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Gabbard’s Treatments of Psychiatric Disorders > Part VI. Anxiety Disorders, Dissociative Disorders, and Adjustment
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Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder
INTRODUCTION
Posttraumatic stress disorder (PTSD) is defined by DSM-IV-TR (American Psychiatric Association
2000) as a mental disorder that follows exposure to a traumatic event in which the person
experienced, witnessed, or was confronted with actual or threatened death or serious injury, or
threat to the physical integrity of self or others, provoking terror, horror, or helplessness at the
time of exposure and resulting in symptoms of reexperiencing, avoidance and numbing, and
hyperarousal lasting more than a month and causing social or occupational dysfunction. Acute
stress disorder (ASD) was added to the diagnostic nomenclature in DSM-IV (American Psychiatric
Association 1994) to describe a syndrome of severe dissociative, intrusion, avoidance, and
hyperarousal symptoms associated with occupational and social dysfunction in the first 4 weeks
after a traumatic stressor. It was included in the nosology because of evidence that a substantial
minority of trauma victims endure these symptoms and that these symptoms are associated with an
elevated risk of progressing to PTSD (Koopman et al. 1994). By definition, PTSD cannot be
diagnosed until 1 month after the occurrence of a traumatic stressor, and the adjustment disorders
were not thought to reflect the severity of either the stressors or the reaction to them. The
diagnosis of ASD requires the presence of at least three dissociative symptoms, in addition to one
each of the intrusion, avoidance, and hyperarousal symptoms seen in PTSD.
Traumatic experiences are extremely common and include sexual and physical assault, natural
disasters, accidents and combat. The National Comorbidity Survey (Kessler et al. 1995) found that
one in two Americans will be exposed to a traumatic event during their lifetime, with 7.8% of
Americans developing PTSD. Interpersonal violence is prevalent, with estimates from an national
random sample indicating that approximately 12 million adult American women (12.9%) have been
raped at least once during their lifetime and about 10 million (11.1%) have been a victim of
aggravated assault (National Victims Center and Crime Victims Research and Treatment Center
1992). In a retrospective study, 35% of rape victims and 39% of aggravated assault victims
reported lifetime PTSD; current PTSD was reported by 13% of the former and by 12% of the latter
(Kilpatrick and Resnick 1993). Other types of trauma also result in high rates of PTSD. More than
15% of the men and 8.5% of the women who served in the Vietnam theater were diagnosed with
current PTSD, approximately 20 years after their service (Kulka et al. 1990). Direct and vicarious
traumatization such as that experienced by paramedics, law enforcement officers, firefighters, and
mental health professionals also results in clinically salient current posttraumatic stress symptoms
in approximately 5%–10% of first responders (Carlier et al. 1997; Marmar et al. 1999, 2006;
McFarlane 1989). Overall, PTSD affects 7.8% of the population (Kessler et al. 1995), and if one
adds subthreshold cases, the combined prevalence amounts to approximately 14%–15% (Davidson
et al. 1991). Thus, the increasing attention the professional community now accords to PTSD is
consistent with the high magnitude of this disorder worldwide, and it highlights the need to develop
effective treatments that are both efficient and enduring.
ACUTE STRESS DISORDER
In his classic paper on acute grief, Lindemann (1944) described a syndrome that we would now
recognize as ASD (Lindemann 1994). He observed symptoms that could be characterized as
dissociative in nature, including numbing and stupor, as well as intrusion, avoidance, and
hyperarousal symptoms. Since Lindemann’s observations, numerous studies have described acute
reactions to traumatic events (Bryant and Harvey 2000; Grinker and Spiegel 1945; Kardiner andPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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Spiegel 1947; Spiegel and Classen 1995). Evidence is accumulating that ASD predicts the later
development of PTSD (Brewin et al. 1999; Bryant and Harvey 1998; Classen et al. 1998; Epstein et
- 1998; Eriksson and Lundin 1996; Harvey and Bryant 1998; Koopman et al. 1994; Marmar et al.
1994; McFarlane 1986; Shalev et al. 1996b; Solomon et al. 1989), although this relation has not
been borne out in all studies (Barton et al. 1996; Dancu et al. 1996). Among those studies that
assessed all ASD criteria, dissociative symptoms were the strongest predictor of PTSD or PTSD
symptoms in most (Bryant and Harvey 1998; Classen et al. 1998; Harvey and Bryant 1998) but not
all (Brewin et al. 1999) investigations.
Given that ASD is a strong predictor of PTSD, it is important to identify risk factors for ASD. In
emergency triage of trauma victims, it is vital to identify those at highest risk for progression to
ASD and PTSD. A promising candidate predictor for ASD is the experience of panic attacks during
and/or immediately after trauma exposure. More than half of those who meet criteria for ASD
report peritraumatic as well as subsequent panic attacks (Nixon and Bryant 2003). Galea et al.
(2002) found peritraumatic panic to be the best predictor of early PTSD in the post-9/11 survey of
1,008 residents living south of 110th Street in Manhattan. This observation is consistent with recent
observations from a study of 747 police officers in which panic reactions and related emotional
distress during exposure were highly predictive of pre-9/11 PTSD symptoms (Brunet et al. 2001).
A second candidate predictor of ASD is peritraumatic dissociation. Numerous studies have found an
association between peritraumatic dissociation and the subsequent development of PTSD
(Koopman et al. 1994; Marmar et al. 1994, 1999; Shalev et al. 1998). Peritraumatic dissociation
refers to a dissociative experience that occurs at the actual time of the traumatic event. One recent
meta-analysis reported that peritraumatic dissociation was the single best predictor (r = 0.35) of
PTSD among trauma-exposed individuals (Ozer et al. 2003), but this view has not been
unanimously supported in longitudinal studies (Dancu et al. 1996; G. N. Marshall and Schell 2002).
Furthermore, peritraumatic dissociation is highly correlated with peritraumatic panic (Brunet et al.
2001; Fikretoglu et al. 2006). Dissociation at the time of a traumatic event may occur when
cognitive capacities to modulate terror and horror are overwhelmed.
Retrospective studies indicate that individuals at greatest risk for developing PTSD following a
traumatic event are those with a personal or family history of psychopathology (Breslau et al.
1991); prior exposure to trauma (Breslau et al. 1999; Nishith et al. 2000); cognitive factors, such as
lower IQ (Saltzman et al. 2006); female gender (Brewin et al. 1999); stressful life events in the
year prior to the traumatic event; poorer social supports; certain preexisting personality traits, such
as proneness to experiencing negative emotions (Brewin et al. 2000); and greater terror, horror,
and dissociation at the time of the event (Brunet et al. 2001; Marmar et al. 2004, 2006).
Preliminary data from a true prospective study of PTSD in police academy recruits (Marmar et al.
2006) support these findings, in that those with greater PTSD symptoms in response to
critical-incident exposure in police service had more of these risk factors.
Psychosocial Treatment of Acute Stress Disorder
General principles common to evidence-based interventions for ASD include the following:
reestablish a sense of safety; rapidly build a therapeutic alliance; provide information; allow
ventilation of emotion only after the objective danger and subjective perceived threat end and
peritraumatic panic subsides; discourage ventilation in those with persistent terror, horror, and
panic; diffuse guilt; facilitate social support; and reinforce the need for self-care. These principles of
acute disaster response are designed to provide immediate contact and comfort, and they utilize
the therapeutic relationship to help acknowledge, bear, and put into perspective recent experiences
and emotions. The cognitive and affective restructuring of a traumatic event entails fitting
experiences into a cognitive framework that alters its meaning, diminishing any inappropriate
sense of personal responsibility for events beyond the person’s control and normalizing intense
emotional reactions to the trauma.
