PTSD Research Paper

Outline

I. Reactions to Traumatic Events

A. Acute Reactions

B. Posttraumatic Stress Disorder

C. Course of PTSD

II. Measures of PTSD

A. Interviews

B. Self-Report Measures

III. Prevalence of PTSD

IV. Vulnerability and Resiliency Factors in PTSD

V. Concomitant Problems Following Trauma

VI. Theories on the Development and Maintenance of PTSD

A. Psychoanalytic Theories

B. Cognitive and Behavioral Theories

C. Psychobiological Approaches

VII. Psychological and Pharmacological Interventions in PTSD

A. Early Interventions

B. Cognitive-Behavioral Therapies

1. Prolonged Exposure (PE)

2. Stress Inoculation Training (SIT)

3. Cognitive Therapy

4. Cognitive Processing Therapy (CPT)

5. Eye Movement Desensitization and Reprocessing (EMDR)

C. Pharmacotherapy

D. Hypnotherapy and Psychodynamic Psychotherapy

VIII. Bibliography

I. Reactions to Traumatic Events

Psychologists and physicians have long been interested in vulnerability and resilience factors in reaction to extreme stress. Earlier accounts of posttrauma reactions focused on descriptions of cases. Spurred by inclusion of Post-traumatic Stress Disorder (PTSD) in the psychiatric diagnosis nomenclature in 1980, experimental research has examined many facets of the phenomenon.

In the Diagnostic and Statistical Manual (DSM-IV) published by the American Psychiatric Association in 1994, a trauma is defined as an experienced or witnessed event that involves threat of death or serious injury, and which evokes feelings of terror, horror, or helplessness. Thus, events such as anticipated death of a loved one, job loss, or divorce would not qualify as a trauma in this formulation. The International Classification of Diseases (ICD-10), published by the World Health Organization in 1992, describes a traumatic event as having an exceptionally threatening or catastrophic nature, which would be likely to cause pervasive distress in almost anyone.

The most common traumas studied are combat, sexual assault, sexual abuse in childhood, criminal victimization, torture, accidents, and natural disasters. Larger-scale traumas, such as mass migration, refugee camp experiences, and holocausts, have not yet been thoroughly researched. Clearly, such mass traumas would be expected to have considerable impact on those individuals directly affected as well as on their children, communities, and cultures.

A. Acute Reactions

A number of physical and psychological symptoms are considered common reactions immediately after a traumatic experience. Many trauma victims report being disoriented and anxious after a trauma and have difficulty sleeping and concentrating. Victims are often reluctant to talk about the trauma or deliberately contemplate it; nevertheless the traumatic memory intrudes on their thoughts quite frequently. In recognition of the severe distress and psychological dysfunction that often occur immediately after a trauma, a new diagnostic classification called Acute Stress Disorder (ASD) was adopted in the DSM-IV in 1994. The focus of this disorder is on dissociative features, and, consequently, the symptom criteria include at least three of the following: a sense of numbing, detachment, or lack of emotional responsiveness, a reduction in awareness of surroundings (e.g., being in a daze), derealization, depersonalization, and dissociative amnesia. Reexperiencing of the trauma, avoidance, and arousal, as defined in the criteria for PTSD, must also exist. A diagnosis of Acute Stress Disorder is warranted when such symptoms last between 2 days and 1 month, occur within 1 month of the trauma, and interfere significantly with daily functioning.

B. Posttraumatic Stress Disorder

Posttraumatic Stress Disorder, as described in DSM-IV, is a set of symptoms that begins after a trauma and persists for at least 1 month. The symptoms fall into three clusters. First, the individual must reexperience the trauma in one of the following ways: nightmares, flashbacks, or intrusive and distressing thoughts about the event; or intense emotional distress or physiological reactivity when reminded of the event. Second, the individual must have three of the following avoidance symptoms: avoidance of thoughts or feelings related to the trauma, avoidance of trauma reminders, psychogenic amnesia, emotional numbing, detachment or estrangement from others, decreased interest in leisure activities, or a sense of foreshortened future. Third, the individual must experience two of the following arousal symptoms: difficulty falling or staying asleep, difficulty concentrating, irritability or outbursts of anger, hypervigilance, or an exaggerated startle response. To meet diagnostic criteria for PTSD, the symptoms must cause significant impairment in daily functioning. These criteria provide a good operational definition of PTSD, as they describe the symptoms seen in most cases. However, the three categories of symptoms are not empirically validated as distinct symptom clusters. For instance, it is not clear that the symptoms of behavioral avoidance and emotional numbing are similar and belong in the same category.

