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Anxiety sensitivity and its impact on pain experiences
and conditions: A state of the art
Sherry H. Stewart
1
and Gordon J. G. Asmundson
2
1
Dalhousie University, Departments of Psychiatry and Psychology, and
2
University of
Regina, Faculty of Kinesiology and Health Studies and Department of Psychology
Abstract. This paper serves as an introduction to the special issue of Cognitive Behaviour Therapy
devoted to the topic of anxiety sensitivity (AS) and its impact on pain experiences and conditions. We
provide a historical overview of relevant cognitive behavioural models of chronic pain, summarize
recent models incorporating the AS construct, and introduce the papers in the special issue. These
papers are organized into two sets – basic laboratory-based investigations and relatively more
applied studies. We attempt to highlight some of the most important findings from each of these
investigations and studies, in turn. Then, we consider several important conclusions derived from the
set of special issue papers and the implications of these for the practice of cognitive-behavioural
interventions with pain populations. Finally, we make several suggestions for directions for future
investigations in this burgeoning area of cognitive behavioural research and practice. Key
words: anxiety sensitivity; experimental pain; cold pressor; fear of pain; pain catastrophizing;
anticipatory anxiety; fear-avoidance models; persistent headache; chronic pain
Correspondence address: Sherry H. Stewart, Ph.D., Department of Psychology, Dalhousie University,
Life Sciences Centre, 1355 Oxford Street, Halifax, Nova Scotia, Canada, B3H 4J1. Tel: (902) 494-
3793; Fax: (902)-494-6585. E-mail: sstewart@dal.ca
Anxiety sensitivity (AS) is a cognitive indivi-
dual difference variable characterized by a
fear of anxiety-related symptoms (Reiss,
1991). For example, people with high levels
of AS may believe that when they are
experiencing difficulty concentrating that
this may portend a loss of control, or they
may expect that when they experience a
racing heart, this could result in a heart
attack. Consistent with the predictions of
Reiss’ (1991) expectancy model of anxiety,
longitudinal research has now established AS
as a risk factor for panic attacks and anxiety
disorders (e.g., Schmidt, Lerew, & Jackson,
1999). More recently, AS has also been
conceptualized as a risk factor for chronic
pain (e.g., Asmundson, 1999). Indeed, studies
have shown that AS is associated with acute
pain experienced in the laboratory and with
persistent or chronic pain conditions (e.g.,
Keogh & Asmundson, 2004).
It is important to place current chronic pain
theories that incorporate AS into historical
context. Philips (1987) expanded on the
foundational work of Fordyce (1976);
Lethem, Slade, Troup, and Bentley (1983);
and Linton, Melin, and Go¨testam (1984) in a
model of chronic pain that emphasized the
roles of avoidance behaviour and cognitive
factors in maintaining the pain condition. She
noted that chronic pain patients are charac-
terized by extensive avoidance, including
avoidance of stimulation, movement, activity,
and social/leisure pursuits. Philips explained
that this avoidance behaviour is not only
ineffective as a longer-term pain management
strategy, but it actually may be harmful in
terms of maintaining or exacerbating pain.
She also recognized the role of a variety of
fear-based cognitive factors (e.g., pain expec-
tancies, pain-related self efficacy, memories of
past aversive/painful experiences) and, thus,
set the stage for later consideration of the role
of AS – a cognitive variable.
Like Philips’ (1987) model, the now popular
fear-avoidance model (e.g., Vlaeyen & Linton,
2000) also emphasizes the role of avoidance
behaviour in maintaining chronic pain. In this
# 2006 Taylor & Francis ISSN 1650-6073
DOI 10.1080/16506070601090457
Cognitive Behaviour Therapy Vol 35, No 4, pp. 185–188, 2006
model, it is the fear of pain (an emotional
variable) that is thought to motivate pain-
related avoidance and escape behaviour
which, in turn, maintains exaggerated percep-
tions of pain through processes such as
deconditioning. Others have since built upon
the fear-avoidance model to incorporate the
role of AS in explaining pain chronicity.