Psychological DebriefingPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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Psychological debriefing during the acute phase following a traumatic event has been propounded
as effective in reducing psychological distress due to trauma. In recent years, however, its
effectiveness has been questioned, and the need for randomized controlled intervention trials is
evident (Raphael et al. 1996). The existing research is plagued with methodological limitations and
contradictory outcomes, with some studies showing benefits (Jenkins 1996; Robinson and Mitchel
1993; Turner et al. 1993), but the majority not (Bisson et al. 1997; Everly and Boyle 1999; Griffiths
and Watts 1992; Hobbs et al. 1996; Hytten and Hasle 1989; Jacobs et al. 2004; Kenardy et al. 1996;
Lee et al. 1996; Matthews 1998; Priest et al. 2003; van Emmerik et al. 2002; Watson and Shalev
2005; Weisaeth 1989).
In a well-designed randomized controlled study, Mayou et al. (2001) found that debriefing recently
hospitalized accident victims was of no benefit in those with low levels of initial distress and
interfered with recovery at 6-month and 3-year follow-up in those who were highly distressed at
the time of debriefing. S. Rose et al. (2003) conducted a systematic review of single-session
debriefing following trauma. Of the 11 randomized controlled trials reviewed, 3 showed positive
outcomes, 6 demonstrated no difference in outcome between intervention and nonintervention
groups, and 2 (which also had the longest follow-up) showed negative outcomes for debriefing.
It has been claimed that critical-incident stress debriefing may work better for emergency response
personnel than for survivors (Jacobs et al. 2004). Given the extreme and frightening nature of
traumatic experiences, it is not unnatural for professional first responders and mental health
clinician volunteers to experience acute stress symptoms in mass-casualty incidents. When the
traumatic event is a natural or manmade disaster, there may be the additional strain of having to
work quickly in an unfamiliar environment with many individuals who are in extreme emotional
states. The toll that this takes on crisis workers has been recognized and has resulted in efforts to
provide debriefing to crisis counselors (Armstrong et al. 1991; Mitchell 1983; Talbot et al. 1992).
Debriefing strategies, used with both victims and crisis workers, involve providing a setting where
individuals can speak about their feelings and reactions to the stressful event. Such interventions,
referred to as “psychological first aid” for trauma survivors, emphasize preventing further harm,
mobilizing family resources, and providing education about available resources, coping strategies,
and communication (Watson and Shalev 2005). As with civilian victims, debriefing with first
responders is of uncertain benefit, with one study in Dutch police officers reporting greater
symptoms 1 week later, despite a positive evaluation by those offered the intervention (Carlier et
- 2000). Caution is necessitated in using emotion-focused approaches in “hot debriefings” with
highly distressed responders.
Combat Stress Reactions
The frontline combat treatment approach is designed for use with military persons who are
experiencing acute combat stress reactions. The three principles are 1) proximity, 2) immediacy,
and 3) expectancy (PIE) (Solomon and Benbenishty 1986). The idea is that soldiers should be
treated 1) close to the combat line, 2) as soon as possible after onset of symptoms, and 3) with the
expectation that they will return to combat (Kardiner and Spiegel 1947). Treatment involves caring
for physical needs by providing sleep, food, and drink for a few days in a safe environment, with
some opportunity to talk about the recent traumatic experiences. This brief intervention was found
to result in lower rates of PTSD. There is an urgent need for controlled studies comparing PIE
treatment with anxiety management including a brief course of beta-blockers for the field
management of combat stress reactions.
Brief Cognitive-Behavioral Therapy for Acute Stress Disorder
The treatment of choice for ASD is brief cognitive-behavioral therapy (CBT). Bryant et al. (2005)
found that a combination of cognitive-behavioral treatment plus hypnosis for ASD resulted in fewer
people meeting criteria for PTSD at 6-month follow-up and that the hypnosis component in
particular reduced reexperiencing symptoms more quickly at follow-up. The utility of hypnosis in
inducing a type of controlled dissociative state similar to that often experienced spontaneously
during trauma (Spiegel and Cardena 1991; Spiegel et al. 1988) was cited as an explanation for this Print: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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effect of hypnosis in amplifying cognitive-behavioral treatment effects in the acute stress setting.
Pharmacotherapy for Acute Stress Disorder
In the first hours after a traumatic event, the highest priority is to reduce peritraumatic terror,
horror, and panic. Prolonged peritraumatic distress increases associational and nonassociational
fear conditioning and memory consolidation, increasing the risk of PTSD. Adrenergic blockers hold
promise for immediate treatment of trauma victims with persistent elevations in heart rate, greater
panic and greater dissociation at the time of traumatic exposure. Pitman et al. (2002) reported that
propranolol given within 6 hours of the traumatic event for 10 days was superior to placebo for
reducing arousal reactions to trauma reminders 1 month after exposure. Vaiva et al. (2003), in a
nonrandomized equivalent-group design, found that immediate treatment with propranolol reduced
PTSD symptoms at 2 months. Large-scale randomized controlled trials are in progress with
propranolol for immediate treatment of trauma victims in emergency room settings. For those
whose acute stress symptoms persist in the first weeks, beta-blockers, mood-stabilizing agents,
and selective serotonin reuptake inhibitors (SSRIs) have been recommended (Shalev and Bonne
2000), along with low-dose trazodone for insomnia and prazosin for nightmares; however,
controlled trials are limited.
POSTTRAUMATIC STRESS DISORDER
Psychosocial Treatments for Posttraumatic Stress Disorder
Cognitive-Behavioral Therapy Emphasizing Prolonged Exposure
More than 25 controlled trials of CBT including prolonged exposure have demonstrated that this
approach is highly effective in ameliorating PTSD symptoms and related psychiatric problems.
Arising from an experimental background, cognitive-behavioral interventions typically have been
subjected to rigorous testing and traditionally involve repeated assessments of target symptoms,
comparison groups, and well-delineated and replicable procedures. CBT for PTSD involves a
combination of education about the normal course of stress response, relaxation and anxiety
management techniques, cognitive therapy to address pathogenic beliefs, imaginal and in vivo
exposure to trauma-related stimuli, and relapse prevention. This method is predicated on
facilitating fear extinction both through repeated exposure in the absence of real threat, leading to
new learning that counters fear conditioning, and through cognitive and somatic management of
response to reminders of the trauma.
The educational component involves describing to the patient aspects of his or her experience that
are typical of the response to traumatic stress, allowing him or her to anticipate future reactions
and find them less alien and frightening. Various relaxation techniques, such as deep diaphragmatic
breathing and progressive muscle relaxation, improve symptoms and modulate arousal responses
during exposure treatment. Cognitive therapy is used to help people avoid overgeneralizing risk
perception, to counter unrealistic responsibility for the traumatic event, and to manage survivor
guilt. They may then be exposed to reminders of the trauma in a manner that, coupled with control
of somatic response, is designed to facilitate fear extinction. Finally, consolidation of change is
sought with the idea of preventing relapse in the face of subsequent minor or major stressors
(Bryant and Harvey 2000).
The most effective component of cognitive-behavioral approaches used with PTSD patients is
prolonged imaginal and in vivo exposure, in which patients confront reminders of the traumatic
event. This approach is designed to activate memories of the trauma in order to modify the
pathological aspects of those memories (Foa and Rothbaum 1998). Obviously, the use of exposure
techniques requires that the patient remember at least some details of the trauma.
