Task 2 - A Total Wreck PDF

Task 2 - A total wreck Learning goals What are DSM-5 diagnostic criteria, prevalence & gender differences of PTSD? What make someone vulnerable to PTSD? What are healthy and unhealthy coping responses to traumatic events? What are the available treatments for PTSD? What is dissociation and how does...

Task 2 - A total wreck Learning goals What are DSM-5 diagnostic criteria, prevalence & gender differences of PTSD? What make someone vulnerable to PTSD? What are healthy and unhealthy coping responses to traumatic events? What are the available treatments for PTSD? What is dissociation and how does it relate to PTSD? Introductory chapters Post-traumatic stress disorder (PTSD) - a set of persistent anxiety-based symptoms that occur after experiencing/witnessing an extremely fear-evoking or life-threatening traumatic event. It is debated if PTSD is an anxiety disorder, a stress-induced fear response, a dissociative disorder, or a trauma and stressor-related disorder. However, the acknowledgement that its primary precipitating cause is a traumatic experience has led to PTSD being placed in its own broader diagnostic category. The traumatic event can be actual/threatened death, serious injury, or sexual violation (DSM-5). Diagnosis and prevalence of trauma and stress-related disorders PTSD is one of the few DSM-5 disorders in which the cause of the disorder is a defining factor (diagnosis of PTSD is considered only if the individual has experienced an extreme trauma prior to symptoms). PTSD symptoms are grouped into 4 categories: Intrusive symptoms - re-experiencing the traumatic event through flashbacks, intrusive thoughts, physiological reactions. Avoidance - e.g. active avoidance of thoughts, memories or situations associated with the trauma. Negative changes in cognition and mood - e.g. persistent fear, horror, anger, guilt or shame, persistent negative beliefs about self, others or world (e.g. 'no one can be trusted', 'I've lost my soul forever'), or dissociative feelings of detachment or estrangement from others. Hypervigilance and chronic arousal - constantly being on guard for the traumatic event to recur, sounds/images remind people of their trauma and can instantly create panic and flight. Once symptoms develop, PTSD is chronic and can last for years. PTSD is associated with depression, guilt, shame, anger, marital problems, physical illness, sexual dysfunction, substance abuse, suicidal thoughts, self-harm and stress-related violence. PTSD symptoms are developed by up to 90% of rape victims, 70-90% of torture victims, >50% of prisoners of war, 20-25% of earthquake and flood survivors, 15% of motor vehicle accident victims. PTSD symptoms can also develop when the stressor has not been life -threatening or has involved simply viewing stressful images of life-threatening traumas. This DSM-5 criterion has been criticized because it makes easier to fake PTSD for financial benefit and may confuse PTSD with merely experiencing stress. ^ DSM-5 summary Lifetime prevalence is 1-3% for the general population, but higher for groups who are at risk of experiencing severe trauma (e.g. 12-33% for civilians living in war zones, 10% for rescue workers). Around 50% of adults experience at least 1 event in their lifetime that may qualify as a PTSD-causing trauma. Women are significantly more likely (2.4 times) than men to develop PTSD after such an event. This could be because women experience triggers more often than men (especially sexual abuse), and the triggers they experience are more often stigmatized, decreasing the social support they receive. Men are more likely to suffer traumas that carry less stigma, such as exposure to war. Culture can play a role in PTSD. Caucasian disaster victims show lower prevalence than Latinos or African Americans. These differences cannot be explained by differences in the frequency of exposure to traumatic experiences. All racial/ethnic minority groups are less likely than whites to seek treatment for trauma-related symptoms, presumably due to lower socioeconomic status and less access to healthcare, or to greater stigmatization against seeking treatment. For some people symptoms can be mild to moderate and permit normal functioning. For others, however, the symptoms can be immobilizing, causing deterioration in their work, family, and social lives. Acute stress disorder (ASD) - a short-term psychological and physical reaction to severe trauma. Symptoms are very similar to PTSD symptoms, but the duration is much shorter (symptoms arise within 1 month of trauma exposure and last no longer than 4 weeks). Although ASD is defined a short-term response to trauma, people who experience it are at high risk of continuing to experience post-traumatic stress symptoms for many months. Psychopathology Page 1 Adjustment disorder - another trauma- and stress-related diagnosis, which consists of emotional and behavioral symptoms (depression, anxiety and/or antisocial behavior) that arise within 3 months of the experience of a stressor. The stressors that lead to adjustment disorder can be of any severity, while those that lead to PTSD and ASD are, by definition, extreme. Adjustment disorder is a diagnosis for people who experience emotional & behavioral symptoms following a stressor who do not meet the criteria for PTSD, ASD, or an anxiety or mood disorder, resulting from stressful experience. The etiology of PTSD The main challenge for any theory of the etiology of PTSD is to explain why only some people develop PTSD symptoms after traumatic experiences. Environmental and social factors The severity, duration and an individual's proximity to a trauma are risk factors for developing PTSD. People who have the emotional support of others after a trauma recover more quickly than people who don't. Biological factors Heritability of PTSD has been estimated to be 0.30 in war veterans. This suggests that PTSD develops as a result of a gene X environment interaction, where a combination of an extreme trauma experience and a genetic predisposition to PTSD are required to generate PTSD symptoms. The following biological vulnerability factors have been proposed for PTSD: A relatively small/underdeveloped hippocampus. The hippocampus is significantly smaller in individuals who developed PTSD. This may be due to overexposure to neurotransmitters and hormones released in the stress response. A smaller hippocampus represents a risk factor for the development of PTSD following a traumatic experience. Failure of brain centers (e.g. ventromedial PFC) to inhibit amygdala activity, which results in inability to control the activation of fear following trauma. Study: