Stress Disorders Research Paper

Stress and Trauma

Stress is usually defined as the product of circumstance that threatens the homeostasis of the organism and requires adjustment to reestablish homeostasis or develop a new cognitive and emotional organization to accommodate the challenging experience or irretrievable loss. Hans Selye (1976) developed a theory of stress, which he considered a syndrome of “nonspecifically-induced changes within a biological system” (p. 64). However, for the purpose of this research paper, the definition of stress by Mason (1971) as a reaction to threatening or unpleasant factors is more appropriate. Selye discussed both psychological and physiological factors and described negative (distress) and positive (eustress) types of stress responses. His work implicated the autonomic nervous system in the stress response, but it had little in the way of cognitive components to it. The stress response was understood to be—in essence—a cortical reflex to stress. Subsequent theories have taken cognitive appraisal of the nature of a stressor into greater account. This later work was facilitated through the development of life event inventories— such as the Holmes-Rahe inventory (Rahe, Meyer, Smith, Kjaer, & Holmes, 1964), which attempted to quantify life stressors and which are being improved by newer approaches (Carson, Butcher, & Mineka, 2000).

Stimuli and circumstances that produce stress are called stressors, and there have been various categorizations of them, including that of frustrations, conflicts, and pressures (Carson et al., 2000). Although there is no absolute demarcation, extreme stressors would include severely intense or chronic frustrations, conflicts, or pressures of any kind, whereas traumatic events can be defined in a more circumscribed way. We consider trauma as an event caused by humans or nature that reduces the individual to an object and challenges deeply held assumptions of safety, fairness, ability to control events, and predictability. The discontinuity of circumstances in trauma contributes to a discontinuity of cognitive, emotional, and somatic experience among the persons who experience it. The 1987 edition of the Diagnostic and Statistical Manual of Mental Disorders–Third Edition– Revised (DSM-III-R; APA, 1987) defined traumas as events outside of the range of typical normal experience, but epidemiological studies have shown that the majority of individuals—even inhabitants of countries not at war—have witnessed or experienced some form of trauma during their lifetime. An example is the study by Norris (1992) in which 69% of respondents had reported at least one traumatic incident during their lifetime.

Partly to correct the false notion that trauma is an uncommon event, the DSM-IV (APA, 1994, 2000) redefined it as experiencing or witnessing events that involve actual or threatened death or injury or jeopardize the physical integrity of self or others. Furthermore, it is required that the individual’s response include intense fear, helplessness, or horror—or agitated or disorganized behavior in children. There are problems with this conceptualization. The first criterion limits trauma to actual or threat of violence and death, but other factors such as property loss and serious medical or psychological disorder can bring about PTSD (McFarlane & de Girolamo, 1996).The second criterion, although it seeks to address the importance of the subjective response, was partly designed for forensic rather than scientific reasons (McFarlane & de Girolano, 1996) and disregards the possibility that an individual may respond initially with numbing and dissociation rather than with intense emotion (Lindemann, 1944; Spiegel & Cardeña, 1991).

Bearing in mind both the limitations of the current DSM-IV definition of trauma and the fact that the posttraumatic response always involves an interaction between the characteristics of the stressor and those of the experiencing individual, we examine now salient dimensions of trauma. Traumatic events vary with regard to their source (e.g., natural vs. human-made victimization), nature (e.g., sexual abuse vs. physical abuse), chronicity (e.g., being a prisoner of war or POWfor a week vs. being a POW for months or years), severity (e.g., being exposed to combat without casualties vs. a combat with multiple casualties), extent of areas affected (e.g., an earthquake that affects only the self or personal property vs. one that produces disruptions in food supplies, transportation, and other resources),typeofexposure(e.g.,witnessinganaccidentvs.personal experience of the grotesque or handling of dead bodies), relationship to perpetrator (e.g., a stranger vs. a parental figure committing sexual abuse), and so on. Although the data are not unequivocal, it has been generally observed that traumatic events with a greater negative impact are instigated by humans, are chronic and severe, affect various living functions and the social network, and involve sexual rather than just physical abuse—especially abuse of an incestuous nature (Dancu, Riggs, Hearst-Ikeda, Shoyer, & Foa, 1996; Freyd, DePrince, & Zurbriggen, 2001; Labbate, Cardeña, Dimitreva, Roy, & Engel, 1998; van der Kolk, McFarlane, & Weisaeth, 1996). Green (1993) has categorized trauma of a violent nature according to eight dimensions: threat to life and limb, severity of physical harm, receiving intentional injury or harm, exposure to the grotesque, violent or sudden loss of a loved one,witnessing or learning of violence to a loved one, learning of exposure to noxious agent, and causing death or severe harm to another.

Individual psychological differences are at least as important as the characteristics of the stressor. Whereas some severe and chronic traumas such as chronic maltreatment as a POW can produce lifetime or current PTSD prevalences as high as 85% and 59%, respectively (Engdahl, Dikel, Eberly, & Blank, 1997; Ursano & Rundell, 1995), there are marked differences in the effect of less severe stressors (Yehuda & McFarlane, 1995). In a recent and important meta-analysis on predictors of PTSD, Brewin, Andrews, and Valentine (2000) found that previous psychiatric history, childhood abuse, family psychiatric history, low socioeconomic status (SES), lack of education, low levels of intelligence, other previous trauma or adverse childhood factors, trauma severity, lack of social support, and life stress were consistent or homogeneous predictors, whereas being a woman, younger, and of minority status seemed to be significant predictors only in some populations.

After extreme stress or trauma has occurred, there is a wide range of possible and sometimes overlapping reactions. Some traumatic events only have a transient effect, whereas others have life-transforming consequences—both positive and negative. Besides the dysfunctional responses that are described in later sections of this research paper, many individuals report positive changes as a result of the struggle with a traumatic event (Calhoun & Tedeschi, 2000). These changes include greater investment in and appreciation of life, interpersonal relationships, spirituality, personal resources, and an immediate or delayed increase in the sense of mastery to deal with difficult situations (Fullerton & Ursano, 1997; Tedeschi & Calhoun, 1995). Such benefits have been found among various populations, including survivors of cancer (e.g., Taylor, 2000), bereavement (Bower, Kemeny, Taylor, & Fahey, 1998), disaster (McMillen, Smith, & Fisher, 1997), combat (Fontana & Rosenheck, 1998), war captivity (Sledge, Boydstun, & Rabe, 1980), and severe accidents (Brickman, Coates, & Janoff-Bulman, 1978). Women tend to report more benefits from traumatic experiences than do men (Cordova, Cunninghman, Carlson, &Andrykowski, 2001).

The majority of people react to most time-limited traumas such as a disaster with transient mild to moderate symptoms (e.g., Cardeña & Spiegel, 1993), but particularly violent events such as rape may have a greater impact (e.g., Dancu et al., 1996; Engdahl et al., 1997). An important area of investigation is the impact of early responses to trauma on current and chronic dysfunction. The scant and not fully consistent data suggest that severe dissociation may jeopardize survival at the time of the stressor (Koopman, Classen, & Spiegel, 1994, 1996), despite its overall possible species survival value (Nijenhuis, 2000). The DSM-IV diagnosis of acute stress disorder (ASD; APA, 1994, 2000) has triggered a growing number of studies of dysfunctional reactions around the time of trauma (i.e., peritraumatic) and their potential to develop into chronic severe psychopathology.

The vast majority of clinical and research attention has focused on severe chronic or delayed-onset symptoms (mostly under the rubric of PTSD). In the sections that follow, we give an overview of ASD, PTSD, and complex PTSD, a proposed variant of PTSD that encompasses broader posttraumatic responses than does simple PTSD, including dysfunctions in areas such as personality structure, identity, and relational abilities. After reviewing these posttraumatic disorders, (ASD and PTSD are included in the anxiety disorders section of the DSM-IV), we cover the literature on dissociative and conversion disorders (currently classified elsewhere in the DSM-IV nosology).