The ICD-IO criteria for PTSD also include some reexperiencing symptoms (nightmares, flashbacks, distress on exposure to reminders), actual or preferred avoidance of trauma reminders, and either an inability to recall important aspects of the trauma or sustained psychological sensitivity and arousal (sleep disturbance, hypervigilance, difficulty concentrating). These three criteria must all be met within 6 months of the traumatic event for a diagnosis to be given.

Several differences between the two definitions can be identified. First, the DSM-IV specifies a minimal number of symptoms that need to be observed to receive the diagnosis, whereas the ICD-IO leaves more freedom for clinical judgment. The advantage of the former approach is its utility in clearly operationalizing the concept of PTSD. The disadvantage is its rigidity and the possibility that one symptom can determine diagnostic membership. Second, the ICD-IO does not recognize the numbing symptoms, which together with flashbacks and nightmares are thought to be cardinal features of PTSD. Third, arousal symptoms are optional in the ICD-IO but are required in the DSM-IE Clinical observation and theoretical accounts of PTSD support the importance of these symptoms and render the ICD-IO diagnostic criteria less satisfactory.

C. Course of PTSD

The course of PTSD is variable. For the majority of individuals, symptoms begin immediately after the trauma, although some appear to have a delayed reaction. During the first 3 months after the trauma, the individual is said to have acute PTSD, whereas chronic PTSD is defined as symptoms persisting beyond 3 months. Symptoms can fluctuate over time between diagnosis of PTSD, subthreshold symptoms, and few or no symptoms. Recovery is affected by a number of factors, including perception of oneself and one’s surroundings, actual social support, life stress, coping style, and personality.

II. Measures of PTSD

A number of measures have been developed to assess PTSD, including clinical interviews and self-report instruments. These measures vary widely in terms of the target symptoms, administration time, and the samples used for ascertaining psychometric properties. Adult assessment tools are reviewed in the next section. Although some measures have also been developed for children, they are outside the scope of this paper.

A. Interviews

The Structured Clinical Interview for DSM (SCID) is believed to be the most widely used diagnostic interview. Its major disadvantage, however, is that it does not provide a measure of symptom severity. Several other interviews that provide information of both diagnostic status and symptom severity are available. Two interviews are becoming quite widely used in PTSD research. The first is the Clinician-Administered PTSD Scale (CAPS) that yields separate scores for frequency and intensity for each symptom. Disadvantages of this interview include a long administration time and validation on military veterans only. The second interview, the PTSD Symptom Scale Interview (PSS-I), includes a combined frequency/severity rating for each of the 17 PTSD symptoms in the DSM-IV and thus yields both a diagnosis and a continuous severity rating. Unlike the CAPS, the PSS-I takes only about 15 to 20 minutes to administer and was validated on female assault victims.

B. Self-Report Measures

Several self-report scales have been developed to assess symptoms of PTSD. The first was the Revised Impact of Events Scale (RIES), which yields two factors: intrusion and avoidance. A revised version of the RIES added hyperarousal items, but has shown mixed results in reliability studies and, like its predecessor, does not correspond fully to the DSM-IV PTSD symptoms. Two scales, the Mississippi Scale and the Penn Inventory, have excellent psychometric properties in veteran samples but do not provide information about diagnostic status because they do not fully correspond to the DSM-IV defining symptoms.

The PTSD Symptom Scale-Self-Report (PSS-SR) and its successor, the PTSD Diagnostic Scale (PDS), provide information about each of the 17 DSM-IV symptoms, yielding both diagnostic and severity information. The PDS is the only self-report instrument that assesses all DSM-IV criteria, including information about the nature of the traumatic event and the level of functional interference, in addition to information about PTSD diagnosis and symptom severity. It was validated in a sample of victims of a wide range of traumas and evidenced sound psychometric properties, and thus can be used in studies of various trauma populations.

