CHAPTER 10
ACUTE STRESS DISORDER AND
POSTTRAUMATIC STRESS DISORDER
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Richard A. Bryant
Acute stress disorder (ASD) is relatively new addition to the diagnostic systems used to describe
stress reactions in the aftermath of trauma. It was
introduced in 1994 in the fourth edition of the
Diagnostic and Statistical Manual of Mental Disorders
(DSM–IV; American Psychiatric Association, 1994).
It has been a notoriously controversial diagnosis
insofar as people have questioned its conceptual
basis, operational definition, and empirical support.
Despite this, the advent of the diagnosis has resulted
in an exponential increase in attention given to
acute trauma reactions and a wealth of new research
that has shed light on how we understand posttraumatic stress responses occurring immediately or
soon after the traumatic event. This chapter reviews
the historical roots of the ASD disorder, tracks its
development to its current understanding in DSM–5
(American Psychiatric Association, 2013), discusses
known mechanisms of ASD, and reviews prevailing
assessment and treatment procedures.
A BRIEF HISTORY OF THE ASD DIAGNOSIS
Throughout the course of the various successive iterations of the posttraumatic stress disorder
(PTSD) diagnosis in DSM, there has been a restriction of 1 month after trauma exposure on how soon
this diagnosis can be made. This stipulation was
instituted because of concerns that a premature
labeling of a maladaptive stress response would
overpathologize normative and transient stress
reactions. This perspective was debated in the lead
up to DSM–IV (American Psychiatric Association,
1994) when commentators felt that this situation
resulted in a diagnostic gap that precluded acutely
distressed people from being accurately identified.
One of the major reasons for this concern was that
in the U.S. health-care system, access to care can be
compromised if a person does not have a formally
recognized diagnosis. Hence, it was proposed that
a diagnosis describing acute stress reactions would
promote pathways to health care within a month of
trauma exposure.
Additionally, a second goal of the new ASD diagnosis was proposed, which was to identify acutely
traumatized people who subsequently will develop
PTSD. As we will discuss, many people will display
acute distress in the initial days after trauma exposure, and this distress can extend to the initial week
or two. Many of these people, however, will not
progress to develop PTSD. Thus, a major challenge
for early intervention always has been to disentangle
those people in the acute phase who have a transient stress response from those displaying the early
signs of a chronic course of PTSD. It was proposed
that ASD would provide a solution, at least to some
degree, to this problem.
ASD was defined by DSM–IV (American Psychiatric Association, 1994) in a format that was generally consistent with the PTSD diagnosis, with some
important distinctions. The individual needed to
be exposed to a traumatic event in which there was
actual or threatened death or serious injury and
must have experienced fear, helplessness, or horror
(Criterion A). In addition, four additional symptom
clusters needed to be satisfied. Cluster B, which
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Richard A. Bryant
is the cluster that distinguished ASD from PTSD,
required at least three of the following dissociative symptoms: (a) a subjective sense of numbing,
detachment, or absence of emotional responsiveness; (b) reduced awareness of surroundings;
(c) derealization; (d) depersonalization; and
(e) dissociative amnesia. These symptoms could
exist either at the time of trauma (often called
peritraumatic dissociation) or in the month afterward. One also needed to exhibit one or more reexperiencing symptoms, such as intrusive thoughts,
images, nightmares, or distress to reminders of the
event (Criterion C), marked avoidance of stimuli
that remind the individual of the trauma must
be present (Criterion D), and marked anxiety or
arousal symptoms (Criterion E). These symptoms
had to cause significant distress or impairment
(Criterion F), and last for a minimum of 2 days and
a maximum of 4 weeks (Criterion G).
CRITICISMS OF THE ASD DIAGNOSIS
When the new ASD diagnosis was introduced,
it was met with much criticism for conceptual,
empirical, and procedural reasons. From a conceptual view, it was considered unusual to have
a diagnosis that had a goal of predicting another
subsequent, and phenomenologically similar, diagnosis (Bryant & Harvey, 2000). Another conceptual concern was that the diagnosis may result in
excessive diagnoses of normative stress responses,
thereby labeling people as disordered when, in
fact, they were simply experiencing understandable stress reactions that would later abate (Marshall, Spitzer, & Liebowitz, 1999). Other criticisms
focused on the dearth of solid evidence for the
criteria to both identify those who were acutely
distressed and predict later PTSD (Bryant & Harvey, 1997). Notably, those who were strong supporters of the new diagnosis recognized that the
link between ASD and later PTSD was “based more
on logical arguments than on empirical research”
(Koopman, Classen, Cardeña, & Spiegel, 1995,
p. 38). The concerns for the lack of empirical evidence for the ASD diagnosis was highlighted by
concerns that the emphasis in the diagnostic criteria on dissociation had a limited empirical base,
162
although more evidence did emerge after the diagnosis was introduced (Marshall et al., 1999).
THE ROLE OF DISSOCIATION
Given the emphasis placed on dissociation in ASD,
it is important to fully understand the rationale
and evidence for this feature of the acute trauma
response. We can see the evolution of the dissociative school of thought commencing in the
seminal work of Janet in the early 20th century in
Paris (Janet, 1907). In his work with people who
developed a range of psychosomatic and hysterical
symptoms following trauma, he observed that some
trauma survivors responded to the trauma by splitting awareness of their distressed state from normal
consciousness. Although this led to short-term
relief, he proposed that this splitting (or dissociation) led to psychological problems because of the
demands this placed on psychological resources. It
is curious that this school of thought did not enjoy
great influence for much of the 20th century, arguably because of the dominance of psychoanalysis
and the rising emergence of behaviorism. In the
latter years of the 21st century, the notion of dissociation being a pivotal role in traumatic stress
response gained momentum, with many commentators believing it was central to the development of
posttraumatic psychopathology (van der Kolk &
van der Hart, 1989). This notion was supported by
evidence of elevated levels of hypnotizability, a trait
associated with dissociation, in people with PTSD
(Spiegel, Hunt, & Dondershine, 1988; Stutman &
Bliss, 1985).
Numerous reports also had indicated that people
with chronic PTSD had higher levels of dissociation,
as measured by dissociative tendencies scales (Bernstein & Putnam, 1986; Bremner et al., 1992; Coons,
Bowman, Pellow, & Schneider, 1989). Relating this
idea to ASD, it was argued by many that dissociative
responses to the trauma in the acute phase resulted
in limited access to the trauma memories, which
subsequently could hinder processing of emotional
experiences and thereby lead to ongoing PTSD
(Spiegel, Koopman, & Classen, 1994). Supporting
this idea, some limited evidence from early studies
indicated that dissociation in the acute phase was
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Acute Stress Disorder and Posttraumatic Stress Disorder
associated with subsequent PTSD (Cardeña &
Spiegel, 1993; Holen, 1993); this finding was replicated numerous times after the introduction of
the ASD diagnosis (Ehlers, Mayou, & Bryant, 1998;
Murray et al., 2002).
Some critics of the emphasis on dissociation
expressed concerns about the mechanism that dissociation was purportedly playing in the acute phase.
In setting out diagnostic criteria for ASD, DSM–IV
(American Psychiatric Association, 1994) allowed
that dissociative symptoms could occur in this syndrome during the trauma or during its aftermath.
The ambiguity over when dissociation arose in ASD
is problematic because when it occurs may lead to
distinct outcomes. For example, dissociative reactions that occur during a trauma may act to limit
encoding of the traumatic experience and, in this
sense, actually may be protective (Horowitz, 1997).
