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Psychosomatic Medicine:
Original Article

Treatment of Posttraumatic Stress Disorder: A Review

Shalev, Arieh Y. MD; Bonne, Omer MD; Eth, Spencer MD

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From the Center for Traumatic Stress, Hadassah University Hospital, Jerusalem, Israel.

Address reprint requests to: Arieh Y. Shalev, MD, Center for Traumatic Stress, Department of Psychiatry, Hadassah University Hospital, P.O. Box 12000, Jerusalem, 91120, Israel.

Received for publication January 17, 1995; revision received August 10, 1995.

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Abstract

This article analyzes the literature on the treatment of posttraumatic stress disorder (PTSD).It briefly exposes the theoretical basis for each treatment modality and extensively examines pharmacological, behavioral, cognitive, and psychodynamic therapies, as well as group and family therapies, hypnosis, inpatient treatment, and rehabilitation. Articles were identified by scanning Medline and PsychLit for all papers in English reporting treatment of PTSD. Anecdotal case reports were, then, excluded. Eighty one articles were identified and categorized as either biological or psychological, with the latter category further divided into behavioral, cognitive, psychodynamic, and other treatment modalities. Information regarding the type of trauma, the sample studied, the treatment method, and the results of the treatment has been extracted from each article and is presented briefly. A synthesis of findings in each area is provided. Most studies explored a single treatment modality (e.g., pharmacological, behavioral). The cumulated evidence from these studies suggests that several treatment protocols reduce PTSD symptoms and improve the patient's quality of life. The magnitude of the results, however, is often limited, and remission is rarely achieved. Given the shortcoming of unidemnsional treatment of PTSD, it is suggested that combining biological, psychological, and psychosocial treatment may yield better results. It is further argued that rehabilitative goals should replace curative techniques in those patients with chronic PTSD. A framework for identifying targets for each treatment modality is presented.

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INTRODUCTION

During the past 300 years, a variety of terms have been applied to the mental sequelae of severe trauma, including: Nostalgia, Soldier's Heart, Railway Spine, Shell Shock, Combat Neurosis, and Combat Fatigue. Each of these names reflected a theoretical view of the cause of mental trauma (e.g., homesickness, mechanical impact, exhaustion, mental conflict) and its nature (neurosis, dysregulated circulation). The current appellation, posttraumatic stress disorder (PTSD) ([1]), points to our current belief in stress as a cause of mental disorders.

In its most recent definition ([1]), PTSD is a pervasive anxiety disorder that follows exposure to stressful events. DSM-IV diagnostic criteria for PTSD ([1]) include: a) exposure or confrontation with a traumatic event accompanied by intense fear, helplessness, or horror; b) persistent reexperiencing of the traumatic event, expressed by at least one of the following: recurrent and intrusive distressing recollections of the event, recurrent distressing dreams, acting or feeling as if the traumatic event were recurring, distress on exposure to cues that symbolize or resemble an aspect of the event, and physiological reactivity on exposure to cues that symbolize or resemble the trauma; c) avoidance of stimuli associated with the trauma and numbing of general responsiveness, expressed by: efforts to avoid thoughts, feelings, or conversations associated with the trauma, efforts to avoid activities, places, or people that arouse recollections of the trauma, inability to recall an important aspect of the trauma, markedly diminished interest in previously significant activities, feeling of detachment or estrangement from others, restricted range of affect, and sense of a foreshortened future (three symptoms required); and d) persistent symptoms of increased arousal, such as difficulty falling or staying asleep, irritability or outbursts of anger, difficulty concentrating, hypervigilance, or exaggerated startle response (two symptoms required). The duration of the disturbance must exceed 1 month, and it should be associated with significant distress or impairment.

Several features of PTSD attest to its inherent complexity: a) Instances of recovery from PTSD regularly occur during the first year of its course ([2]), and 15 to 25% of the survivors of severe traumatic events may suffer from a chronic PTSD ([3,4]); b) PTSD is among the few disorders for which DSM-IV specifies a cause (i.e., the traumatic event). Yet, this requirement implicitly equates common incidents, such as road traffic accidents, with prolonged war exposure or colossal atrocities, such as the Holocaust; c) classified among the anxiety disorders, PTSD has also been considered for inclusion among the dissociative disorders or as part of a separate category of "stress disorders" ([5]); and d) the core clinical features of PTSD, namely reexperiencing and avoidance, closely resemble those observed during normal grief ([6,8]) thereby suggesting that PTSD symptoms may reflect an attempt to deal with the meaning of the trauma and the associated loss. Yet, a strong component of learned conditioning seems to underlay PTSD, and behavioral interventions effectively ameliorate both avoidance and intrusion symptoms in PTSD ([9-11]). Finally, neurobiological research ([12]) offers pertinent insights into the pathophysiology and pathogenesis of this "psychogenic" disorder.