the amygdala of people with PTSD responds more actively to emotional stimuli. Study: the medial PFC, which modulates amygdaloid activity to emotional stimuli, is less active in people with more severe symptoms of PTSD than in people with less severe symptoms. Therefore, the brains of people with PTSD may be both more reactive to emotional stimuli and less able to dampen that reactivity when it occurs. Genetically endowed heightened startle responses and fear-relevant endocrine secretion. Resting levels of cortisol among people with PTSD (when not exposed to trauma reminders) tend to be lower than among people without PTSD. Cortisol reduces sympathetic nervous system activity after stress, so lower levels may result in prolonged activity of the SNS following stress, thus making it easier to develop a conditioned fear of stimuli associated with the trauma and subsequently develop PTSD. Some physiological responses to stress are exaggerated in PTSD sufferers, including elevated heart rate and increased secretion of epinephrine & norepinephrine. In people with PTSD, different components of the stress response may not be working in sync with each other. The hypothalamic-pituitary-adrenal (HPA) axis may be unable to shut down the response of the sympathetic nervous system by secreting necessary levels of cortisol, resulting in overexposure of the brain to epinephrine, norepinephrine, and other neurochemicals. This overexposure may cause memories of the traumatic event to be “overconsolidated,” or planted more firmly in memory. Vulnerability factors Several factors characterize individuals who are likely to develop PTSD after trauma: A tendency to take personal responsibility for the traumatic event and the misfortunes of others involved in the event. Developmental factors such as early separation from parents or an unstable family life during early childhood. A family history of PTSD. Existing high levels of anxiety, depression or a pre-existing psychological disorder. Low intelligence. High IQ is the best predictor of resistance to the development of PTSD. There is a link between IQ and the development of coping strategies to deal with experienced trauma or stress. Self-reported dissociative symptoms at the time of the trauma and a belief that one is about to die. These experiences may relate to how the individual processes and stores information about the trauma at the time, and this isimportant in some specific theories of PTSD symptoms. Maladaptive coping strategies, such as avoidance, dissociation or self-destructive strategies (drinking, self-isolation etc.) Exposure to extreme or chronic stress during childhood may permanently alter children's biological stress response, making them more vulnerable to PTSD & other anxiety disorders & depression. Studies of maltreated children show abnormal cortical responses to stressors and a diminished startle response. Adults abused as children continue to have abnormal cortisol responses and elevated startle & anxiety responses to laboratory stressors, even when they no longer show PTSD or depression symptoms. Avoidance and dissociation The style of coping after any distressing/traumatic experience is critical to subsequent psychological health. Avoidance coping typically does not lead to a beneficial outcome and people who avoid thinking about their trauma are more likely to develop PTSD after a traumatic experience. Dissociation - a psychological process (a feeling that one is detached from both mind and body) that individuals use to detach and distance themselves from trauma. During dissociation, different facets of self, memories, or consciousness become disconnected from one another. Dissociation is associated with an inability to recall important personal information of stressful nature. In the context of PTSD, dissociation may represent an avoidant strategy for coping or confronting painful/stressful memories. Dissociation is a risk factor for PTSD - individuals who experience dissociation either just before or during the trauma are more likely to develop PTSD. People who use dissociation as a coping strategy after the trauma are at risk of chronic long-term PTSD symptoms. Psychopathology Page 2  People who use dissociation as a coping strategy after the trauma are at risk of chronic long-term PTSD symptoms. For some people with PTSD, dissociative symptoms are especially prominent and persistent and they can be diagnosed with the subtype PTSD with prominent dissociative (depersonalization/derealization) symptoms. Conditioning theory Classical conditioning can explain many PTSD symptoms: Trauma (US) becomes associated with the place and time of the trauma (CS). When these cues (or similar ones) are encountered in the future, they elicit the arousal and fear that was experienced during the trauma (conditioned fear response). The sufferer develops both cognitive & physical avoidance responses which distract them from fully processing such cues and therefore does not allow the associations between cues and trauma to extinguish. The reduction in fear resulting from these avoidance responses reinforces those responses and maintains PTSD symptoms. Classical conditioning does not provide a full explanation of PTSD. It does not explain why some individuals who experience trauma develop PTSD and others do not. It cannot explain some symptoms unique to PTSD and not found in other anxiety disorders (e.g. re-experiencing symptoms, dissociative experiences etc.). Emotional processing theory Emotional processing theory - severe traumatic experiences are of such major significance to an individual that they lead to the formation of representations and associations in memory that are quite different to those formed as a result of everyday experience. This theory is similar to the conditioning account, but it also differs in some ways. For example, if severe trauma has become associated with certain cues (e.g. after being assaulted in an alleyway), this experience will override any other positive associations formed as a result of previous experience with that cue (the alleyway). More, severe trauma not only results in cues eliciting very strong fear responses, but also changes the individual's previous beliefs about the safety of the world => many more cues than previously will elicit fear, startle and hypervigilance responses. Emotional processing theory belongs to a broader class of information-processing theories, which explain how fear responses are learnt, stored and triggered, and how the traumatic event changes beliefs about self and the world. These theories have inspired some successful therapeutic procedures for PTSD which address how the