• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of nihpaAbout Author manuscriptsSubmit a manuscriptNIH Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
J Pain. Author manuscript; available in PMC May 1, 2011.
Published in final edited form as:
PMCID: PMC2898132

Situational vs. dispositional measurement of catastrophizing: Associations with pain responses in multiple samples


Catastrophizing is widely recognized as an important risk factor for adverse pain-related outcomes. However, questions remain surrounding the details of its assessment. In particular, recent laboratory studies suggest that evaluation of “situational” catastrophizing (i.e., catastrophizing measured during or directly after the administration of noxious stimulation) may provide information distinct from that obtained by standard, or “dispositional” measures which assess individuals’ recall of catastrophizing in daily life. However, comparatively little research has systematically investigated the inter-relationships and properties of these two different forms of pain-related catastrophizing. The current study evaluated both situational and dispositional catastrophizing measures within multiple samples: healthy individuals (N=84), patients with painful temporomandibular joint disorders (TMD; N=48), and patients with painful arthritis (N=43). All participants first completed the Pain Catastrophizing Scale (PCS)49, and then underwent psychophysical pain testing, which included heat, cold, and pressure pain. Participants then completed a situational catastrophizing measure with reference to the laboratory pain he/she had just undergone. Situational catastrophizing scores were not significantly correlated with dispositional PCS scores in the healthy participants and arthritis patients, though they were associated in TMD patients. Situational catastrophizing was more strongly associated with experimental pain responses than dispositional PCS scores for the healthy subjects and arthritis patients. In general, higher levels of situational catastrophizing were associated with lower pain thresholds and higher pain ratings across all 3 samples. The findings highlight the importance of multi-dimensional assessment of pain-related catastrophizing, and suggests a role for measuring catastrophizing related to specific, definable events.

Keywords: Situational Catastrophizing, Dispositional Catastrophizing, TMD, Arthritis, experimental pain


A substantial literature has demonstrated that catastrophizing, a set of negative emotional/cognitive processes (such as magnification of pain, rumination and pessimism about pain, and feelings of helplessness when in pain) is a critically-important risk factor for adverse pain-related outcomes. It has been positively associated with elevated indices of pain severity, pain behaviors, analgesic use,34 interleukin-6 (a pro-inflammatory cytokine) reactivity,20 length of hospital stay, postoperative recovery time,48 suicidal ideation,22 and physical disability (see 5,50 for reviews of the catastrophizing literature), as well as with the prospective development of pain conditions such as spinal pain and phantom limb pain.7,43,45

In some studies, catastrophizing has also been related to experimental pain responses, with those reporting increased catastrophizing generally showing more sensitivity to calibrated noxious stimuli administered in a controlled setting.50 For example, Edwards and colleagues22 found that increased pain-related catastrophizing was associated with greater supra threshold ratings and elevated temporal summation of noxious thermal stimuli. Moreover, several studies have shown that catastrophizing was associated with greater sensitivity to cold pain (e.g., individuals high in catastrophizing had a lower tolerance for cold pain and rated cold pain intensity more highly).13,17 Two studies of electrical pain responses also found that catastrophizing related to elevated pain sensitivity, though in both cases, only self-reported pain and not nociceptive muscle reflexes, were affected by an individual’s degree of catastrophizing.27,44

One interesting feature of some of these experimental pain studies is that they have assessed catastrophizing specifically with respect to the noxious stimuli that are delivered in the laboratory (i.e., “situational catastrophizing”). In these studies, catastrophizing is measured immediately after a specific pain experience that is shared by all participants. It seems natural to expect that two different measures of pain catastrophizing, a construct with some trait-like characteristics and that is fairly stable over time,53 would be highly inter-correlated. However, previous reports have documented, at best, moderate correlations between scores on a dispositional catastrophizing measure such as the Pain Catastrophizing Scale (PCS; which cues respondents to recall prior pain experiences and then queries their typical degree of catastrophizing) and situational catastrophizing scores. 13,17 Moreover, when the two measures of catastrophizing have been directly compared, situational catastrophizing has been shown to correlate significantly more highly with experimental pain responses. This is consistent with classic research on interactions between individual trait characteristics and environmental circumstances in which expression of a behavioral disposition, such as catastrophizing, depends on existing situational demands.40 Similarly, early coping research has suggested that coping disposition was only weakly associated with coping behaviors in a given situation.9,36

Collectively, these findings suggest that situational measurement of pain-related processes such as catastrophizing, which are captured during or immediately after a specific pain induction procedure, may have greater accuracy and be more relevant to an individual’s experience of pain than dispositional measures of how much an individual recalls responding in general. The PCS49 measure relies on the respondent’s choice of a pain referent (i.e., some previously painful event), and the recall of their response. This can create an important bias, as memory is known to be influenced by emotional processes37,39 and personality factors.8 Recently, findings have emerged in the depression literature, where day-to-day variability in “state” measures of depressed mood was associated with physiologic markers of stress where as a “trait” measure of depressive symptomatology was not.46

