Psychological Services Copyright 2008 by the American Psychological Association

2008, Vol. 5, No. 1, 26 35 1541-1559/08/$12.00 DOI: 10.1037/1541-1559.5.1.26

Negative Emotions, Pain, and Functioning

Gabriel Tan Mark P. Jensen

Michael E. DeBakey VAMC and Baylor College of University of Washington School of Medicine
Medicine
John Thornby Paul A. Sloan
Baylor College of Medicine Michael E. DeBakey VAMC

We used linear structural equations (path model analysis) to examine associations

among negative emotions, pain, and functioning in a large sample (N 511) of
veterans with chronic pain. We postulated and tested a model where pain and func-
tioning affect negative emotions and where negative emotions affect pain and func-
tioning. The findings confirm a strong relationship between negative emotions, pain,
and functioning in our sample, particularly as the variable Pain Interference affects
Depression. In a significant but weaker relationship, we also found that Anxiety has a
direct effect on patients perception of their Disability. Specifically, the data support a
model where increased Pain Interference, Pain Severity, Depression and Anxiety all
lead to increased Disability. Findings that Pain Interference and Depression appear to
play a major role in the relationships between pain and negative emotions support the
need for experimental studies to understand the causal impact of these variables on
patient functioning. In the meantime, the findings suggest that Pain Interference,
Depression, and Anxiety, in addition to Pain Severity, should all be targets of chronic
pain treatment.