III. Prevalence of PTSD

Lifetime prevalence of PTSD in the general population is estimated at 9%, with up to a third of these cases having chronic PTSD. Among trauma victims, the rate is much higher, estimated at 24 %. However, the rates of PTSD tend to vary considerably among different types of trauma. For instance, estimates of the lifetime prevalence of PTSD in Vietnam War veterans range from 27 to 65%; in civilian populations exposed to terrorism and torture, prevalence ranges from 33 to 54%. Between 35% and 94% of victims of violent assaults manifest PTSD. In contrast, accidents and natural disasters appear to produce lower rates of PTSD, 4.6 to 59%, depending on the event studied and the degree of exposure. Even individuals with little or no direct exposure to the trauma can develop PTSD; this phenomenon has been referred to as the “ripples outward” effect. Importantly, certain occupations are at risk for PTSD by virtue of increased probability of repeated direct exposure to trauma; between 9% and 26% of professionals such as police, nurses, and firefighters develop PTSD in reaction to stressors experienced on the job.

Prevalence in certain vulnerable populations is much higher than in the general population, presumably because individuals in these groups have been exposed to more traumatic experiences. These include populations seeking outpatient psychotherapy and those in substance abuse clinics. Women appear to be somewhat more likely than men to develop PTSD after trauma, 10.4 % versus 5 %, respectively. As noted earlier, the prevalence of emotional difficulties after mass traumas, such as refugee camp experiences or holocausts, has not been systematically studied.

IV. Vulnerability and Resiliency Factors in PTSD

Factors implicated in posttrauma reactions can be divided into three categories: pretrauma variables, variables related to the trauma itself, and posttrauma variables.

Research on pretrauma demographic variables has not identified reliable predictors of who will develop chronic PTSD with one exception: women are somewhat more likely to manifest PTSD than men after experiencing a similar trauma. In contrast, it appears that poor psychological and social functioning prior to the trauma renders the individual vulnerable to developing chronic symptoms. For instance, prior hospitalization and a history of drug abuse were found to be associated with a more severe posttrauma reaction. Also, a history of traumatic events in childhood or adulthood predicts a more severe response to a new trauma.

The nature of the trauma itself also appears to affect recovery. First, traumas differ in their likelihood of producing PTSD; rape, for example, is more likely to produce persistent symptoms than a natural disaster. Second, given a specific trauma (e.g., rape), injury and perceived threat of death produce more severe and persistent reactions.

Several posttrauma factors have been found to exacerbate symptoms. It appears that dissociation (emotional numbing, amnesia, depersonalization) shortly after a trauma hinders recovery. Also, on average, assault victims who exhibit more severe initial reactions to the trauma also show more symptoms later on. Thus, individuals seem to differ in how strongly they are affected by a similar trauma, and their initial reaction is associated with later psychopathology.

Evidence on the role of social support as facilitating or hindering recovery is equivocal. It seems that negative reactions from others, such as blame, increase posttrauma psychopathology, but, unfortunately, positive reactions do not show the expected positive effects. Excessive anger or guilt after the trauma also appears to block readjustment. Additional longitudinal research on the factors that promote resilience to trauma are clearly needed.

V. Concomitant Problems Following Trauma

Traumatized individuals not only exhibit ASD or PTSD symptoms, but also depression, substance abuse, anxiety, dissociation, and physical health problems.

The rate of use and abuse of drugs and alcohol, including nicotine, in traumatized individuals is higher than in the general population. There are at least two explanations for this finding. First, traumatized individuals may choose to cope with their symptoms by increasing substance use. Second, substance abuse may increase the risk of being exposed to a traumatic experience.

Many individuals report symptoms of depression after a traumatic event, such as sadness, lack of energy, diminished interest in leisure activities, hopelessness, sleeplessness, and eating disturbances. Although some of these symptoms overlap with the defining symptoms of PTSD (e.g., markedly diminished interest in activities), the two disorders are separate entities and both can develop independently as a response to a traumatic experience.

