
0.06
0.161
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.09
Ba (95% CI)
Betaa
p-Valuea
VIF
26.0 ( 55.8, 3.8) 0.1 ( 1.7, 1.4)
0.23 0.02
0.086 0.857
1.01 1.03
2.6 ( 6.8, 1.7) 0.1 ( 1.0, 0.9)
0.17 0.02
0.228 0.897
1.27 1.29
p-Valuea
VIF
0.366
VIF – variance inflation factor. a Reported coefficients are for final models.
Table 4 Hierarchical regression model for pain intensity at threshold Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to intensity (s)
0.03
0.619
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.19
Ba (95% CI)
Betaa
3.1 ( 13.6, 7.3) 0.3 ( 0.8, 0.3) 0.6 ( 1.2, 0.1)
0.07 0.12 0.20
0.550 0.317 0.099
1.07 1.03 1.08
0.9 ( 0.6, 2.3) 0.4 (0.1, 0.7)
0.176 0.31
0.240 0.021
1.31 1.29
Ba (95% CI)
Betaa
p-Valuea
VIF
0.004
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
Table 5 Hierarchical regression model for pain intensity at tolerance Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to symptom tolerance (s)
0.05
0.354
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.18
0.9 ( 8.3, 6.4) 0.1 ( 0.4, 0.3) 0.1 ( 0.1, 0.1)
0.03 0.02 0.24
0.802 0.868 0.054
1.06 1.03 1.10
0.4 ( 1.4, 0.7) 0.4 (0.1, 0.6)
0.09 0.40
0.482 0.004
1.30 1.29
p-Valuea
VIF
0.011
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
Table 6 Hierarchical regression model for SBP reactivity Variables
R2
Change in R2 (p-value)
1st Block Sex Anxiety (STAI) Time to symptom tolerance (s)
0.11
0.074
2nd Block Pain catastrophizing (CSQ) Fear of pain (FPQ-III)
0.13
Ba (95% CI)
Betaa
0.2 ( 6.2, 6.4) 0.3 (0.1, 0.6) 0.1 ( 0.1, 0.1)
0.01 0.25 0.16
0.962 0.044 0.214
1.06 1.03 1.09
0.3 ( 1.1, 0.6) 0.1 ( 0.1, 0.3)
0.08 0.16
0.567 0.253
1.29 1.29
0.516
Bold font indicates significant contributor to final model. VIF – variance inflation factor. a Reported coefficients are for final models.
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baum et al., 1998). Among the dependent variables (i.e., pain perception measures), there were statistically significant associations between threshold and tolerance time (r = 0.407, p < 0.01), pain intensity at threshold and at tolerance (r = 0.351, p < 0.01), and pain intensity at threshold and the tolerance time (r = 0.273, p < 0.05). These results indicated that the pain perception measures shared a maximum of 16% variance and were appropriate for use as separate dependent variables in our subsequent regression models. 4.1. Regression analyses for tolerance The regression model for tolerance time is summarized in Table 3. Sex and anxiety were not significant predictors of pain behavior, explaining only 6% variance (p = 0.161). The addition of fear of pain and pain catastrophizing explained an additional 3% variance in pain behavior, but this addition was not statistically significant (p = 0.366). These results suggest that the specific psychological components of the FAMEPP did not improve prediction of tolerance. 4.2. Regression analyses for pain intensity The regression models for pain intensity at threshold and tolerance are summarized in Tables 4 and 5, respectively. Sex and anxiety were not significant predictors of pain intensity explaining only 3% variance (p = 0.619) at threshold and 5% variance (p = 0.354) at tolerance. The addition of fear of pain and pain catastrophizing significantly improved (p < 0.05) the prediction of pain intensity for both models, explaining an additional 16% variance at threshold and 13% variance at tolerance. In the final model, fear of pain was the only statistically significant predictor for pain intensity at threshold (b = 0.31, p = 0.021) and tolerance (b = 0.40, p = 0.004). These results suggest that the specific psychological components of the FAMEPP improve the prediction of pain intensity at threshold and tolerance, after considering sex and anxiety. In addition, these results suggest that fear of pain was the only significant individual predictor of pain intensity. 4.3. Regression analyses for SBP reactivity to pain The regression model for SBP reactivity to pain is summarized in Table 6. Sex and anxiety were not significant predictors of SBP reactivity to pain, explaining 11% variance (p = 0.074). The addition of fear of pain and pain catastrophizing explained an additional 2% variance in SBP reactivity to pain (p = 0.516). These results suggest that the specific psychological components of the FAMEPP were not significant predictors of change in SBP. While the final model was not predictive of SBP reactivity to pain, anxiety was a significant indi-
vidual predictor (b = 0.25, p = 0.044) suggesting it alone influenced SBP reactivity to pain.