Acute Stress Disorder

The main reasons to include acute stress disorder (ASD) in the DSM-IV were the lack of a diagnosis for acute and dysfunctional reactions within the first month after trauma, the partial disregard of dissociative symptomatology in the concept and criteria of PTSD, and a greater convergence with the International Classification of Diseases (ICD) classification of acute stress reaction (Cardeña, Lewis-Fernández, Beahr, Pakianathan, & Spiegel, 1996). The original proposal of brief reactive dissociative disorder (Spiegel & Cardeña, 1991) underwent a number of transformations and compromises until it emerged as the current acute stress disorder diagnosis. Its final criteria include exposure to direct or witnessed trauma involving intense negative emotions; at least three dissociative symptoms (e.g., numbing, depersonalization, derealization, being in a daze, and amnesia); reexperiencing or intrusion of the traumatic event (one symptom required); marked avoidance of stimuli related to trauma (one symptom required); marked anxiety or hyperarousal (one symptom required); clinically significant distress or impairment for a minimum of 2 days and a maximum of 4 weeks; and the absence of a direct cause by a psychoactive substance or a general medical condition (APA, 1994, 2000).

Critics of the ASD criteria point out some problems, including the mismatch of ASD and PTSD symptoms (even though the DSM-IV considers that the former, if continuing past 1 month, can be rediagnosed as PTSD), the question of the extent to which dissociative symptoms are as central to the diagnosis as the other criteria are, and the need for greater refinement in diagnostic criteria (e.g., Bryant & Harvey, 1997). A more severe critique of the validity of ASD and of the importance of peritraumatic dissociation as a predictor of PTSD (Marshall, Spitzer, & Leibowitz, 1999) has called for greater accuracy in the diagnosis of acute stress responses, but this critique also seems to have misinterpreted data on the predictive value of peritraumatic dissociative responses (Butler, 2000; Simeon & Guralnik, 2000; Spiegel, Classen, & Cardeña, 2000). The conceptualization of both PTSD and ASD and the nature of their relationship clearly need further elucidation.

The relationship between traumatic stressors and dissociative reactions is quite robust.The current conception of this relationship is based on observations by clinical pioneers such as Breuer and Freud, Charcot, James, Janet, and others (van der Kolk, Weisaeth, & van der Hart, 1996), on extensive literature reviews (Butler, Duran, Jasiukaitis, Koopman, & Spiegel, 1996; Spiegel & Cardeña, 1991), and on international data reanalyses (Cardeña et al., 1998) of reactions to traumatic events that support a strong association between traumatic events and disssociative reactions. Prospective studies assessing dissociation shortly after an earthquake (Cardeña & Spiegel, 1993) and before and after acute stress during military training (Morgan, Hazlett, Richardson, Schnurr, & Southwick, 2001) also challenge the skepticism about a robust trauma-dissociation relationship (Merckelbach & Muris, 2001).

In addition to the commonly reported alterations in memory, perception, and a sense of detachment associated with exposure to human-made or natural trauma (Spiegel & Cardeña, 1991), dissociation and PTSD subscales have a high correlation (Gold & Cardeña, 1998), and more patients with posttraumatic disorders manifest state and trait dissociative symptomatology (e.g., Cardeña, 1998; Hyer, Albrecht, Poudewyns, Woods, & Brandsma, 1993) and show higher hypnotizability than do most other clinical and nonclinical groups (Spiegel, Hunt, & Dondershine, 1988).

The most important finding seems to be that acute dissociative reactions are significant, strong, and independent predictors of long-term psychopathology. Retrospective studies reporting a substantially higher dissociation around the time of trauma for PTSD patients compared with other groups include Vietnam (Bremner et al., 1992) and Gulf War (Cardeña, 1998) veterans, individuals exposed to typhoons (Staab, Grieger, Fullerton, & Ursano, 1996) and emergency rescue workers (Grieger et al., 2000). Prospective studies show similar findings, including numbing as the single best predictor of later PTSD among Israeli soldiers (Cardeña et al., 1998) and dissociative symptoms as significant predictors of later PTSD symptomatology among victims of a firestorm (Koopman et al., 1994, 1996); bystanders of a mass shooting (Classen, Koopman, Hales, & Spiegel, 1998); individuals with mild traumatic brain injury (Bryant & Harvey,1998); survivors of disastrous flooding (Waelde, Koopman, Rierdan, & Spiegel, 2001); and victims of motor vehicle accidents, other accidents, or terrorist attacks (Brewin, Andrews, Rose, & Kirk, 1999; Ehlers, Mayou, & Bryant, 1998; Harvey & Bryant, 1998; Shalev, Peri, Canetti, & Schreiber, 1996). Although there is a dearth of research with children, Saxe and collaborators (Saxe, 2002) have reported that among child burn patients, dissociation as evaluated by adults was a significant predictor of later PTSD symptomatology.

Some studies that have not replicated these findings have methodological problems, including a lack of specific measures to evaluate ASD (Barton, Blanchard, & Hickling, 1996) or low statistical power and a measurement time frame inconsistent with ASD criteria (McFarlane, Atchison, & Yehuda, 1997). Nevertheless, a number of issues about ASD require more investigation, including criteria that might optimize diagnostic sensitivity and specificity of dissociative and other ASD symptoms (Brewin et al., 1999), the biology of peritraumatic dissociation (Griffin, Resick, & Mechanic, 1997), and risk predictors for peritraumatic dissociation (Morgan et al., 2001). Valid and reliable instruments to help this inquiry have been developed (Bryant & Harvey, 1997; Cardeña, Koopman, Classen, Waelder, & Spiegel, 2000). It will be useful to evaluate peritraumatic biological indicators as well, because there is evidence that increased heart rate and lower cortisol levels at that time may predict later PTSD (Yehuda, McFarlane, & Shalev, 1998).

Some evidence indicates that compared with men, women experience—or at least report—greater peritraumatic dissociation. In a reanalysis of our earlier study on professional students exposed to an earthquake (Cardeña & Spiegel, 1993), we found that about 2 weeks after the incident, women reported significantly greater time distortion, derealization, and depersonalization reactions than did men (df 95, p .001), but this difference disappeared 4 months after the incident (p .1). A gender difference was also found in a general sample exposed to a firestorm (Koopman et al., 1996). There is also some evidence that younger people experience or report more peritraumatic dissociation (Marmar, Weiss, Metzler, & Delucchi, 1996). Recently, Koopman and collaborators (2001) reported that minority Vietnam veterans with PTSD reported more peritraumatic dissociation than did nonminority veterans, but that study did not control for SES. Zatzick, Marmar, Weiss, and Metzler (1994) controlled for that factor and found no independent contribution of ethnicity. Marshall and Orlando (2002), in a study on victims of community violence, found evidence that degree of acculturation in their minority Latino sample was negatively correlated to peritraumatic dissociation.