Keywords: pain, negative emotions, pain interference, pain functioning

A number of investigators have studied the
relationships between negative emotions, par-
ticularly depression, and pain. It is well ac-
cepted among pain experts that negative emo-
tions such as depression are related to pain
perception and experience (e.g., Banks & Kerns,
1996; Holzberg, Robinson, Geiser, & Gremil-
lion, 1996). However, questions concerning the
causal associations between pain and negative
emotions (e.g., whether depression and other
negative emotions such as anxiety and anger
result from chronic pain and/or whether nega-
tive emotions exacerbate pain experience) have
remained largely unresolved.
Current models of pain perception argue that
the experience of pain is influenced by emo-
Gabriel Tan, Michael E. DeBakey VAMC and Baylor
College of Medicine; Mark P. Jensen, University of Wash-
ington School of Medicine; John Thornby, Baylor College
of Medicine; Paul A. Sloan, Michael E. DeBakey VAMC.
Correspondence concerning this article should be ad-
dressed to Gabriel Tan, ABPP, Michael E. DeBakey VA
Medical Center, 2002 Holcombe Blvd (145 Anesthesiol-
ogy), Houston, TX 77030, E-mail: tan.gabriel@med.va.gov
26
tional states, and that disability specifically re-
sulting from pain is affected by both pain per-
ception and emotional state. In support of these
models, evidence indicates that states of depres-
sion lead to increases in the report of pain
(Salovey & Birnbaum, 1989), decreases in the
tolerance for experimentally induced pain
(Zelman, Howland, Nichols, & Cleeland,
1991), and interpretation of various sensa-
tions as painful (Pennebaker, 1982). How-
ever, the data are not conclusive, given the
finding that depressed patients can also have a
higher sensory and pain tolerance then non-
depressed patients (for a review and meta-
analysis, see Dickens, McGowan, & Dale,
2003).
The notion that pain is the catalyst for nega-
tive emotional states comes from the belief that
pain causes enough of a disruption in an indi-
viduals life that negative affective states
emerge (see Banks & Kerns, 1996). For exam-
ple, pain can lead to a sense of hopelessness and
helplessness, can interfere with reinforcing or
pleasurable activities, and can lead to isolation,
sleep disturbances, and frustration. All of these
 NEGATIVE EMOTIONS, PAIN, AND FUNCTIONING
effects can increase the likelihood of experiencing
symptoms consistent with depression and anxiety
and are/may be associated with anger or irrita-
bility. Pain may also initiate a sense of loss,
particularly if associated with disability.
Studies that examine the association between
chronic pain severity and depression have
shown mixed results with respect to the concor-
dance rates and the strength of the association,
but most have demonstrated some relationship
(see G. K. Brown, 1990; Magni, 1987; Romano
& Turner, 1985). However, there remains some
controversy over the causal direction(s) of this
relationship. In one early study, G. K. Brown
found that the association between chronic pain
intensity and depression was moderate, and that
a model identifying chronic pain as a precursor
to depression fit better with his data than a
model identifying depression as a precursor for
pain. Rudy, Kerns, and Turk (1988) proposed a
model in which specific cognitive appraisals
that relate to chronic pain, such as perceived life
interference and loss of self-control, are medi-
ating factors that determine if someone with
chronic pain will become depressed, and found
support for this model in their data. In a later
study, Turk, Okifuji, and Scharff (1995) repli-
cated this finding in an elderly population and
also found that age (being over or under age 70)
moderated the relationship between depression
and pain severity.
In addition to depression, anxiety is often
identified as a correlate of chronic pain. There is
evidence that suggests that states of anxiety can
lead to lower pain tolerance (Carter et al., 2002;
James & Hardardottir, 2002; Keogh & Co-
chrane, 2002) and higher perceptions of pain
(Granot & Lavee, 2005; McWilliams, Goodwin,
& Cox, 2004; Pud & Amit, 2005; Tripp, Stan-
ish, Coady, & Reardon, 2004). However, this
relationship may be moderated by several fac-
tors such as gender (Dougher, Goldstien, &
Leight, 1987; Jones & Zachariae, 2004; Jones,
Zachariae, & Arendt-Nielsen, 2003) and atten-
tion (James & Hardardottir, 2002). Sullivan,
Thorn, Rodgers, and Ward (2004) suggested
that trait anxiety leads to higher levels of state
anxiety, which leads to catastrophizing, which
then in turn leads to increased pain perceptions.
A third negative emotion state occasionally
referred to with respect to pain is anger (also
referred to as irritability). Anger, as suggested
by Henry (1986), can result from a perceived
27
challenge to ones control appraisal. It is a con-
comitant of depression (Wade, Price, Hamer, &
Schwartz, 1990) and it has been hypothesized
that anger turned inward leads to increased anx-
iety and depression. Although anger has been
associated with anxiety and depression and has
been hypothesized to be related to pain, the
relationship between anger and pain has not
been explored in research as much as that be-
tween depression or anxiety and pain (Robinson
& Riley, 1999). Speculation about the nature of
the relationship between anger and pain comes
from limited reports indicating that patients
with chronic pain tend to report higher levels of
hostility and anger (F. F. Brown, Robinson,
Riley, & Gremillion, 1996; Gaskin, Greene,
Robinson, & Geisser, 1992). Suggestions about
the nature of this relationship include the con-
cept of elevated cortisol levels, sympathetic
arousal (Fernandez & Turk, 1995) and the idea
that anger triggers somatic reactivity such as
muscle tension that actually causes or increases
pain perception (Flor & Turk, 1989).
Overall, although a number of correlation
studies have examined the associations between
negative mood states, including depression,
anxiety, anger, and pain, the nature of the rela-
tionships among these domains is not well un-
derstood. Four possible relationships among the
variables have been hypothesized (Robinson &
Riley, 1999): (a) that negative emotional states
sensitize a person to experience pain, (b) that
negative emotional states actually cause pain,
(c) that negative emotional states are the result
of the experience of pain, and (d) pain and
negative emotional states are parallel processes
that co-occur because of a root biological cause.
A fifth option is that negative mood states and
pain impact each other, and that the causal
relationship does not lie in only one direction.
There has been some suggestion that the link
between pain and these negative emotions may
be mediated, at least in part, by pains effect on
functioning. However, the concept of function-
ing in the context of chronic pain may consist of
two distinct domains. For example, Dworkin et
al. (2005) suggested that if one were to look at