In contrast, if dissociation persists continuously after
the traumatic event, then it is possible that it serves
the function of limiting access to the trauma memories and their affect. Most dissociative reactions
after trauma abate with time (Davidson, Kudler,
Saunders, & Smith, 1990), which underscores that
persistent dissociation is not common. Furthermore,
the alterations in awareness and perception that
people often experience during a trauma are actually quite common in everyday life (Ross, Joshi, &
Currie, 1990). It appears that these alterations in
awareness are particularly common when we are
highly aroused, and this can be attributed to reduced
working memory capacity, limiting the capacity to
encode normal amounts of information when our
minds are being bombarded by lots of stimuli during
an arousing experience. For example, people taking
part in skydiving for the first time typically find this
to be a frightening experience and also report high
levels of dissociation, but this does not seem pathological because people do not subsequently develop
PTSD (Sterlini & Bryant, 2002). Furthermore, when
people are under threat, evidence indicates that they
narrow their attention onto stimuli that are likely to
be the source of threat, thereby reducing the encoding of other events (Kramer, Buckhout, & Eugenio,
1990; Maass & Köhnken, 1989).
What if dissociative responses are more persistent and do not subside after the initial days
following the traumatic event? This may have an
impact on how the person can access trauma memories and arguably could lead to more psychopathological responses. This view is supported by studies
that have focused on dissociation that occurs during
the trauma and dissociation that persists after the
traumatic event. Across studies, dissociation that
persists after exposure to the trauma is linked to
both acute (Panasetis & Bryant, 2003) and chronic
(Briere, Scott, & Weathers, 2005) posttraumatic
reactions.
Probably the most commonly used measure
of peritraumatic dissociation is the Peritraumatic
Dissociative Experiences Questionnaire (Marmar,
Weiss, & Metzler, 1997); factor analytic studies
have shown that it encompasses two subscales:
reduced awareness and derealization or depersonalization. Although reduced awareness is not
strongly linked to psychopathological responses,
derealization or depersonalization is (Brooks et al.,
2009). This finding highlights that dissociation is
not a uniform construct but rather that different
forms of dissociative experience play distinct roles
in the posttraumatic response. One recent study
that employed latent profile analysis revealed that
acutely traumatized people who are most symptomatic are characterized by elevated dissociation and
avoidance (Hansen, Armour, Wang, Elklit, &
Bryant, 2015). This pattern may suggest that
although dissociation is not prominent in all ASD
individuals, it may feature in those who are particularly distressed.
THE PREDICTIVE POWER OF ASD
Following the introduction of the ASD diagnosis in
DSM–IV (American Psychiatric Association, 1994), a
series of longitudinal studies appeared that assessed
for ASD within the initial month after trauma exposure and subsequently assessed for PTSD. This
increasing body of evidence allowed the field to
better understand how predictive ASD was of later
PTSD. A review of the published longitudinal studies identified 23 investigations (Bryant, 2011). Several major points emerge from these studies. First,
across the majority of these studies, most trauma
survivors with ASD subsequently met criteria for
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Richard A. Bryant
PTSD. That is, the ASD diagnosis appears to be
doing a good job insofar as most people with the disorder do not remit but rather continue to have longterm PTSD. In contrast, the sensitivity in predicting
PTSD was quite poor, meaning that most trauma
survivors who eventually developed PTSD did not
meet the criteria for ASD initially. Put another way,
ASD was failing to identify most people in the acute
phase who would develop PTSD. The emphasis on
dissociation may preclude many distressed people
from inclusion in the ASD diagnosis; although they
manifest re-experiencing, avoidance, and arousal
symptoms, they may not meet the stringent criterion
for dissociation. In fact, several studies assessed
subsyndromal ASD, which typically required meeting three of the four ASD symptom clusters (but not
dissociation). These studies found that the sensitivity in predicting PTSD was better if one used subsyndromal ASD. Even these studies, however, found
only modest sensitivity in predicting PTSD.
An interesting pattern emerges when we look at
the predictive capacity of ASD in children. Consistent with the adult literature, overall PTSD symptoms tend to abate over time in children (Kinzie,
Sack, Angell, Manson, & Rath, 1986; Milgram et al.,
1988). When we peruse the five child studies that
have assessed ASD and PTSD longitudinally (Bryant,
Salmon, Sinclair, & Davidson, 2007; Dalgleish et al.,
2008; Ji, Xiaowei, Chuanlin, & Wei, 2010; KassamAdams & Winston, 2004; Meiser-Stedman, Yule,
Smith, Glucksman, & Dalgleish, 2005), the pattern
suggests that ASD is an even weaker predictor of
PTSD in children than adults. The significant majority of children who develop PTSD after trauma do
not display ASD initially. This may be attributed to
the poor understanding of dissociative responses in
children after trauma.
TRAJECTORIES OF POSTTRAUMATIC
RESPONSE
As researchers have struggled with the predictive
capacity of the ASD diagnosis, they have attempted
to improve prediction by emphasizing certain symptoms, such as re-experiencing (Brewin, Andrews,
Rose, & Kirk, 1999), insomnia (Shalev, Freedman,
et al., 1998), emotional numbing (Harvey & Bryant,
164
1998), different symptom permutations (Brewin
et al., 1999), or the overall level of acute symptoms
(Bryant, Moulds, & Guthrie, 2000). Despite these
attempts, none of these strategies have really provided adequate sensitivity or positive predictive
power for identifying people in the acute phase who
subsequently will develop PTSD.
Why is prediction of PTSD so difficult? Probably the answer to this question is the increasing
evidence that posttraumatic stress responses do not
develop, or maintain, in a linear fashion. Instead,
it appears that people fluctuate enormously over
time in the degree of PTSD symptoms they may
experience. In a large longitudinal study of traumatically injured patients who were assessed in
hospital and again at 3, 12, and 24 months later,
it was found that the rate of PTSD remained fairly
constant over time—but approximately half of
people who had PTSD, or even subsyndromal
PTSD, at any time point had a different status at
the next assessment (Bryant, O’Donnell, Creamer,
McFarlane, & Silove, 2013). For example, of those
who had PTSD at 12 months, 37% had no PTSD at
3 months—suggesting a worsening of symptoms for
many people.
This realization has led the field of traumatic
stress to look beyond simple diagnostic categories
to understand PTSD response because this oversimplifies the condition of the individual. Categorizing individuals as having PTSD or not is arbitrary
because these individuals need to shift by only
1 of a possible 20 symptoms and they instantly
jump from being categorized as a case to a noncase.
