The diagnostic criteria for posttraumatic stress disorder (PTSD) as outlined by the DSM-UI in 1980 provided a more coherent basis for the study and treatment of the mental sequelae known to follow catastrophic experiences. Early historical accounts portrayed the reactions of persons whose world schema had been shattered.1,2 The concept of "railway spine" in the 19th century was linked to the nature of the stressor and the belief that there was an actual physical disruption of the nervous system that accounted for symptoms of anxiety and debilitation.3
Freud's conceptualization of "war neurosis" as "a consequence of an extensive breach being made in the protective shield against stimuli" provided a useful metaphor of the sensory overload that overwhelms the cerebral cortex in the course of its role of processing incoming information.4 His idea of "repetition compulsion" as a way of mastering a trauma has furnished a valuable means of conceptualizing the intrapsychic aspects of the paradoxical and maladaptive responses to stress that are often observed.4 In their studies of World War I combatants, Babinski and Froment reasoned that soldiers were unconsciously exposed to internal or external hypnotic suggestions at the time of the trauma, that later played a role in the onset of psychiatric symptoms.5 in his wrkings on the etiology of war neurosis, Pavlov emphasized the linkage of symbolic stimuli, such as fear and its physiologic symptoms, that become "associated with security to life by the law of conditioned TeAeXeS."6
DIAGNOSTIC CRITERIA FOR PTSD
The publication of the DSM-III in 1980 provided for the first time a taxonomtc description of the entire range of PTSD, including the chronic, unremitting, and sometimes crippling mental conditions that can follow trauma. Prior versions (the DSM in 1952 and the DSM-II in 1968) were limited solely to the description of acute stress conditions.7 The new classification provided a unifying and coherent concept upon which diagnosis, research, and treatment could be based. The DSM-III-R in 1987 defined the nature of the stressor in a more specific fashion, as well as restructuring and clarifying the major criteria of the disorder. The DSM-III-R criteria for PTSD are organized as follows:
* the traumatic event,
* persistent reexperiencing (at least one symptom),
* persistent avoidance of stimuli (at least three symptoms),
* persistent increased arousal (at least two symptoms), and
* duration greater than one month.
The Traumatic Event
The stressor is defined as "an event outside ordinary human experience that would be markedly distressing to almost anyone, including threat of death, loss of body integrity, serious harm or threat to a loved one, sudden destruction of home or community, or witnessing an accidental or violent death or severe injury of another."
As a way of empathizing with the profoundly disorganizing events endured by PTSD patients, it might be helpful to imagine that one's habitual assumptions of trust, reliability, and safety in the world have been suddenly and radically challenged. It is horrifying and disorganizing to the ego for familiar, reliable aspects of our world to shift without warning.8 We expect the walls of buildings to stay in their places, floors to bear our weight, planes to stay aloft, and automobiles to take us on our way. Our personal repertoire of experience has led to these assumptions, and they become a part of our self-system. Shaw reviewed some of the developmental antecedents involved in the dissolution of these basic assumptions, focusing on the experience as an "unmasking of the illusion of safety."9 Anything that disrupts this habitual reliant expectation can create a warp in identity, a sense that one has lost the magically invincible self, which the assumptions of safety, control, or reliability have previously adorned. The attempt to repair the ensuing narcissistic injury becomes a critical factor in the ensuing disease and its treatment.
Symptoms of persistent reexperiencing include at least one of the following:
* recurrent intrusive and distressing recollections (repetitive play in children),
* recurrent, distressing dreams of the event,
* sudden acting or feeling as if the event were recurring (dissociative flashback episodes), and
* intense distress triggered by events that symbolize or resemble the trauma.
Persistent reexperiencing can be seen as a form of hypermnesia - a sharply focused, eidetic memory, unlike the oneiric, hazy recollections of mundane things, such as the nature of last Tuesday morning's breakfast. From this eidetic quality derives the ruminative, inerasable traumatic images so troubling to patients with PTSD. Hypermnesia includes not only the plot of the traumatic script that the victim has endured, but also the intense fear and physiologic arousal that was present at the time the original memories were encoded. One patient, for example, was amnesic for the events of a vehicular crash in which her car began to spin out of control. She later developed a distressing vertiginous feeling that was, in feet, a replay of a frightening somatosensory aspect of the accident . That such reexperiencing may occur without the conscious realization of the individual is also seen in the traumatic repetitious play of children and the symbolic reenactments of trauma seen at all ages.10 While traumatic dreams often involve a close replication of the fateful event along with its affective accoutrements, they also are metaphorically elaborated in terms of the meaning that the trauma has assumed in the patient's self-system.