functioning one should consider both generic
measures, which measure general functioning
and could allow for comparison across debil-
itating conditions (i.e., general disability,
which can result from many different factors),
and disease-specific measures, which assess the
28 TAN, JENSEN, THORNBY, AND SLOAN
impact of a specific disorder on functioning
(e.g., the component of disability that is specif-
ically caused by pain; that is, pain interference).
Pain interference has been defined as the extent
to which pain interferes with day-to-day func-
tioning (Jensen, 2003). Assessing both do-
mains of functioning may help to identify the
role general versus pain-specific dysfunction as
they relate to emotion.
The purpose of the present investigation
was to clarify the relationships between neg-
ative emotional states, particularly depres-
sion, anxiety, and anger with chronic pain and
functioning by testing the hypothesis that
negative emotions (depression, anxiety, and
anger) are significantly associated with pain
and functioning (pain intensity, pain interfer-
ence, and disability) using a structural equations
modeling (LISREL) approach. We made five a
priori hypotheses concerning the causal direc-
tions of associations, given the fact that viable
models exist for a number of different causal
paths (e.g., that emotions can impact pain, that
pain can impact emotions, that emotions and pain
can impact each other). However, we did plan to
examine and test for additional or different possi-
ble causal paths.
Method
Participants
The sample was obtained from the population
of patients with chronic noncancer pain referred
to the Integrated Pain Management Program
(IPMP) of the Houston VA Medical Center, a
tertiary teaching hospital. The IPMP is a mul-
tidisciplinary outpatient pain assessment, con-
sulting, and treatment program that receive re-
ferrals from surgical, medical, and psychiatric
departments within the medical center. Patients
referred to the IPMP typically have an extensive
history of chronic pain and have received prior
treatments for pain. Inclusion criteria for partic-
ipation in the program (and therefore, for par-
ticipating in this study) include: (a) referral
from primary care physicians or other medical
specialists documenting a history of chronic
pain complaints not responsive to treatment
provided by the referral sources; and (b) com-
pleting the intake-questionnaire packet for treat-
ment (detailed below). Patients are excluded
from the program (and therefore from partici-
pation in this study) only if they have not met
the inclusion criteria.
Patients were required to complete a packet
of self-report questionnaires prior to their initial
IPMP assessment. The questionnaire packet
was mailed to patients with a cover letter ex-
plaining that the questionnaires were to be used
primarily for clinical purposes but that the data
might also be used for program evaluation and
research. Prior to analyzing the data for the
current study, approval from the Institutional
Review Board was obtained. Out of the 1,265
packets mailed from 1995 through 1998, 564
packets were returned, with a return rate
of 44.6%. Thus, slightly less than half of all
patients referred to the IPMP followed through
on their referral and completed the necessary
paperwork to receive services.
The demographic characteristics of the par-
ticipant sample were reported in a previous
study comparing responses to two measures of
pain coping administered in the packet (Tan,
Jensen, Robinson-Whelen, Thornby, & Monga,
2001). The mean age of patients completing the
questionnaires was 50.8 years (SD 11.4,
range 22 to 82 years). Most (84.5%) had at least
a high school education; 12% were college
graduates. The majority of the participants were
male (90.3%). Although most were White
(62.4%), 22.6% were Black, 4.6% were His-
panic, 0.5% was other, and 9.9% did not
respond to this item. Approximately half
(50.2%) were married. Almost half of the par-
ticipants (48.0%) were already receiving dis-
ability compensation for a pain-related condi-
tion, and 58.0% indicated disability due to pain
for more than 5 years. Information about spe-
cific pain diagnosis was not collected, but
breakdowns by primary pain sites were as fol-
lows: back (39.0%), limbs (32.0%), neck/
shoulders (19.0%), head (6.0%), and all over
(4.0%). Furthermore, 72% of the patients re-
ported that they had pain at multiple sites.
To evaluate possible response bias, we col-
lected demographic and disability information
on all patients referred between January 1996
and December 1996. Information was obtained
on 94% of the patients and resulted in a sample
of 126 responders and 168 nonresponders. The
responders and nonresponders did not differ
with regard to age (M 54.5 and 53.9 years,
respectively). There was also no significant dif-
ference in gender, 2 1.92, ns, marital status
 NEGATIVE EMOTIONS, PAIN, AND FUNCTIONING
2 0.03, ns, or disability status (i.e., receiving
no disability, service-connected disability, or
nonservice-connected disability) 2 0.68, ns.
Because the data come from a decade old sam-
ple and may be outdated, a comparison was
made with a more recent data set independently
collected for another study (Tan, Jensen,
Thornby, & Shanti, 2004). Results indicated
that the current data set consisted of a somewhat
younger group (M age 50.80 vs. 55.78; p .05;
N 511 and 434, respectively); were less de-
pressed (M score of 14.26 vs. 17.88; p .05);
and reported less pain interference (M interfer-
ence score of 7.19 vs. 7.47; p .05). However,
the two groups do not differ in education, eth-
nicity, gender, or pain intensity scores. The dif-
ferences at p .05 level are likely to be an
artifact of the rather large sample sizes rather
than meaningful sample differences.
Measures
Measures of Negative Emotion
Measures of negative emotions assessed de-
pression, anxiety, and anger symptoms. The
Center for Epidemiological Studies Depression
Scale (CESD; Radloff, 1977) was used to as-
sess depression. The State Anxiety (SAnxiety)
subscale and the State Anger (SAnger) sub-
scale of the StateTrait Personality Inventory
(STPI; Spielberger, 1979) were used to measure
anxiety and anger, respectively.
CESD. The CESD was used as a measure
of psychological functioning in this study. The
CESD was developed to assess the presence
and severity of depressive symptoms in a gen-
eral population. It includes 20 items that are
based on a 4 point scale ranging from 0
(rarely) to 3 (most of the time), resulting in
scores ranging from 0 to 60 (higher scores in-
dicating greater depressive symptoms). The
CESD has been widely used in pain research
(G. K. Brown, 1990; Jensen & Karoly, 1991;
Monga, Tan, Ostermann, Monga, & Grabois,
1998) and has adequate reliability and conver-
gent validity (Radloff & Locke, 1986). Crite-
rion validity has also been established as the
CESD scores of depressed and nondepressed
participants have been found to be significantly
different (Radloff & Locke, 1986).
STPI. SAnger and the SAnxiety sub-