However, to date the associations between different modes of assessing catastrophizing have only been examined in student samples, not in clinical populations in whom catastrophizing might be relatively more important in shaping their experiences of pain. The current analyses combined data from two separate studies, one described in a previous publication19 and one not yet published. Both sought to elucidate the associations of situational and dispositional catastrophizing measures with a variety of experimental pain responses among healthy adults, patients with arthritis pain and patients with temporomandibular joint disorders (TMD), all of whom underwent a standardized array of experimental pain induction procedures. It was hypothesized that measures of situational and dispositional catastrophizing would be more strongly inter-correlated with one another in the patient groups, and that situational catastrophizing would be more strongly associated with experimental pain responses (e.g., pain thresholds, ratings of standardized noxious stimuli) than dispositional catastrophizing across all of the groups. These results were presented in abstract/poster form at the annual meeting of the American Pain Society.6

Materials and Methods

Data from a total of 175 individuals (84 healthy individuals, 48 temporomandibular joint disorder patients, and 43 patients with arthritis pain) were analyzed in this study. Data were pooled from a previous study of sleep and TMD pain19 and a study of stress-immune system responsiveness in arthritis patients (unpublished). Approximately half of the healthy individuals and all of the TMD participants included here were part of the pain and sleep study19 and only baseline pain induction procedures (prior to sleep disturbance) were used in the current analyses. The arthritis patients and the other half of the healthy individuals participated in the stress-immune system study; again only baseline pain procedures were included in the current analyses. All study-related procedures were approved by the Johns Hopkins Hospital Institutional Review Board. All participants were recruited through posted advertisements throughout the medical institution and undergraduate/graduate schools. Potential participants contacted the research coordinators who conducted an extensive telephone screening. Eligibility criteria for healthy participants included having no pain condition or medical disorders. All participants were excluded for an active alcohol or drug abuse problem, or use of narcotics, antidepressants, anticonvulsants, and muscle relaxants. For the two patient groups, individuals reporting primary pain conditions or serious medical disorders other than TMD or arthritis were excluded. Both patient groups were required to report a typical pain severity ≥ 2 out of 10 and minimum symptom duration ≥ 6 months. Interested and potentially eligible individuals were scheduled for a physician assessment of additional eligibility criteria. Potential TMD participants were scheduled to meet with an oral medicine specialist who conducted the research diagnostic criteria [RDC for TMD14]) and confirmed primary diagnosis of TMD (Axis 1 [group I, II, and/or III]). Osteoarthritis (OA) and rheumatoid arthritis (RA) patients also had a physician-confirmed arthritis diagnosis (i.e., many had been evaluated at the Johns Hopkins Arthritis Center). OA of the knee was confirmed using ACR Clinical Classification Criteria (e.g., pain in the knee and radiographic evidence of joint space narrowing or osteophytes). RA was diagnosed using ACR Clinical Classification Criteria, and both groups were combined into one group to generate an adequate sample size for data analyses. Previous catastrophizing work has also combined OA and RA patients,38 and catastrophizing is clinically relevant in both groups.16 In the TMD group, six individuals were deemed ineligible based on RDC/TMD criteria, nine participants were lost to follow-up between their RDC/TMD visit and pain testing sessions and an additional five participants had incomplete pain testing data due to equipment malfunctioning and were thus excluded from these analyses. Three arthritis patients and two healthy participants from the sleep disturbance study did not complete all pain testing measures, again due to equipment issues, and were therefore not included in the final analysis.

Verbal and written informed consent was obtained upon arrival, after which participants completed the Pain Catastrophizing Scale (PCS)49 and the other self-report psychological questionnaires in paper and pencil format. Next, participants underwent psychophysical pain testing, following which he/she completed the situational catastrophizing questionnaire. The laboratory pain induction procedures included pressure, thermal, and cold pressor pain assessment. The pressure and thermal procedures were conducted first in randomized order, followed by the cold pressor procedure.

Psychophysical Pain Testing

Pressure Pain Procedure

A Somedic algometer (Sollentuna, Sweden) was used to assess responses to mechanical pressure using a 0.503-cm2 probe covered with a 1-mm polypropylene material.35 Pressure was gradually increased at an application rate of 30 kPa per second until the subject reported pain threshold (i.e., “first felt pain”), at which point stimulation was terminated. Pressure pain threshold was assessed twice each at the right and left upper trapezius muscles. The four pressure pain thresholds were averaged together.

Thermal procedures

Heat Pain Threshold (HPTh)

A computer-controlled Medoc Thermal Sensory Analyzer (TSA-2001, Ramat Yishai, Israel), a peltier-element-based stimulator with a 30×30 mm surface area, was used to deliver contact heat stimuli. HPTh was assessed three times on the left ventral forearm using an ascending method of limits. The temperature increased from a baseline of 32 °C with a 0.5 °C/s rate of rise, until the participant responded by pressing a button (when he/she first noticed a painful sensation). When the button was pressed, the temperature of the thermode was recorded. Between trials, the positioning of the thermode was moved up the arm slightly to avoid overlapping the testing sites. A 30-s inter-stimulus interval was maintained. The cutoff temperature for all trials was 52 °C to avoid tissue damage. The HPTh was determined as the average of these trials.