The incidence of comorbid anxiety disorders is also elevated among individuals with PTSD. For example, lifetime comorbidity of panic disorder in Vietnam veterans with PTSD was 21% in females and 8% in males, versus 1.5 to 3.5% in the general population. The lifetime prevalence of obsessive-compulsive disorder was found to be 13% in females and 10% in males, as compared with 2.5 % in the general population.

There is a greater frequency of physical health problems among trauma victims than in the general population, especially among those who develop chronic PTSD. Trauma victims have higher rates of gastrointestinal disorders and pelvic or abdominal pain, and visit the doctor more often than the general population. In the aftermath of rape and child sexual abuse, gynecological and psychosexual problems such as vaginal discharge, dysmennorhea, dyspareunia, vaginismus, and pelvic pain have also been noted.

VI. Theories on the Development and Maintenance of PTSD

Reactions to trauma have long captured the interest of theorists of psychopathology. Janet’s 1889 theory of reactions to trauma has influenced both early and contemporary conceptualizations. Janet proposed that when confronted with a traumatic event that besieges the victim with an overabundance of intense thoughts and feelings, too numerous or intense to integrate, some individuals selectively attend away from the trauma to trauma-irrelevant thoughts and feelings. Thus, ideas related to the trauma remain split off or dissociated from normal consciousness and become “fixed.” Although out of consciousness, these “fixed ideas” remain part of the victim’s ideational content, and therefore continue to exert influence over his or her thought, mood, and behavior in the form of fragmented reliving of the trauma such as visual images, somatic states, emotional conditions, or behavioral reenactment.

A. Psychoanalytic Theories

Freud wrestled with understanding the influence of traumatic experiences on the individual’s psyche. In early writings, he was influenced by Janet’s theory on the strength of the emotional reactions that are produced by a traumatic experience and that force the victim to become fixated on the trauma. Later, Freud abandoned the dissociation view and proposed that the persistence of trauma reactions reflects an association between the traumatic event and childhood repressed conflicts, ideas, or impulses, and the efforts to prevent conscious awareness of them. He also coined the concept of “repetition compulsion” to explain trauma reexperiencing, proposing that because of the need to keep it away from consciousness, the individual is forced to repeat aspects of the trauma as a contemporary experience rather than as a memory of it. Influenced by World War I experiences, Freud refocused on the external reality, and, in the spirit of Janet, viewed the emotional upheaval generated by the trauma as the source of traumatic neurosis. He suggested that the intensity of the trauma, the inability to find conscious expressions for it, and the unpreparedness of the individual cause a breach to the stimulus barrier and overwhelm the defense mechanisms. More recent theorists have proposed that the developmental level and ego resources available to the victim are central to the manner in which the trauma is experienced and to the production of symptoms. For instance, a young child, easily overwhelmed and flooded with emotion, may experience complete helplessness in the face of trauma, whereas a mature adult would be more likely to respond through emotional numbing and cognitive constriction. Psychoanalytic theorists and practitioners focus on the need to help the victim acknowledge and bear the trauma and the resulting psychic damage, and develop coping mechanisms such that the memories of the trauma are incorporated into his or her current experience.

B. Cognitive and Behavioral Theories

Several schools of thought inspired cognitive-behavioral theories of PTSD. The first is learning theory, which explains PTSD symptoms in terms of instrumental and classical conditioning. The learning model that most directly influenced cognitive-behavioral treatments (CBT) aimed at anxiety reduction was Mowrer’s two-factor theory. First, Mowrer proposed that fear is acquired through classical conditioning, where a neutral stimulus comes to evoke fear through its pairing with an aversive stimulus. Applying this theory to explain PTSD symptoms, neutral stimuli (e.g., supermarket) that were present during the trauma are presumed to acquire the ability to elicit fear through their associations with the danger stimuli (e.g., gun). Through the processes of generalization and second-order conditioning, stimuli similar to those present during the trauma also come to evoke fear. For instance, the stimuli all men, being alone, and the word rape can all acquire the capacity to cause anxiety. In Mowrer’s second stage, avoidance behavior is established through the process of operant conditioning. That is, an individual learns to reduce trauma-related anxiety through avoidance of, or escape from, the feared stimuli. Escape and avoidance behaviors are negatively reinforced because avoidance diminishes the aversive fear state.

