Extremely stressful or traumatic events, such as combat, natural disasters, and terrorist attacks, place the people who experience them at an increased risk for developing psychological disorders such as posttraumatic stress disorder (PTSD). Throughout much of the 20th century, this disorder was called shell shock and combat neurosis because its symptoms were observed in soldiers who had engaged in wartime combat. By the late 1970s it had become clear that women who had experienced sexual traumas (e.g., rape, domestic battery, and incest) often experienced the same set of symptoms as did soldiers (Herman, 1997). The term posttraumatic stress disorder was developed given that these symptoms could happen to anyone who experienced psychological trauma.
4 Chapter/Lecture 5 Stress Disorders and Dissociative Disorders
Posttraumatic Stress Disorder and Depersonalization and Derealization Disorders.
Section 2: A BROADER DEFINITION OF PTSD
PTSD was listed among the anxiety disorders in previous DSM editions. In DSM-5, it is now listed among a group called Trauma-and-Stressor-Related Disorders. For a person to be diagnosed with PTSD, she be must exposed to, witness, or experience the details of a traumatic experience (e.g., a first responder), one that involves “actual or threatened death, serious injury, or sexual violence” (APA, 2013, p. 271). These experiences can include such events as combat, threatened or actual physical attack, sexual assault, natural disasters, terrorist attacks, and automobile accidents. This criterion makes PTSD the only disorder listed in the DSM in which a cause (extreme trauma) is explicitly specified.
Symptoms of PTSD include intrusive and distressing memories of the event, flashbacks (states that can last from a few seconds to several days, during which the individual relives the event and behaves as if the event were occurring at that moment [APA, 2013]), avoidance of stimuli connected to the event, persistently negative emotional states (e.g., fear, anger, guilt, and shame), feelings of detachment from others, irritability, proneness toward outbursts, and an exaggerated startle response (jumpiness). For PTSD to be diagnosed, these symptoms must occur for at least one month.
Roughly 7% of adults in the United States, including 9.7% of women and 3.6% of men, experience PTSD in their lifetime (National Comorbidity Survey, 2007), with higher rates among people exposed to mass trauma and people whose jobs involve duty-related trauma exposure (e.g., police officers, firefighters, and emergency medical personnel) (APA, 2013). Nearly 21% of residents of areas affected by Hurricane Katrina suffered from PTSD one year following the hurricane (Kessler et al., 2008), and 12.6% of Manhattan residents were observed as having PTSD 2–3 years after the 9/11 terrorist attacks (DiGrande et al., 2008).
Section 3: RISK FACTORS FOR PTSD
Of course, not everyone who experiences a traumatic event will go on to develop PTSD; several factors strongly predict the development of PTSD: trauma experience, greater trauma severity, lack of immediate social support, and more subsequent life stress (Brewin, Andrews, & Valentine, 2000). Traumatic events that involve harm by others (e.g., combat, rape, and sexual molestation) carry greater risk than do other traumas (e.g., natural disasters) (Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Factors that increase the risk of PTSD include female gender, low socioeconomic status, low intelligence, personal history of mental disorders, history of childhood adversity (abuse or other trauma during childhood), and family history of mental disorders (Brewin et al., 2000). Personality characteristics such as neuroticism and somatization (the tendency to experience physical symptoms when one encounters stress) have been shown to elevate the risk of PTSD (Bramsen, Dirkzwager, & van der Ploeg, 2000). People who experience childhood adversity and/or traumatic experiences during adulthood are at significantly higher risk of developing PTSD if they possess one or two short versions of a gene that regulates the neurotransmitter serotonin (Xie et al., 2009). This suggests a possible diathesis-stress interpretation of PTSD: its development is influenced by the interaction of psychosocial and biological factors.