Anxiety Management Training for PTSD
Anxiety management training (AMT) includes a variety of procedures and programs, including
biofeedback, relaxation, cognitive restructuring, positive self-talk, and thought stopping. AMT isPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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used when anxiety pervades patients’ daily functioning. In this technique, the focus is not so much
on modifying the trauma memory as on managing fear by teaching patients skills for controlling
their anxiety. The defining characteristics of PTSD include both specific fears (associational fear
conditioning, including specific phobic reactions to reminders) and general chronic arousal
(nonassociational fear conditioning, including general hypervigilance and concentration
difficulties); therefore, both prolonged exposure and AMT are useful in managing PTSD.
Virtual Reality Exposure for PTSD
Virtual reality exposure (VRE) is a promising medium for conducting prolonged exposure therapy.
VRE presents a computer-generated view of a virtual world that changes in a natural way with head
motion. During VRE sessions, patients wear the head-mounted display with stereo earphones that
provide visual and audio cues consistent with being in a “virtual Vietnam.” Patients in one
investigation were exposed to two virtual environments, a virtual Huey helicopter flying over a
virtual Vietnam and a clearing surrounded by jungle. In this way, patients were repeatedly exposed
to their most traumatic memories but immersed in Vietnam stimuli. In this open trial of 10 male
combat veterans, clinician ratings of PTSD symptoms at 6-month follow-up revealed improvement
on all three symptom clusters (Rothbaum et al. 2001). Difede and Hoffman (2002) reported a single
case vignette of using VRE to treat PTSD in a survivor of the World Trade Center attacks.
Eye Movement Desensitization and Reprocessing for PTSD
Eye movement desensitization and reprocessing (EMDR) (Shapiro 1989a, 1989b, 1995) is a form of
exposure treatment with a strong cognitive component accompanied by saccadic eye movements.
The technique involves the patient’s imagining a scene from the trauma, focusing on the
accompanying cognition and arousal, and tracking the therapist’s rapidly moving finger. The
sequence is repeated until anxiety decreases, at which point the patient is instructed to generate a
positive thought and to associate it with the scene while moving his or her eyes. The efficacy of
EMDR has received support from case reports (for a comprehensive review, see Lohr et al. (1995).
Mixed results have emerged from controlled investigations. In one study, PTSD combat veterans
and sexual assault survivors were assigned to either one session of EMDR or a delayed-treatment
control condition (Shapiro 1989a, 1989b). The average anxiety ratings while imagining the
traumatic scene decreased in the patients who received EMDR, but because posttrauma pathology
was not directly assessed in this study, the efficacy of the EMDR treatment cannot be ascertained.
A controlled study on the efficacy of EMDR with Vietnam veterans (Pitman et al. 1996) found that
the eye movements were unrelated to outcome. Only one study compared EMDR with CBT
consisting of prolonged imaginal exposure, stress inoculation training, and cognitive therapy
(Devilly and Spence 1999). Both treatments were conducted over nine sessions. The results
indicated that CBT was superior to EMDR at follow-up. In summary, several studies report
beneficial effects of EMDR, although other studies report equivocal findings with EMDR not resulting
in significant improvements over control conditions or comparison treatments, especially on blind
standardized PTSD measures. All studies that examined the role of the eye movements themselves
found them unrelated to treatment outcome. Thus, it appears that to the extent that techniques
defined as EMDR are effective, they are so for reasons that involve factors such as reexposure and
working through of traumatic memories with a therapist who responds positively and
constructively, rather than because of any effect of rapid eye movements, rhythmic tapping, or
other physiological manipulations during the treatment.
Stress Inoculation Training for PTSD
Of the various AMT programs, stress inoculation training (SIT) (Kilpatrick et al. 1982), developed
for trauma survivors with chronic disturbances, has received the most attention. The original
program, which included 20 therapy sessions and homework assignments, consisted of two phases:
an educational phase and a coping-skills training phase. Treatment began with the educational
phase, a 2-hour session in which the treatment program rationale and theoretical basis for the
treatment were explained. The second phase of SIT focused on the acquisition and application ofPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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coping skills and included training in deep muscle relaxation, breathing control, role-playing, covert
modeling, thought stopping, and guided self-dialogue that followed Meichenbaum’s (1975) SIT. The
efficacy of SIT has been supported by several reports by Kilpatrick and colleagues (Kilpatrick et al.
1982; Veronen and Kilpatrick 1982, 1983) and by other investigators (Foa et al. 1991, 1999; Resick
et al. 1988).
In a study by Foa et al. (1991), prolonged exposure, SIT, and supportive counseling were compared
with each other and with a wait-list control condition in a controlled study of female rape survivors
with PTSD. All treatments included nine 90-minute sessions delivered biweekly in the individual
format described below. To control for the natural decline in symptoms that occurs following an
assault, the study included only patients who had experienced the target trauma at least 3 months
before treatment. All conditions produced improvement on all measures immediately posttreatment
and at follow-up. At follow-up, prolonged exposure produced superior outcome on PTSD symptoms.
Patients who received prolonged exposure continued to improve after treatment termination,
whereas patients in the SIT and supportive counseling conditions had no change between
posttreatment and follow-up.
Why Is Cognitive Reprocessing Effective for PTSD?
Foa and Kozak (1986) adopted the view of fear as a cognitive structure that contains
representations of the feared stimuli and feared responses as well as the meanings associated with
them. These authors suggested that two conditions are required for the reduction of fear. First, the
fear memory must be activated. Second, new information must be provided that includes elements
incompatible with the erroneous elements in the existing fear structure, so that a corrected
memory can be formed (Foa and Kozak 1986). Exposure procedures, which involve confrontation
with the fear stimuli either imaginally or in vivo, activate the structure (i.e., elicit fear) and provide
an opportunity for corrective information to be integrated and thereby modify the fear structure.
The transformative element in exposure is not desensitization but rather fear extinction, a process
of evolving new learning that overlays and modifies the original trauma-driven fear conditioning.
Indeed, there is evidence from animal research that when memories are retrieved and combined
with new information, they are restored in a transformed manner, analogous to an edited
manuscript replacing its earlier iteration in a computer file (LeDoux 2000, 2002).
Implementation of Prolonged Exposure for PTSD
During imaginal exposure, it is important to have patients vividly reimage the traumatic event in
their mind’s eye, recount the narrative in the first-person present tense, and pay attention to their
physiological reactions (“My heart’s pounding”), appraisals (“I know I’m really in trouble”), and
threat-related thoughts (“He will shoot me”) as well as detailed descriptions of stimuli and action.
The inclusion in imagery scenarios of all of these modes of stimuli and response has been found to
enhance emotional engagement. When only stimuli are described (and not responses), fewer fear
responses are observed. As noted above, evidence indicates that activation of fear is positively
related to treatment gains (Foa and Kozak 1998; Kozak et al. 1988).
Exposure therapy requires PTSD patients to perform two extremely difficult tasks: 1) to
intentionally confront the very memory they have been actively avoiding and 2) to trust the
therapist to assist them throughout this frightening experience. This reluctance to trust others,
combined with the strong tendency in many PTSD patients to dissociate (Foa and Hearst-Ikeda
1996; Marmar et al. 2004; Spiegel 1991; Spiegel and Cardena 1991; Spiegel et al. 1988), may result
in difficulty in engaging emotionally during exposure therapy. Patients may be emotionally
distanced even while recounting the details of their trauma, appearing to tell someone else’s story
rather than their own.
Another issue pertinent to the use of exposure therapy with trauma survivors stems from the
intimate and embarrassing nature of many trauma experiences, which results in increased difficulty
in disclosure. It is less embarrassing to discuss being attacked by a dog than to discuss details of
being raped or of shooting someone at close range. On the one hand, the therapist should makePrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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special efforts to encourage disclosure by asking more probing questions; on the other hand, such
inquiry should be conducted with extra sensitivity to the intimate material being presented. EMDR
offers an alternative in which the imagery is reinvoked without embarrassing disclosure to the
therapist.