Cognitive-behavioral therapy of PTSD has also been influenced by cognitive theory. Cognitive theory assumes that the interpretation of events, rather than events themselves, underlies emotional reactions. Accordingly, an event can be interpreted in different ways and consequently can evoke different emotions. Aaron Beck and colleagues suggest that trauma victims who manifest chronic persistent anxiety are unable to discriminate between safe and unsafe signals, and consequently their thinking is dominated by the perception of danger. They also suggest that traumatic fear can be maintained through a sense of incompetence to handle stressful events.

Other cognitive theorists have postulated that cognitive schemas are disrupted after victimization. A schema is a meaning structure that guides the perception, organization, and interpretation of incoming information. Common to these theories is the supposition that a traumatic experience requires cognitive modification and that such modification is accomplished by assimilation and accommodation. Accordingly, the victim must either assimilate the traumatic experience into preexisting schemas, or, more often, change schemas to accommodate the traumatic experience. In her 1992 book, Janoff-Bulman took the position that people in general hold the assumptions: “the world is benevolent, the world is meaningful, and self is worthy,” and these assumptions are incompatible with a traumatic experience. Building on Janoff-Bulman’s ideas, other theorists suggest that the following areas are of particular relevance: safety, dependency/trust of self and others, power, esteem, intimacy, and independence.

Coming from the psychoanalytic tradition, Horowitz integrated psychoanalytical and information processing notions in his 1986 book, suggesting that people have a basic need to match trauma-related information with their “inner models based on old information.” The process of recovery entails the repeated revision of both trauma-related information and the inner models until they agree, which Horowitz referred to as the “completion tendency.”

Foa and Kozak integrated cognitive and learning theories to explain the development and maintenance of pathological anxiety in what they called emotional processing theory. In their 1986 paper, fear is conceived as a cognitive structure or a program for escaping danger which includes representations of fear stimuli, fear responses, and their meaning. Pathological fear, they suggested, is distinguished from normal fear in that it includes erroneous associations and evaluations. Emotional processing theory views anxiety disorders as representing distinctive fear structures in memory, and the persistence of anxiety symptoms is conceived as reflecting impairment in emotional processing. Accordingly, PTSD is construed as reflecting a fear memory that contains erroneous associations and evaluations, whereas a normal trauma memory reflects associations and evaluations that better match reality. First, a pathological PTSD structure contains excessive response representations that are reflected in the PTSD symptoms. Second, this structure includes erroneous stimulus-stimulus associations that do not accurately represent the world. For example, the pathological fear structure of a woman who was raped at gunpoint by a bald man would contain an association between “bald men” and “gun.” In reality, however, bald men are not more likely to carry guns or to rape than men with a full head of hair. Third, the structure also includes erroneous associations between harmless stimuli such as “bald,” “home, …. suburbs,” and the meaning of “dangerous.” Being raped one time while at home in the suburbs does not tangibly increase the chance of encountering violence in that environment. Fourth, the structure includes erroneous associations between harmless stimuli and escape or avoidance responses. For example, the victim who was raped by the bald man would tend to run away from such men. In reality, however, running away from “bald men” is not likely to enhance safety. These erroneous associations would lead to mistakenly interpreting the world as entirely dangerous.

Another set of erroneous associations and evaluations is the interpretation of the victim’s response representations. It is thought that the victim’s responses during and after the trauma, and in particular the PTSD symptoms, are interpreted to mean self-incompetence. In summary, emotional processing theory hypothesizes that two major pathological concepts underlie PTSD: the world as entirely dangerous, and the self as entirely inept.

C. Psychobiological Approaches

Psychophysiological, neurohormonal, neuroanatomical, and immunological changes have been observed in animals exposed to extreme stress and in trauma victims who developed PTSD (van der Kolk, McFarlane, & Weisaeth, 1996). These changes have been hypothesized to disregulate responses to incoming information and to inhibit successful processing of traumatic memories.