Unlike other disorders, such as major depression, obsessive compulsive disorder (OCD), schizophrenia, or phobias, for which one treatment modality has emerged as being uniquely effective (e.g., antidepressants, specific serotonin reuptake inhibitors (SSRIs), neuroleptics, and desensitization, respectively), PTSD has no such prominent treatment. Given its complexity and given the lack of specific therapy, one may argue that a reasonable approach to the treatment of PTSD involves a multi-dimensional model. Discontent with the therapeutic results of unidimensional treatment approaches ([13,15]) further supports this argument. Barlow ([15]) proposed one such complex model of PTSD, which includes consideration of the role of biological and psychological vulnerabilities, negative life events, fear reactions, perceptions of control, social support, and coping strategies.

In a previous article ([16]), we proposed, on a basis of clinical vignettes, a four-level model based on Engel's ([17]) "biopsychosocial" paradigm. The biological level of this model refers to alterations in neuronal functioning that may be expressed, in affected individuals, as a result of their traumatic exposure. The psychological-behavioral level involves conditioned fear responses acquired during the trauma and reinforced thereafter. The next level incorporates altered networks of meanings as reflected in profound changes in self-concept and interpersonal relations that follow trauma. Finally, the social level includes real and symbolic interactions between the individuals and the society that are involved in the acquisition and maintenance of the trauma, as well as the healing from trauma. Although each of these four interacting levels is a potential target of a specific treatment approach, we have argued that a combined treatment approach, addressing several of these layers, is particularly appropriate for PTSD.

This article expands the multi-level paradigm by critically reviewing the main explanatory models of PTSD and the related literature on treatment of the disorder. We also examine the idea that the neurobiological imprint of psychic trauma may become indelible, such that rehabilitation rather than the curative approach is often indicated.

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THE BIOLOGICAL APPROACH TO PTSD
Biological Formulation and Research

Research into the psychobiology of PTSD has followed two paths. The first consists of a search for commonalties among biological findings in PTSD and those in other mental disorders, and the second involves a quest for specific attributes of PTSD.

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Similarities Between PTSD and Other Mental Disorders

Comorbid panic disorder was found in 13 to 19% of PTSD patients ([18,19]). In other PTSD patients, sudden arousal on exposure to cues reminding the patient of the trauma bears phenomenological resemblance to panic anxiety ([20]). Further, anxiety, dissociation, and flashbacks can be elicited in PTSD patients by experimental procedures that provoke panic attacks in patients with panic disorder (e.g., administration of yohimbine or lactate) ([20,21]). Theoretical formulations based on this analogy assign a role to the locus ceruleus-norepinephrine (LC-NE) "alarm" system in PTSD ([12,21]) and predict a positive effect of anti-panic medication on PTSD symptoms.

Major depression is frequently co-diagnosed in PTSD patients ([22,23]). Depressive symptoms resemble DSM-IV PTSD symptoms of "diminished interest," "restricted range of affect," and "sense of foreshortened future." Treatment and modalities based on that relationship involve antidepressants and MAO inhibitors.

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Specific Biological Attributes of PTSD

Among the "specific" models of PTSD are: a) dysregulation of opioid neuromodulation, b) imprinting and consolidation of traumatic memories, and c) hypothalamic-pituitary-adrenal (HPA) axis dysregulation.

During stress, opioid neuromodulation is responsible for phenomena such as stress-induced analgesia and amnesia ([24]). The "opioid" model of PTSD ([24]) further expands the role of opioides into the chronic condition, suggesting that the presence of distressful and repetitive behavior in PTSD, such as self-inflicted pain, reexposure to danger, or emergence of distressful recollection of the trauma, is due to an inappropriate release of endogenous opioides during adversity. Partial support for this view was provided by a study showing that naloxone, an opiate antagonist, reverses stress-induced analgesia in PTSD ([25]).

The memory imprinting model assumes that the "etching" of traumatic experiences into a neuronal network plays a major role in the etiology of the disorder. Earlier formulations ([26,27]) theorized that stress hormones, secreted during the traumatic event, may mediate the consolidation of traumatic memories. A recent observation ([28]) suggests, indeed, that inhibition of beta-adrenergic transmission by propranolol, during exposure to distressful and neutral audio-visual narratives, reduces the number of distressful items remembered. The relevance of these findings to conditions of extreme stress requires further study.

Emotional memory is of particular interest in PTSD. In a series of animal studies, LeDoux ([29]) showed that the acquisition of fear conditioning is mediated by a dual neuronal pathway that involves a subcortical path, which includes the sensory thalamus and the lateral and central nuclei of the amygdala, and b a thalamocortical path, involving the sensory cortex and similarly leading to the amygdala. Lesions to the cortical pathway, however, did not interfere with the acquisition of conditioned fear. Moreover, such lesions prevented the extinction of fear conditioning thereby suggesting that, in the absence of cortical inhibition, emotional memories may be stored "forever" at subcortical levels of the brain. Clinical features of PTSD (e.g., reactivation of recovered PTSD patients on exposure to new traumata or in aged veterans, delayed onset of PTSD (e.g., ([30-32])) are consistent with the concept of indelible memory: harnessed, but never deleted. Successful treatment of PTSD, accordingly, may not involve an eradication of traumatic memories but rather an enhanced control over previously acquired fear responses.