Additionally, great care must be exercised in selecting situations for in vivo self-exposure for
assault victims. In some environments, such as inner-city ghettos, assaults are quite frequent. The
reality of such survivors’ fears was tragically demonstrated to us when one of our patients was
murdered in her own home hours after her therapy session.
PTSD patients often describe dissociative reactions at the time of the trauma (Marmar et al. 2004;
Spiegel et al. 1988; Terr 1991). Some dissociative responses are minimal (“I don’t really feel it
after that . . . . I hear myself saying it”), but more blatant dissociation or numbing is also common.
Such responses may include a sense of “leaving one’s body and watching it.” An extreme
dissociative reaction involves dissociative amnesia—the inability to recall important aspects of the
situation. In the case of complete amnesia, imaginal exposure cannot be implemented. However,
most trauma survivors remember at least some details of the trauma. With these individuals,
imaginal exposure has been found helpful in aiding recall of details that were previously
inaccessible. For example, during the third session of imaginal exposure, one rape survivor recalled
for the first time that her assailant had cocked the pistol he was holding to her head and threatened
to pull the trigger if she did not perform fellatio. Thereafter, she was able to describe her assault in
detail, and within six sessions her fear had dissipated.
In deciding how to conduct exposure treatment, a therapist must use clinical judgment. For
example, although the therapist may structure imaginal exposure to last for 45–60 minutes, a
shorter period should be implemented if the patient cannot tolerate such a long exposure. If a
gradual decrease in distress does not occur spontaneously, coping statements such as “But you are
going to survive . . . ” may be introduced into the imagery. It is important that the therapist not
encourage avoidance by terminating the imaginal exposure while the patient remains very fearful.
Decision-making guidelines for the use of exposure therapy for PTSD have been established that
take into account patient variables such as tolerance for extreme arousal, imaging ability, and
compliance (Foa and Rothbaum 1998; Jaycox and Foa, in press; Litz et al. 1990). It seems that
survivors who experience extreme distress when remembering their trauma or who show extreme
avoidance of situations, objects, or thoughts that remind them of the trauma would profit from
exposure therapy. However, for some patients, the memories are excruciatingly painful,
overwhelming coping capacities and resulting in resistance in complying with exposure
instructions. In these cases, the therapist may be advised to take a more gradual approach and to
begin therapy skills building, including anxiety management techniques (Cloitre et al. 2002).
Hypnosis for Posttraumatic Stress Disorder
Techniques employing hypnosis can be helpful in reeliciting traumatic memories and in managing
painful affect associated with them (Spiegel and Cardena 1990). The intensely focused
concentration typical of hypnosis is mobilized in order to access and work through traumatic
memories. When the hypnotic induction is ended, the dissociative elements of hypnosis facilitate
putting aside traumatic memories until the next therapeutic intervention. In addition, hypnotic
dissociation facilitates separating somatic from psychological distress. This is done by maintaining
a state of physical relaxation—for example, floating and picturing traumatic memories on an
imaginary screen:
A 32-year-old social worker was brutally assaulted in the early evening as she was returning with bags of
groceries to her apartment. She fought with the assailant, suffering a basilar skull fracture, but managed
to prevent his dragging her into her apartment and raping her. In hypnosis, she was asked to picture the
assailant on one side of an imaginary screen. As she did this with strong emotion, she noted two things
that she had not thought of previously. The first was that he was surprised that she was fighting as hard
as she was. The second was a look on his face that convinced her that his intention was not merely toPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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rape her, but to kill her. On the other side of the screen, she was asked to concentrate not on him, but on
what she had done to protect herself. This enabled her to come to a new recognition that, far from
increasing her injury by fighting with him, which had been her previous thought, she had quite possibly
saved her life. In this way, the hypnosis was used to facilitate her restructuring her memory of the
assault, making it painful but bearable because she had attended to her instinct for self-preservation as
well as the viciousness of his assault (Spiegel 1989).
Psychodynamic Treatment for Posttraumatic Stress Disorder
In one of only a few controlled studies, Brom et al. (1989) randomly assigned 112 individuals with
PTSD to desensitization, hypnotherapy, or brief dynamic psychotherapy. The mean length of
treatment ranged from 14.4 to 18.8 sessions. Brom and colleagues concluded that all treatments
were beneficial, the differences were small, and each modality did not benefit all subjects.
Participants who received psychodynamic treatment showed the least improvement in intrusive
symptoms initially. However, follow-up data indicated that subjects in the psychodynamic group
showed greater improvement during the posttermination phase than did subjects in the other
therapies. This finding suggests that psychodynamic therapy may mobilize coping mechanisms that
continue to function after termination (Horowitz et al. 1986).
In a series of empirical studies in which a manualized brief dynamic treatment was used, Horowitz
and colleagues (Horowitz and Kaltreider 1995; Horowitz et al. 1993, 1994) tested the hypothesis
that survivors of traumatic events experience heightened intrusive and avoidant symptoms related
to traumatic memories and themes. They determined that this dual response is characterized by
intense conflict as the patient attempts to integrate traumatic memories while defending against
external and internal dangers such as painful emotions. Recognition of these responses helps the
patient and therapist to process the conflictual topic and accompanying intrusions, avoidances,
fragmentation of thinking, and stifling of emotional expression. It may also foster awareness of
previous pathological attempts at coping.
Lindy et al. (1988) reported on an open series of 37 Vietnam War veterans with clinical diagnoses
of PTSD who received psychodynamic psychotherapy aimed at processing traumatic war memories.
These veterans were compared with a volunteer sample (n = 200) of Vietnam veterans culled from
clinical and nonclinical sources. After an average of 56 sessions, independent raters noted
significant changes on the Hopkins Symptom Checklist–90 (SCL-90; Derogatis 1977), the Impact of
Event Scale (Horowitz et al. 1979), and the Cincinnati Stress Response Schedule. Intrusive
phenomena, feelings of alienation and depression, and associated hostility and substance abuse
were most notably changed. Numerous other clinical reports (de Wind 1971; Herman 1992; D. S.
Rose 1991; Shengold 1989, 1991) suggested that psychodynamic psychotherapy is effective.
Confrontation of and management of intense rage in the victim are vital according to many of these
reports.
The psychodynamic treatments of PTSD, including individual, group, and family, emphasize safety,
exploration of the trauma, and reconnection. Several groups working with survivors of different
traumas and influenced by different theoretical orientations have proposed models for the
psychodynamic psychotherapy of PTSD: Horowitz (stress response syndromes, including
complicated and traumatic grief [Horowitz 2001; Horowitz et al. 1984]), Herman (incest and sexual
abuse [Herman 1983; Herman and Hirschman 1984]), Lindy (war and disaster [Lindy 1989; Lindy
and Lindy 2004]), Marmar (variations in dynamic therapy for acute, chronic, and complex comorbid
PTSD [Marmar et al. 1996b]), and Pearlman (early childhood abuse [Pearlman and Courtois 2005]).
The models have much in common. All 1) emphasize the clinician–patient therapeutic relationship,
the role of transference and countertransference, and the importance of clear boundaries, 2) use a
supportive-expressive approach, 3) address the safety of the patient, 4) make trauma and its
related cognitive schemata the central focus when possible, 5) relate trauma to developmental
schemas, and 6) facilitate the transformation of reliving and reexperiencing traumatic memories
into a coherent and contained narrative of the trauma. All help the patient move from discontinuityPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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toward continuity of the self and others, from despair to meaning, and from pathological and rigid
defenses toward more flexible defenses and adaptive coping skills.