scales were two of the six subscales of the STPI
29
developed by Spielberger (1979). Although the
STPI was never published, its scales were used
in the subsequent development of the State
Trait Anxiety Inventory and the StateTrait An-
ger Expression Inventory (Spielberger, 1994).
On the STPI, participants were asked to indicate
how they feel at a particular moment by rating
themselves on a 4-point rating scale ranging
from 1 (not at all), 2 (somewhat), 3 (moderately
so), to 4 (very much so). Alpha coefficients were
.84 to .92 for the SAnxiety scale and .90 to .92
for the SAnger scale, showing good internal
consistency. Correlations of the STPI with the
Eysenck Personality Questionnaire (EPQ)
Neuroticism subscale were 0.49/0.46 (for
men/women) for the SAnxiety scale
and 0.44/0.32 (men/women) for the SAnger
scale. Conversely, inverse correlations were
found between the SAnxiety and SAnger
subscales with the EPQ Extraversion sub-
scales: 0.21/ 0.16 (men/women) and
0.07/ 0.10 (men/women), respectively.
Measures of Pain and Functioning
Measures of pain and functioning available
for analysis included: the RolandMorris Dis-
ability Questionnaire (RMDQ; Roland &
Morris, 1983) to assess disability, the Inter-
ference scale of the West HavenYale Multi-
dimensional Pain Inventory (WHYMPI;
Kerns & Turk, 1985) to assess the extent to
which pain interferes with the patients life, and
the Pain Severity scale of the WHYMPI to as-
sess pain severity.
RMDQ. The RMDQ is used to assess over-
all/generalized disability. The RMDQ, derived
from the Sickness Impact Profile, was originally
developed to assess disability associated with
back pain (Roland & Morris, 1983). Items focus
almost exclusively on the physical dimensions
of disability (Deyo & Centor, 1986). Partici-
pants indicate which, if any, of 24 statements
describe them today and are related to their
pain. (e.g., I stay at home most of the time
because of my pain.). Scores range from 0
to 24, with higher scores indicating greater
disability.
Chronic pain treatment centers have found
that the RMDQ is simple to use and provides a
great deal of useful clinical information about
patients disability (Williams, 1988). Research
has supported the validity and reliability of the
30 TAN, JENSEN, THORNBY, AND SLOAN
scale for assessing disability with reference to
persons presenting with mixed chronic pain
problems (Jensen, Strom, Turner, & Romano,
1992), as well as low back pain (Deyo & Cen-
tor, 1986; Lanier & Stockton, 1988).
WHYMP. The WHYMPI (Kerns, Turk, &
Rudy, 1985) is a 56-item measure that assesses
the impact of pain on the patients life, the
patients view of how significant others respond
to their communication of pain, and the pa-
tients general activity level. The validity and
reliability of the WHYMPI has been well estab-
lished (Kerns et al., 1985). The validity of the
WHYMPI has been further supported by the
results of exploratory and confirmatory factor
analytic procedures (Turk & Rudy, 1990). Two
of the scales, Interference and Pain Severity
were used as measures of function and pain for
this study.
The Interference scale of the WHYMPI con-
sists of 11 items that assess the extent to which
pain has interfered with day-to-day activities
and functioning, including the ability to work,
to enjoy family, to participate in social and
recreational activities, and to perform house-
hold chores (Kerns et al., 1985). Scale scores
range from 0 to 66, with higher scores indicat-
ing greater perceived interference over ones
daily functioning. The Interference scale has
been reported to have an excellent internal con-
sistency of 0.90 and a testretest stability
of 0.86 (Kerns et al., 1985).
The Pain Severity subscale of the WHYMPI
was used to assess pain severity and was entered
in the analyses to control for this potential con-
found. The Pain Severity subscale consists of
three items that assess both pain intensity and
suffering. Subscale scores range from 0 to 18,
with higher scores indicating greater intensity
and suffering. The pain severity subscale has an
internal consistency of 0.72 and a testretest
stability of 0.82 (Kerns et al., 1985).
Procedure
The Linear Structural Relations program
(LISREL, Version 8.30; Scientific Software In-
ternational, Inc., 1996) was used to examine the
relationships between the negative emotions
(Anger, Anxiety, and Depression) on the one
hand, and Pain Interference, Disability, and
Pain Severity on the other. Our basic hypothesis
was that all six variables are presumed to be
endogenous: any of the six variables could have
a path to any of the other variables or have a
path leading to it from any of the other vari-
ables. We further hypothesized the existence of
at least one path leading from pain and func-
tioning variables to negative emotions and at
least one path leading in the opposite direction.
This family of relationships neither mandates
nor precludes the possibility of recursive or
nonrecursive models. This is the fifth model as
stated in the Introduction. We will also address
the other four models.
We hypothesized the existence of six specific
paths between variables: Pain Severity to Inter-
ference, Interference to Disability, Interference
to Depression, Depression to Anxiety, Anxiety
to Anger, and Anger to Interference.
LISREL does not prove causal association be-
tween variables, although the results of LISREL
analysis can be viewed as being consistent or
inconsistent with some variables having influ-
ence on other variables. In essence the two sets
of variables, emotion and pain, were hypothe-
sized to act in a nonrecursive manner, in which
the influence of emotion on pain may exist in
one cycle and the reverse may occur in a sub-
sequent cycle. Thus within the same model, the
two sets of variables are allowed to potentially
appear to influence those in the other set as well
as being influenced by them.
Input data in the current application of LISREL
analysis consisted of a covariance matrix among
the six variables, along with estimates of measure-
ment error for each variable. The measurement
errors were estimated using predetermined values
for reliability along with the observed variances in
the present data. When the measurement errors
were applied, the six input variables were replaced
with six latent variables with the same names
but free of measurement error.
The estimation procedure we chose to utilize
in this application followed an iterative process
similar to stepwise regression but with impor-
tant differences. At the initial step a presumed
basic structure was defined, consisting of the six
hypothesized paths among the six latent vari-
ables. At each succeeding step the user has the
option of adding and/or removing particular
paths, based on the significance of paths cur-
rently in the model. A modification index
indicates the approximate significance of add-
ing any path not currently in the model. This
sequence continues until a path model has been
 NEGATIVE EMOTIONS, PAIN, AND FUNCTIONING 31