Symbolic triggering of distressing memories can be experienced on the anniversary of the event or by sensory stimuli that are in any way reminiscent. These stimuli can be auditory, visual, tactile, or olfactory. Survivor guilt, which is no longer a criterion in the DSM-III-R as it was in the DSM-III, is a common finding that may be determined by factors such as the nature of the trauma, cultural background, ' ' and an intrapsychic attempt to maintain the illusion of having been in control.
Persistent Avoidance of Stimuli
Avoidant symptoms consist Of:
* efforts to avoid thoughts or feelings associated with the trauma,
* efforts to avoid activities or situations that arouse recollections of the trauma,
* inability to recall an important aspect of the trauma (psychogenic amnesia),
* markedly diminished interest in significant activities (developmental regression in children),
* feelings of detachment or estrangement from others,
* restricted range of affect, and
* a sense of a foreshortened future.
Avoidant symptoms frequently are responsible for diagnostic difficulties that arise. Patients often have great difficulty discussing their traumatic experience with relatives and health professionals, because of the physiologic arousal and painful memories stimulated when talking about it. Amnesia may play a signiñcant role and is a frequent cause of misdiagnosis. Over-identification with the patient's need to minimize the impact of trauma may result in unconscious collusion with his or her defenses and can result in failure to make a timely diagnosis. Once a diagnosis is made, similar factors may cause reluctance to seek treatment and premature withdrawal from therapy.
Persistent Increased Arousal
Symptoms of persistent increased arousal include:
* difficulty falling or staying asleep,
* irritability or outbursts of anger,
* difficulty concentrating,
* exaggerated startle response, and
* physiologic reactivity upon exposure to events symbolizing or resembling an aspect of the traumatic event.
The marked hyperarousal that accompanies hypermnesic symptoms is frequently responsible for the commonly reported fear of going crazy. Irritability and anger in some patients can be quite intense and when combined with feelings of mistrust and shattered self-esteem can result in the misdiagnosis of paranoid schizophrenia. KoIb reports that dissociative symptoms are seen in approximately 5% of Vietnam veterans with chronic PTSD.12 Dissociative symptoms are seen less commonly following motor vehicle accidents. While dissociation is classified as a hypermnesic flashback, prominent elements of hyperarousal and avoidant withdrawal often are present.
Arousal episodes may be triggered by a variety of somatosensory and ideational stimuli in the clinical or laboratory setting. They are often accompanied by measurable physiologic changes, including heart rate, respiration, muscle trembling, diaphoresis, and galvanic skin response. A number of centers employ such responses to stimuli as diagnostic tools.13 Even without elaborate equipment, careful clinical observation of the patient during anamnesis of traumatic events may reveal visual signs of arousal, including agitation, tremor, flushing, pallor, loss of expressivity in the voice, and a flattening of facial expression.
Onset of hyperarousal, avoidance, diminished ability to engage in fantasy, and impaired expression of emotion manifesting as alexithymia may cause diagnostic confusion with personality disorders in PTSD patients. Careful history and collateral information are necessary to distinguish whether the personality disorder existed prior to the onset of PTSD, or is a secondary manifestation.
SPECIAL DIAGNOSTIC CONSIDERATIONS IN CHILDREN
Posttraumatic play in children involves a serious, repetitive activity that reworks the traumatic experience. Terr has emphasized that these games themselves can have a deleterious effect on playmates who were uninvolved in the original trauma.10 Reenactment behaviors may become a hazardous replaying of the traumatic event. Terr's patient Leslie ran away from home by hitching a ride from a stranger at the age of 11 - three years after her abduction in the Chowchilla kidnapping. She denied the similarity to the traumatic event by stating "the kidnapping was they were taking me . . . the other was that / was going."10 A foreshortened sense of future, a belief in the ability to predict the future, and omen formation were seen in this group as a distortion of time sense.10
Children who felt utterly helpless in their inability to predict the kidnapping, mentally reversed posidiction into prediction. This phenomenon also is seen in adults. If a patient who was driving a car prior to an accident reports having a premonition of the accident prior to its occurrence, the clinician is cautioned against automatically assuming that this was an unconsciously motivated event. The premonition may be a postevent thought transposed into a preevent position in the patient's memory,10 serving as an intrapsychic defense against the helplessness perceived amidst the utter unpredictability of the traumatic event.