The models include three phases of treatment. During the initial phase, trust gradually develops
through conscious and unconscious tests of the therapist’s availability, reliability, interest,
understanding, and boundaries. In the middle phase, maladaptive or pathogenic beliefs arising from
the trauma circumstances are reworked, focusing on pathogenic weak/victim and strong/victimizer
roles and the dynamic relationship between these disparate self-concepts—for example, acting
weak or being self-destructive as punishment for unconscious guilt. This involves facing the past,
linking vulnerable self-concepts from earlier developmental periods to reactivation of these through
trauma, exploring subjective meanings, and mourning the self that was lost. This stage is subject to
distrust and to intense negative trauma-related transferences, which need to be understood and
interpreted. In the final phase, bereavement and reconnection occur, with resultant attribution of
meaning, mastery of the trauma experience, and reinvestment in the future, with appropriate
developmental and life-cycle tasks and a sense of reconnection with the pretrauma self. In all
models, interventions are consistently trauma focused, supportive, empathic, and educational.
Group and Family Treatment for Posttraumatic Stress Disorder
The group as a unit of therapeutic change for individuals with postcombat problems grew in tandem
with increasing recognition of PTSD and the establishment of the self-help movement of the 1970s.
Because veterans with PTSD and survivors of rape trauma experience themselves as alienated,
isolated, and with diminished feelings, a group may provide acceptance, communality, and mutual
commitment. Today, both psychodynamic and cognitive-behavioral group therapy for patients with
PTSD are common. Psychodynamic groups attend to and help consolidate individual members’
anxieties about new meanings of the trauma experience (Koller et al. 1992). The group confronts
irrational assumptions that organize the trauma, such as feelings of omnipotent control,
assumptions of betrayal, and the value of avoidance (Foy et al. 2002).
A large randomized Department of Veterans Affairs (VA) trial of 360 combat veterans compared
trauma-focused versus present-focused group therapy. Intention-to-treat analysis revealed no
significant differences between the two interventions, and about 40% of patients improved in both
arms. The dropout rate was higher in the trauma-focused arm, but among those who persisted with
the trauma-focused therapy there was improvement in avoidance and numbing symptoms (Schnurr
et al. 2003).
The patients’ aloneness and disconnection from other trauma survivors, and their diminished
capacity for sustaining relationships, make the family a vital site and often one in which pain is
experienced. In untreated PTSD patients, families may become disengaged through alienation,
enmeshed through poor boundaries, or chaotic and crisis-driven in response to fears of rage.
Treatment involves 1) a psychoeducational dimension in which understanding the disorder reduces
blame, shame, and stigmatization; 2) some form of disclosure that transforms an unspeakable
event into one that is knowable, approachable, and meaningful; and 3) increased tolerance for the
tension between a compelling past and a real present (Rosenheck et al. 1998).
Summary and Conclusions Regarding Psychosocial Treatments for
Posttraumatic Stress Disorder
Psychodynamic interventions are widely used with trauma survivors, and theoretical accounts of
their use and descriptions of treatment approaches exist. However, this area is limited by a dearth
of well-controlled studies. In contrast, numerous controlled studies of CBT consistently have shown
that both exposure programs and anxiety management techniques are effective in reducing PTSD
symptoms and related problems. The effects of exposure on PTSD symptoms in the studies of
combat veterans appear to be less impressive than with survivors of other traumas. This
differential efficacy may be the result of differences in the populations, the treatment programs,
and the measures. With regard to the populations, the difference in comorbidity between veterans
and other trauma survivors may account for the apparently reduced efficacy of exposure treatmentPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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with veterans. Clinical impressions suggest that Vietnam veterans with PTSD enrolled in VA clinics
have more comorbid Axis I and II disorders than do other trauma survivors with PTSD. In addition,
although both veterans and other trauma survivors often have trauma-related guilt and anxiety, for
some the traumatic memories may be driven more by guilt than by the anxiety that is central to the
memories of other trauma survivors. Guilt-centered trauma memories are more resistant to CBT
treatment (Hembree and Foa 2000).
Although cognitive-behavioral techniques are effective, they should be used with caution. PTSD
patients are particularly avoidant and present many treatment obstacles, especially for exposure
techniques. Stress management techniques appear helpful and cause less anxiety in treatment
sessions; however, when tolerated, exposure-based treatments are associated with the largest
treatment gains. The therapist must always be aware of safety issues. Although the results of the
studies presented above are impressive, clinicians in private practice may encounter more difficult
patients who would be excluded from controlled clinical studies. More vulnerable trauma patients
may dissociate, use substances, become depressed, or leave treatment when prematurely
confronted with trauma work.
Pharmacotherapy for Posttraumatic Stress Disorder
There is agreement in the literature that medication is not usually the primary treatment for ASD
and PTSD (Davidson 1992, 1997; Famularo et al. 1988; Marmar et al. 1993; Shalev et al. 1996a;
Southwick and Yehuda 1993; Turner 1999; van der Kolk 1987). Therefore, it is recommended that
psychopharmacological treatment be used as an adjunct to psychotherapeutic intervention and be
integrated into the psychotherapy (Marmar et al. 1993; Shalev et al. 1996a; Southwick and Yehuda
1993). Symptomatic treatment with medication may be perceived by patients as a means of
isolating their descriptions of violence and other trauma-related material, suppressing them, and
keeping them from the therapist rather than as an empathic means of providing comfort (Southwick
and Yehuda 1993), or it may be interpreted by patients as a sign of failure in recovery (Turner
1999). On the other hand, especially when patients in the immediate aftermath of trauma have
severe hyperarousal symptoms, appropriate psychopharmacological treatment can make patients
more accessible to psychotherapy (Marmar et al. 1993; van der Kolk 1987) and holds promise for
the prevention of chronic PTSD (Pitman et al. 2002; Vaiva et al. 2003).
Theoretical Basis for Pharmacological Interventions in Posttraumatic Stress
Disorder
Fear Conditioning and Fear Extinction Models of PTSD
Basic science research on memory consolidation and fear conditioning has demonstrated that
heightened adrenergic activation can promote the consolidation and retrieval of fear-provoking
memories (Bohus and Lissak 1968). Building on this preclinical work, conditioning models of
trauma response propose that PTSD is the result of strong associative learning whereby individuals
initially react to a traumatic event (unconditioned stimulus) with arousal and fear (unconditioned
response). Individuals with PTSD then continue to show arousal (conditioned response) when
confronted with trauma-related cues (conditioned stimuli). It has been hypothesized that
terror-driven sympathetic arousal at the time of a traumatic event may result in the release of
stress-related neurochemicals (including norepinephrine and epinephrine) in the cortex, mediating
an overconsolidation of trauma memories (Pitman 1989).
In the weeks after trauma exposure, the majority of trauma survivors will engage in extinction
learning, in which they associate the conditioned stimuli with safe consequences and thereby
inhibit the fear response. By contrast, the minority of people who develop PTSD suffer from
impaired extinction learning and overconsolidate memories of the trauma. Both dissociation
(Simeon et al. 2003) and panic reactions (Charney et al. 1993; Southwick et al. 1997) have been
associated with increased catecholamine states. It is likely that those displaying peritraumatic
panic, dissociation, or other forms of intense emotional distress during and immediately after the
traumatic event have higher levels of catecholamines than those who do not respond in thisPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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manner. An enhanced elevation of catecholamines in the immediate aftermath of a traumatic event
may increase the probability of intrusive recollections in the first few days and weeks posttrauma
(Charney et al. 1993), with a feedforward process further intensifying fear conditioning and
memory consolidation.