fear network resulting from traumatic experience can be modified. This account has been recently elaborated to include the fact that individuals who prior to the trauma have relatively fixed views about themselves and the world are actually more vulnerable to PTSD. Mental defeat Mental defeat - a specific frame of mind in which the individual sees themselves as a victim, by processing all information about the trauma negatively, and viewing themselves as unable to act effectively. This negative approach to the traumatic event and its consequences adds to the distress, influences the way the trauma is recalled, and may give rise to maladaptive behavioral and cognitive strategies that maintain the disorder. These individuals believe that they are unable to influence their own fate and do not have the necessary skills to protect themselves from future trauma. They do not fully process the memory of the trauma because of their perceived lack of control over it, and so they do not integrate the event fully into their own autobiographical knowledge. This leads to symptoms such as reexperiencing the trauma, difficulty in recalling events from it, and dissociation between the experience of fear responses and their meaning. PTSD sufferers have negative views of self and the world, including negative interpretations of the trauma, negative interpretations of PTSD symptoms, of the responses of others, and a belief that the trauma has permanently changed their life. Dual representation theory Dual representation theory - explains PTSD as a hybrid disorder involving 2 separate memory systems. Verbally accessible memory system (VAM) - registers memories of the trauma that are consciously processed at the time. These memories are narrative in nature and contain information about the event, its context, and personal evaluations of the experience. They are integrated with other autobiographical memories and can be easily retrieved. Situationally accessible memory system (SAM) - records information from the trauma that may have been too brief to take in consciously, including sights, sounds, and extreme bodily reactions to trauma. It is responsible for the vivid, uncontrollable flashbacks experienced by PTSD sufferers which are difficult to communicate to others (as they are not stored in a narrative form). There is good neuropsychological evidence for the existence of these 2 separate memory systems and their links with the amygdala. Study: when describing their memories, PTSD suffers characterized flashback periods with greater use of detail (especially perceptual detail), by more memories of death, more use of the present tense, more mention of fear, helplessness and horror. In contrast, ordinary memories were characterized by more mention of secondary emotions (e.g. guilt & anger). These findings are consistent with the view that flashbacks are the result of sensory and response information stored in the SAM system. Treatment of PTSD Psychotherapies for PTSD generally have 3 goals: Expose clients to what they fear in order to extinguish that fear. Challenge distorted cognitions that contribute to the symptoms. Help clients reduce stress in their lives. Psychological debriefing Psychological debriefing - a structured way of trying to intervene immediately after trauma (24-72 hours after the traumatic event) in order to prevent the Psychopathology Page 3 Psychological debriefing - a structured way of trying to intervene immediately after trauma (24-72 hours after the traumatic event) in order to prevent the development of PTSD. The most widely used techniques for this are crisis intervention or critical incident stress management (CISM). The purpose of these interventions is to reassure the participants that they are normal people who have experienced an abnormal event, to encourage them to review what has happened to them, to express their feelings about the event, and to discuss & review support and coping strategies in the immediate post-trauma period. There is much criticism of psychological debriefing and its value as an intervention for PTSD. It is not clear if victims will gain any benefit from being counselled by strangers and possibly coerced into revealing thoughts and memories that may be difficult to reveal immediately after the traumatic event. Many of the survivors of severe trauma do not display symptoms of psychological disorders, nor will they develop PTSD. Studies suggest that there is little evidence that debriefing reduces the incidence of PTSD, and in some cases it may impede natural recovery after trauma. Exposure therapies Exposure therapy - the sufferer is helped by the therapist to confront and experience events and stimuli relevant to their trauma and their symptoms. This should achieve 2 goals: Extinguish associations between trauma cues and fear responses. Help the individual disconfirm any symptom-maintaining dysfunctional beliefs that have developed as a result of the trauma (e.g. 'I can't handle any stress'). Exposure to fear triggers is often a difficult step to take for PTSD sufferers and may make symptoms worse in the early stages of treatment. Exposure therapy can take various forms: Asking the client to provide a detailed written narrative of their traumatic experiences. Using VR and computer-generated imagery. Imaginal flooding - asking the client to visualize feared, trauma-related scenes for extended periods of time Imaginal treatments can be followed by in vivo graded exposure to real trauma-related cues. Exposure-based therapies provide therapeutic gains that are superior to medication and social support. Eye movement desensitization and reprocessing (EMDR) - a form of exposure therapy for PTSD in which clients are required to focus their attention on a traumatic image/memory while simultaneously visually following the therapist's finger moving backwards and forwards before their eyes. This continues until the client reports a significant decrease in anxiety to the image or memory. The therapist then encourages the client to restructure the memory positively, by thinking positive thoughts in relation to that image (e.g. 