A variation on the memory imprinting theme is the kindling model of PTSD ([33]). By analogy with the acquisition of kindled seizures in animals, this model postulates that the repeated processing of distressful recollections progressively decreases the threshold for neuronal transmission of similar signals up to the point of inducing an irreversible cycle of spontaneous repetitions. Animal studies have shown that such a process involves a cascade of functional and structural modifications (e.g., early and late gene expression, new protein synthesis, neuronal sprouting) leading to irreversible modifications of synaptic conductivity ([33]).

Important to note, this model extends the time interval for "traumatic imprinting" into the postexposure period. It implies that intense arousal, paired with external or internal cues of the trauma, during a critical period after the event induces neuronal changes that may later be expressed as PTSD. An association between secondary stressors (i.e., those that follow the impact phase of traumatic events) and long term psychopathology is also predicted by this model. Interventions aimed at reducing hyperarousal among recent trauma survivors (e.g., by comforting the patient or preventing further distress or by pharmacological agents) may, therefore, operate as secondary prevention.

Studies of the HPA axis have shown a decreased epinephrine/cortisol ratio, elevated urinary catecholamines, and an increased dexamethsone suppression in PTSD (e.g., [34-36]). Findings of enhanced feedback sensitivity of the HPA axis in PTSD are opposed to those observed in depression. Recently, elevated levels of serum-free triiodothyronine, thyroxin-binding globulin, and total thyroxin levels were found in PTSD ([37]), although findings of decreased thyroid function were reported in survivors of prolonged traumatization ([38]).

Animal research suggests that dopaminergic brain systems could be involved in PTSD ([12]). Preadministration of the dopamine agents, for example, prevents the acquisition of escape deficit (an equivalent of chronic surrender) after inescapable shock ([39]). Yehuda et al. ([40]) found an elevated urinary excretion of dopamine in PTSD, which correlated with PTSD symptom severity. This line of research has not been followed, and the effect of neuroleptics has not been studied systematically in PTSD.

Finally, findings of increased 5HT2 receptor affinity and a decreased number of platelet-binding sites in PTSD ([41]) imply that serotonergic neurotransmission may play a role in PTSD. Preliminary evidence ([42]) suggests that pretreatment paroxetine binding predicts the clinical responses to SSRIs in PTSD patients.

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Biological Treatment of PTSD

Reports of pharmacotherapy of PTSD include all of the families of psychotropic agents ([43-45]). Table 1Table 3summarizes the results of these reports.

Table 1
Table 1
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Table 3
Table 3
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Studies of antidepressants ([46-73]) suggest that these drugs sometimes improve PTSD symptoms of intrusion and avoidance as well as depression, insomnia, and anxiety. The magnitude of the therapeutic response, however, is far less than that obtained in major depression or panic disorder in that no study has shown full remission of PTSD symptoms, as is often the case in the major depression or panic disorder. Moreover placebo-controlled, double-blind studies ([46-48]) and an open trial ([50]) failed to demonstrate a major effect of antidepressants on PTSD symptoms of intrusion and avoidance. Recent studies of fluoxetine, sertraline, and paroxetine ([51-54]) suggest that SSRIs may ameliorate these symptoms to some extent. Van der Kolk's controlled study ([49]) has further shown that survivors of recent traumata (e.g., sexual abuse) benefit from fluoxetine more than Vietnam veterans, in whom fluoxetine did not reduce dissociation, hostility, or intrusion. Other studies imply that the effect of antidepressants on PTSD may be enhanced by lithium ([55]) and clonidine ([56]).

Studies of benzodiazepines have produced mixed results. One controlled investigation ([13]) failed to show a specific effect of alprazolam on PTSD symptoms of intrusion and avoidance, despite a modest effect on anxiety. An open study of clonazepam ([57]) describes, however, improved sleep and reduction in nightmares, flashbacks, and panic attacks. Severe withdrawal symptoms have been described in PTSD patients treated with alprazolam ([58]) whereas clonazepam has not been shown to cause severe withdrawal.

Mood stabilizers such as lithium, sodium valproate, and carbamazepine have been studied in open trials. The results indicate that these drugs reduce irritability and improve impulse control in PTSD ([59,60]). By virtue of their "anti-kindling" effects, clonidine, carbamazepine, and valproate have been touted as particularly promising in PTSD. However, among anti-kindling products, one must distinguish those that prevent the acquisition of kindled seizures (e.g., clonidine) from those that inhibit acquired kindled seizures (e.g., carbamazepine, valproate). The former may be considered for early preventive treatment of PTSD, and the latter may be useful in chronic PTSD.

Pharmacological studies of PTSD have numerous shortcomings. As shown in Table 1Table 3, there are few controlled studies, and the results of these studies are inconsistent. Most of the research has been conducted on male combat veterans with chronic PTSD. The length of potential remissions and the rate of relapse have not been studied. Comorbid personality disorders may create difficulties in compliance with treatment regimen in PTSD. Finally, the effect of early pharmacological intervention should be further examined.