Studies during World War Il indicated that apathy and decreased activity were more common with populations of children during bombing raids than overt anxiety or panic.'4 Children can be "infected" with PTSD by their parents as well as by playmates.15 McFarlane found that parental response following common disaster played a greater role than the child's degree of direct exposure. Mothers who themselves had the highest incidence of posttraumatic imagery were likely to be the most overprotective or anxious around their children.14
There is no age at which children are immune to the psychic and physiologic sequelae of stress. Irritability, masked avoidant behavior, and hormonal changes were found in newborns circumcised without anesthetic.10 PTSD in children carries with it an additional morbidity. The loss of expectant reliability and the shattering of the sense of a safe self before a cohesive ego has formed impairs healthy formation of trust in children and interferes with identity development in adolescents.15
OTHER DIAGNOSTIC ISSUES
The vicissitudes of PTSD are manifold. Symptoms may commence immediately after a trauma and follow a steady progression or may improve spontaneously and later relapse. Overt symptoms can be totally absent for many years following a trauma and then flare up in a full-blown syndrome 40 years later, following a symbolically triggering event.17 As previously mentioned, diagnosis may be confounded by avoidant symptoms. Patients who have a puzzling, refractory mental disorder with a polymorphous appearance of depression, explosive anger, substance abuse, anxiety, somatization, and borderline features should be suspected of suffering from a masked form of PTSD. For this reason, inquiring about traumatic life events is important in every complete psychiatric diagnostic evaluation. Patients who are able to describe a traumatic event, but are inhibited in revealing the extent of the response during verbal questioning, often will reveal additional information on written questionnaires.
I ask suspected PTSD patients to fill out the Impact of Events Scale18 as a supplement to the clinical history. This instrument is also very useful as a longitudinal measure of symptom intensity. Psychological testing, including the MMPI,19 the Millon Clinical Multiaxial Inventory,20 the 16 Personality factor test,20 and the Rorschach test,21 have been studied in populations of PTSD patients, mainly combat veterans. Keane et al developed a PTSD scale as part of the regular MMPl inventory, which has been found somewhat useful diagnostically in groups of combat veterans.19 The applicability of these and other psychological tests requires further study and validation in wider populations of PTSD patients.
Diagnosis of PTSD may be hampered by countertransferential factors. Patients are often irritable (arousal symptoms). They may be amnesic for significant aspects of the clinical history and appear uncooperative (avoidant symptoms). They mistrust clinicians, who as authority figures readily become the target of anger arising from a lost sense of expectant reliability and order. If patients have suffered physical injuries as part of their trauma, it is common for a chronic pain syndrome to develop in which the experience of pain appears to be out of proportion to objectively determined tissue injury.22
The clinician may unconsciously defend against empathie contact for fear of being contaminated by the patient's horrifying experience. An attempt to erroneously blame the victim for his or her fate may be a way of defending against the painful reality that the same terrible thing could befall the clinician.
The former widespread acceptance of the concept of "compensation neurosis," since shown to be invalid,23,24 may have resulted in part from these issues. Until it was shown that the great majority of patients involved in litigation failed to experience a magical recovery following settlement of their case, many patients with PTSD were labelled as malingerers, given unnecessary physical examinations and procedures to prove or disprove the nature of their physical pain, and subjected to the unconscious anger of physicians who reacted negatively to the patient's inability to respond.24
The converse problem of overidentification with the patient's suffering can lead to erroneously minimizing the nature and severity of the PTSD symptoms. The sensitive clinician can inappropriately respond to the anxious plea in the patient's eyes. "Please tell me there's nothing wrong with me, Doctor," and wind up inadvertently colluding with the patient's avoidant defenses. Premature reassurance may hamper proper identification of the disorder and paradoxically can increase anxiety, because it gives a signal to the patient that even the doctor is unable to face the trauma.
OTHER CUNICAL ASPECTS OF PTSD
PTSD is not a rare condition. In a general population study, Heizerand colleagues found a 1% prevalence of PTSD in the total population, 3.5% in civilians exposed to physical attack or noncombat veterans, and 20% in Vietnam combat veterans.25 Predisposition to PTSD and comorbidity with other psychiatric disturbance must be considered in treatment of affected patients. Earlier studies from World War II suggested that 34% to 80% of soldiers developing war neurosis had suffered a previous psychiatric disturbance.3
Later studies of military and civilian populations, using recent diagnostic criteria, have indicated that as the severity of the trauma intensifies, larger percentages of individuals with no prior psychiatric history will develop PTSD and factors of predisposition become less important.2627 An article by Foy et al gives an excellent review of the literature on the relationship of pre- and postcombat factors in PTSD.28 In a prospective study of veterans, Card was able to identify only one precombat factor, namely low self-esteem at age 15, that later correlated with PTSD symptomatology,29 Davidson et al found a 66% history of alcoholism, depression, and anxiety disorders in family members of combat veterans with PTSD, a pattern that more closely resembled the control population with generalized anxiety disorder than their depressed control group.30
Increased severity of PTSD following rape may be related to preexisting psychopathology, substance abuse, and lack of social support.31 Heizer et al found that individuals with PTSD were at increased risk for obsessive compulsive disorder, dysthymia, and bipolar disorder in their general population study.23 Benedikt and KoIb reported that 10% of 225 veterans referred to a chronic pain clinic were later diagnosed with PTSD.22 In a study by Sierles et al, 56% of 25 combat veterans had other psychiatric diagnoses, including alcoholism, drug dependence, antisocial personality, depression, and organic mental disorder.32 A high incidence of substance abuse reported in PTSD patients33 requires further study, as it may be restricted to certain populations, such as combat veterans.