'I can deal with this'). The rationale is that combining eye movements with attention to fearful images encourages rapid deconditioning and restructuring of the feared image. EMDR is more effective than no treatment, supportive listening and relaxation, but some studies have shown that it has a higher relapse rate than CBT. However, recent reviews suggest that EMDR is one of the most effective treatments for PTSD, despite its controversial status. Critics of EMDR argue that it adds nothing to already existing exposure therapies. However, experimental studies have demonstrated that the eye movement component of EMDR is essential for successful treatment regardless of how it's done (e.g. up-down movements are just as effective as side-side movements). It is important that the eye movement task taxes working memory and so weakens traumatic memories. Cognitive restructuring Cognitive restructuring therapies usually attempt to help clients do 2 things: Evaluate and replace intrusive/negative automatic thoughts. Evaluate and change dysfunctional beliefs about the world, themselves and their future that have developed as a result of the trauma. Study: 2 basic dysfunctional beliefs mediate the development & maintenance of PTSD: 'The world is a dangerous place' 'I am totally incompetent' Immediately after a severe trauma, almost all people develop a negative view of the world and themselves, but for most people these beliefs become disconfirmed through daily experience. However, those who avoid trauma-related thoughts will also avoid disconfirming these extreme views. This will foster the development of chronic PTSD. Studies that have analyzed treatments that contain both exposure and cognitive restructuring components suggest that cognitive restructuring does not significantly improve exposure therapy in producing changes in dysfunctional cognitions. Cognitive-behavioral therapy and stress management A major element of CBT for PTSD is systematic desensitization, in which the client identifies thoughts and situations that create anxiety, ranking them from most anxiety-provoking to least. The therapist takes the client through this hierarchy, exposing the client to trauma cues that elicit fear, avoidance, and other PTSD symptoms, sometimes using relaxation techniques to reduce anxiety. The therapist also watches for unhelpful thinking patterns (e.g. survivor guilt) and helps the client challenge these thoughts. Prolonged exposure therapy - a type of CBT for PTSD that focuses on repeated exposure to trauma reminders. Cognitive processing therapy - a type of CBT for PTSD that focuses on reinterpretation of the trauma. Stress inoculation therapy (SIT) - a therapy for clients with PTSD who cannot tolerate exposure to their traumatic memories. Therapists teach clients skills for overcoming problems in their lives that increase stress and problems that may result from PTSD (e.g. marital problems or social isolation). Psychopathology Page 4  problems or social isolation). SIT is efficacious for PTSD, but exposure-based therapies show more consistent outcomes. Newer treatment techniques are also being explored, including mindfulness techniques, yoga and meditation, and VR technology for exposure. Biological therapies SSRIs and to a lesser extent benzodiazepines are used to treat PTSD symptoms, particularly sleep problems, nightmares, and irritability. Some people benefit, but evidence for drug effectiveness is mixed, and some drugs can have significant side effects and addictive potential. Dissociative disorders and PTSD Dissociative symptoms are listed in the diagnostic features of PTSD and these symptoms include amnesia, flashbacks, numbing and depersonalization. PTSD is related to dissociative disorders in at least 3 possible ways: Persistent dissociative symptoms immediately after a traumatic experience are a significant predictor of the subsequent acquisition of full-blown PTSD. Dissociation is a feature of complex/severe PTSD, in which individuals suffer from a range of persistent symptoms, enduring personality changes, affect disruption, somatization (experiencing psychological distress as somatic symptoms), and changes in self-perception. Complex PTSD - a severe form of PTSD, often associated with early-age interpersonal trauma and with dissociative symptoms from that early age. There may exist a specific dissociative subtype of PTSD that is defined by the severity of both PTSD and dissociative symptoms, and which may account for up to 30% of PTSD cases. Emotion- and intrusion-based reasoning in Vietnam veterans with and without chronic PTSD - Engelhard article (2001) Introduction Patients suffering from PTSD and other anxiety disorders tend to prioritize the processing of threatening information. This tendency is significantly related to the severity of PTSD, but less to the degree of trauma exposure. PTSD patients also tend to selectively store and recall threatening information. Emotion-based reasoning (ER) - the tendency to infer danger from one's own anxious response to a situation, rather than from objective situation (i.e. if anxiety, then threat). This tendency has been found in spider phobia, panic disorder, social phobia, and other anxiety disorders. Once PTSD symptoms have emerged, the individual's appraisals of them may be critical, and incite a sense of threat (internal - I'm going crazy or external - The world is dangerous). This sense of threat may make the disorder self-perpetuating by amplifying distress and avoidance strategies. PTSD patients have high anxiety sensitivity - fear of anxiety symptoms arising from beliefs about their negative implications. The negative interpretation of PTSD symptoms has been strongly linked to chronic PTSD, the distress caused by the symptoms, and the use of avoidance strategies. However, these negative appraisals of symptoms involve a sense of internal threat, and it's still unclear if PTSD patients also perceive more external threat on the basis of such symptoms. Intrusion-based reasoning (IR) - inferring danger from the presence of PTSD-related intrusions. The authors hypothesize that PTSD patients also engage in ER, and in addition to that, they engage in IR. They also explore if ER and IR remain after adjusting for the influence of perceived uncontrollability, anxiety and outcome expectations of scenarios. They also explore the link between IR & ER, and whether they are associated with trait anxiety, anxiety sensitivity, the negative interpretation of post- trauma symptoms and intelligence. Method Vietnam War combat veterans with combat-related PTSD were compared with combat veterans who never had PTSD or other anxiety disorders. Participants rated perceived danger of 2 series of brief scenarios: ER-scenarios that were specific for other anxiety disorders, and IR-scenarios that were specific for combat-related PTSD. There were 4 versions of each scenario that started identically, but ended differently: 1. With objective danger information and an anxiety response; 2. With objective danger and a non-anxiety emotional response; 3. With objective safety and anxiety; and 4. With objective safety and a non-anxiety emotional response. ER scenarios were taken from a previous