More recent animal models propose that both associational and nonassociational fear conditioning
play a role in PTSD (Siegmund et al. 2005). In fear conditioning experiments, animals develop both
conditioned associations to previously neutral stimuli when paired with the unconditioned stimulus
(for example, pairing of a light or tone with a footshock) and nonspecific heightened fear responses
to previously neutral stimuli (light or tone) that were never paired with the footshock. The latter
are more rapidly extinguished when the animal is given an SSRI, whereas the former respond to
repeated exposure in the absence of the negative reinforcing stimulus. Taken together, the
associational and nonassociational conditioned fear models suggest that the combination of CBT
and SSRIs offers a broad-spectrum approach for treating both trauma-related triggers for
reexperiencing and general anxious arousal in those with PTSD.
Sensitization
Exposure to a single or repeated stimulus may result in sensitization to subsequent stresses of
lower intensity. Analogously in PTSD, repeated exposure to severely traumatic events or repeated
reexperiencing of that event in memory may ultimately produce a lowered threshold for heightened
reactions to stressors. It follows that medications that can modulate these sensitized circuits might
reduce PTSD symptoms.
Inescapable Shock/Learned Helplessness/Noradrenergic Mechanisms
On the basis of animal experiments, Anisman and Sklar (1979) proposed that learned helplessness
behaviors in response to inescapable stress provided an animal model of depression. However, it
has been proposed that this model has more in common with PTSD (Foa et al. 1992; van der Kolk
1987) but also has its limitations (Yehuda and Antelman 1993). In animals, inescapable stress is
accompanied by mobilization and release of catecholamines (norepinephrine and dopamine) and
serotonin, followed by their depletion. Krystal et al. (1991) related this effect to a disturbance of
the brain’s “alarm center”—the locus coeruleus, a noradrenergically rich region of the brain stem.
Drugs that have antiadrenergic effects, such as beta-blockers and imipramine, and that
downregulate the locus coeruleus prevent the development of learned helplessness in animals that
have been exposed to inescapable shock and likewise are effective in ameliorating the symptoms of
PTSD in humans. Conversely, noradrenergic alpha2-antagonist drugs, such as yohimbine, stimulate
the locus coeruleus and induce symptoms of PTSD in combat veterans with that diagnosis (Charney
et al. 1993). Increased central and peripheral noradrenergic activity may represent the substrate of
some PTSD symptoms, such as increased autonomic arousal, fearfulness, vigilance, and
reexperiencing.
Serotonergic Mechanisms
Growing evidence indicates that serotonin (5-hydroxytryptamine [5-HT]) is important in PTSD.
Conditioned avoidance behavior, characteristic of the “avoidance” cluster of PTSD symptoms (i.e.,
phobic avoidance of trauma or its reminders), is modulated by serotonergic pathways arising in the
dorsal raphe and projecting to the amygdala (Kent et al. 1998). An adaptive pathway (i.e., one that
may strengthen coping responses in the face of stress) also arises in the median raphe and
innervates the hippocampus. In addition, the regulatory effect of serotonin on sleep further
supports the relevance of serotonin to PTSD. Finally, as discussed below, medications that increase
serotonergic transmission are clinically effective in PTSD.
Antidepressants
Tricyclic Antidepressants
Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) were the firstPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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antidepressants to be used for the treatment of PTSD. Clinical trials data with mostly small samples
indicated modest symptom improvement from imipramine (effect size: 0.25) (Frank et al. 1988),
moderate improvement from amitriptyline (effect size: 0.64) (Davidson et al. 1990), and no
advantage from desipramine (effect size: 0.05) (Reist et al. 1989). The TCAs were effective for
reexperiencing and arousal symptoms but not for avoidance and numbing. TCAs are not widely used
because of anticholinergic side effects, in particular cardiotoxicity, relative to the SSRIs and the
atypical antidepressants.
Monoamine Oxidase Inhibitors
A review by Southwick et al. (1994) found the MAOIs to be more effective than the TCAs in the
treatment of PTSD, with improvement in 82% of phenelzine-treated patients compared with 45%
for patients treated with a TCA. Two placebo-controlled studies (Kosten et al. 1991, with a
preliminary report by Frank et al. 1988; Shestatzky et al. 1988) assessed the irreversible MAOI
phenelzine in combat veterans with chronic PTSD. Shestatzky et al. (1988) found no difference
between drug and placebo in a 5-week crossover trial with 13 patients; however, sample size and
treatment duration may have limited statistical power to detect group differences. As an
irreversible, nonselective MAOI, phenelzine has limitations, including hypotension and risk of
hypertension when combined with certain foods and other medications. At present, phenelzine is
generally not recommended as a first-line treatment but should be considered if trials of
better-tolerated medications have failed and the patient can comply with dietary restrictions.
Reversible and selective MAOIs are potentially safer and better tolerated. However, brofaromine
(which selectively inhibits both MAO-A and serotonin transport but is not currently marketed) was
found ineffective in one controlled trial (Baker et al. 1995) and modestly effective in a subgroup of
subjects in a second trial (Katz et al. 1995). Moclobemide (a reversible inhibitor of MAO-A that is
not currently available in the United States) has shown promise in an open trial of 20 patients with
chronic PTSD due to childhood physical and sexual abuse (Neal et al. 1997).
Selective Serotonin Reuptake Inhibitors and New Agents With Serotonergic Activity
Successful open-label and double-blind trials of sertraline (Brady et al. 2000; Davidson et al. 2001b;
Zohar et al. 2002), paroxetine (R. D. Marshall et al. 2001), fluoxetine (van der Kolk et al. 1994),
fluvoxamine (Marmar et al. 1996a), and citalopram (Seedat et al. 2002) have established the SSRIs
as the pharmacological treatment of choice for PTSD. Sertraline and paroxetine are the only
FDA-approved medications for PTSD, having been assessed in large multisite randomized,
double-blind controlled trials. The two sertraline multicenter trials by Brady et al. (2000) and
Davidson et al. (2001b) included a total of 395 civilian trauma victims and demonstrated efficacy
for the reexperiencing, numbing and avoidant, and hyperarousal symptoms of PTSD. A positive
treatment response was defined as having a 30% or greater reduction for the combined
Clinician-Administered PTSD Scale Part 2 (CAPS-2) score plus a Clinical Global
Impressions–Improvement (CGI-I) Scale score of much or very much improved at the end of the
study. By these criteria, 53% and 60% of sertraline-treated patients were responders in the two
respective studies, compared with 32% and 38% of placebo-treated patients. Female patients had
a significantly better response than males, consistent with studies of SSRIs for premenopausal
women with depression. The gender effect has not been replicated in all studies. Zohar et al.
(2002) found that sertraline was effective for both male and female Israeli combat veterans with
PTSD.
- D. Marshall et al. (2001) demonstrated that paroxetine was effective for both men and women
with chronic PTSD. Patients were prescribed either 20 or 40 mg of paroxetine or placebo
throughout the course of the study. In this study there was a 50% reduction on the clinician-rated
PTSD symptom measure using the CAPS-2 for paroxetine-treated patients compared with a 33%
reduction for placebo. The reduction in the CAPS-2 score resulted in an effect size of 0.5, generally
smaller than the effects reported for CBT studies. Of note, American combat veterans with PTSD
generally show less benefit from SSRIs in controlled trials (Friedman et al., in press). Although it is
commonly believed that veterans are reluctant to report clinical improvement because of concernsPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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about losing disability benefits, the primary reason for the negative finding in the sertraline trial
was an unexpectedly large response in the placebo group.
Almost all of the SSRI studies were conducted over a period of 12 weeks or less, with improvement
usually seen in 4–6 weeks. Londborg et al. (2001) conducted a 24 week open-label trial of
sertraline in 249 of the patients who had just completed a 12-week randomized controlled trial
(RCT). Ninety-two percent of the RCT study responders in the sertraline group maintained their
beneficial response. An important finding during the course of this 24-week continuation study was
that patients who had taken sertraline the prior 12 weeks experienced an additional 31% decrease
in symptoms. Surprisingly, 58% of patients classified as nonresponders in the initial 12-week study
converted to responders. Although these observations are confounded by the effect of the passage
of time, they suggest that a longer course of treatment with an SSRI may be required to optimize
therapeutic benefits of SSRIs for chronic PTSD.