Does this shift in one symptom accurately reflect
their clinical condition? We know that it does not
because of much evidence that people with subsyndromal PTSD can suffer as much functional
impairment as those with full PSTD (Stein, Walker,
Hazen, & Forde, 1997). Even when people have
looked beyond diagnostic rates over time and studied severity of PTSD, they have tended to focus on
the average response to a traumatic event—this can
lead to the conclusion that whereas most people
will display some distress initially, they will tend
to adapt in the following weeks or months. More
sophisticated statistical approaches, however, have
now mapped the trajectories by using latent growth
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Acute Stress Disorder and Posttraumatic Stress Disorder
mixture modeling, which permits distinct groups
to be identified so that their overall path of adjustment can be modeled. Put another way, rather than
assuming that
all people follow the same path, it permits different trajectories to be mapped. This approach has
resulted in numerous longitudinal studies being
analyzed, and remarkably, the trajectories that have
been identified show much consistency. Different
researchers have noted (a) a resilient class with consistently few PTSD symptoms, (b) a recovery class
with initial distress then gradual remission,
(c) a delayed reaction class with initial low symptom
levels but increased symptoms over time, and (d) a
chronic distress class with consistently high PTSD
levels. Across all studies, the resilient class is the
most prevalent, with approximately three quarters
of trauma survivors enjoying minimal distress across
time. These patterns have been observed in survivors of traumatic injury (Bryant et al., 2015), severe
acute respiratory syndrome (Bonanno et al., 2008),
women diagnosed with breast cancer (Lam et al.,
2010), disaster (Pietrzak, Van Ness, Fried, Galea, &
Norris, 2013), disaster and terrorist attacks
(Norris, Tracy, & Galea, 2009), and military personnel deployed to the Middle East (Bonanno, Mancini, et al., 2012). These lessons teach us important
lessons about predicting PTSD. First, people will
respond in a variety of ways after trauma, and this
complicates how we will identify these people in the
acute phase. Second, the factors that influence how
a person adapts following trauma can include life
events that occur after the trauma, and so these cannot be assessed in the acute phase. We are only at
the beginning of using this approach to map trajectories, and so the next step is to predict which trajectory people will follow. One study of rape victims
that found two trajectories noted that ASD predicted
membership of the more distressed group (Armour,
Shevlin, Elklit, & Mroczek, 2012). At this point, it
appears that the simplest means to predict who will
require mental health assistance is to identify those
who will be resilient because they typically will be
psychologically healthy over time. This is a different
approach than the one adopted by the ASD diagnosis, which seeks to target those with a specific disorder rather than excluding those who appear healthy.
ASD IN DSM–5
As the field of acute traumatic stress accumulated
greater evidence, it became apparent that the conceptualization and operation of ASD was in need of
revisions in the next edition of DSM. In 2013, the
American Psychiatric Association released DSM–5
and in this iteration the ASD diagnosis underwent
some important changes. One of the most important
shifts in focus was that it no longer was intended to
predict subsequent PTSD (Bryant, Friedman, Spiegel, Ursano, & Strain, 2011). On the basis that the
ASD diagnosis was not identifying most people who
subsequently develop PTSD, it was decided that this
goal should be abandoned. Instead, the emphasis
was placed on identifying people who were experiencing severe stress reactions and who could benefit
from mental health services. In this sense, remember
that the DSM is a U.S. product that needs to accommodate the distinctive needs of U.S. health-care
systems; it was proposed that this diagnosis would
facilitate access to mental services. Although it has
been suggested that the ASD diagnosis was not necessary because the adjustment disorder diagnosis
also could be made to describe people in the initial
month after trauma, the latter diagnosis presents
strong concerns because some health companies do
not recognize this diagnosis like they do ASD, and
it often is perceived as being transient and therefore
not requiring clinical intervention.
The DSM–5 (American Psychiatric Association,
2013) definition of ASD also moved away from the
prior emphasis on dissociation. The DSM–IV (American Psychiatric Association, 1994) ASD definition
required patients to display three dissociative symptoms and to satisfy the re-experiencing, avoidance,
and arousal clusters. Since the introduction of the
ASD diagnosis, it became apparent from crosssectional and longitudinal studies that patients
experienced considerable heterogeneity in their
symptoms, and there was actually little empirical
justification for the specified number of symptoms in
each symptom cluster. Several factor analytic studies
have been conducted on ASD symptoms, with varying
results. Whereas some have supported the DSM–IV
conceptualization of the four factors (Brooks, Silove,
Bryant, O’Donnell, Creamer, & McFarlane, 2008;
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Richard A. Bryant
Cardeña, Koopman, Classen, Waelde, & Spiegel,
2000; Wang et al., 2000), others have found that
this four-factor structure does not readily accommodate acute stress responses (Armour, Elklit, &
Shevlin, 2013; Bryant, Moulds, & Guthrie, 2000).
Accordingly, in DSM–5, a different approach was
adopted that did not require specific symptom
clusters to be present. Instead, it was decided that a
minimum of 9 of a possible 14 symptoms should be
present. This was deemed to reflect people who suffered severe stress reactions that may warrant mental health intervention.
Although the DSM–5 (American Psychiatric
Association, 2013) definition of ASD did not require
symptom clusters to be satisfied, the criteria nonetheless are listed under specific headings to facilitate
clinician use. The initial group of symptoms are the
intrusive symptoms and include (a) recurring intrusive memories of the trauma, (b) recurrent dreams
related to the traumatic experience, (c) flashback
memories that involve some degree of reliving of
the actual experience, and (d) marked psychological distress or physiological reactivity to things that
remind the person of the trauma. The next category
involves negative mood, which contains the single
symptom of persistent inability to experience positive emotions. This used to be termed emotional
numbing (a dissociative symptom in the DSM–IV;
American Psychiatric Association, 1994), but in
DSM–5 the symptom focused more on difficulties in accessing positive emotions (rather than all
emotional responses) because of the evidence that
PTSD is characterized by hyperreactivity to negative
stimuli (Orr, 1997) but not to positive cues
(Litz, Orsillo, Kaloupek, & Weathers, 2000). Next
the dissociative symptoms are itemized, and these
were reduced from the five symptoms listed in
DSM–IV to two. Reduced awareness of one’s surroundings was deleted because it predominantly
pertained to responses occurring during the trauma,
and as noted, this is not associated with ongoing
psychopathology. The symptoms of derealization
and depersonalization that were listed separately in
DSM–IV were combined into a single item in DSM–5
because of the documented overlap between
these two responses in available data (Harvey &
Bryant, 1999a). The remaining dissociative
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symptom is dissociative amnesia. The next symptom heading refers to the avoidance symptoms. One
symptom refers to effortful avoidance of traumarelated thoughts or emotions and the other refers to
avoidance of situations or conversations that remind
the person of the traumatic event. The last symptom
category involves arousal symptoms, which lists five
symptoms: sleep disturbance, irritable or aggressive
behavior, hypervigilance, concentration problems,
and heightened startle response.
DSM–5 (American Psychiatric Association, 2013)
also made a minor shift in the timeframe during
which ASD can be diagnosed. The DSM–IV
(American Psychiatric Association, 1994) stipulation that ASD could be diagnosed 2 days after the
event lacked any empirical base, which is not surprising considering the paucity of research on the
progression of stress symptoms in the initial days
after trauma. Evidence suggests that many people
who will experience stress reactions in the days
immediately following a traumatic event subsequently will report markedly fewer reactions in the
period after (Solomon, Laor, & McFarlane, 1996).
Given this lack of evidence, in DSM–5, the time
required to delay a diagnosis was extended from 2 to
3 days to minimize diagnosing people in the acute
phase when they may be experiencing temporary
stress reactions. It should be noted, however, that
the timeframe of 3 days also lacks evidence to support it.
Incidence of ASD
In terms of the incidence of ASD, the temporary
nature of the condition hinders proper epidemiological analysis of population rates. Perusing
large-scale psychiatric studies of population mental
health typically leads to the conclusion that ASD
often is not included in the surveys because of the
focus on more chronic disorders. Accordingly, our
knowledge of how frequently ASD exists is limited
to studies of trauma-exposed populations in which
researchers have assessed for ASD within 1 month.