study. IR scenarios were PTSD-specific scenarios tailored to the participants using case-reports of Vietnam War veterans. Example PTSD scenario: It’s a fourth of July holiday, and you’re on your way to meet some friends. You’re looking forward to seeing them, but you’re running late. As you’re driving your car, several children toss firecrackers under the wheels of your car. Continuation of danger and intrusions scenario: You hit the accelerator, but lose control of the wheel. The car stalls in the wrong lane. The oncoming traffic moves quickly towards you. You hear more firecrackers. The sudden noise triggers upsetting thoughts about Vietnam. Continuation of danger and no intrusions scenario: You hit the accelerator, but lose control of the wheel. The car stalls in the wrong lane. The oncoming traffic moves quickly towards you. You hear more firecrackers. The sudden noise makes you angry, but then you laugh to yourself and think: ‘Well, at least I’ve got a good Psychopathology Page 5  makes you angry, but then you laugh to yourself and think: ‘Well, at least I’ve got a good excuse now for being late’. Continuation of safety and intrusions: The sudden noise triggers upsetting thoughts about Vietnam. Continuation of safety and no intrusions: The sudden noise makes you angry, but then you laugh to yourself and think: ‘Well, at least I’ve got a good excuse now for being late’. Participants are instructed to identify themselves as well as possible with the main character of each scenario and to rate 5 scales: degree of danger of the scenario (dependent variable), safety, uncontrollability, anxiety, and positive vs. negative outcome. Participants also complete questionnaires on PTSD severity, anxiety trait, anxiety severity, intelligence, and a questionnaire used to measure the negative appraisals of PTSD symptoms. Results The PTSD group reported more PTSD symptoms, more trait anxiety, more negative interpretations of symptoms, and higher anxiety sensitivity compared to the non-PTSD group. Compared to the control group, the PTSD group showed higher danger ratings on scenarios with anxiety information relative to scenarios without anxiety. Compared to the control group, the PTSD groups also showed higher danger ratings on scenarios with intrusions relative to scenarios without intrusions. These effects remained intact after controlling for anxiety and outcome expectations. After adjustment for uncontrollability, the effect for both ER & IR scenarios dropped, but remained substantial => they were only partly due to perceptions of uncontrollability. ER and IR were defined as the difference in danger ratings between scenarios with and without information about anxiety and intrusions. These variables were moderately related (r = 0.35). IQ was significantly related to IR (r = -0.89). Discussion As predicted, Vietnam combat veterans with PTSD (compared to healthy combat veterans) interpret anxiety responses and PTSD-intrusions as predictors of impending threat. These 2 effects are only moderately correlated, suggesting that they are loosely coupled (this could also be due to unreliable measurement). The ER/IR effects may be partly explained by the following 2 explanations: Individuals who perceive anxious and post-traumatic symptoms as unpredictable and uncontrollable may believe that lack of control over emotional responses makes them vulnerable to external threat during such emotional episodes (supported by the fact that uncontrollability accounted for part of the effects). Lower pre-trauma intelligence, expressed in limited abstract thinking and higher order reasoning skills may impede coping with acute PTSD symptoms and make trauma victims more vulnerable to IR (supported by the fact that IQ was negatively related to IR). However, inconsistent with this argument, IQ was not related to ER. The results of this cross-sectional study cannot determine causality between PTSD and IR/ER. However, there is evidence that healthy individuals high in ER have more difficulty distinguishing safety from danger signals. There are several ways in which ER & IR can contribute to the persistence of PTSD. Because the common experiences of intrusions and anxiety as taken as evidence that doom is still/again impending and that the world is unsafe. By fostering avoidance of cues that lead to the experience of anxiety. Avoidance strategies impede emotional processing and modification of the fear structure. By amplifying distress, which increases the frequency of intrusive thoughts. By motivating PTSD patients to search selectively for danger-confirming information (confirmation bias). Psychopathology Page 6  A longitudinal study of intrusion-based reasoning and PTSD after exposure to a train disaster - Engelhard article (2002) This study aims to replicate the IR findings from the previous study above and elucidate causality. Method Residents of a Belgian town who witnessed a tragic train crash were administered a modified IR paradigm within 1 month post-trauma and were reassessed for PTSD at 3.5 months. Control residents, who lived in the same community, but did not witness the crash directly, were also tested for IR. Hypothesis 1: the directly exposed individuals would display IR to a greater degree than controls, and greater IR would be related to more acute PTSD symptoms. Hypothesis 2: The early tendency to allow distressing intrusions to influence danger inferences would predict the presence & intensity of chronic PTSD. Results The directly exposed group showed IR, which is reflected by greater ratings of danger to scenarios in which intrusions were included relative to the same scenarios in which intrusions were excluded (steeper slopes in the figure). IR was significantly related to acute & chronic PTSD symptoms, and the latter 2 were also significantly related with each other. The figure to the right shows danger ratings of individuals with and without (partial) PTSD at 3.5 months after the accident. Discussion The results suggest that intrusions may serve as contextual cues indicating that a different stimulus predicts harm. IR did not significantly contribute to chronic PTSD over and above acute PTSD symptoms. This could be due to the small sample size. The results are similar for previously found associations between negative interpretations of initial PTSD symptoms and chronic PTSD symptoms controlled for initial symptoms (r between 0.10 and 0.36). In sum, although the correlation of IR with chronic PTSD symptoms was attenuated by acute PTSD symptoms, the correlations of IR with both acute and chronic PTSD symptoms were quite robust and suggest a strong relationship. Reviewing the potential of psychedelics for the treatment of PTSD - Krediet article (2020) Introduction Psychopathology Page 7 Introduction Due to limited efficacy of pharmacological interventions, exposure-based psychotherapy is currently the first-line treatment for PTSD. However, even after several modalities of psychotherapy, PTSD often remains a chronic illness, with significant psychiatric & medical comorbidity. 