Posttraumatic Stress Disorder

History

Although posttraumatic pathology has been described for centuries, it was not until the twentiethcentury that systematic research and theory started in earnest. Some earlier antecedents of the PTSD construct include so-called traumatic neurosis, soldier’s heart, and shell shock (van der Kolk, Weisaeth, et al., 1996). Some of the great clinical pioneers— Charcot, Janet, and Freud among them—wrote on posttraumatic conditions, and the psychiatrist Stierlin concluded in the early part of the twentieth century that posttraumatic reactions (fright neurosis) were not rare and did not require a psychopathological predisposition (van der Kolk, Weisaeth, et al., 1996). World War I brought forth important theoretical and clinical work by Charles Myers and W. H. Rivers in Great Britain; this work continued being developed during World War II by Kardiner, Grinker and Spiegel, and other eminent figures. At about the same time, Lindemann (1944), in his classic paper on the symptomatology and management of acute grief, documented the fundamental categories of PTSD symptoms—intrusion, avoidance, and hyperarousal—that form the basis of the diagnostic criteria today (APA, 1994). He noted that the severe disruption that followed trauma, with physical agitation, emotional distress, and disturbed patterns of sleep, seemed to be a necessary processing of loss—a kind of grief work that prepared the traumatized individual to reenter life and relationships. Later, Horowitz (1986) noted the importance of affective dysregulation in the posttraumatic period. Related symptoms were either undermodulated, as with intrusion and hyperarousal symptoms, or overmodulated, as with avoidance symptoms, and both could occur in sequence in the same person.

Symptomatology

The DSM-IV (APA, 1994, 2000) diagnostic criteria for PTSD include—in addition to exposure to the criterion stressor criteria discussed previously—at least one intrusion, three numbing, and two hyperarousal symptoms. The intrusion symptoms include recurrent and intrusive distressing recollections of the traumatic event, dreams or nightmares about the event, reliving the experience, flashback episodes, illusions or hallucinations (related to the event), intense distress at exposure to cues that represent an aspect of the traumatic event, and physiological reactivity on exposure to cues concerning the event (APA, 1994, 2000). The numbingavoidance symptoms include 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 or participation in significant activities, feelings of detachment or estrangement from others, restricted range of affect (e.g., inability to have loving feelings), and sense of a foreshortened future (APA, 1994, 2000). The hyperarousal symptoms include difficulty falling or staying asleep, irritability or outbursts of anger, difficulty concentrating, hypervigilance, and exaggerated startle response (APA, 1994, 2000). The disorder must also last at least 1 month. It is considered acute if it lasts less than 3 months and chronic if it lasts more than 3 months. It must cause significant distress or impairment in social, occupational, or other important areas of functioning.

Those with PTSD often have other comorbid psychiatric symptoms and disorders, such as social anxiety (e.g., Crowson, Frueh, Beidel, & Turner, 1998), other anxiety and mood disorders (e.g., Breslau & Davis, 1992), suicide attempts (e.g., Davidson, Hughes, Blazer, & George, 1991), dissociative symptoms (Yehuda et al., 1996), substance abuse (e.g., Cottler, Compton, Mager, Spitznagel, & Janca, 1992; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995), and personality disorders (e.g., Southwick, Yehuda, & Giller, 1993).

Etiology

Ideas about the etiology of PTSD have fluctuated between an emphasis on the nature of the stressed person and the nature of the stressor. In the middle of the twentieth century, psychiatry in the United States came under the increasing domination of psychoanalytic theory. Freud had postulated that combat neurosis was a variation of other neuroses arising from unresolved dynamic conflicts based on problems in psychosexual development (Freud, Ferenczi, Abraham, Caligor, & Jones, 1921). His theory held that early life difficulties in development determined psychopathology more than did the combat trauma itself. This perspective led to attempts to link combat trauma to what are now called personality disorders (Henderson & Moore, 1944). Freud developed his metapsychology (Freud, 1916–1917/1963) after he abandoned the trauma theory of the etiology of the neuroses. He formulated symptoms as expressions of dynamic unconscious conflict between incestuous libidinal wishes and harsh superego strictures against such wishes. The linking of personality disorders to posttraumatic symptomatology had the disadvantage of scapegoating emotional casualties of combat—in essence, blaming the victims rather than the combat trauma for the disorder.

There is a fundamental conflict between the psychodynamic and the PTSD models. Preoccupation with early childhood development and the world of the unconscious tends to minimize the importance of the role of trauma and the intrusion of reality later in life—that is, unconscious language tends to be extreme and dramatic, blurring the distinction between fantasy and reality. Initially, one of the reasons that the diagnosis of PTSD was overlooked or minimized was a prevailing assumption that the diathesis was more important than the stress—that people who developed symptoms after trauma such as combat had serious psychiatric problems, especially personality disorders, prior to the trauma that accounted for the response to it. From this point of view, the trauma was merely a trigger for an exacerbation of symptoms of a preexisting disorder.

Reaction to this viewpoint spawned several decades of research with the opposite point of view—that is, that PTSD developed in a minority of normal individuals who were subjected to serious physical stress independent of their personality or early life experience. A study of World War II veterans found that only a quarter of acute psychiatric casualties of combat had a preexisting psychiatric diagnosis (Torrie, 1944), and some later studies posited no relationship between prior psychopathology and PTSD (e.g., Ursano, 1981).

More recently, however, the pendulum has begun to swing a bit back to the earlier position. Several studies indicate that a history of previous PTSD due to earlier life trauma does sensitize individuals to the reoccurrence of PTSD when they endure subsequent trauma (Brewin et al., 2000). These individuals may be asymptomatic prior to the trauma, but they seem to retain a vulnerability that may elicit memories and symptoms related to earlier life trauma. For example, Baider and colleagues (Baider, Peretz, & Kaplan De-Nour, 1992) observed that Holocaust survivors who develop cancer often experience a recrudescence of their long-dormant posttraumatic stress symptoms.

Even though early life trauma may predispose individuals to the development of PTSD in the wake of subsequent trauma, this phenomenon does not reduce the salience of the stress itself in the production of PTSD symptoms (Figley, 1978; Spiegel et al., 1988). There is growing evidence that exposure to traumatic stressors is almost the norm rather than the exception. In one study of 1,007 young adults from an HMO practice in Detroit, Breslau and collaborators (Breslau, Davis, Andreski, & Peterson, 1991) found a high lifetime prevalence of exposure to traumatic events of 39.1%. The rate of PTSD among those exposed was 23.6%, yielding a lifetime prevalence of PTSD in this sample of 9.2%. Those with PTSD also suffered increased risk for anxiety and mood disorders. A similar prevalence rate of combat-related PTSD (Keane & Fairbank, 1983) provides compelling evidence that trauma exposure frequently leads to PTSD. However, such data leave open the question of what differentiates those who were symptomatic from the three out of four who are exposed but did not develop PTSD symptoms. A comprehensive meta-analysis of risk factors (Brewin et al., 2000) concluded that pretrauma factors have a consistent but weak relationship to subsequent PTSD, whereas such posttrauma factors as lack of social support may have a higher impact.

Sensitization theory (Silver & Wortman, 1980) holds that prior exposure to trauma takes a toll on an individual’s resources for coping with subsequent trauma. This can occur by a reactivation of memories of prior trauma during exposure to subsequent trauma, adding to its burden. Indeed, it has been commonly observed in Vietnam veterans that even comparatively mild subsequent stressors, such as a minor auto accident, can elicit major traumatic responses (Spiegel, 1981), especially in those with previous significant trauma exposure (Breslau, Chilcoat, Kessler, & Davis, 1999). Even the unexposed offspring of Holocaust survivors show physiological and psychological signs of PTSD sensitization (Yehuda, Halligan, & Bierer, 2001).

There is also fascinating recent evidence of permanent hypothalamic-pituitary-adrenal (HPA) dysregulation in adults who suffered sexual and physical abuse as children and have symptoms of depression and PTSD (Heim et al., 2000).Avast number of psychobiological abnormalities involving psychophysiology, neurohormonal systems, and neuroanatomical and immunological effects have been related to PTSD (van der Kolk, 1996). One of the areas that has received more attention is hippocampal atrophy among individuals with PTSD. Various studies have found decreased dendritic branching and smaller hippocampal volume among these individuals, although not every study has replicated these results (Bremner, 2002).