A difference in the nature of PTSD following combat and civilian trauma may explain some of the variation in these studies, as emphasized by Burstein et al, who compared Vietnam veteran outpatients with PTSD to patients developing PTSD from motor vehicle accidents.34 Veterans were more likely to have intense dissociative reexperiencing episodes, to be males traumatized in late adolescence, to be of lower social class, to be self-referred, to have a better awareness of their diagnosis, to have been ill for a longer period before the onset of treatment, and to have been more refractory to treatment. While a more substantial number of motor vehicle accident patients were able to complete treatment with acceptable symptom relief, even this group had a dropout rate of 81 .8% when the delay in seeking treatment exceeded 40 weeks.
Recent review articles have summarized a variety of biological and psychophysiological findings in PTSD patients, indicating that they exhibit high autonomic arousal from exposure to specific stimuli measured by heart rate and galvanic skin response, and that they generally manifest increased noradrenergic output, diminished endogenous opioids, and impaired adrenal cortical output.35·36 Findings have been conflicting at times, and most populations studied have been combat veterans. Sleep EEG studies are few in number and show mixed results.37,38
These and other findings have generated a number of fascinating theories regarding the etiology of PTSD and provide a rationale for research employing new treatment modalities. Van der Kolk linked the vivid, inerasable quality of traumatic hypermnesia to an increased outflow from the locus ceruleus to the hippocampus and amygdaloid complex, which are structurés involved in short-term memory encoding.39 From the rat model of inescapable shock and its associated increase in beta-endorphin receptor sensitivity, which causes an effective state of opiate tolerance, he postulated that "addiction to trauma" could be an attempt to relieve a relative paucity of endorphins at the opiate receptors.39 KoIb reasoned that traumatic experiences, which have been shown to be selectively neurotoxic, suppress cortical functioning (primarily the temporal -amygdaloid complex) and lead to a disinhibition of activated brain stem structures.40 Pitman suggested that the neuropeptides vasopressin or ACTH "etch" a traumatic experience into memory by increasing norepinephrine turnover.41 Conversely, he suggested that oxytocin and opioid peptide given at the time of trauma might prevent the onset of PTSD by acting as endogenous amnesic agents.41
In the behavioral literature, Keane et al, like Pavlov, have postulated that PTSD symptoms result from the linkage of a traumatic event as an unconditioned stimulus with a previously neutral event, the conditioned stimulus.42 Spiegel et al emphasized the dissociative aspects of PTSD, and like Babinski, its similarity to the hypnotic state.43 In a recent study, his group found that Vietnam veterans with PTSD scored higher than controls on the Hypnotic Induction Profile.45
TREATMENT OF PTSD
A variety of treatment approaches have been employed for patients with PTSD, including psychodynamic psychotherapy,44 behavioral therapy,45,46 cognitive therapy,46 group therapy,12,46 hypnosis,4648 narcosynthesis,12 and pharmacotherapy.39,49 Depending on the needs of the patient, the particular features of the disorder, the presence of external support, and cultural factors, any combination of methods may be required. Early identification and education of the patient as to the nature of the disorder probably improves prognosis.50 Chronicity can result in an extended course of illness and may be crippling.12 The high rate of noncompliance and treatment dropout in PTSD patients mandates that strategies for dealing with this aspect of the disorder be considered from the outset.
