2. catastrophizers and noncatastrophizers, most research
treats catastrophizing as a continuous, normally distrib-
uted variable (1). In our database of patients with pain,
there is wide variability around the mean catastrophizing
score (Figure 2). Catastrophizing also exists on a contin-
uum in healthy, pain-free individuals (9); indeed, higher
catastrophizing, assessed in pain-free adults, predicts the
future development of chronic pain and pain-related
health care utilization (10,11). A rich area of debate has
centered on whether catastrophizing is best conceptual-
ized as a stable and enduring trait, such as a dimension of
personality, or as a modifiable characteristic (1,12), with
some evidence supporting both positions. Several studies
report a high test–retest stability of catastrophizing mea-
sured over time frames of up to a year in patients with RA
and in other samples (7,13). In contrast, catastrophizing
often decreases when patients undergo cognitive-behav-
ioral therapy (CBT; a set of psychologist-delivered inter-
ventions designed to facilitate the development of self-
management skills, including regulating one’s thoughts,
emotions, and behaviors) (14,15), indicating that cata-
strophizing can be altered by treatment.
Adverse Outcomes of Catastrophizing
Pain severity. Cross-sectionally, catastrophizing relates
to higher pain severity among patients with RA (16–18)
and OA (19,20). High levels of catastrophizing are also
associated with more severe and widespread pain and
more emotional disturbance among individuals with FM
(21–24) and scleroderma (25). In general, these associa-
tions persist even after statistically controlling for depres-
sion, anxiety, or neuroticism (20,26). Several prospective
studies have illustrated the longitudinal association of
catastrophizing with pain in RA. In daily diary studies,
patients with RA who exhibited greater catastrophizing
reported more day-to-day pain and attention to pain than
low catastrophizers (26,27). Findings from another pro-
spective study suggested that baseline catastrophizing
scores predicted enhanced pain and depression in patients
with RA at 1-year followup (28). Catastrophizing may also
influence the success of pain-related treatments in patients
with musculoskeletal disease. In studies of patients with
OA recovering from knee surgery (29,30), higher preoper-
ative levels of catastrophizing were associated with more
pain and disability up to 6 months postoperatively.
Whether catastrophizing predicts the onset of painful
rheumatic conditions is not known, although high cata-
strophizing was shown to be a risk factor for the onset of
low back pain and disability in a population-based study
(10,11).
Pain sensitivity. Catastrophizing shows positive associ-
ations with tender point counts in both population studies
of musculoskeletal tenderness and clinic-based samples of
patients with FM (24,31–33). Hyperalgesia, or enhanced
responsiveness to painful stimuli, is a defining feature of
FM but has also been noted in patients with RA (34–39)
and OA (40–42). Catastrophizing may be correlated with
some of these hyperalgesic responses. For example, cata-
strophizing was associated with decreased heat pain
threshold and tolerance in women with FM (43), reduced
pain tolerance during a cold pressor test in patients with
juvenile rheumatoid arthritis (JRA) (44,45), and lower pain
threshold and tolerance in response to electrical stimula-
tion among patients with OA (46). Recent evidence from
our laboratory suggests that higher catastrophizing relates
to greater central nervous system (CNS) sensitization dur-
ing sustained pain (47), which may account for the con-
sistent positive relationship between catastrophizing and
pain sensitivity.
Figure 2. Distribution of Coping Strategies Questionnaire (CSQ)
catastrophizing subscale scores in a sample of 2,257 patients
experiencing heterogeneous chronic pain syndromes (unpub-
lished data). Scores on the CSQ catastrophizing subscale range
from 0 to 6.
Figure 1. The Pain Catastrophizing Scale (7). Total scores range
from 0 to 52.
326 Edwards et al
3. Depression. In general, catastrophizing is strongly asso-
ciated with measures of negative affect (1). Multiple inves-
tigators have documented positive associations between
catastrophizing and depressive symptoms in FM (21,
23,43). Similar findings have been reported in patients
with RA (16), and we have observed a significant Pearson’s
correlation (r ϭ 0.65) between catastrophizing and scores
on the Beck Depression Inventory in several hundred in-
dividuals with scleroderma. Prospective studies have doc-
umented the association of high catastrophizing at base-
line with increases in depressive symptoms over periods
of up to 1 year in patients with RA (13) and FM (28). In a
recent diary study of patients with OA, catastrophizing
showed concurrent and prospective relationships with
more intense negative mood (i.e., increases in catastroph-
izing on a given day related to worsened mood that same
day and on the next day) (19). Taken together, these find-
ings suggest that in the context of chronic pain, catastroph-
izing may contribute to depressed mood on a short- and
long-term basis. Interestingly, virtually no research to date
has examined associations between pain-related cata-
strophizing and formally assessed (e.g., by structured in-
terview) psychiatric diagnoses such as posttraumatic
stress disorder, generalized anxiety disorder, etc., which
represents an important avenue for future catastrophizing
research.