5. Discussion This study investigated specific psychological components of the FAMEPP for their influence on acute pain perception during application of a standardized pain stimulus. This stimulus produced a tonic experimental pain, which we believed to be of sufficient duration to allow psychological and coping parameters to operate (Geisser et al., 1992; Sullivan et al., 1995, 2000). In addition, the use of such a laboratory setting allowed subjects to complete psychological questionnaires prior to pain onset, which allowed for variation in pain perception to be attributed to psychological factors of interest. This methodology also allowed for a multidimensional definition of pain perception to be studied including the measurement of tolerance, pain intensity, and SBP reactivity. Neither fear of pain nor pain catastrophizing improved the prediction of tolerance during the cold pressor task. This unexpected finding contrasts with the majority of clinical studies linking these factors with avoidance behavior (Al Obaidi et al., 2000, 2003; Crombez et al., 1999; Geisser et al., 1992; McNeil and Rainwater, 1998; Sullivan et al., 2002; Vlaeyen et al., 1995a). However, previous studies involving patients with chronic LBP were primarily cross-sectional, unable to distinguish if fear of pain or pain catastrophizing preceded or followed avoidance behavior (Al Obaidi et al., 2000, 2003; Crombez et al., 1999; Sullivan et al., 2002; Vlaeyen et al., 1995a). The previous studies involving tolerance in pain free individuals did not include both fear of pain and pain catastrophizing measures (Geisser et al., 1992; McNeil and Rainwater, 1998) and one of these studies examined observation of a painful procedure instead of administration of controlled pain stimulus (McNeil and Rainwater, 1998). The poor prediction by fear of pain and pain catastrophizing in this study suggests that other factors may influence tolerance during the acute stage of pain. Future studies should consider alternative factors that have recently been highlighted in the experimental pain literature, for example, gender role expectations of pain (Robinson et al., 2003, 2004; Wise et al., 2002). A competing explanation for not predicting tolerance is that the pain stimulus was not threatening enough to elicit avoidance behavior from fear of pain or pain catastrophizing, despite the fact that the cold pressor is believed to be an acceptable model for musculoskeletal pain (Price et al., 1987; Rainville et al., 1992). There is support for this contention in the literature as Gracely et al. (2004) have hypothesized that the influence of pain catastrophizing on pain perception may be weakened
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with the use of low threat stimuli commonly used in experimental studies. In the present study, subjects spent a relatively short time (mean = 78.9 s) experiencing pain in a low threat condition (their mean threat levels = 1.9 cm on a 10-cm VAS) with little variation (SD = 1.6 cm) in these ratings. Therefore, this study provides circumstantial evidence that the cold pressor stimuli may actually have not elicited cognitions related to fear of pain and pain catastrophizing that influenced pain behavior. However, further study directly testing this assertion is warranted. Previous studies of the FAMEPP have not considered the role of threat despite the fact that, ‘‘threatening illness information’’ is hypothesized to be involved with the development of an exaggerated pain perception (Vlaeyen and Linton, 2000). Future clinical and experimental FAMEPP studies should measure perceived clinical threat and the threat of other experimental models (e.g., intra-muscular saline injections (Arendt-Nielsen et al., 1996; Moseley et al., 2004), delayed onset muscle soreness (Dannecker et al., 2002, 2003), capsaicin (Frot et al., 2004)), or ischemia should be assessed. Perhaps experimental studies could ethically manipulate the level of threat (i.e., through instructional set) by including a debriefing session that offset any deleterious effects of the instructional set. This methodology would also allow for the interaction of threat with fear of pain and pain catastrophizing to be empirically investigated. Elevated fear of pain before the onset of pain was predictive of elevated pain intensity ratings during acute pain perception, which is consistent with a clinical report indicating fear of pain was likely to have an early influence on pain intensity (Sieben et al., 2002). Pain catastrophizing is also known to predict acute pain perception from experimental stimuli (Geisser et al., 1992; Sullivan et al., 1995, 2000), but this study suggests it does not influence pain intensity when fear of pain is considered. This issue is relevant to the validity of the FAMEPP and has not been previously reported for acute pain perception. It is also noteworthy that these results converge with those from a study involving patients with chronic LBP, demonstrating that pain related fear was the only significant predictor of pain related disability when pain related fear, catastrophizing, and appraisal of control were considered (Woby et al., 2004). While this study suggests that acute pain intensity was only predicted by fear of pain, the literature linking pain catastrophizing with clinical and experimental pain perception should not be ignored (Geisser et al., 1994; Gracely et al., 2004; Severeijns et al., 2001, 2002; Sullivan et al., 1995, 2000, 2002). The current study considered pain catastrophizingÕs influence on pain intensity before pain was experienced, not while subjects were actually experiencing pain. This methodological approach may have limited pain catastrophizingÕs influence on pain intensity as a recent study involving acute dental pain