Another compelling theory is that certain personality characteristics such as neuroticism and extroversion predispose some to trauma exposure and therefore to a higher prevalence of PTSD (Breslau, Davis, & Andreski, 1995). Secondary losses and gains subsequent to trauma may either reinforce or diminish the odds that a transient symptom picture will become chronic. We now turn our attention to a proposed and severe variant of PTSD that is spawning a wealth of research, clinical observations, and treatment strategies.

Complex PTSD

Concept

Historically, PTSD has been defined as a syndromic response to a specific delimited traumatic event (APA, 1994), with the symptom constellation and comorbidity mentioned previously. However, in 1992, Judith Herman proposed that the traditional diagnostic categories neither suited nor captured the features associated with conditions of extreme and protracted traumatic stress, such as some cases of childhood sexual and physical abuse, prolonged persecution or captivity as a hostage or POW, or chronic domestic battery. Herman (1992a) noted that there were three broad areas of disturbance among such patients: the complexity and tenacity of their symptom profiles, the event-related characterological changes they undergo that undermine their experience of relatedness and identity, and their vulnerability to repeated selfor other-inflicted harm. Conventional diagnostic groupings, including PTSD symptom criteria, either simply overlooked these aspects or fitted such clinical presentations into traditional categories. Thus, Herman (1992a, 1992b) proposed a new diagnostic category, complex PTSD, noting that “responses to trauma are best understood as a spectrum of conditions rather than a single disorder. They range from a brief stress reaction that gets better by itself and never qualifies for a diagnosis, to classic or simple post-traumatic stress disorder, to the complex syndrome of prolonged, repeated trauma” (Herman, 1992b, p. 119).

Herman’s proposal addressed observations made and issues raised by earlier commentators, including clinical reflections that the simple PTSD concept was inadequate to describe or account for the severity and multiplicity of effects seen in Holocaust survivors or refugees (Kroll et al., 1989; Niederland, 1968). Additionally, Terr (1991) had observed that childhood traumatic stressor events came in two types: “single-blow” traumas (Type I; p. 14) and traumas that result from “long-standing or repeated ordeals” (Type II; p. 11) and that each was associated with a different constellation of emotional, cognitive, and behavioral symptoms. Similarly, in reviewing the long-term effects of childhood sexual abuse, Finkelhor (1988) argued that PTSD was not the appropriate diagnostic label for these outcomes because it did not capture the functional impairment and other abuse-specific symptomatology present in the condition.

Diagnosis

The diagnosis of complex PTSD (also known within the literature as a disorder of extreme stress not otherwise specified; DESNOS) that Herman (1992b) proposed required that the individual must have suffered a history of subjection to totalitarian control over a prolonged period. Additionally, it included diagnostic symptomatic and characterological features not addressed in the classic PTSD diagnosis:

• Alterations in affect regulation, including persistent dysphoria, suicidal preoccupation, self-injury, under- or overregulated anger, and compulsive or inhibited sexuality.
• Alterations in consciousness, including memory disturbances, transient dissociative experiences, depersonalization-derealization, and reliving experiences.
• Alterations in self-perception, including feelings of helplessness; paralysis of initiative; defilement; stigma; difference from others; and shame, guilt, and self-blame.
• Alterations in perception of the perpetrator, including preoccupation with the relationship, idealization or paradoxical gratitude, a sense of a special or supernatural relationship, unrealistic attribution of total power to perpetrator, and acceptance of the belief system or rationalizations of the perpetrator.
• Alterations in relations with others, including isolation and withdrawal, disruption of romantic relationships, distrust, repeated failures of self-protection, and repeated search for a rescuer.
• Alterations in systems of meaning, which may manifest as a loss of sustaining faith, a sense of hopelessness and despair, or both.
• Disturbances in somatic functioning, such as somatization symptoms, a central feature of this disorder often not included in measures of complex PTSD and DESNOS (Herman, 1992a; Pelcovitz et al., 1997; Roth, Newman, Pelcovitz, van der Kolk, & Mandel, 1997; van der Kolk, 1996).

Empirical support for this new diagnosis has come from a number of studies. Zlotnick and colleagues (1996) found that women with a history of childhood sexual abuse showed increased severity of symptoms of somatization, dissociation, hostility, anxiety, alexithymia, social dysfunction, maladaptive schemas, self-destruction, and adult victimization when compared to women without such histories. van der Kolk, Pelcovitz, and colleagues (1996) found that participants in the DSM-IV field trial for PTSD who had experienced physical or sexual assaults in childhood (before age 14) were significantly more likely than were participants who had experienced a disaster at some time in their lives to report difficulties with all three of the following DESNOS symptom areas: affect regulation, dissociation, and somatization; they were also more likely to endorse various individual DESNOS-related items.

There is also evidence that a DESNOS diagnosis has different treatment implications. Ford (1999) found that the DESNOS (but not the PTSD) classification was associated with early childhood trauma, extreme levels of reexperiencing, impaired characterological functioning, and use of intensive psychiatric services in military veterans seeking inpatient PTSD treatment (see also Newman, Orsillo, Herman, Niles, & Litz, 1995). Ford and Kidd (1998) reported that a DESNOS diagnosis predicted poor PTSD treatment outcome independent of the effects of a PTSD diagnosis or early childhood trauma history, indicating that the presence of DESNOS should be assessed and considered in planning treatment for those with chronic PTSD. Ford (1999) concluded that although PTSD and DESNOS are often comorbid, they are distinct syndromes.

The DSM-IV PTSD field trial (Pelcovitz et al., 1997; Roth et al., 1997; van der Kolk, Pelcovitz, et al., 1996) also sought to evaluate the feasibility and utility of the complex PTSD and DESNOS categorization. Preliminary findings from a study of 234 participants with a history of sexual abuse, physical abuse, or both (Roth et al., 1997) found that for women, sexual abuse—particularly in combination with physical abuse—was a risk factor for complex PTSD (see also Hall, 1999). Patients with a history of both sexual and physical abuse were 14.5 times more likely to warrant a complex PTSD diagnosis than were patients who had not experienced both types of abuse. In addition, preliminary findings in the trials indicated that complex PTSD was rarely found among non-trauma-exposed survivors (those who did not meet the stressor criterion for PTSD) and rarely occurred without concurrent PTSD. In the same field trials, a useful, psychometrically sound, structured interview for disorders of extreme stress was developed (Pelcovitz et al., 1997).

Although Herman’s (1992a, 1992b) classification was not included in DSM-IV (APA, 1994), 9 of 12 of the associated features listed for PTSD are derived from her formulation (Roth et al., 1996). Additionally, the International Classification of Diseases–10th Revision (ICD-10; World Health Organization), published in 1992, included a similar disorder named enduring personality change after catastrophic experience. Commenting on the inclusion of this disorder, Kinzie and Goetz (1996) observed, “the absence of a similar disorder in the DSM-IV is puzzling” (p. 173). Given the growing evidence supporting the plurality of traumatic stress responses and the demonstrated utility of assessing complex PTSD or DESNOS in some traumatized samples, it seems likely that complex PTSD will be incorporated into future American psychiatric nosologies; it is already informing clinicians who treat patients with histories of extreme, repeated trauma.

Dissociative and Conversion Disorders

What are now called the dissociative and conversion disorders in DSM-IV would map quite directly onto the hysterical symptoms that were a central concern of the clinical pioneers in France, Austria, and the United States at the end of the nineteenth century (Spiegel & Cardeña, 1991). Nonetheless, the investigation of pathological (or normal) alterations of consciousness and their relationship to somatic functioning were neglected during later decades and have just recently gained preeminence among many clinicians and researchers (Cardeña, 1997a; Hilgard, 1994). This interest, however, has not gone unchallenged; some critics have questioned the validity of dissociative amnesia and dissociative identity disorder (DID).We discuss these controversies later in this research paper.