Commentators ([43,45]) have opined that pharmacological treatment of PTSD may require prolonged periods before being effective. In an 8-week study, Davidson et al. ([48]) showed, in fact, that symptoms of anxiety, intrusion, and avoidance continue to improve between Week 4 and Week 8. Despite such improvement, however, the authors found no evidence for drug effects on the structured interview for PTSD. Furthermore, 64% of the amitriptyline group and 72% of controls still met diagnostic criteria for PTSD on completion of the study.

As suggested by previous reviewers (e.g., [45]), pharmacotherapy alone is rarely sufficient to cure PTSD. Many PTSD patients, however, find their symptoms intolerable, and some seek relief by self-medicating with alcohol or illicit drugs or by engaging in life-threatening behavior, including suicide ([73]). The relief provided from prescribed medication may reduce the tendency of PTSD patients to self-medicate, as well as the risk of violent behavior and suicide. Furthermore, symptom relief provided by medication may facilitate participation in psychotherapy ([16,45,60]).

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THE PSYCHOLOGICAL APPROACH TO PTSD
The Behavioral Model

The core behavioral conceptualization of PTSD identifies classic conditioning as the mechanism linking the symptoms of PTSD to the precipitating trauma. Subjects who originally react to a traumatic event (unconditioned stimulus (UCS)) with fear and arousal (unconditioned response (UCR)) will, according to this model, continue to show the same "conditioned" response (CR) to cues (conditioned stimuli (CS)) that have been paired with the stressful exposure.

Contrary to simple conditioning, however, the learned response (CR) in PTSD does not extinguish over time. To explain the lack of spontaneous extinction over time, Mowrer's ([74]) two-factor model was applied to PTSD ([75]). In this model, the initial "simple" conditioning (resulting in avoidance of cues immediately present during the trauma, such as combat sounds) is followed by operant conditioning, in which avoidance of a variety of internal and external cues that are loosely associated with the trauma (such as any memory of combat or any sound with similar properties) is rewarded by reduction in distress. The reinforcement of such avoidance would prevent the extinction of the conditioned response over time and expand the avoidant behavior to secondary and tertiary cues. Psychophysiological studies showing increased responses to cues reminiscent of the trauma have provided the necessary experimental support for the emotional conditioning construct ([76,77]).

Foa and colleagues' cognitive-behavioral model ([10,78,79]) integrates the meaning attributed to the trauma by the subject with conditioning. These authors considered the possibility that the perception of controllability and predictability and the subsequent attributions of threat are central to the development of the conditioned responses involved in PTSD. Such perceptions of the trauma should be addressed in therapy along with desensitization or flooding.

Behavior Therapy. Interventions based on behavioral theory are designed to undo CR to CS that have been paired with the trauma. Behavior therapy proceeds either by gradual (desensitization) or by massive (flooding) re-exposure to the CS. Another distinction is between live exposure (i.e., to real objects and situations) and imaginal exposure.

Four controlled studies indicated that flooding may reduce PTSD symptoms. Keane et al. ([80]) found a significant effect of flooding on reexperiencing, anxiety, and depression. Boudewyns and Hyer ([81]) showed that flooding positively affected adjustment in Vietnam veterans. Boudewyns and Hyer ([82]) also indicated that clinical improvement, regardless of treatment modality, is associated with a reduction in physiological responses to traumatic imagery. Cooper and Clum ([83]) described a positive interaction between flooding and interpersonal treatment. Foa et al. ([84]) compared a treatment condition combining behavioral and cognitive techniques, the stress inoculation therapy (SIT), with prolonged exposure (PE), counseling, and waiting list control. PE had greater efficacy in reducing PTSD symptoms at the 3.5-month follow-up. Other open studies are summarized in Table 2Table 4Table 5 ([85,86]).

Table 2
Table 2
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Table 4
Table 4
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Table 5
Table 5
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Contrasting with the above, Pitman et al. ([14]) reported an exacerbation of depression and panic anxiety, increased alcohol consumption, and mobilization of negative appraisal during flooding therapy. In 50 Vietnam veterans, Hyer et al. ([87]) similarly reported that 17 of 20 subscales of the Millon Clinical Multiaxial Inventory worsened after 5 weeks of exposure to revivified Vietnam experience.