obtained containing the minimum number of
significant paths, although no path not currently
in the model would contribute significantly to
the model. After the final solution is obtained,
the latent variables can then be standardized to
variables with unit variance as an option.
The degrees of freedom for the t tests of the
significance of each path in the model and chi-
square for error are related to the number of
variables in the covariance matrix and the num-
ber of parameters estimated. In the present ap-
plication, because the covariance matrix con-
sists of six variables, the degrees of freedom in
the final solution were equal to 6*7/2 minus 6
(to account for estimates of the variances of
the 6 latent variables) minus the number of
paths estimated.
Results
Table 1 shows basic descriptive statistics
for all study variables. The means and stan-
dard deviations represent values for the 511
patients used in this study. Reliabilities had
been calculated previously from other data,
and the measurement errors were estimated
from the formula:
Measurement error (variance
in the sample) * (1 reliability).
Table 2 shows the correlation matrix
among all six variables. Although all correla-
tions were significant, the strength of the as-
sociations was variable. For example the cor-
relations within the pain variables and within
the emotional variables were all larger than
all of the correlations between pain and emo-
tional variables. Of particular interest is the
observation that Pain Severity had lower cor-
relations with each of the emotional variables
than did Interference and Disability. Similarly
Anger had lower correlations with Interfer-
ence, Disability, and Pain Severity than did
Depression and Anxiety. On the other hand
the emotional variables tended to be more
strongly associated with each other than did
the pain and functioning variables. These ob-
servations are reflected in the derived paths.
Figure 1 represents the path model with the
most support derived from this process. The
weighted least squares chi-square for er-
ror 5.78 with 8 degrees of freedom ( p
.67). Illustrated are the seven estimated paths,
the path coefficients for the standardized so-
lution and the statistical significance of each
path. There are a total of eight paths, where
no variable except Pain Severity has both a
direct or indirect path leading away from it-
self and a direct or indirect path leading back
to itself. A unique aspect of this model is that
it contains both a path from pain to emotion
and a path from emotion to pain. The path
from Anxiety to Disability is the weakest of
the paths ( p .01) while the path from
Anxiety to Anger is the strongest ( p
0.001). All variables but Anger have a direct
or indirect path ultimately leading to Disabil-
ity. This final model contains five of the six
paths in our hypothesis. The hypothesized
path from Anger to Interference has been
replaced with the path from Anxiety to Dis-
ability, and a path from Disability to Pain
Severity has been added.
We further investigated the possibility of
finding a model that consists of paths among the
three pain-associated variables and among the
three emotion variables without crossing to or
from either group. The best such model con-