Ratings of Supra Threshold Heat Stimuli

Two series of brief, repetitive noxious thermal stimuli were administered in ascending order to the left ventral forearm. Within each series there were 10 stimuli. The target temperatures were 49 and 51 °C. Each stimulus was delivered for a 0.5-s duration, with a 3-s inter-pulse interval. Participants provided intensity ratings for each of the ten stimuli using a 0–100 scale (where 0 = no pain and 100 = the most intense pain imaginable). The trial was terminated if the subject said “stop” at any point, or if he/she provided a rating of 100. Additionally, participants were asked to rate painful after-sensations 15 seconds following the final pulse.

Cold Pressor Pain

Cold pressor pain was assessed by having the subjects immerse their right hand up to the wrist in 4 °C water. The water temperature was maintained (±0.1 °C) by a refrigeration unit (Neslab, Portsmouth, NH), and was constantly circulated to prevent local warming around the submerged hand. The participant was prompted to rate their hand pain on the 0–100 scale at 20 seconds post-submersion. Participants were instructed to remove their hand from the water following this brief procedure (or at any time if intolerable). Participants also rated their maximum level of hand pain during this procedure. Cold water immersion was repeated twice and ratings were averaged together.

Psychological measures

Depression Measures

The Beck Depression Inventory (BDI) is one of the most commonly-used measures of depressive symptomatology. It assesses the frequency and severity of a variety of cognitive, affective, physiological, and motivational symptoms of depression.2 Each item is scored on a four-point scale (0–3) with higher scores reflecting more severe symptoms. The BDI has been shown to be a reliable and valid index of depressive symptomatology in general and clinical populations.1 It correlates highly with the diagnosis of depression using structured clinical interviews.28

The Brief Symptom Inventory (BSI) is a well-normed, 53-item self-report measure of multiple dimensions of psychological symptoms.12 Each item is scored on a 5-point Likert scale, with responses ranging from 0 (not at all) to 4 (extremely). The six-item depression subscale was used in the current analysis. This measure is widely used and has been shown to be reliable and valid in both general and clinical populations.11 Data for the current analysis is a combination of two studies in which one (the immunity study) used the BDI and the other used the BSI-depression subscale (sleep study). Therefore, these measures were z-scored within their respective samples. The subsequent Z-scores were used in the regression analyses

Catastrophizing Measures

The Pain Catastrophizing Scale (PCS)49 consists of 13 items rated on a 5-point scale ranging from 0 (not at all) to 4 (all the time). Participants are instructed to indicate the degree to which he/she has specific thoughts and feelings when experiencing pain. The measure assesses three dimensions of catastrophizing: rumination, magnification, and helplessness. The PCS has been validated for both clinical and nonclinical samples.41,49

The Situational Catastrophizing Questionnaire (SCQ) is a six question adaptation of the PCS (described above). It has been used by our group in other studies and has been described more fully by Edwards et al.22 It is included in Appendix 1. Participants completed this questionnaire immediately following the pain induction procedures described above and were instructed to reference the pain procedures while answering. On the other hand, the depression measure and PCS were completed prior to conducting pain testing.

Data Analysis

All analyses were conducted using SPSS 16. Pain testing measures were z-scored separately in each participant group and combined into components based on Principal Component analysis with varimax rotation which yielded 3 factors: pain threshold (including thermal and pressure pain thresholds), supra threshold pain ratings (ratings of 49 and 51°C stimuli, and cold pressor pain ratings), and painful after-sensations (following both supra threshold heat stimulations) see supplementary Table 1. Chi-Square tests were used to compare demographic variables between the three participant groups. To examine the relationship between situational and traditional catastrophizing measures with the other variables of interest, Pearson partial correlations were conducted (controlling for sex, age) to examine the associations between psychological variables and experimental pain components. A sensitivity analysis was also conducted to examine whether combining data from the two studies was appropriate.

A series of hierarchical linear regressions were then performed to examine the relationship between catastrophizing measures and each pain testing component for each of the three participant groups. Hierarchical regression was chosen as the most appropriate assessment, given our goal of elucidating the association between pain responses and catastrophizing measures within groups. To control for potential confounds related to demographic variables and overlap between depression and catastrophizing characteristics, sex, age and ethnicity (coded as white/nonwhite for data analysis purposes) were entered into the first block, the depression z-score was entered into the second, and both catastrophizing measures were entered into the third block simultaneously.

In order to statistically test whether the two measures of catastrophizing (dispositional [PCS] and situational [SCQ]) differed significantly in their unique association with pain responses, the difference in unstandardized beta coefficients between the dispositional PCS and the SCQ was calculated via the studentized nonparametric bootstrap method. This technique10,23 allows statistical comparison of the difference in beta weights between two independent (predictor) variables in a regression equation, permitting conclusions regarding whether the observed associations with the dependent variable are significantly different.