Consistent with patterns of findings in studies of
chronic PTSD, these studies have led to varied rates
of ASD. For example, ASD has been reported following motor vehicle accidents (13–21%), mild traumatic brain injury (14%), assault (16–19%), burns
Acute Stress Disorder and Posttraumatic Stress Disorder
(10%), industrial accidents (6%), and witnessing a
mass shooting (33%; Harvey & Bryant, 2002).
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Cognitive Models of ASD
One of the most influential models in PTSD involves
the cognitive mechanisms that occur during and
immediately after trauma exposure. Exemplifying
this approach is Ehlers and Clark’s (2000) model,
which posited that traumatic stress is affected
strongly by two cognitive processes: maladaptive
appraisals about the trauma and its aftermath, and
autobiographical memories. Regarding appraisals,
this model proposes that how we respond to trauma
is influenced strongly by how we interpret what it
means for our safety, our future, and our worth as a
person. Central to this idea is that people can generalize from appraisals of the trauma to other life
events, which can result in pervasive fear or other
negative affective states. These appraisals can focus
on one’s vulnerability (e.g., “I can never feel safe
again”), one’s role in the trauma (e.g., “the attack
was my fault”), or one’s capacity to cope with the
aftermath (e.g., “I am a terrible mother for not coping better”). Such appraisals heighten the sense of
threat that one can experience after the trauma,
which fuels more stress symptoms and leads to PTSD.
A large body of evidence supports the proposition that maladaptive appraisals in the acute phase
play an important role in posttraumatic adjustment.
It is worth noting that people with chronic PTSD
often display distorted appraisals of the trauma
(Dunmore, Clark, & Ehlers, 1997; Foa, Ehlers,
Clark, Tolin, & Orsillo, 1999) and also the extent
to which having these symptoms reflect negatively
on the trauma survivor (e.g., having flashback
memories may be interpreted as a sign of losing
one’s mind; Ehlers et al., 1998; Ehlers & Steil, 1995;
Steil & Ehlers, 2000). Similarly, people with ASD
tend to exaggerate both the probability of negative
events happening to them as well as the severity
of how adverse those events would be (Warda &
Bryant, 1998). ASD patients also tend to exaggerate information related to external harm, somatic
stimuli, and social events in ways that suggest these
things are harmful (Smith & Bryant, 2000). In terms
of predicting later posttraumatic stress, negative
appraisals shortly after the trauma are predictive of
subsequent PTSD (Dunmore, Clark, & Ehlers, 2001;
Engelhard, van den Hout, Arntz, & McNally, 2002;
Halligan, Michael, Clark, & Ehlers, 2003; Kleim,
Ehlers, & Glucksman, 2007; Mayou, Ehlers, & Bryant, 2002; Murray, Ehlers, & Mayou, 2002; Wikman, Molloy, Randall, & Steptoe, 2011). As distinct
from the content of appraisals, people’s cognitive
styles also predict subsequent functioning—for
example, ruminating after a traumatic event is
predictive of later PTSD (Ehlers, Mayou, & Bryant,
2003; Kleim et al., 2007; Mayou et al., 2002).
Ehlers and Clark (2000) also emphasized the
importance of autobiographical memories, insofar
as the trauma experience needs to be integrated
into one’s normal autobiographical base for it to
be contextualized and processed. It is proposed
that the strong fear and arousal associated with
trauma results in information being encoded in a
predominantly sensory (and often visual) manner,
which results in poor intentional memory of certain aspects of the trauma. For example, an assault
victim may have recurring images of an attacker’s
face but have patchy recall of the sequence of events
as they occurred. Termed data-driven processing,
these fragmented memories of the trauma purportedly maintain a sense of nowness in that the person
recalls the memory as if it is still in present rather
than being able to contextualize it as being oriented
in the past.
Consistent with this perspective, it has been
found that data-driven processing is linked with
intrusive memories and PTSD (Ehring, Ehlers, &
Glucksman, 2008; Halligan, Clark, & Ehlers,
2002; Halligan et al., 2003). Further support for
this proposal is found in acute stress populations.
Data-driven processing in the month after trauma
is linked with heart rate increase in response to
trauma-related cues (Ehlers et al., 2010). Children
with ASD report more sensory-laden memories of
their trauma, which in turn mediate the relationship
between perceived threat of a trauma and severity
of ASD (Meiser-Stedman, Dalgleish, Smith, Yule, &
Glucksman, 2007). Also consistent with cognitive
models is evidence that trauma memories tend to be
fragmented in both those with chronic PTSD (Amir,
Stafford, Freshman, & Foa, 1998; Foa, Molnar, &
Cashman, 1995; Foa & Riggs, 1993; van der Kolk &
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Richard A. Bryant
Fisler, 1995) and those with ASD (Harvey & Bryant,
1999b). It also has been shown that when people
with ASD receive exposure therapy, the increased
organization is associated with decreased dissociative content of their memories (Moulds & Bryant,
2005).
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Biological Models of ASD
The other major model of ASD focuses on biological processes. In this context, the most influential
model involves fear conditioning, which posits that
the traumatic experience promotes noradrenergic
and glucocorticoid activation, which in turn contributes to consolidation of trauma memories. Trauma
researchers have relied on this model to postulate
that trauma survivors respond to a trauma with
extreme fear (this is the unconditioned response).
The fear experienced at the time of trauma results
in strong associative conditioning between the fear
and many stimuli associated with the trauma (these
are the conditioned stimuli). When one is confronted
with these reminders of the trauma, conditioned
responses are triggered, which can include the range
of re-experiencing symptoms, such intrusive memories and physiological reactivity (Pitman, 1989;
Rauch, Shin, & Phelps, 2006). Supporting this
model is extremely robust evidence that emotional
and physiological reactivity is activated in patients
with PTSD when they are exposed to trauma
reminders (Blanchard, Kolb, Gerardi, Ryan, & Pallmeyer, 1986; Orr et al., 1998; Orr, Pitman, Lasko, &
Herz, 1993).
Central to biological conceptualizations of
recovery from a traumatic experience is the notion
of extinction learning. This term refers to recurrent exposure to the conditioned stimuli but in the
absence of any aversive outcomes—in such situations, there is new learning that the previously conditioned reminders now signal safely and thereby
override initial conditioning (Milad, Rauch, Pitman, & Quirk, 2006). In most traumatic situations,
people often report marked posttraumatic stress
in the initial days after exposure; however, these
reactions often abate in the days and weeks that follow. It is possible that during this period people are
experiencing many trials of extinction learning such
that they are being exposed to trauma reminders,
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but the traumatic outcome is not occurring, and so
there is new learning of safety. For example, motor
vehicle accident survivors who initially are frightened by the sounds of traffic and smell of petrol
may learn in the weeks after the accident that each
time they drive and are exposed to each of these
reminders that they do not have an accident. In this
sense, PTSD is regarded in conditioning models as
an example of failed extinction learning because
the minority of people who go onto develop PTSD
apparently do not learn that the conditioned stimuli
no longer need to be feared (Myers & Davis, 2007).
As noted earlier, people follow diverse trajectories of posttraumatic stress response over time,
with some people showing exacerbation of their
condition. One feature of conditioning models that
may account for this is fear reinstatement, which
involves the return of fear reactions after initial
conditioning has been extinguished because of reexposure to the initial unconditioned stimulus conditions (Bouton, 2004). This process underscores
the finding that initial conditioning is not erased
with extinction learning and can be reinstated if
the appropriate conditions are met. Following from
many experimental studies attesting to the process
of fear reinstatement, this mechanism can explain
symptom return in anxiety (Norrholm et al., 2006).