Disability. Catastrophizing shows robust associations
with self-reported disability and with more objective indi-
ces of function such as returning to work. In patients with
OA, catastrophizing relates to higher levels of observed
pain behaviors and functional limitations during standard-
ized activity tests (20). Among patients with OA undergo-
ing knee surgery, catastrophizing prospectively predicted
postsurgical disability, even after controlling for other psy-
chosocial factors (29). Importantly, although pain severity
is often a primary determinant of disability, RA studies
have established that catastrophizing predicts disability
even after controlling for pain severity (16,48). Finally,
catastrophizing and other indices of poor pain coping are
prospectively associated with reductions in objectively
measured mobility and muscle strength over periods of up
to 5 years in patients with RA (49,50). These findings are
consistent with studies of low back pain (51–53) in which
catastrophizers reported more pain and reduced function
during standardized physical tasks (e.g., range-of-motion
exercises, etc.).
Physiologic indices of disease activity in RA. Multiple
RA studies have reported positive relationships between
catastrophizing (or helplessness, one component of cata-
strophizing) and elevated disease activity (54–58). Al-
though much of this research is cross-sectional, at least 1
longitudinal RA study has shown that catastrophizing pro-
spectively predicted worsening disease activity (defined
by erythrocyte sedimentation rate [ESR] and joint counts)
(26). Among patients with JRA, catastrophizing directly
influences physicians’ global assessments of disease (59),
with higher catastrophizing predicting more severe dis-
ease assessment. Whereas most of these studies did not
control for symptoms of anxiety or depression, a recent RA
study concluded that although helplessness was strongly
positively associated (i.e., 15% shared variance) with ele-
vated high-sensitivity C-reactive protein (CRP) levels, anx-
iety and depression were either unrelated or only mod-
estly related to CRP (60). Finally, prospective RA research
has also revealed that baseline helplessness predicts future
increases in ESR (61) as well as mortality (62,63), even
when controlling for baseline disease severity. Whether
catastrophizing directly impacts other physiologic systems
such as the sympathetic nervous system or the hypotha-
lamic–pituitary–adrenal axis is uncertain; cold pressor
studies have demonstrated that high catastrophizing does
not predict cortisol reactivity to pain (64), but does predict
sustained increases in myocardial contractility (65), a po-
tential index of sympathetic activity. Although it is un-
clear how catastrophizing influences disease severity,
helplessness does correlate with less effective medication
use (66) and less positive health behavior such as exercise
(67), suggesting several plausible pathways by which cata-
strophizing could enhance disease, reduce physical
health, and promote mortality.
Additional outcomes. The impact of catastrophizing on
outcomes can be fairly broad (i.e., not limited to pain). For
example, catastrophizing is related to greater reports of
fatigue among women with breast cancer (68,69), in-
creased constitutional symptoms such as nausea in indi-
viduals with infections (70), reduced maternal social in-
volvement among new mothers (71), and dissatisfaction
with treatment among patients being treated for gastroin-
testinal symptoms (72). From a societal perspective, cata-
strophizing is an important variable to understand because
it relates to greater health care utilization and use of pain-
related medications in the general population (11,73),
even after controlling for pain intensity.
Hypothesized Mechanisms of Action
Catastrophizing interferes with pain-coping and bene-
ficial health behaviors. Perceptions of helplessness and
pessimism may diminish the likelihood that high cata-
strophizers anticipate positive outcomes from other cop-
ing efforts, which may therefore be underutilized (1). In 2
experimental pain studies, individuals who were high
catastrophizers reported using fewer active coping strate-
gies (e.g., distraction, relaxation, etc.) during a cold pressor
test (7,74). Catastrophizing also relates to lower coping
efficacy in patients with OA (19) and RA (18); indeed, in
this latter study, higher levels of catastrophizing were as-
sociated with reduced perceptions of coping self efficacy
on the part of both the patient and his or her spouse.