Because AS reflects a general propensity to
develop fears (Reiss, 1991), Asmundson,
Norton, and Norton (1999) proposed that
AS plays a key role in the onset and
maintenance of chronic pain by amplifying
the tendency to develop fear of pain. The fear
of pain then elevates pain-related avoidance,
leading to deconditioning and increased pain
experiences. These increased pain experiences
result in further avoidance and negative
expectancies regarding pain, as described in
earlier models. Later, as the role of ‘‘pain
catastrophizing’’ (another cognitive variable)
became increasingly recognized (see Sullivan
et al., 2001), the fear-avoidance model was
amended. The amended model conceptualizes
cognitive variables of appraisal and expectan-
cies of pain as feeding into pain castrophizing
which, in turn, leads to pain-related fear and
associated avoidance (Norton & Asmundson,
2004). Asmundson et al. (2000) further su-
ggested that AS (particularly the physical
concerns component) promotes catastrophic
cognitions regarding pain. Thus, in the
amended model, AS was seen to exert its
actions on pain via effects on pain catastro-
phizing. Additional refinements to the fear-
avoidance model are outlined by Asmundson,
Norton, and Vlayen (2004).
Other theorists have focused on attempting
to explain the role of AS in contributing to the
severity of acute pain experiences. Schmidt
and Cook (1999) suggested that AS should
enhance pain intensity by increasing a person’s
vulnerability to experiencing anxiety which, in
turn, should promote increased pain experi-
ences. In this model, AS is seen as a distal,
trait measure, and anxiety as a proximal, state
measure. Similarly, Watt and Stewart (2000)
suggested that AS may represent a general
tendency to perceive any source of arousal as
threatening. Thus, AS should amplify the
experience of bodily sensations related to a
wide range of somatic events, including pain.
The current special issue involves papers
representing the state-of-the-art in this area of
research. They are divided into two main sets –
basic laboratory-based and relatively more
applied studies. The first four papers consist
of basic, laboratory-based investigations with
non-clinical populations where the focus is on
understanding the nature of the relation
between AS and the pain experience. All of
these laboratory-based investigations make use
of experimental pain-induction methods and
involve consideration of the mechanisms
underlying the known association between
AS and aspects of acute pain. The first paper,
by Uman, Stewart, Watt, and Johnston, links
AS to specific aspects of the pain experience
(i.e., pain intensity and fear of pain) in a
laboratory-based cold pressor investigation
with university women. This investigation
shows that the relationship of AS to pain
intensity is mediated through the association of
AS with a fearful response to the pain stimulus.
The second paper, by Keogh, Barlow, Mounce,
and Bond, also used the cold pressor to
confirm that AS is related to experimentally-
induced pain. Their findings suggest that there
may be gender differences in how AS relates to
pain. AS appears related to self-report mea-
sures of pain in women and to behavioural
measures of pain in men. The third paper, by
Tsao, Lu, Kim, and Zeltzer, describes the
results of an investigation using the cold
pressor and two other types of laboratory pain
stimuli (thermal pain and pressure pain) to
investigate underlying mechanisms relating AS
to pain experience in children. Their work
shows that the relation of AS to pain intensity
operates indirectly through the association of
AS to anticipatory anxiety while children await
painful stimuli. Further, their work contributes
to a fledgling body of research that extends the
relation of AS and pain from adults to
children. The last paper in this section, by
Conrod, describes an investigation linking AS
to increased anticipatory anxiety when await-
ing a painful stimulus in the laboratory.
Through the inclusion of a social stressor
control condition, this investigation also
shows that the elevated anticipatory anxiety
of high AS participants is not specific to pain
situations.
The second set of papers are relatively more
applied than the first set in terms of the type of
pain investigated (e.g., persistent headache
pain), the population investigated (e.g.,
chronic musculoskeletal pain patients), or the
186 Stewart and Asmundson COGNITIVE BEHAVIOUR THERAPY
treatment focus of the investigation (e.g., an
intervention study). In the first paper of this
second set, Drahovzal, Stewart, and Sullivan
describe the results of a survey study with
undergraduates that investigated the relations
between AS and pain catastrophizing and their
relative contributions to various aspects of
persistent headache pain. Their results suggest
that although AS and pain catastrophizing are
highly correlated, they are separable psycho-
metrically, and they independently contribute
to the prediction of persistent headache pain.
The next paper, by Carleton, Asmundson,
Collimore, and Ellwanger, examined differ-
ences between chronic musculoskeletal pain
patients and controls on responses to a startle
probe paradigm tapping automatic and stra-
tegic attention allocation to several types of
pain-schema relevant words. One result from
this investigation was that chronic pain
patients with high AS appear to have more
difficulty disengaging attention from words
indicative of physical harm. In the final paper,
Watt, Stewart, Lefaivre, and Uman present on
the results of a randomized controlled trial.