Furthermore, this process may offer an explanation
for the finding that posttraumatic stressors can contribute to delayed-onset PTSD (Bryant, O’Donnell,
Creamer, McFarlane, & Silove, 2013; Smid et al.,
2012). This occurs commonly in the acute period
after trauma because people are exposed to many
related stressors, such as hospital visits, legal inquiries, and confrontations with people involved in the
traumatic event.
Much research has explored the role of fearconditioning processes during the acute period
after trauma. A series of studies have assessed resting heart rate immediately after trauma exposure
because this can reflect sympathetic arousal and
may be one sign of the level of fear conditioning the
trauma survivor experiences. Across numerous studies with both adults and children, it has been found
that higher resting heart rates in the initial days after
trauma exposure predict subsequent PTSD (Bryant,
Creamer, O’Donnell, Silove, & McFarlane, 2008;
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Acute Stress Disorder and Posttraumatic Stress Disorder
Kassam-Adams, Garcia-España, Fein, & Winston,
2005; Shalev, Freedman, et al., 1998). This pattern
has even been found in people who suffer severe
brain injury and who are amnesic of the traumatic
event—suggesting that fear conditioning may occur
at levels below full awareness (Bryant, Marosszeky,
Crooks, & Gurka, 2004). Further support of the
role of increased arousal after trauma is that elevated
respiration rate in the first 48 hours predicts PTSD
(Bryant, Creamer, et al., 2008). More direct support for the process of fear conditioning is a finding
that phasic increases in heart rate in response to
trauma reminders are a stronger predictor of PTSD
than resting state heart rate (O’Donnell, Creamer,
Elliott, & Bryant, 2007). In the context of extreme
arousal after trauma, it is worth noting that nearly
all people with ASD reported having panic symptoms during the trauma, and most of these persist in
the weeks after the event (Nixon & Bryant, 2003).
It seems that people are particularly vulnerable to the effects of trauma exposure if they were
predisposed to enhanced conditioning or impaired
extinction before the trauma exposure. In an early
prospective study, newly recruited firefighters
who at the time of assessment were in class-based
training and had not commenced active duty were
assessed on paradigms relevant to conditioning
models. This study found that recruits’ skin conductance and eye blink startle reactions in response
to startling tones predicted their level of acute
stress symptoms within a month of subsequently
being exposed to a traumatic event as a firefighter
(Guthrie & Bryant, 2005). This finding may suggest the tendency to be reactive to stressors, which
may increase vulnerability to fear conditioning.
In a related study, this research assessed extinction learning before trauma exposure by having
the recruits receive electric shocks when they were
presented with a particularly colored shape but
not when presented with a different color. They
subsequently were presented with extinction trials;
level of PTSD 2 years after commencing firefighting
duties was predicted by impoverished extinction
learning as a recruit (Guthrie & Bryant, 2006). This
finding appears robust because it has been replicated
both in first responders and military personnel who
were assessed before exposure to traumatic events
(Lommen, Engelhard, Sijbrandij, van den Hout, &
Hermans, 2013; Orr et al., 2012). These data point
to individual differences in extinction learning being
pivotal in modulating vulnerability to PTSD.
When humans are exposed to a traumatic event,
they respond with two distinct stress systems. One
is the fast-acting autonomic nervous system, and the
other is the slower-acting hypothalamic-pituitaryadrenal (HPA) axis. An initial sympathetic response
secretes adrenaline and noradrenaline, which leads
to increases in heart rate, respiration rate, and blood
pressure; these responses are needed to engage in
either fight or flight from a threat. There is also a
slower HPA response, in which there is a cascade
of HPA axis activity involving the hypothalamus
secreting corticotropin-releasing hormone, which
in turn leads to the anterior pituitary generating
adrenocorticotropic hormone (ACTH). ACTH then
elicits secretion of glucocorticoids (this is cortisol
in humans), and importantly, this provides negative
feedback to the hypothalamus, which inhibits further activation of corticotropin-releasing hormone
(Radley et al., 2011). The role of the latter reaction
is to restabilize the system by promoting homeostasis once the threat has passed.
Many have argued that PTSD is characterized by
diminished feedback emanating from the HPA axis,
thereby leading to prolonged arousal in PTSD, with
evidence that PTSD patients have lower cortisol
levels (Yehuda, Boisoneau, Mason, & Giller, 1993;
Yehuda et al., 1995; Yehuda et al., 1990). Supporting this proposal is that some evidence exists that
lower cortisol levels shortly after trauma predict
later PTSD (Delahanty, Raimonde, & Spoonster,
2000; Resnick, Yehuda, Pitman, & Foy, 1995). This
evidence is not straightforward, however, because
evidence also exists that acute levels of cortisol
after trauma can be higher than in those who later
develop PTSD (Delahanty, Nugent, Christopher, &
Walsh, 2005).
Further support for this notion comes from some
research that has attempted to prevent PTSD by
enhancing cortisol levels in the acute period after
trauma exposure. This line of research builds on
animal studies that have found that administering
hydrocortisone to rats shortly after stressing them
results in less fear behavior than administering a
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Richard A. Bryant
placebo (Cohen, Matar, Buskila, Kaplan, & Zohar,
2008). Consistent with this finding, administering
cortisol shortly after an experimentally induced
stressor has been shown to result in fewer traumatic memories (Schelling et al., 2001; Schelling
et al., 2004). In terms of clinical applications, one
early study has found that giving trauma-exposed
survivors cortisol within hours of trauma exposure
can limit subsequent PTSD (Zohar et al., 2011).
Although this research is new and has yet to be replicated, it does seem that the glucocorticoid system
plays an important role in acute traumatic stress,
and it contributes to ongoing arousal.
The noradrenergic system is critically important
in the acute stress response. One of the reasons for
its pivotal role is that it underpins consolidation of
emotional memories. In animal studies, it has been
shown repeatedly that levels of adrenomedullary
stress hormones during or immediately after learning are associated with enhanced memory (Liang,
Juler, & McGaugh, 1986; Sternberg, Isaacs, Gold, &
McGaugh, 1985). Levels of endogenous noradrenergic activation also are associated with memory
for emotional material in humans (Segal & Cahill,
2009). Moreover, administering humans yohimbine
(which is an adrenergic agonist) leads to greater
memory for emotional stimuli (Southwick et al.,
2002), yet β-adrenergic blockades decrease amygdala activation and impair memory for emotional
(but not neutral) stimuli (Cahill & van Stegeren,
2003; O’Carroll, Drysdale, Cahill, Shajahan, &
Ebmeier, 1999). Some evidence also shows that
epinephrine and norepinephrine 1 month after
trauma exposure are associated with PTSD severity
in men (Hawk, Dougall, Ursano, & Baum, 2000),
although another study has not replicated this finding (Videlock et al., 2008).
This line of research has led to attempts to
limit PTSD development by reducing noradrenergic release in the acute period after trauma exposure. Pitman and colleagues (2002) administered
propranolol or placebo within 6 hours of trauma
exposure to people admitted to an emergency
department; although patients who received propranolol did not display different PTSD levels relative to placebo 3 months later, those who initially
received propranolol displayed less reactivity to
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trauma reminders 3 months later (Pitman et al.,
2002). Consistent with this result, another study
increased the dosage of propranolol to 240 mg a day
for 19 days, commencing within 12 hours (E. A.