Chi-Square tests revealed that the sex and age distribution differed significantly between groups. More women were in the TMD and arthritis groups than the healthy participants, and arthritis patients were generally older than the other two groups. Demographic information, means (SD), Cronbach’s alpha coefficients for situational and dispositional catastrophizing, and the raw pain data for each of the participant groups are presented in Table 1. Overall, situational catastrophizing scores (F = 4.2, p = .02) and PCS scores (F = 5.1, p = .007) were significantly different between the three groups. Situational catastrophizing differed significantly between arthritis patients and healthy participants (p = .006) as well as arthritis and TMD patients (p = .015), controlling for age and sex. Situational scores did not differ between healthy and TMD participants (p > .05). A significant difference on PCS scores emerged between healthy participants and both of the patient groups (TMD, p = .01; arthritis, p = .009), controlling for age and sex. No difference was observed between TMD and arthritis patients on the PCS. Internal consistency was adequate for both the situational and dispositional PCS measures for each group. Sensitivity analysis revealed that healthy individuals recruited to each study differed on age, as the immune response study sought to recruit arthritis patients and it was important that the healthy sample be more representative and comparable in age with the arthritis patients. No differences emerged between the two healthy groups on any experimental pain measures controlling for age.

Table 1
Demographic Information, Cronbach’s Alpha for situational catastrophizing and PCS Questionnaires and raw experimental pain scores for each group.

Associations Between Measures

As reported in Table 2, situational catastrophizing scores were not correlated with dispositional PCS scores in the healthy participants and arthritis patients, though there was a significant positive association in the TMD patients. The dispositional PCS was significantly associated with depression scores in the healthy group and arthritis patients, while situational catastrophizing was correlated with depression in TMD patients. Moreover, at a univariate level, situational catastrophizing was generally more strongly associated with experimental pain responses (e.g. pain threshold, supra threshold pain ratings) than dispositional PCS scores, though these results varied by pain testing modality (see Table 2).

Table 2
Pearson Partial Correlation Matrix (controlling for sex and age) between questionnaire data and experimental pain measures for each participant group.

Hierarchical Regressions

Hierarchical linear regressions revealed that, after controlling for sex, age, ethnicity, depression and the dispositional catastrophizing measure, situational catastrophizing predicted pain threshold in healthy participants and arthritis patients (Tables 3a and 3b respectively) but not in TMD patients (Table 3c), though a trend toward significance was observed in this group (p = .07). Dispositional PCS did not significantly predict pain threshold after adjusting for these variables in any of the three participant groups. Additionally, beta weight calculations revealed that situational catastrophizing was a significantly better predictor than the dispositional PCS measure in both the healthy and arthritis groups (ps < .05). The situational measure also predicted supra threshold responses in healthy participants (Table 4a) after controlling for sex, age, ethnicity, depression and dispositional PCS, while the dispositional PCS measure did not (after controlling for demographics and situational catastrophizing). A significant difference between dispositional and situational catastrophizing measures observed in healthy participants (p = .05). This relationship was not found in the arthritis patients (Table 4b). The situational measure did predict supra threshold responses in TMD patients (Table 4c) after controlling for sex, age, ethnicity, depression and dispositional PCS, while the dispositional PCS measure did not; however a significant difference between dispositional and situational catastrophizing measures was not observed in this group. Interestingly, situational catastrophizing predicted after-sensation pain ratings in each of the three groups (Tables 5a, 5b and 5c) controlling for demographics as well as depression and dispositional PCS; again however, the situational measure was only significantly different from the dispositional PCS in healthy participants (p = .04). Dispositional PCS scores were not predictive of any pain responses measured for any of the three groups of participants although PCS beta weights approached significance as predictors among the TMD patients (threshold p = .08; supra threshold p = .06; after-sensation p = .1). The variance in pain responses accounted for by the construct of catastrophizing (including both situational and dispositional) ranged between 6 – 13% for healthy participants, 15 – 21% for TMD patients, and 3 – 16% for arthritis patients.


The current study sought to extend recent work on the assessment of catastrophizing by examining both dispositional and situational responses in different populations. The situational catastrophizing measure (reported in22) uses questions derived from PCS items, which were modified to apply to laboratory-based pain testing. In general, findings indicate that the situational catastrophizing was significantly associated with experimental pain measures, though these relationships evidenced a variable response pattern across participant groups. Situational catastrophizing significantly correlated with threshold (healthy and arthritis), supra threshold (TMD), and after-sensations (healthy, arthritis, and TMD), whereas the dispositional PCS measure did not significantly add to the models (adjusted for situational catastrophizing) in any participant group. Statistical trends were observed for associations between the dispositional PCS and pain thresholds and supra threshold ratings in TMD participants. The magnitude of the association between situational catastrophizing and pain responses is likely to be clinically significant. For the regressions in which situational catastrophizing is a significant predictor of pain responses, the betas range in absolute value from .05 to .08. In our previous work, we have reported that individuals who are low in situational catastrophizing differ from those who are high in situational catastrophizing by 8–10 points on this scale. 22 To simplify, by taking a 10-point “change” in that situational catastrophizing scale, going from low to high in situational catastrophizing is associated with a “unique change” in pain responses of between ½ and ¾ of a standard deviation in pain response. This is true after accounting for the influence of demographic factors, depressive symptoms, and dispositional catastrophizing. We have previously noted that individual differences in pain sensitivity have important clinical implications for the development of clinical pain,15,21 and the present data suggest that individual differences in situational catastrophizing may be an important contributor to that variability.