Section 4: SUPPORT FOR SUFFERERS OF PTSD
Research has shown that social support following a traumatic event can reduce the likelihood of PTSD (Ozer, Best, Lipsey, & Weiss, 2003). Social support is often defined as the comfort, advice, and assistance received from relatives, friends, and neighbors. Social support can help individuals cope during difficult times by allowing them to discuss feelings and experiences and providing a sense of being loved and appreciated. A 14-year study of 1,377 American Legionnaires who had served in the Vietnam War found that those who perceived less social support when they came home were more likely to develop PTSD than were those who perceived greater support (Figure). In addition, those who became involved in the community were less likely to develop PTSD, and they were more likely to experience a remission of PTSD than were those who were less involved (Koenen, Stellman, Stellman, & Sommer, 2003).
Section 5: LEARNING AND THE DEVELOPMENT OF PTSD
Cognitive factors are important in the development and maintenance of PTSD. One model suggests that two key processes are crucial: disturbances in memory for the event, and negative appraisals of the trauma and its aftermath (Ehlers & Clark, 2000). According to this theory, some people who experience traumas do not form coherent memories of the trauma; memories of the traumatic event are poorly encoded and, thus, are fragmented, disorganized, and lacking in detail. Therefore, these individuals are unable remember the event in a way that gives it meaning and context. A rape victim who cannot coherently remember the event may remember only bits and pieces (e.g., the attacker repeatedly telling her she is stupid); because she was unable to develop a fully integrated memory, the fragmentary memory tends to stand out. Although unable to retrieve a complete memory of the event, she may be haunted by intrusive fragments involuntarily triggered by stimuli associated with the event (e.g., memories of the attacker’s comments when encountering a person who resembles the attacker). This interpretation fits previously discussed material concerning PTSD and conditioning. The model also proposes that negative appraisals of the event (“I deserved to be raped because I’m stupid”) may lead to dysfunctional behavioral strategies (e.g., avoiding social activities where men are likely to be present) that maintain PTSD symptoms by preventing both a change in the nature of the memory and a change in the problematic appraisals.
Dissociative disorders are a group of disorders categorized by symptoms of disruption in consciousness, memory, identity, emotion, perception, motor control, or behavior (APA, 2013). These symptoms are likely to appear following a significant stressor or years of ongoing stress (i.e. abuse; Maldonadao & Spiegel, 2014). Occasionally, one may experience temporary dissociative symptoms due to lack of sleep or ingestion of a substance, however, these would not qualify as a dissociative disorder due to the lack of impairment in functioning. Furthermore, individuals with acute stress disorder and post-traumatic stress disorder (PTSD) often experience dissociative symptoms, such as amnesia, flashbacks, depersonalization and/or derealization; however, because of the identifiable stressor (and lack of additional symptoms listed below), they meet diagnostic criteria for a stress disorder as opposed to a dissociative disorder.
There are 3 main types of dissociative disorders that will be described in the next three sections: Depersonalization/Derealization Disorder, Dissociative Amnesia, and Dissociative Identity Disorder.
Depersonalization/Derealization Disorder
Clinical Description
Depersonalization/Derealization disorder is categorized by recurrent episodes of depersonalization and/or derealization. Depersonalization can be defined as a feeling of unreality or detachment from oneself. Individuals describe this feeling as an out-of-body experience where they are an outside observer of their thoughts, feelings, and physical being. Furthermore, some people report feeling as though they lack speech or motor control, thus feeling at times like a robot. Distortions of one’s physical body has also been reported, with various body parts appearing enlarged or shrunken. Individuals may also feel detached from their own feelings.
Symptoms of derealization include feelings of unreality or detachment from the world—whether it be individuals, objects, or their surroundings. For example, people experiencing derealization may feel as though they are unfamiliar with their surroundings, even though they are in a place they have been to many times before. Feeling emotionally disconnected from close friends or family members whom they have strong feelings for is another common symptom experienced during derealization episodes. Sensory changes have also been reported such as feeling as though the environment is distorted, blurry, or even artificial. Distortions of time, distance, and size/shape of objects may also occur.
These episodes can last anywhere from a few hours to days, weeks, or even months (APA, 2013). The onset is generally sudden, and similar to the other dissociative disorders, is often triggered by a intense stress or trauma. As one can imagine, depersonalization/derealization disorder can cause significant emotional distress, as well as impairment in one’s daily functioning (APA, 2013).