Our review emphasizes dissociative disorders among adults, although there is a small but growing literature on children and adolescents (e.g., Putnam, 1994) going back at least to the eighteenth century. Because the term dissociation is used to signify different areas of inquiry in psychology and other disciplines, it is worthwhile to establish some distinctions at the beginning. In cognitive psychology, general dissociation implies differential performance in apparently related cognitive tasks such as comprehension of nouns and adjectives. For our purposes in clinical and personality psychology, the term dissociation has three main senses (Cardeña, 1994):

1. It is a descriptive construct for a lack of association between psychological processes that should be integrated and cannot be explained merely by overlearning or inattention (e.g., he cannot recall his name even though there is no neurological damage that can explain this amnesia).
2. It is a descriptive construct for an alteration of consciousness characterized by experiential detachment from the self or the environment (e.g., I felt that my body was moving on its own).
3. It is an explanatory construct denoting an intentional defense mechanism (e.g., she dissociated her body sensation to tolerate the rape while it was occurring; see Nemiah, 1995).

Other distinctions can also be made. Dissociative phenomena are not necessarily pathological and can occur in benign contexts such as hypnosis, meditation, or religious rituals (Cardeña, 1997b). Distressing or dysfunctional dissociative symptoms can be secondary symptoms of neurological (e.g., seizure disorder) or psychiatric conditions (e.g., panic attacks), whereas dissociative disorders, which we cover in this research paper, involve dissociative symptoms as the main presenting problem and have a mainly psychological rather than neurological etiology.

Dissociation can occur in every major psychological process, including the sense of self, sense of the environment, or both (e.g., depersonalization, derealization); emotions (e.g., disconnection between emotional behaviors and awareness of them); physical sensations and agency (e.g., conversion disorders); memory (e.g., psychogenic or dissociative amnesia); and identity (e.g., DID; Butler et al., 1996; Cardeña, 1997b). One final distinction, first made by Pierre Janet, distinguishes positive symptoms (exaggerations or additions to normal processes such as the flashbacks in PTSD) and negative symptoms (diminution of normal processes, such as lack of memory for one’s name; Janet, 1907/1965). The DSM-IV defines a dissociative disorder as a “disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment” (APA, 1994, p. 477) that is distressing, impairs basic areas of functioning, or both.

Repression and dissociation have often been used interchangeably to explain the same manifestations (e.g., the inability to remember a traumatic event), with some authors defining repression as a defense mechanism to ward off internal pressures and dissociation as an alteration in consciousness to deflect the overwhelming impact of ongoing trauma. The first term is readily identifiable with Sigmund Freud, whereas dissociation is closely linked to the work of Pierre Janet. In the view of Janet, as elaborated by Hilgard, dissociation refers to a different model of mental structure in which information is stored in units that are separate from but relatively accessible to consciousness, unlike the traditional psychodynamic repression model that views the contents of the unconscious as disguised and in need of translation (Hilgard, 1994). Notwithstanding these perspectives, dissociation can be used to describe the lack of integration among psychological processes such as memory or identity or to refer to an experienced disconnection with the self or the environment, without necessarily having to endorse either Janet’s or Freud’s position.

Etiology

The DSM-IV, following decades of clinical observations and studies, asserts that the dissociative disorders are commonly linked to severe stress (e.g., serious emotional conflict) and traumatic events (e.g., early abuse, especially if the events are chronic and severe; e.g., Terr, 1991). Nonetheless, they do not constitute a sufficient cause; otherwise, every seriously traumatized individual would end up having a dissociative disorder, which is clearly not the case. It should also be noted that, for instance, a home where abuse occurs is also one where neglect and chaos can be expected (Widom, 1999), so it is difficult to disentangle traumatic events from related circumstances. Nonetheless, there is new and strong evidence, based on an extensive twin study, that reported childhood sexual abuse has various deleterious consequences, even after controlling for family background (Nelson et al., 2002). Proposed diatheses for development of dissociative disorders include an inborn disposition to dissociate (Jang, Paris, Zweig-Frank, & Livesley, 1998; but see Waller & Ross, 1997) or to be highly hypnotizable (Butler et al., 1996). More recently, a growing database has been providing compelling evidence that specific forms of early attachment (especially avoidant and disorganized) are strong predictors of pathological dissociation (e.g., Ogawa, Sroufe, Weinfield, Carlson, & Egeland, 1997).

The account of dissociative symptoms and disorders originating—at least in part—in actual experiences of trauma (or traumatogenic theory) has been challenged by skeptics of the validity of dissociative amnesia and DID. This latter account posits that these disorders are brought about by the shaping and reinforcement of symptoms by therapists (the iatrogenic theory) or the culture (the sociocognitive theory). We address these proposals in the sections for amnesia and dissociative identity disorders.

Epidemiology and Demographics

Regrettably, major nationwide epidemiological surveys have not systematically evaluated the prevalence of the dissociative disorders, probably following the conclusion by Mezzich, Fabrega, Coffman, and Haley (1989) that such disorders are rare even in a psychiatric population; however, more recent studies with community and clinical samples show that this is not the case. Gleaves (1996) reviewed studies on the prevalence of dissociative disorders among various clinical populations, which ranged between 10% (clients with obsessive-compulsive anxiety disorder) and 88% (women reporting sexual abuse). Studies in countries other than the United States have also found significant rates of dissociative disorders, including 10% in a Turkish university clinic (Tutkun, Sar, Yargic, Ozpulat, Yanik, & Kiziltan, 1998), and 8% in a Dutch clinical sample (Friedl & Draijer, 2000). Ross (1991) sampled a nonclinical Canadian population (n = 454) and found that 11% seemed to have a dissociative disorder of some type, although this latter figure may be an inflated estimate of the actual prevalence in a nonclinical population, at least using DSM-IV criteria.

With respect to age, various studies in the United States and Europe (Vanderlinden, van der Hart, & Varga, 1996) suggest that dissociation reaches its peak somewhere in early adolescence and then gradually declines in a manner similar to that of hypnotizability (Hilgard, 1968).

Moving to the impact of SES on the prevalence of dissociative phenomena, a study with a Canadian community sample found no significant relationship (Ross, 1991; see also Vanderlinden et al., 1996). With respect to peritraumatic dissociation, one study (Koopman et al., 2001) found a significant effect for ethnicity; however, in another study that controlled for SES, the difference disappeared (Zatzick et al., 1994). With respect to the culture-bound syndromes with a dissociative component, both pathological spirit possession and ataque de nervios are predominantly found among women of lower SES, whereas amok, berserk and similar assault conditions are mostly found among men (LewisFernández, 1994; Simons & Hughes, 1985).

Other than those for DID, wherein the vast majority of identified clients are female, findings do not appear to be consistent as to the gender distribution of other dissociative disorders (e.g., Varnderlinden et al., 1996). Nonetheless, Kluft (1996) cautions that the reported ratio of about 9:1 female to male DID patients may be skewed because some males with DID end up in the legal system and are not assessed in epidemiological studies (see also Lewis, Yeager, Swica, Pincus, & Lewis, 1997). Although it has not been studied systematically, there are reports that DID patients seem to come from middle- to low-SES groups (Barach, personal communication, 1996; Coons, 1996).

Disorders

Many varieties of dissociative manifestations in technological and nontechnological cultures are unrelated to distress or dysfunction (Cardeña, 1997b). In the following sections, we confine our discussion to the dissociative pathological manifestations included in the DSM-IV: Dissociative amnesia and dissociative fugue, DID, depersonalization, DDNOS, and the related conversion disorder.