Finally, as noted above, helplessness (one component of
catastrophizing) correlates with reduced adherence to
medication regimens (66) and less positive health behav-
iors such as exercise (67), each of which could potentially
lead to increases in musculoskeletal pain symptoms.
Catastrophizing increases attention to pain. Some re-
search has also examined the hypothesis that catastroph-
izing enhances the experience of pain via its effects on
Catastrophizing and Pain 327
4. attentional processes. That is, high levels of catastrophiz-
ing may lead individuals to attend selectively and in-
tensely to pain-related stimuli. Catastrophizers experience
more difficulty controlling or suppressing pain-related
thoughts than do noncatastrophizers, they ruminate more
about their pain, and their cognitive and physical perfor-
mance are more disrupted by anticipation of pain (51,75–
77). In patients with FM, catastrophizing is strongly cor-
related with increased attention to pain (78) and greater
vigilance to bodily sensations (36,79).
Catastrophizing amplifies pain processing in the CNS.
Incoming signals in the CNS are subject to modulation at a
variety of sites from the spinal cord to the cortex (80). One
hypothesized mechanism by which catastrophizing im-
pacts the experience of pain promotes sensitization or
interfering with pain inhibition in the CNS (1,21,43,47).
An early study suggested that reducing catastrophizing
resulted in the activation of descending endogenous opi-
oid systems that inhibited nociception (81). A more recent
functional magnetic resonance imaging study of patients
with FM indicated that high catastrophizers showed en-
hanced activity in cortical regions involved in the affective
processing of pain, such as the anterior cingulate cortex
and insular cortex, during the experience of acute pain
(21). Recent data from our laboratory also suggest that
catastrophizing may be directly associated with CNS pain-
facilitatory processes in the spinal cord (82). Overall, pre-
liminary evidence indicates that catastrophizing may am-
plify pain processing at multiple CNS loci, with some
researchers postulating that bidirectional relationships be-
tween catastrophizing and nociceptive processing may
contribute to the chronicity of many pain conditions (1).
Catastrophizing has a maladaptive impact on the social
environment. The communal coping model of catastroph-
izing postulates that expressions of catastrophizing func-
tion to maximize access to supportive responses from oth-
ers, and that these social responses may then reinforce
displays of pain and expressions of catastrophizing
(1,83,84). In support of the model, catastrophizers are per-
ceived by others as less able to manage pain, and are more
likely to seek social support (18,48,85,86). It is interesting
to consider that daily diary studies of patients with RA
suggest that expressing emotions and seeking social sup-
port, which may reflect catastrophizing, are prospectively
associated with greater arthritis pain (87–90). Also note-
worthy is the finding that high levels of catastrophizing are
associated with greater perceived stress and less non–
pain-related social support within the social network
(86,91), suggesting that more frequent catastrophizing may
have paradoxical effects by both eliciting more solicitous
responses to pain (92) and reducing the general availabil-
ity of support, potentially by enhancing distress in others
(93).
Implications for Treatment
Screening for psychosocial risk factors that predict poor
treatment outcome is not widespread, but it may hold
promise as a low-cost means to identify individuals who
would benefit most from adjunctive treatments. For exam-
ple, given that catastrophizing is a risk factor for poor
surgical outcomes (29,30), long-term treatment success
may be maximized by offering CBT either presurgery or
concurrently with surgery to those who exhibit high levels
of catastrophizing. We should also note that reducing cata-
strophizing is particularly important in the context of pre-
venting disability. As several RA studies have demon-
strated, the degree of physical disability exhibited by
patients is a function not solely of pain frequency or in-
tensity, but also of the degree of catastrophizing, suggest-
ing that simple pain reduction is not an adequate treat-
ment goal. In this regard, exposure paradigms are an
important part of behavioral treatments for painful condi-
tions such as FM, RA, and OA; interventions designed to
increase physical activity levels may result in greater pain
in the short term, but by reducing catastrophizing and
enhancing self efficacy, these interventions are likely to
reduce long-term pain and disability (94,95).