Imaginal desensitization has been the object of three controlled trials ([11,88,89]) and several open studies ([90-92]). The treatment condition in Peniston's controlled study ([88]) was associated with reduction in nightmares, flashbacks, muscle tension, and readmission rates. Brom et al. ([89]) compared desensitization with brief dynamic therapy, hypnosis, and waiting list controls. All active treatments produced measurable improvement. In a recent study, Richards et al. ([11]) randomly assigned 14 civilian PTSD patients to either four sessions of imaginal exposure followed by four sessions of live exposure or the opposite sequence. Treatment sessions were followed by self-exposure homework assignment. Both protocols and both treatment modalities effectively reduced symptoms of PTSD, depression, fear, and general health, as well as work and social adjustment. The resulting improvement was of significant magnitude, reaching up to 60 to 85% of initial target behavior. Live exposure yielded more improvement on phobic avoidance. A follow-up evaluation, conducted 12 months later (N = 11), showed further improvement in most areas

In many patients, PTSD is the result of exposure to complex events, such as wars, torture, or captivity. Desensitization, however, is often limited to the results of a single event (e.g., a particular combat, a rape). The capacity of PTSD patients to extend their response to behavioral treatment to other traumata has been questioned. Two studies ([85,91]) evaluated physiological responses to mental imagery of the trauma before and after behavior therapy and showed that desensitization of one traumatic incidents does not extend to other traumatic incidents engendered by the same event. The usefulness of behavior therapy in survivors of prolonged traumatization requires, therefore, further studies.

A comprehensive study of live exposure ([93]) has assessed the effects of a complex rehabilitation and training program conducted by the Israel Defense Force 4 years after the 1982 Lebanon war in an effort to change the pervasive course of PTSD in veterans of that war. The program included a month-long exposure to military cues (e.g., rifle range, artillery fire) within a military milieu along with cognitive, behavioral, and supportive interventions. The study compared 40 participants of the program with 40 PTSD controls who did not participate using measures of PTSD, general psychiatric symptomatology, self-efficacy, and social and psychological adjustment. Within-individual changes, induced by the program, were also evaluated. The results showed that, immediately and 9 months after the program, participants in the program fared worse than controls and worse than their own initial scores. In another direct reexposure study, Scurfield et al. ([94]) used a "helicopter ride therapy" with Vietnam veterans with PTSD. That exposure was similarly associated with intrusive painful memories and "inflight reactions," but it improved group cohesion and provided a degree of desensitization. Contrasting with the rather negative results reported above are positive results of two studies (e.g., [11]) that addressed subjects with more recent PTSD.

Overall, studies of behavioral treatment in PTSD report a significant but partial improvement. Clearly, an undoing of a "conditioned response" is insufficient, thereby suggesting that the pathophysiology of PTSD encompasses more than learned conditioning. Moreover, direct exposure and flooding may result in reactivation and worsening of symptoms and behavior.

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Cognitive Formulations of PTSD

The cognitive view of PTSD ([79,95,96]) postulates that basic assumptions that normally underlie one's expectations, appraisal, and behavior may be revealed as inaccurate, insufficient, or inadequate by traumatic experiences. Such critical events may then lead to dysfunctional thinking and therefore to depression, anxiety, and PTSD.

Cognitive psychology (e.g., [79]) suggests that knowledge acquired throughout life is represented in memory in the form of knowledge structures (alias schemata) and that such structures inspire the encoding and the interpretation of new information. Cognitive schemata allow smooth adaptation to changing reality while preserving one's personal perspective and values. In healthy individuals, cognitive schemata can be modified by progressive assimilation of new experiences.

Traumatic events, in contrast, may be followed by a breach in previously held assumptions such that the novelty of the event sharply contrasts with previous schemata and can neither be adapted to nor be assimilated. For example, belief in one's personal strength may be replaced by a sense of extreme vulnerability. Belief in one's capacity to reasonably predict reality may turn into fearful expectation of indiscriminate harm. Finally, preexisting negative self-schemata can be reinforced by trauma. Janoff and Bulman ([95]) proposed that victimization specifically violates the assumptions that the world is benevolent and meaningful and that the self is worthy.

Appraisal of the world as eminently dangerous and of oneself as everlastingly incompetent and vulnerable interferes with recovery from trauma. Cognitive therapists explore and challenge such inadequate schemata, discourage their generalization to the patients' whole life, and foster the re-building of a viable sense of personal worth, competence, and safety.

Cognitive Therapy. Three controlled studies looked at the effect of cognitive techniques in subjects who had suffered from either rape or sexual assault and showed that these techniques are followed by a significant improvements. In the above mentioned study by Foa et al. ([84]), the stress inoculation technique produced a significant reduction of PTSD symptoms immediately after treatment. Resick and Shenicke ([97]) compared group cognitive processing therapy, which comprised of education, exposure, and cognitive components, with waiting list control. Subjects in the treatment group improved in measures of depression and maintained the improvement for 6 months. Finally, Resick et al. ([98]) compared three treatment conditions (stress inoculation, assertion training, and supportive psychotherapy) in 37 rape victims. All three treatment conditions reduced symptoms of distress, avoidance, and intrusion and improved self-expression and self-concept. The results were maintained 3 and 6 months after treatment.

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Psychodynamic Formulations of PTSD

Psychodynamic formulations of PTSD and of its predecessor, the "Traumatic Neurosis," are complex and multifaceted. Two generic metaphors have been advanced, including damage to a component of the mental apparatus and incomplete processing of traumatic experiences.