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suggested that pain catastrophizing promotes sensitization processes that result in enhanced pain sensitivity or reduced pain tolerance (Edwards et al., 2004). Other recent reports suggest that ‘‘in vivo’’ (i.e., while experiencing pain) catastrophizing was correlated with pain intensity ratings and tolerance, while catastrophizing measures were not associated with pain sensitivity when taken before pain was experienced (Dixon et al., 2004; Edwards et al., 2005). Future experimental studies that consider pain catastrophizingÕs influence before and during application of noxious stimuli are necessary to help clarify this potentially important issue. The use of the CSQ could have also limited pain castastrophizingÕs influence on pain intensity, although the CSQ has discriminated between subjects that were pain sensitive or tolerant to the cold pressor stimuli in a previous study (Geisser et al., 1992). The CSQ could have limited the predictive ability of pain catastrophizing in the current study because it is comprised of cognitions (i.e., pessimism and helplessness) that might not be expected to assert much influence on responses to nonthreatening pain stimuli. Therefore, the CSQ may have lacked the necessary sensitivity to predict pain intensity in response to the cold pressor. Future studies of the FAMEPP in experimental settings should consider the Pain Catastrophizing Scale (PCS), which in addition to helplessness, assesses cognitions related to magnification and rumination. The PCS has been associated with pain intensity during a cold pressor task in previous studies (Sullivan et al., 1995, 2000), and it may potentially be a more appropriate measure than the CSQ to consider pain catastrophizingÕs influence on responses to standard noxious stimuli. The direct clinical implications of these results are limited, but this study provides circumstantial support in two areas. First, this study adds to the literature that suggests pre-morbid psychological factors, like fear of pain, have the potential to adversely influence the clinical presentation of musculoskeletal pain disorders (Carragee et al., 2000; Croft et al., 1995; Papageorgiou et al., 1997). Second, these results provide theoretical support for pain reducing cognitive/behavioral interventions applied during the acute stage of an injury. These results suggest that mitigating patientsÕ fear of pain should be the focus of such interventions, instead of emphasizing adaptive cognitive coping styles as an alternative to pain catastrophizing. Indeed, this study converges with recent clinical trials that have demonstrated the efficacy of fear-reduction interventions for patients with LBP (Burton et al., 1999; George et al., 2003; Klaber Moffett et al., 2004). However, as previously acknowledged, the direct application of the results of this study to clinical pain is limited. The FAMEPP hypothesizes that there are observable physiological consequences associated with fear of pain and avoidance behavior (Vlaeyen and Linton, 2000), but this topic has not been extensively reported in the
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literature. In the current study, fear of pain and pain catastrophizing did not predict SBP reactivity at tolerance. Anxiety was a significant individual predictor of SBP reactivity, but not enough variance was explained to support the significance of the entire regression model. This finding was despite a mean SBP increase of 15.4 mmHG from baseline, which is comparable to what has been previously reported in the literature when using the cold pressor (Lowery et al., 2003; Myers et al., 2001). Thus, preliminary evidence exists that the FAMEPP may not be associated with immediate blood pressure reactivity in response to acute pain. However, additional research in this area is needed to determine what role (if any) fear of pain and/or pain catastrophizing play in contributing to the physiological response to pain.
6. Conclusion Our hypotheses that specific psychological components of the FAMEPP (fear of pain and pain catastrophizing) would predict tolerance, pain intensity, and SBP reactivity were partially supported by these results. The FAMEPP was a significant predictor for pain intensity, but not tolerance or SBP reactivity. These results suggest that fear of pain may have a stronger influence on acute pain intensity when compared to pain catastrophizing, while neither of the factors predicted tolerance or blood pressure reactivity to pain.
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