Our findings parallel those of Dixon et al13 and Edwards and colleagues17 who found that situational reports of catastrophizing were more strongly associated with experimental pain report as compared to dispositional assessment of catastrophizing. Geisser and colleagues29 modified the Coping Strategies Questionnaire (CSQ) in a similar fashion (i.e., changing questions to past tense and excluding inappropriate items) and administered the questionnaire following a cold pressor task. While the study did not include a comparison of the standard CSQ measure to the situational version, pain tolerant individuals had significantly lower catastrophizing subscale scores than a pain sensitive group. Bruehl and colleagues3 also used a modified CSQ questionnaire (which they termed “CSQ-acute”); however, they did not examine the catastrophizing subscale. Clearly, situational and dispositional assessment of catastrophizing yield somewhat different information.

Potential mechanisms underlying these differences include a distinction between “trait” measurement (i.e., the dispositional PCS measures a person’s general tendency to catastrophize when in pain) and “state” measurement (i.e., the situational scale measures only an individual’s degree of catastrophizing in a specific situation, over an approximately 1-hour time span). While the state/trait distinction is to some degree artificial (e.g., recent findings suggest that purportedly “trait” measures of personality change as a function of treatment in patients with chronic pain),25 it is likely that the PCS assesses a more broad, dispositional construct than the presumably situation-specific catastrophizing measure. It is also likely that the dispositional PCS measures different pain experiences than the situational scale, since there is no standard referent or time frame for subjects completing the PCS to use when thinking about their pain experience. These pain experiences may have occurred in the distant past in the case of healthy subjects and may include a summary of multiple pain experiences, including recent pain, in the clinical groups. Thus, dispositional PCS scores may relate only minimally to experimental pain responses because of the artificiality of the laboratory environment; that is, standard PCS scores may be driven by past experiences with clinical pain in daily life, whereas in a novel laboratory environment, participants have no relevant prior experience to draw on as they undergo the pain induction procedures. Additionally, the dispositional PCS may be more subject to distortion as a function of memory biases, which have been well-documented in the field of pain research.31 While this issue is perhaps less likely to apply to clinical populations, as a number of studies have shown strong associations between standard PCS scores and pain outcomes in the context of chronic pain, it may be relevant for healthy participants who have no experience with daily pain or whose pain experience is not known to the researcher. Finally, the possibility exists that situational catastrophizing scores are driven by individual differences in pain sensitivity, such that those who are more pain-sensitive experience more pain from the procedures and catastrophize more. Future studies may wish to examine how potential mechanisms influence the relationships between situational and dispositional catastrophizing for a better conceptual understanding of these measures.

It is interesting to note the differences in catastrophizing and its associations across groups after statistically controlling for sex, age, and ethnicity. Consistent with prior research, both groups of patients with persistent pain had higher dispositional PCS scores than generally healthy adults free from chronic pain. This is a common finding4,26,54 in cross-sectional comparisons of patients and healthy participants, although it is unclear whether such differences are due to catastrophizing acting as a risk factor for the development of pain or whether catastrophizing generally increases after a pain condition develops. While situational catastrophizing scores were highest in the arthritis patients, associations between situational catastrophizing and dispositional PCS scores were most strongly related among TMD patients. Thus, our original hypothesis that measures of situational and dispositional catastrophizing would be more strongly inter-correlated with one another in the patient groups was only partially confirmed. Although the cause of this variability is unknown, one potential explanation may be differences in the degree or nature of clinical pain experiences in the two groups. While ethnicity was controlled within the analyses, ethnic differences within the samples may represent another potential explanatory factor.

While bi-directional associations between catastrophizing and nociceptive processing have been proposed,50 the mechanisms underlying catastrophizing’s effects on pain are yet unknown. One theory proposes that catastrophizing amplifies pain processing in the central nervous system 47 by facilitating sensitization and/or interfering with pain inhibition. Our group has shown that situational measures of catastrophizing are associated with increased temporal summation of pain, a primary marker for central nervous system sensitizability associated with endogenous opioid function.22 We have also recently found that situational catastrophizing is associated with greater IL-6 reactivity, suggesting that catastrophizing may influence the pro-inflammatory immune system.20 Some preliminary data may suggest that catastrophizing correlates with a dysregulation of opioid-based pain-control systems.24,34,55 Greater catastrophizing has been associated with reduced analgesic benefit of an IV kappa opioid agonist.24 This hypothesis is additionally supported by an experiment in which high-catastrophizing participants demonstrated less effective functioning of endogenous pain-inhibitory systems, measured using a Diffuse Noxious Inhibitory Controls (DNIC) paradigm.55 While these studies use indirect measures of the endogenous opioid system, they suggest a link between the use of certain pain-coping techniques and opioid-mediated endogenous pain modulation. Catastrophizing does not appear to engage regulatory mechanisms that alter pain transmission in the spinal cord prior to brain processing, as it has no influence on the nociceptive flexion reflex, a spinally mediated withdrawal reflex.27,44 However, catastrophizing predicts increased myocardial contractility after a cold pressor task,18 influencing the relationship between muscle tension, cardiovascular stress, and pain responses.56