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The Metaphor of Damage to the Mental Apparatus

Commenting on the repetitive and distressful nightmares of patients with traumatic neurosis, Freud ([99]) suggested that war trauma creates a breach in a hypothetical "stimulus barrier" that normally protects the mental apparatus from excessive amounts of "excitation." As a result of this structural impairment, the mental apparatus abruptly modifies its operational rules by relaxing the domination of homeostasis-based dynamics exemplified by the "pleasure principle." Instead, the psyche becomes subjugated to a hypothetical "repetition compulsion": a "primitive" and more "biological" set of functional rules. Individuals with traumatic neuroses, accordingly, are captive of the dynamics of a ceaseless repetition compulsion.

The essence of this forgotten, yet most powerful, insight of Freud's formulation is that the repetitive phenomena, in traumatic neuroses, do not necessarily contribute to self-healing and may often express a posttraumatic surrender of the psychic apparatus to a new and dysfunctional set of rules.

Recent structural formulations metaphorically reiterate Freud's original stance. At the heart of these formulations is the appraisal that extreme trauma alters the rules of mental functioning rather than injects new content to old conflicts. In today's parlance, this alteration is referred to as "traumatized self" ([100,101]) or "collapse of structures" ([102]). The practical implication of such formulations is the recognition that the self-healing capacity of PTSD patients is impaired. Consequently, the therapy of PTSD should include ego-supportive maneuvers, address vulnerability in character structure, and involve the therapist in the role of participant rather than neutral observer.

Krystal's ([103]) description, in survivors of massive trauma, of "loss of affective modulation" is another variation on the theme of "psychic damage." Krystal argued that the fact of psychological surrender, typical to situations of prolonged subjugation to extreme adversity, leads to a permanent impairment of the survivor's affective life (e.g., inability to respond to subtle affective cues). This impairment resembles alexithymia, a mental condition in which the person is unable to recognize and use internal states of affect. Research has confirmed the presence of alexithymic traits in war veterans with PTSD (e.g., [104,105]).

McCann and Pearlman's ([96]) constructivist self-development model offers a bridge between self- and cognitive psychology. According to this model, three aspects of the self are affected by trauma: a) self-capacities, or the ability to tolerate intense affect and regulate self-esteem; b) cognitive schemata, or beliefs and expectations about self and others; and c) intrusive trauma memories and related distressing affect.

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The Metaphor of Unresolved Mental Processing of the Event

This psychodynamic model stems from the paradigm of loss, mourning, and grief. Relating to the similarities between symptoms of intrusion and avoidance observed in posttraumatic individuals and those defined by Freud ([6]) and described by Lindemann ([7]) in the early phase of normal grief, Horowitz ([8]) hypothesized that the "stress response syndrome," an early equivalent of PTSD, results from incomplete mental processing of the traumatic event.

From a practical point of view, this concept suggests that PTSD might resolve if the patient is encouraged to work through these conflicts. Such is the main thrust of traditional psychodynamic psychotherapy of trauma-related disorders. However, the experience of extreme arousal and panic associated with the reactivation of traumatic memories, the advent of dissociative reactions during psychodynamic exploration of the trauma, and the extent of psychic avoidance observed in some PTSD patients complicates explorative techniques in many cases.

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Psychodynamic Psychotherapy

Borrowing Lindy's definition ([106]), psychodynamic psychotherapy specifically addresses the meaning of trauma-related symptoms and behavior and the meaning of the traumatic event. The analytic psychotherapist hopes that insight regarding the meaning of symptoms, both conscious and unconscious, can help the patient master inner experiences and repair and restore the integrity of life. In their review of the field, Marmar et al. ([107]) emphasize the importance of establishing a therapeutic alliance and the intrinsic difficulty of that task. Handling transference and counter transference reactions, both related to the enduring effect of traumatization, is emphasized by several authors ([108-110]).

Most of the literature on psychodynamic therapy for PTSD consists of case reports and addresses theoretical and technical aspects of the treatment. The abovementioned controlled study by Brom et al. ([89]) compared brief dynamic psychotherapy with hypnotherapy, desensitization, and a waiting list control. All active treatment groups improved significantly. In a well documented treatment project ([111]), 21 Vietnam veterans with PTSD participated in individual psychoanalytic psychotherapy for 1 year. Decreases in intrusive phenomena and depression were recorded in those patients who completed their treatment. Other reports ([112-115]) are summarized in Table 2Table 4Table 5

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OTHER TREATMENT MODALITIES AND TECHNIQUES
Group Therapy

Historically, the "rap" groups that followed the Vietnam war preceded many other therapies of traumatized combat veterans ([116]). The rap group sessions consisted of disclosure of common experiences, validation of feelings, and sharing of existential distress among fellow veterans. In fact, PTSD patients often perceive their life experiences as fundamentally different from and incomprehensible by nonvictims. Alienation, isolation, helplessness, and mistrust are major psychological components of PTSD, along with restricted affect, emotional dyscontrol, irritability, and depression. These features reduce PTSD patients' interpersonal and social competence. Group therapies have, therefore, a major role in the comprehensive psychiatric treatment of PTSD.