Chronic pain and disability are increasingly managed by
multidisciplinary means; analgesic regimens are fre-
quently supplemented by physical therapy or psychologi-
cal interventions for individuals experiencing persistent
pain from rheumatic diseases (96–98). Indeed, for patients
with FM, nonpharmacologic adjunctive therapies may
demonstrate benefits superior to those provided by anal-
gesic medications (96,99). Emerging evidence indicates
that catastrophizing may be an important mediating vari-
able contributing directly to the outcomes of such treat-
ments. In 2 previous studies, decreases in catastrophizing
correlated with reductions in levels of depression and pain
behaviors (such as distorted mobility and verbal and non-
verbal complaints) among patients undergoing pain treat-
ment (14,100). Subsequent work using more sophisticated
analytic techniques has extended these findings; during
multidisciplinary pain treatment, early reductions in cata-
strophizing are associated with greater improvements in
pain later in treatment, whereas individuals whose cata-
strophizing does not change demonstrate few or no bene-
fits from multidisciplinary interventions (15,101–103).
Previous studies of cognitive and behavioral interventions
for pain suggest that these methods are effective in de-
creasing pain-related catastrophizing (14,15,104), and
based on these findings, it may be of great importance to
target catastrophizing early in the multidisciplinary man-
agement of pain. Future treatment studies in patients with
rheumatic disease may benefit from the assessment of cata-
strophizing pre- and posttreatment, the consideration of
catastrophizing as a mediator or moderator of treatment
effects, and a more fine-grained analysis of the pathways
by which catastrophizing impacts important outcomes.
A crucial unanswered question is whether catastrophiz-
ing is a cause or consequence of chronic pain (1,12). Some
indirect evidence bears on this issue, although no longitu-
dinal studies have yet examined whether catastrophizing
changes following the development of chronic pain. First,
catastrophizing tends to be stable over time in both healthy
adults and patients with pain, showing high test–retest
reliability measured over weeks or months (7,13). Recent
data have also suggested that catastrophizing, measured
initially when patients were experiencing acute pain and
328 Edwards et al
5. remeasured several weeks later when they were pain free,
did not change when patients’ pain was alleviated (47). In
contrast, as noted above, self report of catastrophizing
often decreases when patients undergo CBT (14,15), indi-
cating that it may be substantially modifiable. Finally,
studies using daily diary methodologies offer a unique
opportunity to examine the dynamic properties of cata-
strophizing because these methodologies allow assess-
ment of variability both within persons (i.e., variation from
time point to time point) and between persons. A recent
diary study in patients with chronic pain highlighted the
short-term stability of catastrophizing: individuals dif-
fered substantially in how much they catastrophized, but a
given person was likely to show similar levels of cata-
strophizing across the 2-week period, despite fluctuations
in pain (105). Collectively, catastrophizing appears to de-
velop relatively early in life (106,107) and to possess many
stable, trait-like characteristics, but it is clearly also ame-
nable to reduction by certain types of psychosocial treat-
ment.
Conclusions
Catastrophizing shows strong influences on many pain-
related outcomes in patients with rheumatic disease, with
multiple mechanisms of action accounting for its effects
(Figure 3). Because it is robustly correlated with treatment
success, catastrophizing represents an appealing target for
multidisciplinary pain-management interventions. Be-
cause catastrophizing may act via numerous pathways,
multimodal treatments incorporating pharmacologic, cog-
nitive, behavioral, and potentially social interventions are
perhaps most likely to succeed in ameliorating its effects.
Unfortunately, no published studies have evaluated the
efficacy of pharmacologic interventions in the reduction of
catastrophizing, which represents an important area for
future research. However, CBT and multidisciplinary
treatments consistently reduce catastrophizing, even in
samples of patients with long-standing complaints. For
example, in patients reporting chronic pain for Ͼ12 years,
a 4-week group CBT intervention delivered by a psychol-
ogist improved PCS scores by ϳ40% from pre- to posttreat-
ment (108). At present, little information is available on
the management of catastrophizing in patients with rheu-
matic disease, although based on the broader chronic pain
literature, patients with high levels of catastrophizing are
likely to benefit from referrals to a pain psychologist or to
other health professionals with expertise in CBT. Finally,
given that catastrophizing relates to enhanced inflamma-
tory processes and disease activity in RA, the refinement
and application of cognitive, behavioral, and other inter-
ventions designed to diminish catastrophizing in patients
with arthritis would potentially represent an important
development in disease management.
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