Dissociative Amnesia

According to the DSM-IV, dissociative amnesia (previously called psychogenic amnesia) is characterized by one or more instances of amnesia for important personal information that cannot be explained by ordinary forgetfulness, the common developmental amnesia for the first years of life, or an organic condition. Dissociative amnesia typically involves problems with explicit memory (awareness of personal information or previous experience), whereas implicit memory (i.e., general knowledge such as language, habits, conditioned responses, etc.) is generally but not always preserved (van der Hart & Nijenhuis, 2001).Another general distinction is that dissociative amnesia is typically partially or fully reversible, whereas amnesias with a neurological etiology generally show no (or very gradual and slight) recovery. Careful research does not support a malingering explanation for this condition.

Episodes of amnesia can differ with regard to frequency, extent, and temporal parameters. Patients can have one or few episodes of amnesia, or they can have a chronic condition. The episodic type may involve an individual’s sudden forgetfulness of some or most aspects of his or her life, often after a severe traumatic event. In contrast to this presentation, Coons and Milstein (1992) described chronic forms of amnesia typically associated with reported history of early abuse and involving one or more of the following: episodes of missing time, unexplainable forgetfulness, chronic amnesia for periods that should be remembered (e.g., not remembering events before the person was 13 years of age), and so on.

Amnesic episodes can also be characterized as generalized, selective, localized, or systematized. Generalized amnesia involves amnesia for all or most personal information, including name and personal history, whereas selective amnesia involves forgetting some (but not all) aspects of an event (e.g., remembering just some aspects of a rape incident). Localized amnesia refers to amnesia for a certain period of time—hours, days, or longer. Finally, systematized amnesia refers to the inability to remember certain categories of information, such as all memories about one’s family. Coons and Milstein (1992), in a study with 25 patients, found that the majority of cases were chronic and selective. The loss of memory following a traumatic event is typically concurrent or retrograde to the event, and the person is still able to learn new material. This pattern contrasts with a number of neurologically caused amnesias in which the inability to remember new information is continuous (e.g., various dementias, alcohol amnestic syndrome).

The onset of dissociative amnesia is closely related to severe stress or exposure to trauma, including war experiences, natural disaster, violence, childhood abuse, serious legal or marital problems, depression, and suicide attempts (Coons & Milstein, 1992; Loewenstein, 1991). The precipitating event(s) for dissociative amnesia can be complex and involve idiosyncratic elements; the traumatic events ma yinteract with a preexisting tendency to dissociate and with personal psychodynamics.

As with the other dissociative disorders, comorbid symptomatology of dissociative amnesia frequently includes depression, anxiety, and episodes of depersonalization and unawareness of the surroundings. If there is a history of early and chronic abuse, a more complex syndrome that also includes self-injurious behavior, substance abuse, and sexual problems may be present (Cardeña & Spiegel, 1996; see also this research paper’s section on complex PTSD).

The differential diagnosis of dissociative amnesia includes other dissociative disorders that are superordinate to amnesia (i.e., dissociative fugue, DID, ASD, PTSD, and somatization). Medical conditions that can produce amnesias should also be considered, including transient global amnesia (Rollinson, 1978), amnestic alcohol or Korsakoff’s syndrome, head injury, epilepsy, dementia, amnesic stroke, postoperative amnesia, postinfectious amnesia, alcoholic blackout, and anoxic amnesia (Kopelman, 1987; Sivec & Lynn, 1995). The effect of psychoactive drugs and malingering, when likely, should also be ruled out (Good, 1993). The clinician should be mindful that amnesia may not be a presenting problem because clients may have amnesia for the amnesic episodes, or they may assume that these episodes of forgetfulness are shared by everybody else.

Earlier reports of dissociative amnesia and fugue concentrated on male soldiers in time of war, whereas more recent work (e.g., Coons & Milstein, 1992) has reported a preponderance of females. As with the other dissociative disorders, dissociative amnesia seems to be a condition affecting mostly young adults (Cardeña & Spiegel, 1996).

A thorough discussion of the current controversy about what have been called recovered memories is beyond the scope of this research paper, but notwithstanding some skepticism (e.g., Loftus, 1993), there is considerable evidence confirming the existence of this clinical phenomenon. First, the literature contains dozens of studies—retrospective, prospective, and using various samples, types of trauma, and measurements, including current videotaping (Corwin & Olafson, 1997)— that support the reality of dissociative amnesia and the recovery of corroborated previously forgotten memories (Brown, Scheflin, & Hammond, 1998; van der Hart & Nijenhuis, 2001). Second, the triggers to recover memories involve many mechanisms other than therapy (e.g., Herman & Harvey, 1997).Third, it is more useful to consider the amnesia process as fluctuating and involving different levels of awareness of the forgotten material (Kopelman, Christensen, Puffett, & Stanhope, 1994; Schooler, 1994) than it is to think of such memories as completely irretrievable. Fourth, there are both cognitive (Schooler, 1994) and neurophysiological (Bremner, Krystal, Southwick, & Charney, 1995) mechanisms that may explain both dissociative amnesia and the recovery of the forgotten material. Fifth, the external validity of some recovered memories does not in any way negate the reality of confabulation and suggestive influences on memory (Loftus, 1993). In fact, both processes are two sides of the same coin, showing the malleability of memory and the effect of suggestive influences (self- or other-generated) to forget matters that did occur or remember matters that did not occur (Butler & Spiegel, 1997).

Dissociative Fugue

Some use the term fugue to describe temporary unawareness of surroundings, but the term has a different connotation in psychopathology. Dissociative fugue is defined by the DSMIV (APA, 1994, 2000) as a sudden wandering away from home or place of employment; it is associated with global amnesia for one’s past and confusion about personal identity or adoption of a new identity. The DSM-IV follows the tradition of presenting amnesia and fugue as distinct diagnoses, although it can be argued that dissociative fugue is simply a variant of generalized amnesia.

Before the DSM-IV, the diagnosis was restricted to individuals who actually adopted a new identity, as in William James’description of the ReverendAnsel Bourne, who left his hometown, adopted a new name and profession, and did not recall his previous identity until much later (Kenny, 1986). Although it is not too uncommon to read in newspapers of modern-day Bournes, recent studies show that the most common presentation is confusion about one’s identity rather than adoption of a new one (Loewenstein, 1991; Riether & Stoudemire, 1988). Of course, an undetected and unresolved case of identity confusion may develop a new identity.

As for the nature of this confusion of identity, William James (1890/1923) saw it as a long-lasting trance, and Stengel (1941, in Loewenstein, 1991, p. 255) described it as “states of altered or narrowed consciousness with the impulse to wander,” consistent with Janet’s view of dissociation as involving a focusing and narrowing of consciousness (van der Kolk, Weisaeth, et al., 1996) and with some more recent studies (Cardeña & Spiegel, 1993; Christianson & Loftus, 1987). As in the case of amnesia, traumatic events and severe stress are the common precipitants of this condition. Older Bibliography: on dissociative amnesia and fugue centered on soldiers at time of war (e.g., Grinker & Spiegel, 1945; Kardiner & Spiegel, 1947), but most current cases involve civilians fleeing the terrors of urban life. In a comprehensive review, Loewenstein (1991) noted that in our nomadic modern societies, some patients do not complain of fugue unless they are queried about it, and some abused individuals may have episodes of fugue without anybody noticing it.

Regarding differential diagnosis, a DID diagnosis is superordinate to that of fugue. Conditions that should be ruled out include postictal episodes of aimless wandering or socalled poriomania (Mayeux, Alexander, Benson, Brandt, & Rosen, 1979), which are typically of shorter duration; manic and psychotic episodes accompanied by traveling; neurological conditions such as brain tumors; and drug-related episodes of amnesia and wandering.