Despite the above information, data concerning the efficacy of group therapy are mostly descriptive. A few of the numerous studies of group therapies in PTSD are summarized in Table 2Table 4Table 5 ([117-121]). common denominators of all group approaches to PTSD are attempts to reverse isolation and to reduce helplessness and alienation. Most authors also underscore the need to: establish an effective working alliance, facilitate disclosure, and enhance communication and mutual support among group members. More specific goals have been set according to the theoretical orientation and to the type of trauma. Self-awareness and integration are emphasized by cognitive group therapists (e.g., [122]), and working through traumatic experiences is typical of psychodynamic groups ([119,121]). Anger control ([118]) and empathic understanding of combat nightmares ([119]) are other specific goals.

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Family Therapy

The impact of PTSD extends beyond individual patients to affect their spouses, children, and the larger network of relatives, friends, and co-workers. Intimate family and social relationships may all suffer as a result of inappropriate interactions with persons exhibiting PTSD ([123,124]). In particular, isolation, hypervigilance, irritability, and a propensity for loss of impulse control can contribute to a deterioration of interpersonal functioning. Expression of violence, fear, suspiciousness, or tension within families of PTSD patients may extend to future generations. Family members' reactions may reciprocally exacerbate the patient's condition.

Family therapy offers the opportunity to confer benefits on both the identified patient and the family ([125]). Most of the published literature on family and couple therapy in PTSD, however, consists of anecdotal reports and theoretical formulation. Because of the excessive divorce rate in Vietnam veterans and other PTSD patients, couple therapy may be essential to salvage precarious marital ties ([125]). A recent program involved the application of behavioral family therapy, developed initially for use in schizophrenics, to PTSD patients and their spouses ([126]). Empirical studies are required to assess and document the immediate and long term effect of family therapy in PTSD.

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Hypnosis

Hypnotic induction and other suggestive techniques have been widely used in the treatment of combat stress reactions (e.g., [128]). Studies indicate that Vietnam veterans with PTSD are more hypnotizable than normal controls ([129-132]). In a study by Brom et al. ([90]), hypnotherapy was more effective than waiting list control in improving avoidance and distress in PTSD patients. Our own clinical experience indicates that some PTSD patients resist hypnotic suggestion, often as a way to remain in control, and others respond to hypnotic induction by developing severe dissociative states ([16]). Hypnosis, therefore, must be used with care and only as a component of an overall treatment plan.

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Inpatient Treatment

Some PTSD patients, generally those with high levels of symptomatology, may require hospitalization, often in response to depression, substance dependence, violence, or suicidal behavior. Four studies of inpatient programs have been reported ([133-136]), and two studies evaluated behavioral treatment during the hospitalization of Vietnam veterans with chronic PTSD. The programs included a variety of interventions, such as group and milieu therapy, individual therapy, counseling, behavior therapy, and pharmacotherapy. The length of stay varied among the studies, reaching up to 140 days ([135]). Positive changes in self-esteem, interpersonal relations, and symptoms of numbing and arousal have been reported by Scurfield et al. ([134]). However, in a 12- to 26-month follow-up study of PTSD inpatients released from hospital treatment, Perconte ([136]) showed that symptomatic relapse was the rule. Some improvement (e.g., in employment status) may, nevertheless, persist. Inpatient treatment, therefore, does not markedly affect the course of PTSD but may effectively address crises and comorbidity.

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Vocational Rehabilitation

Data concerning the chronic course of PTSD along with the limited effectiveness of current treatments strongly suggest that rehabilitation should be a major approach to this disorder. Grunert et al.'s study of graded work exposure ([137]) showed that efforts to implement specific rehabilitation programs can be very productive; 90% of 51 patients with PTSD after work-related hand injuries returned to work, often with a new employer, and about 84% were still working 6 months later. Moreover, among subjects who suffered from flashbacks, 73% successfully returned to work. The presence of such flashbacks had previously been associated with a 90% failure to return to work.

At this point in time, however, the literature on rehabilitation of PTSD patients is scarce. Data concerning specific impairments related to PTSD, such as short term memory deficit (e.g., [138]), stimulus sensitivity, reduced attention span, are unavailable. Systematic delineation of such impairments is an important step toward implementing rational rehabilitation programs for PTSD patients.

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DISCUSSION

As attested by this review, efforts to treat PTSD have been extensive, reflecting the wide recognition by clinician and researchers of the disorder's validity and the associated distress and dysfunction. Having started with series of anecdotal reports, treatment studies are becoming more sophisticated, involving controlled designs and larger samples of patients. On the other hand, and in the absence of accepted pathophysiological theory, almost any treatment modality, including ones that have not been covered in this review, could be implemented and assessed in PTSD. This heterogeneity, as well as the feeling that "everything goes," is not serving the field well.