Epidemiology
While many individuals experience brief episodes of depersonalization/derealization throughout their life (about 50% of adults have experienced depersonalization/derealization at least once), the estimated number of individuals who experiences these symptoms to the degree of clinical significance is estimated to be 2%, with an equal ratio of men and women experiencing these symptoms (APA, 2013). The mean age of onset is 16 years, with only a minority developing the disorder after the age of 25. About 1/3 of people with the disorder have discrete episodes, 1/3 have continuous symptoms from their onset, and 1/3 have an episodic course that progresses to continuous.
Comorbidity
Depersonalization/derealization disorder has been found to be comorbid with depression and anxiety disorders. With respect to the personality disorders, depersonalization/derealization disorder is most commonly comorbid with avoidant, borderline, and obsessive-compulsive personality disorders. Some evidence indicates that comorbidity with post-traumatic stress disorder is low (APA, 2013).
Epidemiology
The causes of depersonalization/derealization disorder are largely unknown. Very little is understood about the potential genetic underpinnings; however, there is some suggestion that heritability rates for dissociative experiences range from 50-60% (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011). However, as with other psychological disorders, it is suggested that the combination of genetic and environmental factors may play a larger role in the development of dissociative disorders than genetics alone (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011).
There are clear associations between all of the dissociative disorders and childhood trauma and abuse but the association is slightly weaker for depersonalization/derealization disorder than it is for the other dissociative disorders (i.e., dissociative amnesia and dissociative identity disorder). Emotional abuse, emotional neglect, physical abuse, witnessing domestic violence, being raised by a parent who is seriously impaired and/or mentally ill, and experiencing the unexpected death or suicide of a family member or close friend are early-life stressors that have been identified to be associated with the disorder. The onset of the disorder is commonly triggered by severe stress, depression, anxiety, panic attacks, and drug use (particularly cannabis, hallucinogens, ketamine, ecstasy, and salvia).
Treatment
Depersonalization/derealization disorder symptoms generally occur for an extensive period of time before the individual seeks out treatment. Because of this, there is some evidence to support that the diagnosis alone is effective in reducing symptom intensity, as it also relieves the individual’s anxiety surrounding the baffling nature of the symptoms (Medford, Sierra, Baker, & David, 2005).
Due to the high comorbidity of depersonalization/derealization disorder and anxiety/depression, the goal of treatment is often alleviating these secondary mental health symptoms related to the depersonalization/derealization symptoms. While there has been some evidence to suggest treatment with an SSRI is effective in improving mood, the evidence for a combined treatment method of psychopharmacological and psychological treatment is even more compelling (Medford, Sierra, Baker, & David, 2005). The psychological treatment of preference is cognitive-behavioral therapy as it addresses the negative attributions and appraisals contributing to the depersonalization/derealization symptoms (Medford, Sierra, Baker, & David, 2005). By challenging these catastrophic attributions in response to stressful situations, the individual is able to reduce overall anxiety levels, which in return, reduces depersonalization/derealization symptoms.
Dissociative Amnesia
Clinical Description
Dissociative amnesia is identified by amnesia for autobiographical information, particularly for traumatic events. This type of amnesia is different from what one would consider a permanent amnesia in that the information was successfully stored in memory, however, the individual cannot retrieve it. Additionally, individuals experiencing permanent amnesia often have a neurobiological cause, whereas dissociative amnesia does not (APA, 2013).
There are a few types of amnesia that people with dissociative amnesia can experience. Localized amnesia, the most common type of dissociative amnesia, is the inability to recall events during a specific period of time. The length of time within a localized amnesia episode can vary—it can be as short as the time immediately surrounding a traumatic event, to months or years, should the traumatic event occur that long (as commonly seen in abuse and combat situations). Selective amnesia is in a sense, a component of localized amnesia in that the individual can recall some, but not all, of the details during a specific time period. For example, a soldier may experience dissociative amnesia during the time they were deployed, yet still, have some memories of positive experiences such as celebrating Thanksgiving dinner or Christmas dinner with their unit. The onset of localized and selective amnesia may immediately follow the acute stress or be delayed for hours, days, or longer.