Several limitations should be considered when interpreting these findings. First, two datasets were combined in this study in order to compare findings across participant groups. This could be problematic due to minor variations in location and timing of testing. However, the questionnaires and psychophysical tests were the same for all participants. Second, our analysis did not assess fear of pain or other potentially overlapping constructs. A recent study by Hirsh and colleagues,33 examined dispositional and situational measures of both PCS and CSQ catastrophizing as well as fear of pain in a sample of healthy volunteers undergoing a cold pressor test. They found that pain-related fear was a stronger predictor of cold pressor pain response than either dispositional or situational catastrophizing. While the current assessment did not evaluate fear of pain, considerable evidence has demonstrated that both catastrophizing and fear of pain participate in shaping the pain response.32,42 In contrast, other previous evidence suggests that catastrophizing is a stronger predictor than fear of pain in influencing pain responses51, although this is not consistent across studies.33 Third, we did not probe participants’ dispositional PCS responses to determine what referent they used when indicating how much they “typically” catastrophized. Thus, it is difficult to determine why the correlations between situational and dispositional PCS scores are weak, particularly for the arthritis patients who experience ongoing pain. Fourth, our sample sizes, particularly in the TMD and arthritis groups were small and it is unclear how these findings generalize to other samples of patients with arthritis and TMD or other pain populations. Fifth, we are unable to definitively determine the direction of the association between pain responses and situational catastrophizing in this study. This final point is especially important for future studies of situational catastrophizing in order to begin to establish the causal pathway linking catastrophizing to heightened pain responses. Future studies in this area may benefit from the manipulation of either the degree of pain experienced during laboratory testing (and the impact of this manipulation on situational catastrophizing) or the degree of catastrophizing during a standardized pain experience (and the impact on pain report).

These limitations notwithstanding, the current findings emphasize the importance of assessing catastrophizing related to proximal, specific and known, painful events. Such measures may produce more relevant information, at least when examining laboratory pain responses, particularly with healthy volunteers for whom pain is not a current complaint. The construct of situational catastrophizing is particularly useful when comparing healthy participants to patient groups, as is frequently done in experimental pain studies.

Supplementary Material

1 - appendix 1

2- suppl table 1


This work was supported by NIH Grant K23 AR051315 (to RRE), K23NS047168 (to MTS), R21 NS048593, R24 AT004641, by awards from the American College of Rheumatology and Arthritis Foundation, as well as the Johns Hopkins General Clinical Research Center (M01-RR002719), and with resources from T32 MH75884 and F32 NS063624.



This study adds to a growing literature examining catastrophizing. Our findings highlight the potential importance of the multi-dimensional assessment of pain-related catastrophizing, and suggest a role for measuring catastrophizing related to specific, definable events.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.