Several assessment tools were widely used across studies (e.g., the IES, MMPI), enabling comparisons among them and with our experience. However, despite the large number of studies, the inclusion of survivors of a variety of events, the difficulties in identifying control groups, and the heterogeneity in initial symptom severity and in the duration of PTSD before treatment clearly indicate that the lessons learned from these studies are still preliminary.

Most studies reported substantial alleviation of suffering, but many still had the mark of pioneering enthusiasm and lacked self-critique. In controlled studies, the effect size was often limited, and symptoms of depression, detachment, and anxiety improved more than those of intrusion and avoidance. No study claimed to have achieved durable remission in chronic PTSD, thereby reflecting many clinicians' belief that the disorder is rather unresponsive to any form of treatment. Altogether, the cumulated evidence suggests that patients with PTSD can expect to receive substantial help from therapists but probably not a definite cure.

Given these limitations, several indications emerge from reading the available data. First, evidence tends to support the superior effectiveness of early treatment, whether pharmacotherapy or cognitive-behavioral therapy. Second, some success had been documented in almost every treatment modality, and such partial improvement can often be of great significance for the patient. Third, no agreement has emerged as to a hierarchy of applying treatment modalities in PTSD. Finally, evidence of synergetic effects of pharmacotherapy and psychotherapy has been reported ([61]) in up to 70% of the patients ([64]). The following paragraphs attempt to translate these indications into practical guidelines

Rather than orienting the clinician toward a specific treatment modality, the diagnosis of PTSD suggests that several treatment approaches could be successfully combined. Within PTSD, therefore, the clinician must identify the current sources of distress and dysfunction and evaluate their accessibility to treatment.

Particular PTSD symptoms may point the therapist toward appropriate levels of impairment ([16,139]). The presence of conditioned emotional responses is reflected by: efforts to avoid thoughts, feelings, or conversations associated with the trauma; efforts to avoid activities, places, or people that arouse recollections of the trauma; intense psychological distress at exposure to cues evoking the traumatic event; and physiological reactivity upon exposure to such cues. Altered networks of meaning are often reflected in profound changes in the patients' life trajectory, self-concept, sense of security, and appraisal of others. Symptomatic behavior related to these changes is reflected in the DSM-IV criteria of feelings of detachment or estrangement from others, markedly diminished interest in significant activities, restricted range of affects, and a sense of a foreshortened future. The degree to which such symptoms reflect comorbid depression should be weighed. Other DSM-IV criteria (i.e., inability to recall an important aspect of the trauma, acting or feeling as if the traumatic event were recurring) may reflect the preferential use of the defense mechanisms of denial, dissociation, or repression. Symptoms reflecting dysregulation of arousal are those included in the "D" criteria of DSM-IV: hypervigilance, exaggerated startle response, irritability, difficulty concentrating, and sleep disturbances.

In evaluating the accessibility of these symptoms to treatment, one must consider first that PTSD symptoms may reflect different mental processes at successive phases of the disorder. While perhaps indicating a normal healing process in the early stages of the disorder, recurrent and intrusive recollections of the trauma may "age" with time and come to represent an obsessively repetitive dysfunction of memory. Attempts to explore, elaborate, and work through these memories at later stages may often aggravate rather than cure. Conditioned fear responses may, similarly, become indelible and thereby inaccessible to eradication through desensitization or flooding.

A second important principle is to evaluate the extent to which one level of impairment interferes with attempts to address other levels. Making a hierarchical decision, in the proposed multi-level model, involves knowing where to start, as in the following examples.

Not every PTSD patient is extremely aroused. Those who are, however, and those who have developed a pattern of dissociative responses to any reminder of the trauma are poor candidates for therapy that requires exploration, exposure, or any additional demand. Treatment aimed at reducing the underlying arousal or at better controlling dissociative responses should precede, in such patients, the more explorative approaches. Treatment of severe depression, insomnia, or alcohol or substance abuse may take precedence at some stages of the disorder over social and interpersonal rehabilitation. Patients who are extremely avoidant of memories of the trauma may better respond to interpersonal therapy once their sensitivity to recalling the trauma is addressed. The treatment of these patients could start by imagery desensitization. Marital disputes and work pressures often aggravate, to a critical point, the patient's irritability and emotional dyscontrol. Couple therapy and intervention in the work place may be preferred, as a first step, in such subjects. Finally, each PTSD patient has a unique rhythm of developing trust, of sharing, and of forging a therapeutic alliance.

As a final note, one should remember that, to some extent, the imprint is indelible and hence immutable by current methods. The evidence provided by this review shows that attempts to cure chronic PTSD by reversing its "etiological" mechanisms should be reconsidered and replaced by more realistic goals (e.g., vocational rehabilitation, family counseling, and control of adverse health practices). Defining the parameters of the disability associated with PTSD and assessing the effect of combined treatment programs are important challenges for the future.

The authors thank Ms. Sarah Freedman for her valuable work in reviewing and editing this manuscript.

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Keywords:

biopsychosocial framework, posttraumatic stress disorder.

Copyright © 1996 by American Psychosomatic Society

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