Davidson et al. (2001a) conducted a separate 28-week discontinuation trial of sertraline treatment
with 84 patients, drawn from the Londborg study cohort (Londborg et al. 2001), who had a
sustained beneficial response for 36 weeks. There was a 26% relapse rate for those patients placed
on placebo, compared with 5% of patients who continued on sertraline. Davidson et al.’s findings
support the benefit of continuation therapy observed in the Londborg study and suggest the need to
maintain treatment responders on SSRIs for at least 1 year. Clinical practice suggests that
discontinuation of an SSRI should be initiated 12–18 months after treatment initiation and
accomplished by a gradual taper with careful observation, especially during the first 2 months, the
period of highest risk of relapse in the Londborg study.
In several open trials, other medications such as trazodone (Hertzberg et al. 1996), nefazodone
(reviewed in Hidalgo et al. 1999), and mirtazapine (Connor et al. 1999) also appear promising but
require controlled study. Although no trials have compared two or more serotonergic compounds in
PTSD, anecdotal experience and studies from major depression suggest that if one SSRI is not well
tolerated, another might be clinically effective.
Mood Stabilizers
Mood-stabilizing medications used in clinical trials to treat chronic PTSD include carbamazepine,
valproate, topiramate, lamotrigine, gabapentin, and lithium. Carbamazepine has strong antikindling
properties. In small open clinical trials, carbamazepine decreased reexperiencing symptoms,
insomnia, hyperarousal symptoms, impulsivity, and violent behavior (Keck et al. 1992; Lipper et al.
1986; Looff et al. 1995). Valproate has a less potent antikindling action than does carbamazepine.
In one open-label trial in Vietnam veterans with PTSD, valproate was associated with improvement
in avoidance and arousal but not reexperiencing symptoms (Fesler 1991). Topiramate, an
anticonvulsant with gamma-aminobutyric acid (GABA)–enhancing properties, was found to reduce
PTSD symptoms (including nightmares) in an open-label study in 35 chronic PTSD patients
unresponsive to prior medication treatment (Berlant and van Kammen 2002). Lamotrigine, an
anticonvulsant that is a glutamate antagonist, was found to be promising in a small 12-week
double-blind, controlled trial; however, the small sample size limited the power to detect an effect
(Hertzberg et al. 1999). Careful attention should be paid to the emergence of a serious rash with
lamotrigine. In a retrospective review, adjunctive treatment with gabapentin was found to be
helpful for sleep disturbances, including frequency of nightmares (Hamner et al. 2001). One
additional agent of interest for PTSD is lithium, a mood stabilizer that alters serotonin transport.
Two small open trials of lithium in PTSD reported improvement in hyperarousal symptoms (Kitchner
and Greenstein 1983; van der Kolk 1991), suggesting that lithium augmentation may be helpful for
treatment-resistant anger and irritability (Forster et al. 1995).
Adrenergic-Inhibiting Agents
Adrenergic dysregulation is a key biomarker for ASD and PTSD (Kolb et al. 1984; Southwick et al.
1999). Individuals with PTSD have elevated plasma norepinephrine at rest (Yehuda et al. 1998) and
greater increases after exposure to trauma reminders. Downregulation of platelet norepinephrinePrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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receptors is further evidence for chronic increases in adrenergic activity. As noted above, prolonged
terror leading to sustained peritraumatic adrenergic activity increases the risk for PTSD because of
greater fear conditioning and greater memory consolidation. Propranolol, a nonselective
beta-adrenergic blocker that crosses the blood-brain barrier, decreases memory consolidation for
emotional memories (Cahill et al. 1994), suggesting that treatment with propranolol in the first
hours following traumatic exposure may be warranted. In a double-blind controlled trial by Pitman
et al. (2002), 41 trauma victims were placed on a 10-day course of propranolol or placebo within 6
hours of the traumatic event. At 1 month, 18% of the propranolol patients met the criteria for
PTSD, compared with 30% of the placebo patients. At 3 months, there was no statistical difference
in PTSD symptom levels between the two groups; however, in 22 of 41 participants tested, 0% of
the propranolol patients, compared with 43% of the placebo patients, were physiological
responders to a trauma narrative script. Vaiva et al. (2003), in a nonrandomized contrast group
design, initiated propranolol treatment for 11 accident and assault victims 2–20 hours after
traumatic exposure. Propranolol 40 mg three times a day was provided for 7 days, followed by an
8- to 12-day taper period. These 11 patients were compared with 8 participants who declined
propranolol but agreed to be followed. The two groups were equivalent on demographics, exposure,
injury severity, and peritraumatic responses. Inclusion criteria included resting heart rate higher
than 90 beats per minute shortly following the trauma. Two months following the trauma, the
propranolol group had lower PTSD symptoms, with 1 propranolol patient meeting the criteria for
PTSD, compared with 3 subjects in the group that did not take propranolol. These two studies
suggest that propranolol may be a useful early intervention for preventing the development of
chronic PTSD.
Clonidine is an alpha2 agonist that slows firing of the adrenergic neurons in the locus coeruleus and
reduces adrenergic activity in PTSD (Davidson 1992). It has been shown to reduce impulsive
behavior and intrusive symptoms but not to decrease avoidance and numbing (Kinzie and Leung
1989; van der Kolk 1987). Kolb et al. (1984) reported a reduction in intrusion and sleep disturbance
in Vietnam veterans given a combination of clonidine and a TCA. Clonidine dosages are initiated at
0.1 mg once to twice a day and increased to a maximum of 0.6 mg/day (Silver et al. 1990). An open
trial of the clonidine patch in inpatient children ages 3–6 years with severe PTSD reported
improvement in aggression, lability, insomnia, nightmares, and dissociation (Harmon and Riggs
1996).
Prazosin is an alpha1 postsynaptic receptor antagonist. Raskind et al. (2003) studied the efficacy of
prazosin for PTSD in 10 Vietnam combat veterans in a 20-week double-blind crossover protocol
with a 2-week drug washout to allow for return to baseline. Prazosin patients had a robust
improvement in overall sleep quality and nightmares, with improvement also for other
reexperiencing symptoms, and also for avoidance and numbing and hyperarousal. A related study
examined 11 participants with civilian trauma–related PTSD who continued to experience daytime
PTSD symptoms despite a stable bedtime prazosin dose that suppressed trauma-related
nightmares. Adding daytime prazosin reduced psychological distress specifically to trauma cues
(Taylor et al. 2006).
Benzodiazepines
Benzodiazepines potentiate the effects of GABA. The GABAA receptor is the most common receptor
in the brain and inhibits the activation of most neurons. Benzodiazepines reduce activity of
norepinephrine cell bodies in the locus coeruleus and also play an inhibitory role in the central
nucleus of the amygdala. Surprisingly, the few small-N studies that have been conducted suggest
that benzodiazepines are of limited value in treating the core symptoms of PTSD. Benzodiazepines
interfere with fear extinction, which may explain their limited utility in PTSD. A history of
alcoholism or abuse of sedatives or benzodiazepine drugs is a contraindication to the use of
benzodiazepines in ASD. However, appropriate use of benzodiazepines may reduce the likelihood of
inappropriate alcohol use in the aftermath of trauma (van der Kolk 1983).
In a nonrandomized early intervention trial of Israeli accident and terrorism survivors, alprazolamPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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and clonazepam were compared with a no-benzodiazepine treatment-as-usual group (Gelpin et al.