Conversely, some individuals experience generalized amnesia where they have a complete loss of memory of their entire life history, including their own identity. Individuals who experience this type of amnesia experience deficits in both semantic and procedural knowledge. This means that individuals have no common knowledge of the world (i.e. cannot identify songs, the current president, or names of colors) nor do they have the ability to engage in learned skills (i.e. typing shoes, driving car). The onset of generalized amnesia is typically acute.
While generalized amnesia is extremely rare, it is also extremely frightening. The onset is acute, and the individual is often found wandering in a state of disorientation. Many times, these individuals are brought into emergency rooms by law enforcement following a dangerous situation such as an individual walking aimlessly on a busy road.
Dissociative fugue is considered to be the most extreme type of dissociative amnesia where not only does an individual forget personal information, but they also flee to a different location (APA, 2013). The degree of the fugue varies among individuals – with some experiencing symptoms for a short time (only hours) to others lasting years, affording individuals to take on new identities, careers, and even relationships. Similar to their sudden onset, dissociative fugues also end abruptly. Post dissociative fugue, the individual generally regains most of their memory. Emotional adjustment after the fugue is dependent on the time the individual spent in the fugue – with those having been in a fugue state longer experiencing more emotional distress than those who experienced a shorter fugue (Kopelman, 2002).
Epidemiology
A large community sample suggested dissociative amnesia occurs in approximately 1.8% of the population with females being about 2.5 times more likely to be diagnosed than males (APA, 2013). Similar to trauma-related disorders, it is believed that more women experience dissociative amnesia due to the increased chances of a woman to experience significant stress/trauma compared to that of men.
Comorbidity
Given that dissociative amnesia is often precipitated by a traumatic experience, many people develop PTSD after the traumatic events are finally recalled. Similarly, a wide range of emotions related to their inability to recall memories during the episode often presents once their memories return (APA, 2013). These emotions often contribute to the development of a depressive episode.
Due to the rarity of these disorders with respect to other mental health disorders, it is often difficult to truly determine comorbid diagnoses. There has been some evidence of comorbid somatic symptom disorder and conversion disorder. Furthermore, dependent, avoidant, and borderline personality disorders have all been suspected as co-occurring disorders among the dissociative disorder family.
Etiology
Biological
As previously indicated, heritability rates for dissociative experiences range from 50-60% (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011). However, it is suggested that the combination of genetic and environmental factors may play a larger role in the development of dissociative disorders than genetics alone (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011).
Cognitive
One proposed cognitive theory of dissociative amnesia proposed by Kopelman (2000) is that the combination of psychological stress and various other biopsychosocial predispositions affects the frontal lobe’s executive system’s ability to retrieve autobiographical memories (Picard et al., 2013). Neuroimaging studies have supported this theory by showing deficits to several prefrontal regions, which is one area responsible for memory retrieval (Picard et al., 2013). Despite these findings, there is still some debate over which specific brain regions within the executive system are responsible for the retrieval difficulties, as research studies have reported mixed findings.
Environmental/Behavioral
Severe trauma and/or stress commonly precipitate the disorder. The most common precipitating stressors for fugues are marital discord, financial and occupational problems, natural disasters, and combat in war. The likelihood that dissociative amnesia is experienced increases with higher numbers of adverse childhood experiences (e.g., physical and/or sexual abuse), and more severe and frequent interpersonal violence. According to the behavioral perspective, the amnesia is negatively reinforced by avoiding/removing the distressing thoughts and feelings associated with the trauma/stressor.
Psychodynamic
The psychodynamic theory of dissociative amnesia assumes that dissociative disorders are caused by an individual’s repressed thoughts and feelings related to an unpleasant or traumatic event (Richardson, 1998). In blocking, or dissociating from, these thoughts and feelings, the individual is subconsciously protecting himself from painful memories.