Table 1
Descriptive Data for Self-Report Measures of Pain and Emotion
Variable Range of possible scores M (SD) Reliability Measurement error (Variance)
Interference 0 to 6 5.03 (0.89) 0.853 0.1157
Disability 0 to 24 16.19 (4.97) 0.701 7.3952
Pain severity 0 to 6 5.08 (0.85) 0.718 0.2047
Depression 0 to 60 28.32 (12.15) 0.886 16.7583
Anxiety 10 to 40 23.51 (7.22) 0.889 5.7854
Anger 10 to 40 15.85 (7.30) 0.936 3.3893
Note. N 511.
32 TAN, JENSEN, THORNBY, AND SLOAN

Table 2
Pearson Product-Moment Correlations Between Self-Report Measures of Depression, Anxiety, Pain
Interference, Disability, and Pain Severity
Interference Disability Pain severity Depression Anxiety
*
Disability 0.54
Pain Severity 0.49* 0.43*
Depression 0.39* 0.34* 0.26*
Anxiety 0.30* 0.29* 0.23* 0.62*
Anger 0.24* 0.23* 0.22* 0.52* 0.69*
*
p .001.

sisted of three paths connecting the pain vari-
ables and three paths connecting the emotion
variables, with chi-square for error 102.64
and 9 degrees of freedom, p .001. The strong
direct relationship between Interference and
Depression is evident in both the correlation
matrix and in our final path model.
Discussion
The purpose of the present investigation was
to examine the relationships between negative
emotional states (specifically depression, anxiety,
and anger) and pain and functioning measures
(Pain Severity, Pain Interference, and Disabil-
ity). We hypothesized that measures of negative
emotion and measures of pain and functioning
would be significantly associated with one another,
and we further hypothesized certain limitations
on the directions of influence as exemplified by
paths in a LISREL model. The findings are
consistent with our hypotheses and confirm the
common finding that negative emotional states
are associated with pain and functioning. In
particular the findings support a model suggest-
ing that pain severity directly affects interfer-
ence, and indirectly also affects disability, de-
pression, anxiety, and anger. We also found that

0.430***
Pain Interference Depression

0.467***
0.519*** 0.699***

0.186**
Disability Anxiety

0.421*** 0.757***

Pain Severity Anger

** p < 0.01
*** p < 0.001

Note: X2 for error = 5.78; df = 8; p = 0.67

Figure 1. Path diagram for the standardized solution.