40-60% of PTSD patients do not respond adequately to psychotherapy. Targeting 1 specific neurotransmitter system with drugs in PTSD is insufficient. PTSD treatment may benefit from drug-induced changes in the capacity to engage with traumatic material in psychotherapy (because many PTSD patients are emotionally challenged in exposure therapy and may be unable to complete sessions and eventually drop out). Psychedelic drugs may be particularly suitable for such a substance-assisted psychotherapy approach, because they may increase the capacity for emotional & cognitive processing. This article reviews the potential of 4 psychedelic compounds in treating PTSD: 3,4-methylenedioxymethamphetamine (MDMA), ketamine, classical psychedelics (e.g. psilocybin & LSD), and some cannabinoids. Psychedelic drugs in the treatment of PTSD Psychedelic drugs - a category of compounds that can induce a wide range of psychological, cognitive, emotional and physical effects, usually including the capacity for inducing an altered or opening of the sense of self. MDMA MDMA-assisted psychotherapy has been designated as a break-through therapy for the treatment of PTSD in 2017. MDMA acts as a catalyst to psychotherapy by reducing the fear response to anxiety-provoking stimuli, including previous trauma. MDMA also enhances introspection and increases interpersonal trust, which can benefit the therapeutic alliance. MDMA alters cognition very slightly, produces only mild sensory alterations, and does not include a clouding of consciousness, while patients sustain a clear memory of the experience. MDMA increases emotional empathy, prosocial behavior, pleasantness of affective touch, and subjective ratings of closeness to others, openness and trust. MDMA-assisted psychotherapy has shown the ability to induce lasting changes in some personality traits. Increases in Big 5 Openness play a moderating role between treatment with MDMA-assisted psychotherapy and reductions in PTSD symptoms. MDMA attenuates amygdala activity while activating the frontal cortex, whose activity is often impaired in PTSD patients. MDMA increases oxytocin levels, which may contribute to increased interpersonal trust. A single dose of MDMA in mice reopens the critical period for social reward learning, which requires activation of oxytocin receptors in the nucleus accumbens, and persists even after the drug's acute effects. MDMA use is usually included within a psychotherapeutic treatment, with several non-drug preparatory sessions preceding and multiple integrative therapy sessions following each MDMA session. Sessions are carried out in a clinical, but aesthetically pleasing setting, and last 5-8 hours. Patients are accompanied by 2 therapists whose role is to facilitate an introspective process in which the patient may revisit past experiences. Nondirective approach: the client's own process is allowed to unfold, rather than there being a constant interruption/direction by the therapists. Music has been shown to play a central role in psychedelic-assisted psychotherapy and several playlists have been composed to assist & enhance the therapeutic process. Study: 6 women with chronic PTSD secondary to sexual assault receive a low MDMA dose combined with several 90-minute nondrug psychotherapy sessions before and after the MDMA sessions. Reductions of PTSD symptoms were observed, but the sample size is too small to generalize. The important conclusion is that the administration of MDMA in this population is both physically & psychologically safe. Study: 12 treatment-resistant patients with PTSD receive 2 sessions with MDMA, while 8 patients receive a placebo. 83% of the patients in the MDMA group did not meet the criteria for PTSD anymore, compared with 25% in the placebo group. Treatment effects were stable over a 3.5-year period. These results were replicated in 2 other studies. A pooled analysis of 105 patients from 6 randomized control trials shows that patients who received MDMA experienced significantly greater reductions in PTSD symptoms than patients in the control group. After 2 MDMA sessions, 54.2% of patients no longer met PTSD diagnostic criteria compared with 22.6% in the control group. MDMA-assisted psychotherapy shows higher effect sizes and significantly lower dropout rates than paroxetine and sertraline therapy. Side effects from MDMA include anxiety, tight jaw, headache and fatigue. Episodes of anxiety can occur when the first effects of MDMA become noticeable and can easily be coped with by psychotherapeutic support. Ketamine Ketamine has very rapid effects in the treatment of depression, by acting on glutamatergic and other pathways. One hypothesis about PTSD is that it is a synaptic disconnection syndrome. The therapeutic effects of psychedelic drugs like ketamine may be partially explained by their ability to rapidly increase synaptic & neuronal plasticity. Ketamine may also target PTSD symptoms by its glutamatergic effects. The glutamate system plays an important role in memory processes, e.g. consolidation & extinction learning. Ketamine enhances fear extinction in rodents and has the ability to block memory reconsolidation. Due to its plasticity-enhancing effects, ketamine may also increase receptiveness to psychotherapy in the days following administration. The acute psychoactive effects of ketamine (sensory distortions, hallucinations, transformations in self-concept, emotional attitudes to self & others and Psychopathology Page 8 The acute psychoactive effects of ketamine (sensory distortions, hallucinations, transformations in self-concept, emotional attitudes to self & others and changes in life values and purposes) could catalyze engagement in psychotherapy. Study: a single infusion of ketamine is compared with an infusion of midazolam in 41 patients with chronic PTSD and associated depressive symptoms. Ketamine infusion led to a significant and rapid reduction of PTSD symptoms, which remained significant up until 7 days after this single infusion. These short-term improvement suggest a temporary neurobiological mechanism, similar to that observed in the use of ketamine for depression. The strength & duration of the therapeutic effects of ketamine of PTSD can be enhanced with repeated infusions. Study: administration of ketamine is combined