Hoge et al., 2012); with this approach, it was found
that when analyses were restricted to participants
who complied with medication, there was less psychophysiological responding to reminders in those
who received propranolol than among those receiving a placebo. A subsequent uncontrolled study in
France found that trauma survivors administered
propranolol immediately after trauma had fewer
PTSD symptoms 2 months later (Vaiva et al., 2003).
The role of propranolol in limiting subsequent
PTSD seems complicated, however, because several
studies have not reported significant findings. One
study of medical records found that propranolol
given in the first month after burn trauma did not
reduce ASD symptoms in children (Sharp, Thomas,
Rosenberg, Rosenberg, & Meyer, 2010). A controlled trial of patients in the emergency department
found that acute propranolol did not limit subsequent PTSD development when administered within
48 hours after trauma (Stein, Kerridge, Dimsdale, &
Hoyt, 2007). It also may be that the impact of stress
hormones on emotional memory consolidation is
influenced by gender, as one study found that propranolol had less benefit in female children than
male children (Nugent et al., 2010).
Further evidence for the importance of noradrenergic response in the acute phase after trauma
comes from research using morphine to limit development of PTSD. Studies with animals indicate
that morphine injections into the amygdala impair
acquisition of fear conditioning (Clark, Jović, Ornellas, & Weller, 1972) and also impair memory for
fear conditioning (McNally & Westbrook, 2003).
In the context of human trauma, an early study of
child burn victims found that that morphine dose
in the acute period was inversely related to severity
of subsequent PTSD (Saxe et al., 2001). Subsequent
studies found that administering morphine in the 48
hours immediately after trauma also was associated
with lower subsequent PTSD levels in injured adults
(Bryant, Creamer, O’Donnell, Silove, & McFarlane,
2009) and children (Nixon et al., 2010). A large
study of U.S. troops deployed in Afghanistan found
Acute Stress Disorder and Posttraumatic Stress Disorder
that morphine use following injury in theater was
linked to reduced PTSD (Holbrook, Galarneau, Dye,
Quinn, & Dougherty, 2010). None of these studies
represent controlled trials, so caution when interpreting any causal relationship is essential; however,
these reports are consistent with the notion that
noradrenergic response is highly relevant in acute
stress reactions.
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Assessment of ASD
Since the introduction of the ASD diagnosis, several
assessment instruments have been introduced to
index ASD symptoms. A structured clinical interview, the Acute Stress Disorder Interview (ASDI),
was developed based on the initial DSM–IV (American Psychiatric Association, 1994) items (Bryant,
Harvey, Dang, & Sackville, 1998). This interview
contained 19 dichotomously scored items based on
the DSM–IV dissociative (Cluster B, 5 items),
re-experiencing (Cluster C, 4 items), avoidance
(Cluster D, 4 items), and arousal (Cluster E, 6
items) symptoms. It possessed good internal consistency (r = .90), test–retest reliability (r = .88),
sensitivity (91%) and specificity (93%) relative to
independent clinician diagnosis of ASD, based on
DSM–IV criteria (Bryant, Harvey, Dang, & Sackville,
1998). Confirmatory factor analysis indicated that
the structure of the ASDI was best described by the
four ASD symptom clusters in the DSM–IV (Brooks
et al., 2008). Following the changes to the ASD
diagnosis in DSM–5 (American Psychiatric Association, 2013), the interview was modified so that the
symptoms matched the DSM–5 criteria. The DSM–5
scoring requires 9 of the possible 14 symptoms to be
satisfied, as described by DSM–5.
In terms of self-report measures, the earliest
measure was the Stanford Acute Stress Reaction
Questionnaire (SASRQ; Cardeña, Classen, &
Spiegel, 1991). This measure has gone through
several iterations and has included dissociative,
intrusive, somatic anxiety, hyperarousal, attention disturbance, and sleep disturbance symptoms
(Cardeña & Spiegel, 1993; Classen, Koopman,
Hales, & Spiegel, 1998; Koopman, Classen, &
Spiegel, 1994). Each item asks respondents to
indicate the frequency of each symptom on a
6-point Likert scale from 0 (not experienced) to
5 (very often experienced) that can occur during and immediately following a trauma. It has
been shown to possess high internal consistency
(Cronbach’s alpha = .90 and .91 for dissociative
and anxiety symptoms, respectively) and concurrent validity with scores on the Impact of Event
Scale (r = .52–.69; Cardeña et al., 2000; Koopman et al., 1994). The more recent version of the
SASRQ is a 30-item self-report inventory that
encompasses each of the DSM–IV ASD symptoms
(Cardeña et al., 2000).
The other major self-report measure is the Acute
Stress Disorder Scale (ASDS), which is based on the
same items and wording as the ASDI. Each item is
scored on a 5-point scale to index symptom severity
(Bryant, Moulds, & Guthrie, 2000). Test–retest reliability between 2 and 7 days was strong (r = .94).
Predictive ability of the ASDS has been reported
using a cutoff score of 56 on the ASDS, predicting
91% of those who developed PTSD and 93% of those
who did not. ASDS also has been updated to incorporate DSM–5 (American Psychiatric Association,
2013) changes.
Other measures have been developed to assess
acute stress reactions. Depression is a common
posttraumatic stress response (Bryant et al., 2010;
Shalev, Sahar, et al., 1998), and so one measure
was developed to screen for depression and acute
stress in the period shortly after trauma. The
Posttraumatic Adjustment Scale (PAS; O’Donnell
et al., 2008) includes 10 items that are each
scored on a 5-point scale with the goal of identifying recently trauma-exposed people who are
at risk of developing PTSD or depression. The
PAS includes 10 items that are each scored on a
5-point scale. This scale was developed such that
a summation of scores of all 10 items was predictive of PTSD (PAS–P), and the summation of 5 of
these items was predictive of subsequent depression (PAS–D). In terms of predicting subsequent
PTSD 12 months after trauma, the PAS–P has
been shown to have strong sensitivity (.82) and
specificity (.84), but modest positive predictive
power of (.28). In terms of predicting subsequent
depression, the PAS–D had a sensitivity of .72 and
a specificity of .74, and positive predictive power
of .30 (O’Donnell et al., 2008).
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Richard A. Bryant
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TREATING ASD
The most compelling evidence for effective treatment for ASD involves trauma-focused cognitive–
behavior therapy (CBT). Most treatment guidelines
around the world recommend it as a frontline treatment for the condition (Foa, Keane, Friedman, &
Cohen, 2009; Forbes et al., 2007). In short, this
treatment approach begins with education about
common psychological responses to trauma and
then focuses on three major strategies: anxiety management, exposure, and cognitive restructuring.
Education usually attempts to normalize the trauma
response by informing the patient about the common reactions following a traumatic event and discusses the way in which the core symptoms will be
treated during the course of therapy. Anxiety management strategies aim to reduce arousal through
related techniques, such as breathing retraining,
relaxation skills, and self-talk. Exposure therapy
can involve both imaginal and in vivo exposure.
Imaginal exposure (also called prolonged exposure)
requires the patient to vividly imagine their traumatic experience for prolonged periods, usually for
at least 30 minutes. The therapist asks the patient
to provide a narrative of their traumatic experience
in a way that emphasizes all relevant details with
the goal of the heightening emotional engagement.