The normal stress response upon exposure to a high-magnitude stressor is a complex neurohormonal response, including the release of catecholamines (e.g., epinephrine and norepinephrine), serotonin, endogenous opioids, and hormones of the hypothalamus, pituitary, or adrenal gland (e.g., cortisol, vasopressin, oxytocin). Normally, the introduction of a stressor produces intense and rapid stress responses, and these dissipate quickly after the removal of the stressor. However, after prolonged exposure to stress, the stress responses become disregulated.

Theorists propose that PTSD reflects a failure to regulate autonomic reactions to stimuli such that the individual either experiences hyperreactivity or “shutting down” and emotional numbing. Individuals with PTSD show hyperreactivity, as measured by heart rate, skin conductance, and blood pressure, in reaction to reminders of traumatic events. This disregulation of the emotional and physiological responsiveness occurs with specific reminders of the trauma as well as in reaction to intense but neutral stimuli, signifying a loss of stimulus discrimination. In addition, the individual may come to fear his or her emotional reactions because of being able to do little to control them.

Neurohormonal changes in individuals with PTSD have also been found. First, prolonged stress causes depletion of the noradrenergic system, such that receptors become hypersensitive to any new release of norepinephrine. This noradrenergic hyperreactivity is linked to the increased arousal and startle of PTSD. The high levels of norepinephrine are proposed to inhibit the release of corticotrophin-releasing hormone and thereby inhibit the entire hypothalamic-pituitaryadrenocortical axis. This inhibition, in turn, produces a deficiency in endogenous opioids. Some theories postulate that the reexperiencing symptoms of PTSD cause a burst in the release of endogenous opioids and therefore make up for this deficiency. These endogenous opioids are thought to produce an artificial numbing or calmness, another hallmark of PTSD. Additional theories propose that cortisol responses are lowered in retraumatized individuals and that serotonin levels may decrease in response to prolonged inescapable stress.

In addition to psychophysiological and neurohormonal factors, specific brain abnormalities have recently been detected in individuals with PTSD. One system that is implicated in the disorder is the limbic system, which is thought to function in memory and in emotional reactions to incoming stimuli. One area in the limbic system, the hippocampus, is presumed to record spatial and temporal aspects of experiences in memory. Researchers have noted decreased hippocampal volume in trauma victims with PTSD compared with those without PTSD. One possible explanation for this finding is that individuals with smaller hippocampuses are more likely to develop PTSD; a more likely interpretation of these results is that increased cortisol activity causes shrinkage, because cortisol is toxic to the hippocampus.

A second area in the limbic system, the amygdala, also appears to be altered in individuals with PTSD. The amygdala is thought to assign meaning to incoming stimulation by integrating memory images with emotional experiences associated with those memories, guiding emotional behavior. A single intense stimulation of the amygdala appears to alter the limbic physiology such that a “kindling” effect occurs. That is, the behavior that follows may be predominantly either “fight” or “flight,” and a pattern of conditioned behavior is set up such that there is limited processing of incoming information before the response is initiated.

VII. Psychological and Pharmacological Interventions in PTSD

Several psychological interventions have been used with trauma victims, including supportive counseling individually or in groups, brief dynamic psychotherapy, hypnotherapy, pharmacotherapy, and cognitivebehavioral therapy. As recently reviewed by Foa and Meadows, although a variety of psychological interventions are used routinely with trauma victims, controlled outcome studies have tended to focus on cognitive-behavioral treatments such as systematic desensitization, exposure, and anxiety management. Nevertheless, hypnotherapy and psychodynamic therapy have also shown promise in the few studies examining their efficacy.

A. Early Interventions

The popular supposition among trauma theories is that for recovery to occur after a traumatic experience, special processing efforts should take place. This view has prompted the development of early intervention programs. These programs have focused on education, debriefing after trauma, and training professionals at risk (e.g., police). Usually, “critical incident stress debriefing” is conducted in groups, such as emergency workers, and focuses on education about common reactions to traumatic experiences, encouraging trauma victims to process their experiences in a group setting. Although such programs have become routine in many places, little is known about their efficacy. In fact, some experts have raised concerns that such programs could interfere with rather than facilitate the natural recovery process.