Treatment
Treatment for dissociative amnesia is limited in part because many individuals recover on their own without any type of intervention. Occasionally treatment is sought out after recovery due to the traumatic nature of memory loss. Further, the rarity of the disorder has offered limited opportunities for research on both the development and effectiveness of treatment methods. While there is no evidence-based treatment for dissociative amnesia, both hypnosis and treatment with barbituates have been shown to produce some positive effects in clients with dissociative amnesia.
Hypnosis. One theory of dissociative amnesia is that it is a form of self-hypnosis and that individuals hypnotize themselves to forget information or events that are unpleasant (Dell, 2010). Based on this theory, one type of treatment that has routinely been implemented for individuals with dissociative amnesia is hypnosis. Through hypnosis, the clinician can help the individual contain, modulate, and reduce the intensity of the amnesia symptoms, thus allowing them to process the traumatic or unpleasant events underlying the amnesia episode (Maldonadao & Spiegel, 2014). To do this, the clinician will encourage the client to think of memories just prior to the amnesic episode as though it was the present time. The clinician will then slowly walk them through the events during the amnesic time period in efforts to reorient the individual to experience these events. This technique is essentially a way to encourage a controlled recall of dissociated memories, something that is particularly helpful when the memories include traumatic experiences (Maldonadao & Spiegel, 2014).
Another form of “hypnosis” is the use of barbiturates, also known as “truth serums,” to help relax the individual and free their inhibitions. Although not always effective, the theory is that these drugs reduce the anxiety surrounding the unpleasant events enough to allow the individual to recall and process these memories in a safe environment (Ahern et al., 2000).
Dissociative Identity Disorder
Clinical Description
Dissociative Identity Disorder (DID) is what people commonly refer to as multiple personality disorder, as it was labeled as such in the DSM III. The key diagnostic criteria for DID is the presence of two or more distinct personality states or expressions. The identities are distinct in that they often have their own tone of voice, engage in different physical gestures (including different gait), and have their own behaviors – ranging anywhere from cooperative and sweet to defiant and aggressive. Additionally, the identities can be of varying ages and gender.
While personalities can present at any time, there is generally a dominant or primary personality that is present majority of the time. From there, an individual may have several alternate personality states or alters. Although it is hard to identify how many alters an individual may have at one time, it is believed that there are on average 15 alters for women and 8 for men (APA, 2000).
The presentation of switching between alternate personality states varies among individuals and can be as simple as the individual appearing to fall asleep to very dramatic, involving excessive bodily movements. While often sudden and unexpected, switching is generally precipitated by a significant stressor, as the alter is best equipped to handle the current stressor will present. The relationship between alters varies between individuals – with some individuals reporting knowledge of other alters while others have a one-way amnesic relationship with alters, meaning they are not aware of other personality states (Barlow & Chu, 2014). These individuals will experience episodes of “amnesia” when the primary personality is not present.
Epidemiology
Dissociative disorders were once believed to be extremely rare; however, more recent research suggests that they may be more present in the general population than once believed. Estimates for the prevalence rate of DID is 1.5% (APA, 2013), with more women experiencing the disorder. Due to the high comorbidity between childhood abuse and DID, it is believed that symptoms begin in early childhood following the repeated exposure to abuse; however, full onset of the disorder may not be observed (or noticed by others) until adolescence (Sar et al., 2014) or later in life. Over 70% of people with DID have attempted suicide and other self-injurious behaviors are common (APA, 2013).
Comorbidity
People with DID commonly experience a large number of comorbid disorders including PTSD and other trauma and stressor-related disorders, depressive disorders, somatic symptom disorders (e.g., conversion disorder), eating disorders, substance-related disorders, obsessive-compulsive disorder, sleep disturbances, as well as avoidant personality disorder and borderline personality disorder.
Etiology
Biological
Once again, heritability rates for dissociation rage from 50-60% (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011). However, it is suggested that the combination of genetic and environmental factors may play a larger role in the development of dissociative disorders than genetics alone (Pieper, Out, Bakermans-Kranenburg, Van Ijzendoorn, 2011).