In vivo involves graded exposure to feared stimuli
in which the patient is asked to remain in proximity to mildly fearful reminders of the trauma and
then to repeat this exercise with increasingly fearful situations until they feel comfortable with most
reminders of their experience. Cognitive restructuring teaches patients to identify and evaluate the
evidence for negative automatic thoughts, with
particular focus on beliefs about the trauma, the self,
the world, and the future (Foa, Rothbaum, &
Steketee, 1993).
The fundamental basis of this approach draws on
both fear conditioning and cognitive models. From a
conditioning perspective, it is posited that recovery
from trauma involves extinction learning, including
repeated exposure to stimuli that are associated with
the trauma reminders until new learning is achieved
that trauma reminders is no longer signaling danger
(Davis & Myers, 2002). Through recurrent reliving of
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the trauma memory in the safety of the therapy context
as well as approaching feared stimuli during in vivo
exposure, it is hoped that the patient diminishes the
conditioned response. In terms of cognitive processes,
the emphasis is on altering appraisals so that the person
has a more realistic interpretation of their role in the
trauma and of possible future harm (Ehlers & Clark,
2000; for a detailed discussion of prolonged exposure,
see Volume 2, Chapter 8, this handbook).
There is actually a long history of early interventions for posttraumatic stress responses. More than
30 years ago, people began to adapt behavioral principles to limit subsequent PTSD reactions. These
interventions showed some promising results, but
their conclusions were restricted by methodological shortcomings (Brom, Kleber, & Hofman, 1993;
Kilpatrick & Veronen, 1983). Exemplifying this
approach was a trial in which four sessions of CBT
were given to assault victims shortly after assault
and their responses were compared with others
(who were not randomized to this condition) who
received repeated assessments (Foa, Hearst Ikeda, &
Perry, 1995). Although 10% of those who received
CBT met criteria for PTSD at 2 months, 70% of
the control group had PTSD; there were no differences between groups at 5 months (although the
CBT group was less depressed); one implication
of this study is that CBT may accelerate natural
recovery from trauma. In a better-controlled trial
by the same research team, several weeks after their
trauma, assault survivors with acute PTSD were
randomly allocated to four weekly sessions of CBT,
repeated assessment, or supportive counseling (SC;
Foa, Zoellner, & Feeny, 2006). Nine months later
approximately 30% of participants in each group
met criteria for PTSD. Again, this study may not
have found a relative advantage in early provision of
CBT because of the focus on PTSD rather than ASD
patients. One common theme in these attempts at
secondary prevention of PTSD was that they offered
treatment to all distressed trauma survivors in the
acute phase, thereby enhancing the likelihood that
the effects of intervention would be confused with
natural remission of symptoms that can occur in the
weeks after exposure (Bryant, 2003).
In the first study to focus on trauma survivors
who met criteria for ASD, motor vehicle accident
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Acute Stress Disorder and Posttraumatic Stress Disorder
or nonsexual assault survivors with ASD were
randomly allocated to either CBT or SC (Bryant,
Harvey, Dang, Sackville, & Basten, 1998). The CBT
program included education about posttraumatic
reactions, relaxation training, cognitive restructuring, and imaginal and in vivo exposure that
was conducted in five 1.5-hour weekly individual
therapy sessions. The SC condition included trauma
education and more general problem-solving skills
training that occurred at the same frequency as CBT.
Six months after treatment, there were fewer participants in the CBT group (20%) who met diagnostic
criteria for PTSD compared with SC participants
(67%). Extending this work was another study that
attempted to disentangle the most active ingredients of CBT for ASD in which 45 civilian trauma
survivors with ASD were randomly allocated to five
sessions of either (a) CBT (prolonged exposure,
cognitive therapy, anxiety management), (b) prolonged exposure combined with cognitive therapy,
or (c) supportive counseling (Bryant, Sackville,
Dang, Moulds, & Guthrie, 1999). Six months after
treatment, patients in both CBT programs had less
PTSD (20%) than those in the SC condition (67%).
This finding indicates that exposure and cognitive
restructuring can achieve comparable therapy gains
without the addition of anxiety management strategies. A follow-up that assessed the patients who participated in these two studies 2 years after treatment
found that the treatment gains of those who received
CBT were maintained 4 years after treatment (Bryant, Moulds, & Nixon, 2003).
Other studies by the same research group provide further support for trauma-focused CBT for
ASD. Some commentators had argued that because
of the pivotal role of dissociative responses in ASD
and the potential for this feature of the condition to
impede recovery, hypnosis may be useful to facilitate the emotional processing in the treatment of
ASD (Spiegel, 1996). Accordingly, a study was conducted in 89 ASD patients following civilian trauma
were randomly allocated to either CBT, CBT associated with hypnosis, or supportive counseling (Bryant, Moulds, Guthrie, & Nixon, 2005). To facilitate
emotional processing, a hypnotic suggestion was
provided immediately before imaginal exposure that
the patient would engage fully with the emotional
memory. In terms of treatment completers, more
participants in the supportive counseling condition
(57%) met PTSD criteria at 6-month follow-up than
those in the CBT (21%) or CBT plus hypnosis (22%)
condition. Participants in the CBT plus hypnosis
condition reported fewer re-experiencing symptoms
at posttreatment than those in the CBT condition,
possibly suggesting that hypnosis may have facilitated treatment gains.
One of the most topical issues in the field of
traumatic stress in recent years has been the impact
of mild traumatic brain injury on stress responses,
with numerous accounts in military (C. W. Hoge
et al., 2008) and civilian (Bryant et al., 2010) settings indicating that sustaining a mild brain injury
can increase the risk for PTSD. In a small pilot study
(but the only one available to date), 24 ASD participants who sustained a mild traumatic brain injury
following motor vehicle accidents were randomized
to CBT or SC (Bryant, Moulds, Guthrie, & Nixon,
2003). This study was particularly interested in
testing whether CBT was efficacious in treating this
condition because, by definition, these patients are
at least partially amnesic of their traumatic experience (Bryant, 2001). Consistent with previous
findings, more participants receiving SC (58%) met
criteria for PTSD at 6-month follow-up than those
receiving CBT (8%).
One of the issues that clinicians often consider is
the relative weight that should be given to exposure
versus cognitive restructuring in the course of treatment. To address this issue, one study randomized
90 trauma survivors to either five weekly sessions
of (a) imaginal and in vivo exposure, (b) cognitive
restructuring, or (c) assessment only (Bryant, Mastrodomenico, et al., 2008). This study found that
immediately after treatment and also at the 6-month
follow-up, those patients who received exposure
therapy had lower levels of PTSD, depression, and
anxiety than those in the other conditions. This
finding provides strong support for the argument
that emotional processing of the trauma memories
is beneficial if ASD patients are to achieve optimal
treatment response.