with a mindfulness-based cognitive therapy in patients with refractory PTSD. Patients receive an infusion of ketamine over 40 minutes. Before the infusion, traumatic memories are activated by making patients reflect on a personalized narrative of their trauma. During the infusion period, 2 cycles (10 minutes each) of a mindfulness exercise were practiced, aimed to facilitate the extinction of traumatic memories and the reconsolidation of novel calming memories. Ketamine-induced relaxation and dissociation augmented a state of not reacting fearfully to the traumatic memories but accepting them passively as they come. The ketamine group showed a significantly more durable reduction in PTSD symptoms (34 days) than patients in the placebo group (14 days). Ketamine side effects include drowsiness, dizziness, nausea, perceptual alterations, dissociative effects. Anxiety can be reduced by supportive clinical settings. Classical psychedelics Classical psychedelics include psylocibin, LSD & DMT. They act mainly as 5-HT2a receptor (serotonin receptor) agonists. Classical psychedelics induce several neurobiological changes that may be useful in the treatment of PTSD. Psilocybin & DMT facilitate fear extinction in animal studies and promote neural plasticity in vivo and vitro, increasing neurogenesis, spinogenesis and synaptogenesis. These plasticity-promoting effects may contribute to the drugs' antidepressant and anxiolytic effects. Classical psychedelics decrease amygdala reactivity during emotional processing. Patients with PTSD often show heightened amygdala reactivity => this effect may increase the ability to process traumatic memories. Classical psychedelics increase emotional empathy, mindfulness, insightfulness, acceptance & connectedness and reduce avoidance. Classical psychedelics promote long-term increases in Openness and emotional breakthrough experiences, which have been shown to be a key mediator in long-term psychological change in other mental disorders. Classical psychedelics induce mystical experiences, which mediate therapeutic effects of psilocybin in nicotine addiction, reductions in anxiety, depression and existential distress in patients with a life-threatening diagnosis. The setting in which classical psychedelics are used is very similar to those of MDMA. In the 20th century, many traumatized patients were treated with classical psychedelics. However, they were not diagnosed with PTSD because that diagnosis did not exists at the time. Ayahuasca - a DMT-containing plant that has been used for centuries by indigenous Amazonian people for medicinal, spiritual & other purposes. Ayahuasca has been proposed for the treatment of PTSD and there are also plans to study its effects. Classical psychedelics can induce psychologically challenging experiences (e.g. anxiety & confusion), but they can be part of the therapeutic process. Some patients feel emotionally vulnerable during the days after the experiment, which stresses the importance of psychological support afterwards. Cannabinoids Cannabis contains more than 100 cannabinoids, of which tetrahydrocannabinol (THC) & cannabidiol (CBD) are the most studied. Cannabinoids act on the endocannabinoid system, which plays a central role in emotional memories & is a crucial mediator of t he hypothalamic-pituitary- adrenal response under stress. Exposure to chronic stress causes a downregulation of cannabinoid type 1 receptors; several PTSD symptoms (hyperarousal, sleeping problems, intrusive memories) are facilitated by decreased endocannabinoid signaling. Cannabinoids are mainly used & studied for the temporary relief of PTSD symptoms, but they may also have potential for substance-assisted psychotherapy. Several cannabinoids (including THC & CBD) increase fear extinction and disrupt fear memory reconsolidation. THC can reduce amygdala activity to threatening stimuli, which may facilitate processing of traumatic memories. Therefore, the efficacy of exposure therapies could possibly be enhanced with the targeted use of certain cannabinoids. Cannabinoids are used in a variety of contexts (even as a take-home medication for daily use). Study: 10 PTSD patients from the Canadian military who were experiencing trauma-related nightmares receive nabilone (a synthetic THC-mimicking cannabinoid) in a placebo-controlled trial. After receiving nabilone for 7 weeks, patients showed significantly stronger improvements in distressing dreams & global well-being compared with when they received a placebo for 7 weeks. Nabilone has also shown beneficial effects on several PTSD symptoms, nightmares and sleeping problems in a study of male inmates. The use of cannabinoids may be an additional risk factor for the development of psychotic disorders in susceptible individuals. How does EMDR work? - van den Hout article (2012) History and effects of EMDR EMDR has been criticized because its initial rationale was quite implausible (catalysing a rebalancing of the nervous system, which leads to a shifting of information that is dysfunctionally locked in the nervous system). Psychopathology Page 9 information that is dysfunctionally locked in the nervous system). The eye movements were increasingly replaced by other bilateral stimuli (e.g. alternating left & right beeps). Criticisms include that the eye movements are not a necessary component at all. However, substantial evidence shows that EMDR is just as efficacious as CBT for treating PTSD and that the eye movements add to its beneficial effects. A model of EMDR The following model can be used to test hypotheses about EMDR: Healthy volunteers recall unpleasant memories for a few seconds. They rate the memories in vividness and emotionality (unpleasantness). Then they recall the memories for a longer time (e.g. several periods of 24s). During this 2nd recall, there is either no dual task (recall only) or the participant makes eye movements while recalling the memories (recall + eye movements) by visually tracking a white circle that moves side to side on a computer screen. After a break (few minutes to few days), the memory is recalled under the same conditions and its rated again in terms of vividness and emotionality. Hypothesis 1: EMDR works by recalling aversive memories and eye movements to do not contribute anything If EMDR is nothing more than an imaginal exposure therapy, and eye movements are unnecessary, then 'recall only' should have the same effects as 'recall + eye movements'. Otherwise, vividness and/or emotionality should decrease more after 'recall + eye movements' The authors summarize 16 experiments that measure vividness & emotionality. In all of them, at least one of the measures