Dissociative Identity Disorder

By far the most widely studied and controversial dissociative condition is DID, a new term for what used to be called multiple personality disorder. According to the DSM-IV, it involves the presence within the person of two or more identities or personality states (also known as alters)— with characteristic behaviors, moods, memories, and other characteristics—that recurrently manifest themselves to take control of the individual (APA, 1994, 2000). Psychogenic amnesia is another criterion, although in the case of DID the issue of amnesia is complex because an alter may claim to remember events that another alter cannot recall. The interalter amnesia is both complex and inconsistent with a simple malingering hypothesis (Eich, Macaulay, Loewenstein, & Patrice, 1997). As with the other diagnoses, the symptoms must produce distress or impairment.

There were two main reasons that the name of this condition was changed from multiple personality disorder to DID in the DSM-IV. The first was that the older term emphasized the concept of various personalities (as though different people inhabited the same body), whereas the current view is that DID patients experience a failure in the integration of aspects of their personality into a complex and multifaceted integrated identity. The International Society for the Study of Dissociation (1997) states it this way: “The DID patient is a single person who experiences himself/herself as having separate parts of the mind that function with some autonomy. The patient is not a collection of separate people sharing the same body.”

Another reason for the name change is that the term personality refers to characteristic pattern of thoughts, feelings, moods, and behaviors of the whole individual. The fact that patients with DID consistently switch between different identities, behavior styles, and so on is a feature of the individual’s overall personality. Other phrasing changes in diagnostic criteria clarified that although alters may be personalized by the individual, they are not to be considered as having an objective, independent existence.

It is generally considered that DID is the most severe of the dissociative disorders, and it is certainly the most studied. Originally only a few authors were responsible for most of the research in this area, but there has been a steady growth in the number of contributors to the field. Although it may be true that the majority of clinicians have not treated a DID patient, acceptance of the diagnosis among psychologists and psychiatrists is considerable (Dunn, Paolo, Ryan, & van Fleet, 1994).

DID is the most controversial of all of the dissociative disorders, partly because of the recent increase in its diagnosis (Boor, 1982). Positions range from those who believe that the condition is mostly or completely iatrogenic (e.g., AldridgeMorris, 1989), produced by naive therapists and the media; to those who state that the condition is not necessarily iatrogenic but is molded by cultural expectations and social roles and strategies (e.g., Spanos, 1994); to those who believe that DID is a valid and specific diagnosis (e.g., Putnam, 1989).

Proponents of the iatrogenic explanation point out that DID patients show significantly higher hypnotizability than do other clinical groups and normal individuals (Frischholz, Lipman, Braun, & Sachs, 1992) and are thus prone to follow manifest or subtle suggestions provided by hypnotists probing for possible hidden personalities or alters. At least two studies (Putnam, Guroff, Silberman, Barban, & Post, 1986; Ross, Norton, & Fraser, 1989) have answered this objection by showing that neither the use of hypnosis nor other proposed therapist characteristics account for who gets a DID diagnosis. Also, if the majority of DID patients were just following clinicians’ suggestions, they would have adopted other diagnoses or their symptoms would have been suggested away because the vast majority of such patients had received a number of other previous diagnoses, and many clinicians do not believe in or use the DID diagnosis (Coons, Bowman, & Milstein, 1988; Putnam et al., 1986). In a balanced overview of the DID controversy, Horevitz (1994, p. 447) stated that “critics who claim multiple personality disorder [DID] is nonexistent, rare, iatrogenic, or overdiagnosed may be right or they may be wrong. However, no data at present exists to directly support these contentions” (see also Gleaves, 1996). In fact, there is good evidence for the diagnostic validity of DID using standard clinical criteria (Gleaves, May, & Cardeña, 2001). Also, recent studies using brain imaging technology provide independent corroboration for the reality of switching from one alter to another (Tsai, Condie, Wu, & Chang, 1999) and for the diagnosis as a whole (Sar, Unal, Kiziltan, Kundakci, & Ozturk, 2001).

The fact remains, however, that DID is more frequently diagnosed in the United States than it is in other countries, although there is growing evidence for its validity, reliable diagnosis, and similar prevalence in other places (e.g., Boon & Draijer, 1991; Coons, Bowman, Kluft, & Milstein, 1991; Tutkun et al., 1998). In addition to the iatrogenetic account of this phenomenon, there are other possible explanations, including (a) clinicians in the United States may have greater knowledge of diagnosis and treatment of this disorder, whereas other countries are lagging behind; (b) the etiological circumstances that spawn the condition—namely childhood sexual and other abuse—may be more common in the United States than in other places; or (c) DID may be a more acceptable idiom of distress, so to speak, in the United States than in other countries.

It is also worth noting that a number of studies have found independent corroboration (e.g., medical or legal records; corroboration from family members) for DID patients’ reports of abuse (Coons, 1994; Lewis et al., 1997). This does not mean, of course, that all reports, or all details of every report, are valid or accurate, but it shows that at least a significant proportion of DID patients have verifiable histories of abuse.

The course and prognosis of DID depend on the symptom severity and characterological fragility of the patient, and there is evidence of a wide variety of recovery trajectories (Kluft, 1994). It is widely accepted that therapy for these patients typically takes a number of years (Putnam & Loewenstein, 1993). There is substantial comorbidity between DID, depression, affective lability (including self-injury attempts), anxiety, conversion and other somatoform disorders (headaches are almost always found among DIDs), personality disorders (especially avoidant and borderline) and schizophrenic-like first rank symptoms; substance abuse and eating disorders are not infrequent in DID either (Cardeña & Spiegel, 1996). By definition, DID includes psychogenic amnesia, and this condition is also associated with other dissociative symptoms, including fugue, depersonalization, and “trancelike” states. Although individuals with DID report some first rank symptoms such as auditory hallucinations, they typically have adequate reality testing outside of specific events such as fugues or flashbacks, and they do not usually present the negative symptoms of schizophrenia.

Depersonalization

The DSM-IV (APA, 1994) defines depersonalization as clinically significant persistent or recurrent experiences of feeling detached from one’s mental processes or body, without loss of realitytesting.Thepersonmayexperienceasenseofbeingunreal, dead, or unfeeling. Whereas psychotic episodes involve delusional beliefs, depersonalization episodes describe experiences of alienation from the self but without the impairment in reality testing encountered in psychosis. A depersonalized individual may feel like a robot or as if body movements are mechanical, whereas psychosis might entail holding delusional beliefs that one is turning into metal. Although it is sometimes used interchangeably with depersonalization— and typically co-occurs with it—derealization refers to a sense of unreality about the environment rather than the self.

The range of phenomena that involve alteration in the sense of self is very broad (Cardeña, 1997b), and some authors have tried to distinguish between various self-experience alterations such as out-of-body experiences, autoscopy, and depersonalization proper (Gabbard, Twemlow, & Jones, 1982). Jacobs and Bovasso (1992) proposed five different types of depersonalization: inauthenticity, self-negation, self-objectification, derealization, and body detachment. In their sample of students, self-objectification was more closely related to psychological disorganization than the other types were. The four most common features of depersonalization may be (a) an altered sense of self (e.g., my body doesn’t belong to me), (b) a precipitating event (e.g., an accident, marijuana use), (c) a senseofunrealityoradreamlikestate(e.g.,nothingseemsreal; I’m not real), and (d) sensory alterations (e.g., colors are less vibrant; voices sound strange; Cardeña, 1997b).

Depersonalization disorder should be distinguished from isolated or transient symptoms. The former involves psychologically caused depersonalization as the predominant disturbance, with recurrent and chronic episodes that cause distress or maladjustment. Depression and anxiety frequently co-occur with the condition. In contrast, depersonalization symptoms may be part of a larger clinical syndrome (e.g., DID, panic attacks) or may be unrelated to clinically significant distress or dysfunction. They may have psychological or neurological etiology (e.g., seizure disorders; Litwin & Cardeña, 2000). When depersonalization symptoms occur exclusively in the presence of another psychological disorder, the latter is the superordinate diagnosis. Depersonalization episodes are not uncommon among nonclinical populations and frequently occur during or shortly after a traumatic event (Koopman, Classen, Cardeña, & Spiegel, 1995; Noyes & Kletti, 1977) or as a byproduct of meditation (Lazarus, 1976), hypnosis (Cardeña & Spiegel, 1991), or the use of psychoactive substances (Good, 1993).