1. Beck AT, Steer RA, Carbin MG. Psychometric properties of the Beck Depression Inventory: Twenty-five years of evaluation. Clinical Psychology Review. 1988;8:77–100.
2. Beck AT, Ward C, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Archives of General Psychiatry. 2009;4:561–571. [PubMed]
3. Bruehl S, Carlson CR, Wilson JF, Norton JA, Colclough G, Brady MJ, Sherman JJ, McCubbin JA. Psychological coping with acute pain: an examination of the role of endogenous opioid mechanisms. J Behav Med. 1996;19:129–142. [PubMed]
4. Buenaver LF, Edwards RR, Smith MT, Gramling SE, Haythornthwaite JA. Catastrophizing and pain- coping in young adults: associations with depressive symptoms and headache pain. J Pain. 2008;9:311–319. [PubMed]
5. Campbell CM, Edwards RR. Mind-body interactions in pain: the neurophysiology of anxious and catastrophic pain-related thoughts. Transl Res. 2009;153:97–101. [PMC free article] [PubMed]
6. Campbell CM, Kronfli T, Buenaver LF, Haythornthwaite JA, Smith MT, Edwards RR. In vivo vs. standard catastrophizing in multiple pain measures among healthy, TMD and arthritis patients. Journal of Pain. 2008;9:56.
7. Carroll LJ, Cassidy JD, Cote P. The role of pain coping strategies in prognosis after whiplash injury: passive coping predicts slowed recovery. Pain. 2006;124:18–26. [PubMed]
8. Chan SW, Goodwin GM, Harmer CJ. Highly neurotic never-depressed students have negative biases in information processing. Psychol Med. 2007;37:1281–1291. [PubMed]
9. Cohen F, Lazarus RS. Active coping processes, coping dispositions, and recovery from surgery. Psychosom Med. 1973;35:375–389. [PubMed]
10. Davison AC, Hinkley DV. Bootstrap Methods and Their Application. Cambridge University Press; Cambridge: 1997.
11. Derogatis LR. BSI Brief Symptom Inventory. Administration, scoring, and Procedures Manual. 4. National Computer Systems; Minneapolis, MN: 1993.
12. Derogatis LR, Melisaratos N. The Brief Symptom Inventory: an introductory report. Psychol Med. 1983;13:595– 605. [PubMed]
13. Dixon KE, Thorn BE, Ward LC. An evaluation of sex differences in psychological and physiological responses to experimentally-induced pain: a path analytic description. Pain. 2004;112:188–196. [PubMed]
14. Dworkin SF, LeResche L. Research diagnostic criteria for temporomandibular disorders. J Craniomandib Disord. 1992;6:302–355. [PubMed]
15. Edwards RR. Individual differences in endogenous pain modulation as a risk factor for chronic pain. Neurology. 2005;65:437–443. [PubMed]
16. Edwards RR, Bingham CO, III, Bathon J, Haythornthwaite JA. Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases. Arthritis Rheum. 2006;55:325–332. [PubMed]
17. Edwards RR, Campbell CM, Fillingim RB. Catastrophizing and experimental pain sensitivity: only in vivo reports of catastrophic cognitions correlate with pain responses. J Pain. 2005;6:338–339. [PubMed]
18. Edwards RR, Fillingim RB. Styles of pain coping predict cardiovascular function following a cold pressor test. Pain Res Manag. 2005;10:219–222. [PubMed]
19. Edwards RR, Grace E, Peterson S, Klick B, Haythornthwaite JA, Smith MT. Sleep continuity and architecture: Associations with pain-inhibitory processes in patients with temporomandibular joint disorder. Eur J Pain. 2009 Jan; [Epub ahead of print] [PMC free article] [PubMed]
20. Edwards RR, Kronfli T, Haythornthwaite JA, Smith MT, McGuire L, Page GG. Association of catastrophizing with interleukin-6 responses to acute pain. Pain. 2008;140:135–144. [PMC free article] [PubMed]
21. Edwards RR, Sarlani E, Wesselmann U, Fillingim RB. Quantitative assessment of experimental pain perception: multiple domains of clinical relevance. Pain. 2005;114:315–319. [PubMed]
22. Edwards RR, Smith MT, Stonerock G, Haythornthwaite JA. Pain-related catastrophizing in healthy women is associated with greater temporal summation of and reduced habituation to thermal pain. Clin J Pain. 2006;22:730–737. [PubMed]
23. Efron B, Tibshirani RJ. An Introduction to the Bootstrap (Monographs on Statistics and Applied Probability) Chapman & Hall/CRC; Boca Raton: 1997.
24. Fillingim RB, Hastie BA, Ness TJ, Glover TL, Campbell CM, Staud R. Sex-related psychological predictors of baseline pain perception and analgesic responses to pentazocine. Biological Psychology. 2005;69:97–112. [PubMed]
25. Fishbain DA, Cole B, Cutler RB, Lewis J, Rosomoff HL, Rosomoff RS. Chronic pain and the measurement of personality: do states influence traits? Pain Med. 2006;7:509–529. [PubMed]
26. Flor H, Behle DJ, Birbaumer N. Assessment of pain-related cognitions in chronic pain patients. Behav Res Ther. 1993;31:63–73. [PubMed]
27. France CR, France JL, al’Absi M, Ring C, McIntyre D. Catastrophizing is related to pain ratings, but not nociceptive flexion reflex threshold. Pain. 2002;99:459–463. [PMC free article] [PubMed]
28. Freedland KE, Skala JA, Carney RM, Raczynski JM, Taylor CB, Mendes de Leon CF, Ironson G, Youngblood ME, Krishnan KR, Veith RC. The Depression Interview and Structured Hamilton (DISH): rationale, development, characteristics, and clinical validity. Psychosom Med. 2002;64:897–905. [PubMed]