The recognition that victims who exhibit severe reactions immediately after the trauma are more likely to develop chronic dysfunction has prompted researchers to implement interventions that aim to prevent chronic PTSD. Foa and colleagues conducted a study to compare PTSD severity of female assault victims, who received a brief prevention program (four individual therapy sessions), to that of victims who underwent an assessment procedure. Victims who received the brief prevention program had less severe PTSD and depressive symptoms 2 months after the assault. Clearly, more studies of this type are needed before confidence in prevention efforts can be established.

B. Cognitive-Behavioral Therapies

Currently, five cognitive-behavioral interventions are in use for PTSD: Prolonged Exposure, cognitive therapy, Stress Inoculation Training, Cognitive Processing Therapy, and Eye Movement Desensitization and Reprocessing.

1. Prolonged Exposure (PE)

This is a set of procedures that involves confrontation with feared stimuli, either in vivo or in imagination. With PTSD, exposure therapy typically includes repeated reliving of the traumatic event in imagination and actual confrontation with feared situations and objects that have been avoided because they are reminders of the trauma but are not intrinsically dangerous.

As discussed earlier, the theoretical basis of PE lies in learning and emotional-processing theories. Foa and Kozak have proposed that successful therapy involves correcting the pathological elements of the fear structure, and that this corrective process is the essence of emotional processing. They further suggest that regardless of the type of therapeutic intervention used, two conditions are required for fear reduction. First, the fear structure must be activated through introduction of fear-relevant information. If the fear structure is not activated (fear is not evoked), the structure would not be available for modification. Second, during exposure, information that is incompatible with the existing pathological elements (e.g., fear reduction) must be provided so that the pathological fear structure can be corrected. Specifically, exposure researchers hypothesize that repeated reliving promotes several cognitive changes. First, it promotes habituation of anxiety associated with the trauma memory, and this habituation disconfirms the victim’s erroneous belief that anxiety will stay forever and therefore lead to disastrous consequences. Second, reliving promotes discrimination between “remembering” the trauma and “encountering” it again, thus reinforcing the realization that remembering itself is not dangerous. Third, repeated exposure promotes differentiation between the trauma and similar but safe situations, disconfirming the idea that the world is extremely dangerous. Fourth, it promotes the association between PTSD symptoms and a sense of mastery, rather than incompetence. Finally, repeated recounting of the trauma narrative helps to organize the narrative and thereby to facilitate the integration of the trauma memory.

Several controlled studies on exposure have shown their usefulness in treating PTSD. Whereas studies on veterans showed only modest improvement, two studies with female rape victims showed more improvement. Foa and colleagues found that exposure (imaginal and in vivo) was effective in eliminating PTSD in 55% of rape victims with chronic PTSD compared with 45% of those who received supportive counseling. Superior results were found in a second study: about 70% of victims who received Prolonged Exposure lost their PTSD diagnosis, and none of the women in a wait-list group lost their diagnosis. These treatment effects were maintained at 6-month follow-up.

2. Stress Inoculation Training (SIT)

This intervention consists of training victims to handle anxiety with several skills for anxiety management: relaxation, thought stopping, assertiveness, cognitive therapy, coping self-statements, and guided imagery. Although the direct goal of anxiety management techniques is to teach patients techniques to manage their anxiety, the successful acquisition of such techniques can have indirect effects on the victim’s schemas of self and the world. Specifically, the victim’s experience of being able to control the anxiety fosters a more positive self-image and thereby modifies the perception of the world as overwhelmingly dangerous. Several studies point to the efficacy of this program used alone or in combination with other techniques. For example, the two studies on rape victims reported earlier found that SIT significantly reduced PTSD, to a degree comparable to that of exposure.

Researchers believed that if PE and SIT are quite, but not completely, successful in ameliorating PTSD symptoms, a program that combined these two treatments would yield superior results. However, research does not support this view: combined programs were helpful for female assault victims, but not more than exposure or stress inoculation alone.