It is important that adequate time be provided to enable the patient to describe the traumatic experiences as fully as possible. Efforts should be made to elicit the presence of any affective and psychophysiological symptoms that occurred at the time of the trauma and to ascertain the precise nature of any injury to the sense of self. In acute cases, unrealistic ruminations of guilt often may be relieved rapidly, by explaining to the patient that self-blame may be a retrospective attempt to deny the experience of utter helplessness. Dietz's patient, a police officer who developed PTSD following a gun duel with a felon, illustrates this issue.51 His patient developed the mental equation that vulnerability (during the exchange of gunfire) equaled a fear of penetration, loss of masculine identity, impotence, and loss of the esteemed self. Feldmann used Kohut's framework to explain the presence of violence in PTSD patients.52 It can be seen as a byproduct of the fragmenting self, a method that an individual may use to relieve the disintegrative experience that is set in motion by the helplessness experienced during the traumatic event. He suggested empathie acknowledgment of how discombobulating this loss of control can be for the patient and that violence is a comforting but maladaptive attempt to feel better. This concept can also be helpful as a psychotherapeutic approach for patients who have a need to reenact dangerous repetitions of the trauma. Ulman and Brothers have employed a psychoanalytic treatment of PTSD, focusing on the empathie resolution of traumatically shattered narcissistic fantasies that emanate from the patient's unmodified archaic parental identifications.53
A series of reports using behavioral therapy46,54,55 have shown promising results with use of imaginai flooding derived from specific cues in the traumatic experience. Saigh successfully treated a 6year-old Lebanese boy with this approach.54 After making an initial determination of the specific memory cues that comprised the traumatic event, muscle relaxation and visualization of peaceful scenes were interspersed with guided images of five specific aspects of the trauma scene.
Scrignar advised a combined approach of cognitive and behavioral methods assisted by hypnotherapeutic techniques in both an individual and group setting.46 He used an educative process initially geared to facilitate understanding of the nature of PTSD and later to help the patient separate the memory of the trauma from the associated physiologic reactivity which had become inextricably linked to it through conditioning. Progressive muscle relaxation, sometimes assisted by formal hypnosis, was used to help the patient suppress physiologic arousal. This provided a foundation for specific desensitization techniques, in which the patient was asked to vividly imagine various aspects of the trauma. Graded intensification of this in vitro exposure was interspersed with thought stopping, peaceful images, and previously learned relaxation techniques. Maladaptive cognitions that fostered the patient's belief in his or her own helplessness were systematically challenged during states of relaxation. Some maladaptive cognitions employed by PTSD patients included: "1 can't do anything ... I cannot control my thoughts about the trauma ... 1 cannot influence what I dream ... my personality is irreversibly changed."46 According to Horowitz, progressive desensitization was a more effective behavioral approach for patients with a hysteric disposition, while flooding was more beneficial for obsessionals.44
Spiegel used hypnotic induction to promote a "structured intensification" of his patients' traumatic memories to assist them in working through the grief emanating from their horrifying experiences.48 Improvement in a series of four cases appeared related to degree of hypnotizability, and the patient's ability to gain a sense of control in reexperiencing the trauma.
Common to each .of these disparate treatment methods was a therapeutic effort to assist the patient to focus on aspects of the traumatic experience in a way that would help to restructure a realistic sense of organization and coherence from the rubble of his or her shattered sense of mastery.
To the author's knowledge, there have been only three placebo-controlled, double-blind medication studies for patients with PTSD.56"58 While medication alone usually does not provide a complete treatment, it can be extremely useful in reducing symptoms to the point that a patient can cooperate with psychotherapeutic and behavioral methods. Even partial relief can provide significant restoration of a sense of inner order and control.
Tricyclic and heterocyclic antidepressants have been found useful in relieving sleep disturbance, hyperalertness, panic, increased startle response, impaired concentration, and nightmares, but were not particularly helpful for avoidant symptoms.56,59,60 Conflicting reports regarding the efficacy of phenelzine have appeared.36,57 Carbamazepine has been effective in reducing impulsivity in Vietnam veterans with PTSD.61,61 Lithium carbonate, in low doses of 300 to 600 mg/day, relieved symptoms of inappropriate anger, irritability, and anxiety in previously treatment-resistant Vietnam veterans with PTSD.63 One case report of a patient whose symptoms presented a diagnostic problem indicated that lithium treatment at standard dosage effectuated the unforeseen and spontaneous unmasking of a posttraumatic memory.64
Kolb separately administered Clonidine and propranolol to combat veterans and found both to be effective agents.12 Clonidine, an alpha-2 agonist, downregulates activation outflow from the locus ceruleus. Famularo et al reported that propanolol significantly relieved some of the acute symptoms of PTSD in abused children.65 Benzodiazepines have a high acceptance among PTSD patients because of their rapid anxiolytic effect. The ability of benzodiazepines to inhibit kindling phenomena, which could play a role in PTSD, indicates that they may have a useful pharmacologic role.49 Nevertheless, many clinicians are reluctant to use these agents because of their high potential for tolerance and addiction in a patient group that may be especially vulnerable to substance abuse.
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