It is worth noting that other studies have been
conducted that have not adhered strictly to the
ASD criteria, but their findings are relevant to
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Richard A. Bryant
considering the treatment of acute stress. A large
trial conducted in Jerusalem asked whether early
intervention led to better results than later intervention (Shalev et al., 2012). This study randomized
242 patients admitted to an emergency department,
and who met criteria for either full or subsyndromal
ASD to either prolonged exposure, cognitive restructuring, wait list (who were then randomized to
exposure or cognitive restructuring after 12 weeks),
escitalopram (a selective serotonin reuptake inhibitor [SSRI]), or placebo (Shalev et al., 2012). Nine
months after treatment, PTSD rates were comparable across exposure (21%) and restructuring (22%)
conditions, relative to the much higher rates in the
SSRI (42%) and placebo (47%) conditions. A noteworthy finding to emerge from this study was that
there were no long-term differences between participants who received the early or later provision of
CBT. This outcome is consistent with the observation that effect sizes found in most CBT treatments
of ASD or early PTSD are comparable to effect sizes
of CBT for chronic PTSD (Foa et al., 2009).
In terms of other controlled trials that have
applied CBT to patients with acute PTSD, results
have been mixed. In a British study, 152 traumatic
injury survivors were randomized to receive four
sessions of CBT or no intervention several weeks
after civilian trauma (Bisson, Shepherd, Joy, Probert, & Newcombe, 2004). Although there were no
group differences in anxiety or depression 1 year
after treatment, patients who received CBT had
fewer PTSD symptoms. A less encouraging finding
was reported in a Dutch study in which 143 patients
with acute PTSD were randomized within 3 months
of trauma exposure to either four sessions of CBT
or wait list (Sijbrandij et al., 2007). Although CBT
resulted in greater PTSD reduction after treatment,
this difference was not evident 4 months later.
Mixed findings emerged from a study of 40
recent trauma victims who met criteria for ASD
and were randomized to receive three sessions of
psychoeducation and progressive relaxation and
were randomized to additionally receive either
exposure or supportive counseling (Freyth, Elsesser,
Lohrmann, & Sartory, 2010). Although both groups
displayed comparable symptom reduction 4 years
after treatment, those participants who received
174
exposure displayed reduced heart rate increase in
response to trauma reminders relative to those who
received supportive counseling.
Another British study tested whether providing
therapist-delivered CBT differed from a self-help
program in which patients were given the same elements in the form of a treatment manual. To reduce
the potential confound of natural remission of
symptoms, this study had recently trauma-exposed
patients complete a 3-week self-monitoring phase
before enrolling in the trial, and if they displayed
acute PTSD at the end of the period, they were
randomized to receive either (a) up to 12 weekly
sessions of CBT, (b) a self-help condition (one session with a clinician and a self-help booklet), or
(c) repeated assessments of PTSD symptoms
(Ehlers, Clark, et al., 2003). Consistent with the
cognitive model of PTSD (Ehlers & Clark, 2000),
this adaptation of CBT placed much emphasis on
altering maladaptive appraisals, but it also incorporated exposure elements. This study found at both
posttreatment and at follow-up that CBT delivered
by a therapist achieved greater reductions of PTSD
relative to both the self-help and repeated assessment conditions. Reflecting the overall evidence
reviewed in this chapter is the conclusion of a metaanalysis of four studies of CBT for ASD relative to
supportive counseling. This meta-analysis reported
the relative risk for a PTSD diagnosis was (.36; 95%
confidence interval [CI], .17–.78), supporting the
evidence for the utility of brief CBT for ASD (Kornør
et al., 2008). Notably, a distinct meta-analysis that
focused on a larger range of studies of early intervention, including studies with patients meeting
criteria for ASD or acute PTSD, came to a similar
conclusion (Roberts, Kitchiner, Kenardy, & Bisson,
2009).
Other psychotherapeutic methods have been
adopted to prevent PTSD, but these have tried to
abort the psychopathological process in the early
phases of trauma response. These usually commence
with hours or days of trauma exposure and so they
do not use ASD as the entry criteria to the study.
One such study provided just two sessions of CBT
intended to promote adaptive memory reconstruction in 17 accident survivors who in the emergency
room had heart rates of at least 94 beats per minute
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Acute Stress Disorder and Posttraumatic Stress Disorder
(Gidron et al., 2001); this criterion was based on
the work reviewed earlier indicating that elevated
heart rate levels in the acute period is predictive
of subsequent PTSD (Bryant, Harvey, Guthrie, &
Moulds, 2000; Shalev, Freedman, et al., 1998). This
study provided the telephone-administered CBT 1–3
days after the accident and found that patients who
received CBT had greater reductions in severity of
PTSD symptoms 3–4 months after the trauma than
did those who received two sessions of supportive
listening. In a similar vein, another study randomized 137 patients admitted to the emergency room
to either three sessions of prolonged exposure or
an assessment control condition (Rothbaum et al.,
2012). The imaginal exposure therapy commenced
in the emergency room and was repeated 1 and 2
weeks following the initial session. Patients in the
exposure condition had significantly lower PTSD
scores 12 weeks following the injury relative to
those who received the assessment alone. This is
an interesting study because it not only shows that
early intervention that promotes emotional processing can be efficacious but also highlights that commencing this intervention soon after trauma can be
done safely.
In contrast to the wealth of studies in adults
with ASD, there is relatively little evidence when it
comes to children. In one study, 30 child survivors
of assault with ASD were randomly allocated to
either cognitive processing therapy or supportive
counseling (Nixon, 2012). Cognitive processing
therapy is a variant of CBT insofar as it requires
the participant to write their traumatic experience
and then devotes much therapy time on addressing unhelpful appraisals that the person has about
their experience (Resick & Schnicke, 1992); there
is considerable evidence for positive outcomes with
this modality (Resick et al., 2008; Resick, Nishith,
Weaver, Astin, & Feuer, 2002). This study of ASD
found that at posttreatment and 6-month follow-up,
both interventions were comparably effective. The
generalizability of this study is clearly hampered by
its small sample size, and so there is a need for replication with larger samples.
Whereas we know quite a bit about psychotherapeutic interventions for ASD, relatively scare information pertains to pharmacological interventions.
The previously reviewed Jerusalem study is presently the most robust pharmacological study in the
literature. It suggests that (a) escitalopram does not
perform markedly better than placebo, and (b) the
use of an SSRI is inferior to that of trauma-focused
psychotherapy for ASD. In terms of pharmacological
interventions with children, one randomized trial
reported that 7 days of treatment with imipramine
was more effective in treating symptoms of ASD in
25 child and adolescent burn victims than chloral
hydrate (Robert, Blakeney, Villarreal, Rosenberg, &
Meyer, 1999).
CONCLUSION
The diagnosis of ASD has resulted in an explosion
of novel research into the acute stress reactions after
trauma, and our knowledge is much greater than
what it was two decades ago. Since its introduction,
our knowledge about trajectories of posttraumatic
stress following the acute phase has grown enormously, which has challenged earlier views that
a linear course of adaptation can be predicted in
the acute phase. As we noted, longitudinal studies
indicate that the course of posttraumatic recovery
is complex and fluctuates over time (Bryant et al.,
2013). Moreover, as growth mixture modeling
has indicated, there are at least four pathways that
people tend to follow after adversity (Bonanno,
Kennedy, Galatzer-Levy, Lude, & Elfström, 2012;
Bryant et al., 2015). These patterns challenge previous expectations that the diagnosis of ASD can accurately identify those at risk of PTSD in some linear
way. Nonetheless, the current definition of ASD in
DSM–5 (American Psychiatric Association, 2013)
does seem to capture many of those who can benefit
from interventions in the acute phase. As research
continues to develop more novel psychotherapeutic
and pharmacological methods to abort psychopathological responses, these early interventions hopefully will improve our current levels of success in
secondary prevention of posttraumatic stress.
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