3. Cognitive Therapy

Cognitive techniques are often incorporated into anxiety management programs that teach patients to examine and change systematically maladaptive thoughts that can lead to negative responses. Cognitive therapy involves the use of discourse, in which the patient is taught to identify the beliefs underlying the fear, to examine whether they are distorted or accurately reflect reality, and to replace mistaken or dysfunctional beliefs with more realistic, functional ideas about the ability of the patient to cope with stress and the dangerousness of the world. One possible benefit of cognitive restructuring is that it addresses directly beliefs underlying emotions other than fear, such as anger and guilt. Early investigations of this technique revealed some promise in the use of this therapy to reduce symptoms of PTSD in rape victims.

4. Cognitive Processing Therapy (CPT)

Another cognitive-behavioral program called Cognitive Processing Therapy is described in Resick and Schnicke’s 1992 book. It involves cognitive restructuring and exposure through writing about the trauma. The cognitive therapy is geared toward correcting maladaptive cognitions associated with rape, such as power, safety, and esteem. In one study, on the average, victims who received CPT reported 40% symptom reduction, and these gains were maintained over time. More studies are needed to establish the efficacy of this relatively new treatment.

5. Eye Movement Desensitization and Reprocessing (EMDR)

This therapy, described by Shapiro in 1995, is a form of exposure with a cognitive emphasis, accompanied by guided eye movements. The studies that have evaluated the efficacy of this treatment produced equivocal results. Some show good results, but others show no improvement. Because these studies have many methodological problems, it is difficult to determine the validity of the findings. Further well-controlled studies are needed before a definite conclusion about the value of EMDR can be made.

C. Pharmacotherapy

Many medications have been used for the treatment of PTSD, but only a few have been systematically studied. Most of these have used male combat veterans, and thus the efficacy of pharmacotherapy for other traumatized populations is largely unknown. Tricyclic antidepressants have been used in an attempt to reduce locus coeruleus overactivity and noradrenergic disregulation found in PTSD, with equivocal results. Amitriptyline and imipramine have shown modest reductions in PTSD symptoms in comparison with placebo in double-blind studies with male veterans. In contrast, desipramine failed to show efficacy. One study of fluoxetine, a selective serotonin reuptake inhibitor used to regulate serotonergic dysfunction in individuals with PTSD, found it to be effective in reducing symptoms of PTSD, especially in trauma victims other than Vietnam veterans.

Other medications that have been tested include anticonvulsants such as carbamazepine and valproic acid; but no double-blind studies have been conducted to date. Beta-adrenergic blockers such as propanolol have shown promise in reducing aggressivity and arousal symptoms in open studies, and alpha2-adrenergic agonists, such as clonidine, appear to be effective through their suppression of locus coeruleus activity.

Finally, benzodiazepines have been widely used to suppress anxiety and are believed to reduce PTSD symptoms by reducing limbic system kindling and reversing neurochemical changes in the locus coeruleus and hypothalamus. However, the rebound anxiety and withdrawal symptoms associated with benzodiazepines can be problematic.

In summary, most of our knowledge about efficacy of pharmacotherapy for PTSD is confounded by the restricted samples used in existing studies. Most were conducted on Vietnam veterans, whose symptoms are particularly resistant to all types of treatments, and therefore the present results may underestimate the efficacy of this treatment.

D. Hypnotherapy and Psychodynamic Psychotherapy

Hypnotherapy uses heightened concentration and focused attention to facilitate treatment related to trauma. It is based on the supposition that individuals with PTSD are unknowingly entering trance states when they reexperience the trauma and that hypnotherapy can help them learn how to control their trance states and digest the dissociated traumatic experience in a controlled manner. One study found hypnosis to be as effective as psychodynamic psychotherapy and a type of exposure called systematic desensitization. More studies of this technique are needed before conclusions can be drawn about the usefulness of hypnotherapy.

Psychodynamic psychotherapy has also been used to help individuals recover from trauma. It focuses on intrapsychic conflict about the trauma rather than on resolution of specific symptoms of PTSD. The methods used are in some respects similar to those used in cognitive-behavioral therapy, as these interventions focus on helping the victims process the traumatic experience and on teaching them how to tolerate anxiety. Both individual and group therapies have been used, and some preliminary studies suggest the utility of these interventions.

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