29. Geisser ME, Robinson ME, Pickren WE. Differences in cognitive coping strategies among pain-sensitive and pain-tolerant individuals on the cold pressor test. Beh Ther. 1992;23:31–42.
30. Geisser ME, Robinson ME, Riley JL., III Pain beliefs, coping, and adjustment to chronic pain: let’s focus more on the negative. Pain Forum. 1999;8:161–168.
31. Gendreau M, Hufford MR, Stone AA. Measuring clinical pain in chronic widespread pain: selected methodological issues. Best Pract Res Clin Rheumatol. 2003;17:575–592. [PubMed]
32. Goubert L, Crombez G, Van DS. The role of neuroticism, pain catastrophizing and pain-related fear in vigilance to pain: a structural equations approach. Pain. 2004;107:234–241. [PubMed]
33. Hirsh AT, George SZ, Bialosky JE, Robinson ME. Fear of Pain, Pain Catastrophizing, and Acute Pain Perception: Relative Prediction and Timing of Assessment. Journal of Pain. 2008;9:806–812. [PMC free article] [PubMed]
34. Jacobsen PB, Butler RW. Relation of cognitive coping and catastrophizing to acute pain and analgesic use following breast cancer surgery. J Behav Med. 1996;19:17–29. [PubMed]
35. Jensen K, Andersen HO, Olesen J, Lindblom U. Pressure-pain threshold in human temporal region. Evaluation of a new pressure algometer. Pain. 1986;25:313–323. [PubMed]
36. Kaloupek DG, White H, Wong M. Multiple assessment of coping strategies used by volunteer blood donors: implications for preparatory training. J Behav Med. 1984;7:35–60. [PubMed]
37. Leppanen JM. Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Curr Opin Psychiatry. 2006;19:34–39. [PubMed]
38. Li X, Gignac MA, Anis AH. Workplace, psychosocial factors, and depressive symptoms among working people with arthritis: a longitudinal study. J Rheumatol. 2006;33:1849–1855. [PubMed]
39. Merens W, Willem Van der Does AJ, Spinhoven P. The effects of serotonin manipulations on emotional information processing and mood. J Affect Disord. 2007;103:43–62. [PubMed]
40. Mischel W, Peake PK. Beyond dejá vu in the search for cross-situational consistency. Psychol Rev. 1982;89:730–755.
41. Osman A, Barrios FX, Gutierrez PM, Kopper BA, Merrifield T, Grittmann L. The Pain Catastrophizing Scale: further psychometric evaluation with adult samples. J Behav Med. 2000;23:351–365. [PubMed]
42. Peters ML, Vlaeyen JW, Weber WE. The joint contribution of physical pathology, pain-related fear and catastrophizing to chronic back pain disability. Pain. 2005;113:45–50. [PubMed]
43. Picavet HS, Vlaeyen JW, Schouten JS. Pain catastrophizing and kinesiophobia: predictors of chronic low back pain. Am J Epidemiol. 2002;156:1028–1034. [PubMed]
44. Rhudy JL, Maynard LJ, Russell JL. Does in vivo catastrophizing engage descending modulation of spinal nociception? J Pain. 2007;8:325–333. [PubMed]
45. Richardson C, Glenn S, Horgan M, Nurmikko T. A prospective study of factors associated with the presence of phantom limb pain six months after major lower limb amputation in patients with peripheral vascular disease. J Pain. 2007;8:793–801. [PubMed]
46. Rohleder N, Miller GE. Acute deviations from long-term trait depressive symptoms predict systemic inflammatory activity. Brain Behav Immun. 2008;22:709–716. [PubMed]
47. Siddall PJ, Cousins MJ. Persistent pain as a disease entity: implications for clinical management. Anesth Analg. 2004;99:510–520. [PubMed]
48. Stephens MA, Druley JA, Zautra AJ. Older adults’ recovery from surgery for osteoarthritis of the knee: psychosocial resources and constraints as predictors of outcomes. Health Psychol. 2002;21:377–383. [PubMed]
49. Sullivan MJ, Bishop S, Pivik J. The Pain Catastrophizing Scale: development and validation. Psychological Assessment. 1995;7:524–532.
50. Sullivan MJ, Thorn B, Haythornthwaite JA, Keefe F, Martin M, Bradley LA, Lefebvre JC. Theoretical perspectives on the relation between catastrophizing and pain. Clin J Pain. 2001;17:52–64. [PubMed]
51. Sullivan MJ, Thorn B, Rodgers W, Ward LC. Path model of psychological antecedents to pain experience: experimental and clinical findings. Clin J Pain. 2004;20:164–173. [PubMed]
52. Thorn BE, Clements KL, Ward LC, Dixon KE, Kersh BC, Boothby JL, Chaplin WF. Personality factors in the explanation of sex differences in pain catastrophizing and response to experimental pain. Clin J Pain. 2004;20:275–282. [PubMed]
53. Turner JA, Mancl L, Aaron LA. Pain-related catastrophizing: a daily process study. Pain. 2004;110:103–111. [PubMed]
54. Vangronsveld K, Van DS, Peters M, Vlaeyen J, Goossens M, Crombez G. An experimental investigation on attentional interference by threatening fixations of the neck in patients with chronic whiplash syndrome. Pain. 2007;127:121–128. [PubMed]
55. Weissman-Fogel I, Sprecher E, Pud D. Effects of catastrophizing on pain perception and pain modulation. Exp Brain Res. 2007;186:79–85. [PubMed]
56. Wolff B, Burns JW, Quartana PJ, Lofland K, Bruehl S, Chung OY. Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models. J Behav Med. 2007;31:105–114. [PubMed]


Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...


  • MedGen
    Related information in MedGen
  • PubMed
    PubMed citations for these articles

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...