Their findings show that high AS participants
randomized to a cognitive behavioural inter-
vention focused on reducing AS levels, dis-
played concomitant reductions in fear of pain.
There are several common conclusions that
emerge from the results of this set of papers.
The first involves the intervening or mediating
role of more proximal state anxiety-type
constructs in explaining the previously-estab-
lished relationship between the more distal trait
variable of AS and the pain experience. The
findings of Uman et al., Tsao et al., and
Conrod – all consistent with the theoretical
predictions of Schmidt and Cook (1999) –
suggest that fear of pain and anxiety when
anticipating painful stimulation should be
targets of intervention in cognitive behavioural
interventions for high AS chronic pain
patients. This suggestion is consistent with
emerging clinical interventions for chronic pain
(Asmundson, Vlaeyen, & Crombez, 2004).
A second conclusion is that the indirect
relationship of AS to increased pain experi-
ence, via increased state anxiety, generalizes
across a variety of different pain induction
methods. Although most studies in the first
section of this special issue made use of the
traditional cold pressor task, Tsao et al.
extended these findings to thermal and
pressure pain and Conrod extended them to
pain induced by mild electric shock. We can
have more confidence in this set of findings
knowing that they generalize across a wide
range of types of pain experience.
The findings also converge in suggesting
that the role of AS in pain experiences and
conditions may be more complex than origin-
ally conceptualized. On the one hand, the
results of Watt et al. are consistent with the
position of Asmundson et al. (1999) that AS
drives the fear of pain, because an interven-
tion focused on AS-reduction resulted in
concomitant reductions in fear of pain. On
the other hand, the findings of Drahovzal et
al. are not entirely consistent with predictions
of the amended Vlaeyen-Linton fear-avoid-
ance model that AS exerts its effects on pain
via its effects on pain catastrophizing. If this
were the case, pain catastrophizing would
have been the only significant predictor of
persistent headache when both AS and pain
catastrophizing were simultaneously entered
as predictors in the regression. Instead, AS
must have some additional influences on
persistent pain that are not mediated through
effects on pain catastrophizing. These effects
might be mediated through other cognitive
processes, such as the difficulties disengaging
attention from general physical threat cues
identified by Carleton et al.
There are several interesting avenues for
future research that emanate from the results
of the present set of papers. For example,
more research is needed on the underlying
mechanisms to explain how elevated state
anxiety contributes to increased pain in high
AS individuals. One possibility is that elevated
anticipatory anxiety contributes to increased
physiological arousal (e.g., increased muscle
tension) which contributes to an increased
pain experience. Conrod’s study tested this
possibility and did not provide support for an
intervening role of increased physiological
arousal. Future research might consider the
role of cognitive variables, including attention
(see Carleton et al.).
The question of whether the relation of AS
to pain experiences and conditions varies by
gender also deserves further study. One study
in the special issue that directly tested for
gender effects found important differences in
the relation of AS to manifestations of pain in
women versus men (i.e., Keogh et al.).
VOL 35, NO 4, 2006 187
However, two other studies that directly
tested for gender effects failed to provide
support for any differences in the relation of
AS to pain constructs in males versus females
(i.e., Conrod; Tsao et al.). Future research
should systematically examine the conditions
under which gender moderation effects are
and are not observed. For example, do such
gender differences emerge with development?
Finally, the Watt et al. study suggests novel
avenues for intervention research. Watt et al.
showed that by intervening at the level of AS
via cognitive-behavioural methods, one could
also impact fear of pain in a non-clinical
sample. Important next steps would be to
determine whether these results: extend to the
treatment of chronic pain patients; apply to a
wider range of outcomes (e.g., perceived
disability, pain self-efficacy, pain catastrophiz-
ing); and persist at longer-term follow-up.
Moreover, future investigations should com-
pare Watt et al.’s new ‘AS-reduction approach’
to ‘graded in vivo exposure treatment’ which
involves exposure to movements and tasks that
chronic pain patients have avoided due to
fear of (re)injury (see de Jong et al., 2005).
Watt et al.’s recommended focus on AS in
treatment fits well with recent findings
(Greenberg & Burns, 2003) that pain anxiety
is better viewed as a manifestation of AS
than as a specific phobia of pain (since the
latter position would favour a focus on
reducing avoidance behaviour, as in graded
in vivo exposure treatment). Only future
randomized controlled trials will tell which
of these approaches produces the greatest
benefit in the cognitive behavioural treat-
ment of chronic pain, or whether these two
approaches can be usefully combined.
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