1996). The 13 patients who received a benzodiazepine did not experience reduced symptoms of
PTSD compared with the 13 control subjects. At 6-month follow-up, those receiving
benzodiazepines exhibited a trend toward higher rates of PTSD. Braun et al. (1990) conducted a 12
week double-blind crossover trial with 16 chronic PTSD patients. A 2-week drug washout allowed
for a return to baseline before entering the second phase of the study. After 5 weeks of treatment
with alprazolam, there were no significant reductions of symptoms of intrusion, numbing, and
avoidance. Risse et al. (1990) reported significant withdrawal symptoms following gradual
discontinuation of alprazolam in combat-related PTSD in participants with a history of alcohol abuse
or benzodiazepine dependence, underscoring concerns about the risk for developing dependence
with alprazolam. Sustained-release formulations of alprazolam may prove to be better tolerated
and more effective.
Antipsychotics
There is growing interest in the use of atypical antipsychotic agents for chronic treatment-resistant
PTSD. Atypical antipsychotics are often prescribed in PTSD with disorganized behavior and marked
dissociative symptoms, or with explosive, aggressive, or violent behavior. Risperidone, an
antipsychotic with D2 and 5 HT2 antagonism effects was studied as an adjunctive treatment using a
6-week double-blind controlled design in 15 patients with combat-related PTSD (Monnelly and
Ciraulo 1999). There was improvement in intrusive thinking, irritability, and total PTSD symptoms.
Hamner et al. (2003b) evaluated risperidone as an adjunctive treatment in 40 combat veterans with
PTSD and comorbid psychotic symptoms using a 5-week prospective, randomized, double-blind,
placebo-controlled design. There was a modest reduction in psychotic symptoms. There was also a
modest improvement in reexperiencing symptoms.
Petty et al. (2001) conducted an open clinical trial with olanzapine with 48 veterans diagnosed with
combat-related PTSD. Olanzapine was found to be effective for all three symptom clusters of PTSD,
with a 30% reduction in overall clinician ratings. In a 10-week double-blind, placebo-controlled
trial of 15 patients, Butterfield et al. (2001) reported no advantage of olanzapine compared with
placebo. There was a high placebo response rate, with olanzapine and placebo groups showing
symptom reductions comparable to those in other active-drug treatment trials. In a double-blind,
randomized controlled study of 19 veterans with combat-related PTSD, Stein et al. (2002) reported
that olanzapine was effective when used as an adjunctive treatment for PTSD with associated
depression and sleep problems that had not previously responded well to an SSRI. The olanzapine
group also improved on depression and sleep disturbance.
Quetiapine is an antipsychotic that antagonizes alpha1-adrenergic, 5-HT2A, and histamine (H1)
receptors in addition to its dopamine (D2) blocking effect. This profile suggests that quetiapine may
be helpful for PTSD sleep disturbances as well as overall PTSD symptoms. Compared with
olanzapine quetiapine has a more favorable side-effect profile with regard to weight gain and
metabolic syndrome. In a retrospective chart review of 68 veterans with combat-related PTSD,
low-dose quetiapine was found to be helpful as an adjunctive treatment for patients who had not
responded to two or more psychotropic agents. Quetiapine was also studied in a 6-week open
clinical trial with 20 veterans with combat-related PTSD (Hamner et al. 2003a). There was
improvement in clinician ratings of PTSD symptoms, as well as for psychotic symptoms. Larger
controlled trials are needed to determine the efficacy of atypical antipsychotic agents for
treatment-resistant PTSD.
Summary Regarding Pharmacotherapy for Posttraumatic Stress Disorder
Based on large multisite controlled clinical trials, SSRIs are the medication of first choice for the
treatment of PTSD. Anti-adrenergic agents are promising for immediate treatment in the emergency
medical setting as a secondary prevention for chronic PTSD. Mood stabilizers have a role in
reducing the limbic system sensitization thought to occur in the first weeks and months following
exposure to a traumatic event. They also appear to be helpful in cases of chronic PTSD where
impulsive, aggressive behavior and affect-regulation problems are resistant to first-line SSRIPrint: Chapter 32. Posttraumatic Stress Disorder and Acute Stress Disorder http://www.psychiatryonline.com/popup.aspx?aID=258639&print=yes…
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treatments. Atypical antipsychotics are promising for severe treatment-refractory PTSD with
disorganized behavior and for those with comorbid psychotic symptoms. Patients with more severe
symptoms and with complex patterns of comorbidity may require combinations of pharmacotherapy
agents, with longer-term psychosocial treatment emphasizing affect regulation and social skills
building, cognitive processing, and graduated in vivo exposure (R. D. Marshall and Cloitre 2000;
Schoenfeld et al. 2004).
CONCLUSION
Immediately after exposure, the priorities are reducing terror, horror, and helplessness; restoring a
sense of safety; and mobilizing social support. Debriefing of acutely distressed patients in the first
hours after exposure risks intensifying fear conditioning and memory consolidation, complicating
recovery. Beta-blockers hold promise for treating trauma victims who are highly distressed in the
first hours after exposure. Treatment of ASD during the first weeks after exposure constitutes an
opportunity for rapid amelioration of intense distress, as well as effective prevention of later
illness, including PTSD and depression. Brief cognitive-behavioral interventions, alone and in
combination with adrenergic-blocking agents or SSRIs, may prevent the development of chronic
PTSD symptoms. These disorders, in turn, are also treatable, but individuals with these disorders
frequently avoid treatment or cannot find appropriate psychotherapy and pharmacotherapy.
For chronic PTSD, several psychotherapies have been shown to be effective, and treatment is often
enhanced with judicious use of medication. CBT emphasizing imaginal and in vivo exposure and
cognitive reprocessing are the best-validated treatments for ASD and PTSD. Several variants of
CBT, including cognitive processing therapy and EMDR, have been shown to be effective in
replicated controlled trials. Other psychotherapies that show promise but require further validation
include trauma-focused brief dynamic psychotherapy and combined CBT and hypnotherapy.
SSRIs are the best-validated pharmacotherapies for PTSD and are effective for treating
reexperiencing, avoidance and numbing, and hyperarousal symptoms. Prazosin is useful for
treatment-resistant nightmares. Although controlled trial data are lacking, clinical practice suggests
that low-dose trazodone is well tolerated for insomnia. Benzodiazepines are widely prescribed for
ASD and PTSD but have not been shown to be effective, and they may interfere with fear extinction,
and risk dependence and withdrawal.
For more disturbed patients who are not well stabilized, the initial focus is on improving current
functioning through anxiety and anger management and social skills training, alone and in
combination with atypical antipsychotics, mood-stabilizing agents, and SSRIs. When the more
vulnerable patient is stabilized, trauma-focused therapies, including cognitive processing therapy in
combination with graduated in vivo exposure, may permit a safe exploration and mastery of the
trauma. Caution should be exercised in the use of prolonged imaginal exposure in more disturbed
patients because of the risks of overwhelming anxiety, intensification of anger outbursts and
impulsivity, dissociation, and increased alcohol and drug use.
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Copyright © 2009 American Psychiatric Publishing, Inc. All Rights Reserved.
Course Content
Introduction to Stress Disorders
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Understanding Stress Disorders
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Historical Context and Evolution of PTSD
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Key Concepts in Stress Disorders
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Biological and Psychological Underpinnings of Stress Disorders
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Historical and Biological Perspectives Quiz
Understanding Post-Traumatic Stress Disorder (PTSD)
Exploring Acute Stress Disorder: Symptoms and Causes
Advanced Techniques for Managing Stress Disorders
Conclusion and Future Directions in Stress Disorder Treatment
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