 NEGATIVE EMOTIONS, PAIN, AND FUNCTIONING
depression indirectly, and anxiety directly af-
fects disability. The findings would indicate that
pain sufferers become disabled when they report
increased Pain Interference and Anxiety, and
indirectly increased pain severity and Depression.
This finding is consistent with the idea that a
person suffering from pain may avoid work
due to a fear of exacerbation. The more a
person reports anxiety, depression, pain se-
verity and pain interference due to their pain,
the more disabled the person is likely to be-
come; thus the notion of a cycle of avoidance
and fear playing a central role in disability
(Crombez, Vlaeyen, Heuts, & Lysens, 1999;
van den Hout, Vlaeyen, Houben, Soeters, &
Peters, 2001; Vlaeyen, Kole-Snijders, Boeren, &
van Eek, 1995) is supported.
Our findings that negative emotions are
strongly correlated with each other and that
depression appears to be the source from which
other negative emotions (anxiety and anger)
evolve for our chronic pain population would
suggest that efforts to decrease any of these
negative emotions would not only lead to cor-
responding reduction in the other negative emo-
tions, but that efforts to decrease depression
would likely produce the most effective results.
Initially targeting pain severity would likely
produce the most effective immediate outcome
in alleviating pain and its debilitating effects, if
effective interventions that directly influence
pain severity are available (a significant chal-
lenge, given that the lack of availability of such
interventions that do not themselves produce
adverse events, is one of the primary reasons
that chronic pain remains a significant prob-
lem). Another option is to target pain interfer-
ence, which would appear to then alleviate the
emotional effects associated with pain.
In terms of the hypotheses stated in the In-
troduction, we could not test Hypothesis 1 be-
cause the concept of sensitizing a person to
experience pain could not be easily operation-
alized. Our findings do not indicate a one-way
causal direction between negative emotions and
pain; therefore, Hypotheses 2 and 3 were not
supported in favor of the fifth option of negative
emotions and pain as mutually impacting each
other. Hypothesis 4 (pain and negative emotions
are parallel processes that co-occur because of a
root biological cause) was not supported by our
findings since that would imply that negative
emotions and pain are not significantly corre-
33
lated and do not impact each other; these were
simply not the case based on our findings and
clinical practice.
Limitations
Several issues limit the generalizability of
our findings. First, the participant sample con-
sisted entirely of veterans. Moreover, 90% were
men, and most of the sample had a long history
of severe chronic pain (e.g., 58% have been
disabled due to pain for more than 5 years).
Therefore, any generalization of results to non-
veterans, women, and those with less severe
pain conditions should be made with caution.
Another possible limitation is the fact that the
data set is a decade old, although comparison
with a more recent data set reveals only minor
differences in some demographic and pain-
related variables.
Also, it should be reiterated that LISREL
cannot be used to prove causal associations
between variables. In LISREL, the researcher
specifies the model in which one set of variables
is assumed to predict another set of variables.
LISREL then computes and estimates the
strength and directionality of the relations be-
tween the variables that would best explain the
specified model. Thus, although the current
findings are consistent with the hypothesis that
Pain Interference with function is a key medi-
ating variable in the pain-mood relationship;
experimental research is needed to confirm this
hypothesis. The same holds true for the finding
that Depression (through Anxiety) also has an
indirect effect on Disability, Pain Severity and
Pain Interference, and that it is also a key me-
diating variable in the pain-mood relationship.
Despite the limitations of the current find-
ings, the results point to Pain Severity, Depres-
sion, Anxiety, and Pain Interference as key fac-
tors that appear to contribute to Disability. Until
experimental studies test and confirm the causal
impact of these variables on each other, clini-
cians would do well to target each factor to
maximize patient functioning. Although iden-
tifying effective treatments that impact pain
intensity (without other adverse events) is a
significant challenge, there are treatments for
depression (e.g., antidepressants and cogni-
tive behavior therapy), anxiety (e.g., antianx-
iety medications, in vivo desensitization; cf.
Vlaeyen et al., 1995), and anger (e.g., psy-
34 TAN, JENSEN, THORNBY, AND SLOAN
chotropic medications, anger management),
and pain interference (e.g., operant condition-
ing, Fordyce, 1976). Adequate treatment of
chronic pain requires that each of these treat-
ment options should continue to be made avail-
able to individuals with chronic pain and sig-
nificant disability.
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Received March 2, 2006
Revision received August 1, 2007
Accepted August 21, 2007