Cognitive
Neuroimaging studies have revealed differences in hippocampus activation between alters (Tsai, Condie, Wu & Chang, 1999). As you may recall, the hippocampus is responsible for storing information from short-term to long-term memory. It is hypothesized that this brain region is responsible for the generation of dissociative states and amnesia (Staniloiu & Markowitsch, 2010).
Sociocultural
The sociocultural model of dissociative disorders has largely been influenced by Lilienfeld and colleagues (1999) who argue that the influence of mass media and its publications of dissociative disorders, provide a model for individuals to not only learn about dissociative disorders but also engage in similar dissociative behaviors. This theory has been supported by the significant increase in DID cases after the publication of Sybil, a documentation of a woman’s 16 personalities (Goff & Simms, 1993).
These mass media productions are not just suggestive to patients; mass media also influences the way clinicians gather information regarding dissociative symptoms of patients. For example, therapists may unconsciously use questions or techniques in sessions that evoke dissociative types of problems in their patients following exposure to a media source discussing dissociative disorders.
Psychodynamic
Once again, the psychodynamic theory of dissociative disorders assumes that dissociative disorders are caused by an individual’s repressed thoughts and feelings related to an unpleasant or traumatic event (Richardson, 1998). In blocking these thoughts and feelings, the individual is subconsciously protecting himself from painful memories.
While dissociative amnesia may be explained by a single repression, psychodynamic theorists believe that DID results from repeated exposure to traumatic experiences, such as severe childhood abuse, neglect, or abandonment (Dalenberg et al., 2012). According to the psychodynamic perspective, children who experience repeated traumatic events such as physical abuse or parental neglect lack the support and resources to cope with these experiences. In efforts to escape from their current situations, children develop different personalities to essentially flee the dangerous situation they are in. While there is limited scientific evidence to support this theory, the nature of severe childhood psychological trauma is consistent with this theory, as individuals with DID have the highest rate of childhood psychological trauma compared to all other psychiatric disorders (Sar, 2011).
Treatment
The ultimate treatment goal for DID is integration of alternate personalities to a point of final fusion (Chu et al., 2011). Integration refers to the ongoing process of merging alternate personalities into one personality. Psychoeducation is paramount for integration, as the individual must have an understanding of their disorder, as well as acknowledge their alternate personalities. Like mentioned above, many individuals have a one-way amnesic relationship with their alters, meaning they are not aware of one another. Therefore, the clinician must first make the individual aware of the various alters that present across different situations.
Achieving integration requires several steps. First, the clinician needs to build a relationship and strong rapport with the primary personality. From there, the clinician can begin to encourage gradual communication and coordination between the alternate personalities. Making the alternate personalities aware of one another, as well as addressing their conflicts, is an essential component of the integration of these personalities, and the core of DID treatment (Chu et al., 2011).
Once the individual is aware of their personalities, treatment can continue with the goal of fusion. Fusion occurs when two or more alternate identities join together (Chu et al., 2011). When this happens, there is a complete loss of separateness. Depending on the number of personalities, this process can take quite a while. Once all alternate personalities are fused together and the individual identifies themselves as one unified self, it is believed the patient has reached final fusion.
It should be noted that final fusion is difficult to obtain. As you can imagine, some clients do not find final fusion as a desirable outcome, particularly those with extremely painful histories; chronic, serious stressors; advanced age; and comorbid medical and psychiatric disorders to name a few. For individuals where final fusion is not the treatment goal, the clinician may work toward resolution or sufficient integration and coordination of alternate personalities that allows the individual to function independently (Chu et al., 2011). Unfortunately, individuals that do not achieve final fusion are at greater risk for relapse of symptoms, particularly those with whose DID appears to stem from traumatic experiences.
Once an individual reaches final fusion, ongoing treatment is essential to maintain this status. In general, treatment focuses on social and positive coping skills. These skills are particularly helpful for individuals with a history of traumatic events, as it can help them process these events, as well as help to prevent future relapses.