Because of the co-occurrence of depersonalization and anxiety symptoms, there has been discussion as to the validity of the depersonalization diagnosis, but recent systematic research (Simeon et al., 1997) has supported this construct.

Until recently, there was a dearth of systematic research on this condition (Coons, 1996), but in the last few years Simeon and collaborators have carried out a series of important studies. Their findings about depersonalization include related attentional and memory problems (Guralnik, Schmeidler, & Simeon, 2000), functional abnormalities in cortical areas associated with sensory integration and body schema (Simeon, Guralnik, Hazlett, et al., 2000), and hypothalamic pituitary-adrenal dysregulation (Simeon, Guralnik, Knutelska, Hollander, & Schmeidler, 2001). Consistent with the clinical literature, these authors have also concluded that reports of early abuse—especially emotional abuse—are strongly associated with later depersonalization (Simeon, Guralnik, Schmeidler, Sirof, & Knutelska, 2000).

Dissociative Disorders Not Otherwise Specified

This category includes dissociative pathologies of consciousness, identity, memory, or perception that do not fulfill the criteria of the disorders described so far. Examples from the DSM-IV include cases similar to DID that do not fulfill all the criteria, derealization without depersonalization, dissociative states produced by coercion, dissociative trance disorder, loss of consciousness without a medical condition, and Ganser’s syndrome. Many dissociative diagnoses in this and other cultures fall under this category. For instance, in a large general psychiatric sample (N 11,292), Mezzich et al. (1989) found the majority (57%) of dissociative disorder diagnoses to be atypical (a pre-DSM-IV designation of DDNOS). This figure is very similar (60%) to the one obtained by Saxe and collaborators (1993) in a subgroup of general psychiatric patients reporting clinical levels of dissociation. However, the epidemiological research by Ross (1991) did not find a large percentage of DDNOS diagnoses in that sample.

The studies of Lynn and Rhue (1988), H. Spiegel (1974), and Hartmann (1984) have respectively described subgroups of high fantasizers, hypnotic virtuosos, and thin-boundaried individuals who are vulnerable to distressing fantasies, excessive suggestibility, and uncontrolled loss of boundaries— traits that increase their risk for psychopathology. Some of these individuals may fulfill criteria for DDNOS because uncontrolled and disorganized fluctuations of consciousness are associated with psychopathology in this and other cultures (Cardeña, 1992). Nonetheless, the mere presence of unusual experiences is not indicative of psychological dysfunction (Cardeña, Lynn, & Krippner, 2000).

A substantial proportion of dissociative patients in other cultures have presentations that differ from the ones described so far, including unwanted and uncontrolled spirit possession (Cardeña et al., 1996; Saxena & Prasad, 1989) and medically unexplained loss of consciousness (van Ommeren et al., 2001). There are also various culture-bound syndromes that have dissociation as a central component, including ataque de nervios (which includes paresthesias, unawareness of surroundings and amnesia), startle responses such as latah, and emotional dysregulation syndromes such as amok (Simons & Hughes, 1985). Athorough consideration of social, political, gender, and cultural variables is required to understand these syndromes (Littlewood, 1998).

Conversion Disorder

Conversion disorder is included under the somatoform disorders section of the DSM-IV. This section groups syndromes suggestive of a general medical condition but whose etiology is judged to be primarily psychological. Although we only discuss conversion disorder, much of the research literature we review in the following also applies to other somatoform conditions, such as somatization disorder (similar to the earlier Briquet’s syndrome) and at least some forms of somatoform pain disorder. The DSM-IV criteria for conversion include one or more symptoms or deficits affecting voluntary motor (e.g., seizure-like movement or paralysis) or sensory function (e.g., somesthesias) that suggest a medical condition and psychological factors associated with the symptoms. These symptoms should not be intentionally produced or feigned and cannot be fully explained by a medical condition, the effects of a substance, or culturally sanctioned behavior or experience.

As mentioned previously, many of the so-called hysterical cases described at the turn of the century involved the joint presentation of somatoform and dissociative phenomena (Kihlstrom, 1994). The DSM taxonomy kept these phenomena as a hysterical neurosis of either dissociative or conversion disorder until its third edition, when it subsumed conversion types of reactions under the somatoform disorders (APA, 1980). The avowed reason was to alert clinicians to “the need to exclude occult general medical conditions or substance-induced etiologies for the bodily symptoms” (APA, 2000, p. 485).

Critics of this decision have adduced historical, conceptual, and empirical reasons to challenge this view (Cardeña, 1994; Kihlstrom, 1994; Nemiah, 1991). In support of this position, some studies have reported a substantial overlap of the somatization disorders, trauma history, and dissociative symptomatology in Western (e.g., Pribor, Yutzi, Dean, & Wetzel, 1993; Saxe et al., 1994) and non-Western (van Ommeren et al., 2001) cultures. The most formidable challenge to the separation of conversion and dissociative phenomena has come from the programmatic research of Ellert Nijenhuis and his collaborators (reviewed in Nijenhuis, 2000; see also Cardeña & Nijenhuis, 2000). Advancing the work originally described by Pierre Janet, W. H. Rivers, Charles Myers, and others, Nijenhuis has developed the Somatoform Dissociation Questionnaire, proposed an evolutionary account (based on animal defensive reactions), and carried out various studies showing the relationship between what he calls psychoform (i.e., cognitive and experiential dissociative phenomena) and somatoform dissociation (e.g., somatic dissociative phenomena such as anesthesia, immobility, and pain) and trauma. As is the case with depersonalization, programmatic research on somatoform dissociation has produced a qualitative advance in our understanding of this and related areas.

Conclusions

The previous sections provide an overview of the posttraumatic, dissociative, and conversion disorders. Considering the brief span in which systematic research on the disorders of extreme stress has been conducted, it is impressive how much information has accumulated on these disorders, so it is likely that the conception of their diagnosis and treatment may change in the future. Some of these changes will come out of programmatic research and new brain imaging techniques, whereas others may follow a reconceptualizaton of disorders of extreme stress in particular and psychopathology in general. For instance, it can be argued that the categorical-prototypal scheme for psychological disturbances that the DSM adopts may not be as valuable as a dimensional approach. In the latter, rather than having a set of criteria that need to be present for a diagnosis, the individual is evaluated quantitatively (i.e., dimensionally) with respect to symptoms related to a particular problem. Although the dimensional approach to diagnosis has been most developed in relation to various dimensions of depression, anxiety, and personality disorders (Mineka, Watson, & Clark, 1998; Widiger & Clark, 2001), it could be used for posttraumatic conditions.

More specific problems remain, including the relationship between ASD and PTSD criteria (e.g., the latter minimizes dissociative reactions) and their relationship to other symptoms such as depression. Furthermore, as we have mentioned, the value of separating somatoform dissociative phenomena from psychological forms can be challenged in various ways. The dissociative disorders have been mired in controversy for a number of years, but empirical investigation on such areas as the psychophysiology of DID and depersonalization has been gradually replacing uninformed speculation. Nonetheless, a number of areas remain open for systematic research, among them the longitudinal courses of posttraumatic reactions, the personal characteristics that predispose individuals to react to trauma with dissociation rather than with other symptoms, the encoding of traumatic memories, and so on.

In a world of never-ending disasters, violence, and increasingly sophisticated terrorism, the study of the disorders of extreme stress and trauma remains a vital human endeavor.

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