improved more when using eye movements. Other meta-analyses have also suggested that eye movements have an additive effect => this hypothesis can be dismissed. Hypothesis 2: EMDR works by stimulating "interhemispheric communication" Many people believe that eye movements increase communication between the left & right brain hemispheres, thereby enhancing the ability to remember an aversive event while not being negatively aroused. Therefore, it would not matter which sensory channels are used to stimulate "interhemispheric communication" as long as the stimulus is alternating and rhythmically left-right. Therefore, if eye movements need to be horizontal to decrease the vividness of memories, then vertical eye movements would have no or less effect. Study: participants recall unpleasant memories under 3 conditions: eyes fixated, horizontal movements, or vertical movements. Recall only had no effect. Vividness and emotionality decreased equally in the other 2 conditions. This is evidence against the interhemispheric communication hypothesis. More evidence against this hypothesis is the evidence below of usage of dual tasks other than eye movements. Hypothesis 3: EMDR works by taxing working memory during recall When we multitask, each task competes for WM capacity. Therefore, recalling an emotional memory while doing another task should leave less WM capacity for processing the memory. As a consequence, the memory should become less vivid & emotional. This should apply to both traumatic and mildly negative memories. Imagination inflation effect - when a person tries to form a vivid & detailed image during recall, the original memory will be reconsolidated as vivid & more realistic. When a suspect/witness has visualized a scenario several times, the level of vividness and credibility of the original memory change, affecting the next recall. The 'recall + eye movement' combination will lead to imagination deflation. Therefore eye movements, which tax WM, cause the memory to be reconsolidated less vividly. Other tasks The WM theory predicts that any taxing task should attenuate the vividness & emotionality of the memory. Auditory shadowing, copying a complex figure, playing Tetris, mental arithmetic, calculating out loud, and mindful breathing have all been shown to work in the same way as eye movements in EMDR. Positive memories WM theory predicts that all (even positive) memories should lose their vividness if WM is taxed during recall. Study: making eye movements during activation of positive thoughts rendered these thoughts less vivid and less positive, irrespective whether the movements were horizontal or vertical. Prospective memory and flash-forwards Many patients with anxiety disorders, eating disorders & depression have disturbing images and thoughts about possible future events (prospective memories). Like retrospective memories, these prospective memories can induce flashbacks (in this case flash-forwards about future social, financial, medical or family catastrophes). Psychopathology Page 10 WM theory says that flash-forwards can be stripped of their impact in the same way as flashbacks. Study: compared to the effects of ‘recall only’, ‘recall + eye movements’ led to flash-forwards becoming less vivid and emotional. Similar effects were found in an analogue study of students suffering from performance anxiety, but the effects were weaker in a study of students suffering from intrusive images related to all kinds of idiosyncratic events. This flash-forwards research may provide a rational basis for applying EMDR for disorders other than PTSD. How do we know if and how much WM is taxed? Reaction time (RT) task - task A is administered, where the participant responds as quickly as possible to a prompt, and the RT is measured. Then task B is added to task A. The degree to which task the RT to task A slows down is an index of the amount of cognitive capacity required by B. When participants are asked to respond to high versus low tones by saying 'high'/'low', the RT is about 600ms. When people simultaneously make EMDR-like eye movements, the RT increases to 700ms. Low working memory capacity? Benefit from EMDR WM theory predicts that people with low WM capacity should benefit more from making eye movements. Study: WM capacity is significantly correlated with reduction in vividness and emotionality of memories as a result of 'recall + eye movements' (r = -.44, r = -.43), 'recall + auditory shadowing' (r = -.69, r = -.59), and 'recall + drawing' (r = -.58, r = -.49). Therefore, individuals who are distracted more by dual tasks benefit more from EMDR-type procedures. Inverted U The link between taxing WM and memory effects has the form of an inverted U: too little and too much taxing both have little or no effect. For distraction to happen, there needs to be a minimum degree of taxing. However, if this taxing exceeds a certain level, there will be too little room left for recall. The effect of beeps Theories of bilateral stimulation and interhemispheric stimulation have inspired clinicians to replace eye movements with other forms of bilateral stimulation. A popular method is to have patients listen to alternating left & right beeps through headphones during the recall. However, registering beeps is a passive task that may not even tax WM. Beeps have a very low impact on WM and also a very low effect of reducing emotionality & vividness of memories (1/3 of the effect observed with eye movements). Study: 12 patients with severe PTSD recalled the most distressing traumatic image during the first EMDR session 6 times: twice without a dual task (recall only), twice while making eye movements (recall + eye movements) and twice while hearing beeps (recall + beeps). The largest decreases in vividness & aversiveness were found for recall + eye movements, and there was no effect for recall + beeps. Patients mentioned that they prefer the beeps, because the eye movements were 'distracting' and 'tiring'. Mindfulness and mindful breathing Mindfulness-based cognitive therapy (MBCT) is effective for depression treatment & preventing relapse after treatment. Mindful breathing (MB) is a crucial part of MBCT in the same way that eye movements are a crucial element of EMDR. In MBCT patients are taught to focus their attention on breathing. They don't analyze images/thoughts, but instead accept them and slowly draw their attention back to breathing. This procedural similarity raises the question of whether WM theory can explain how MB works in MBCT. The authors conducted studies that suggest that MB and eye movements tax WM to the same degree and both techniques affect vividness and emotionality of unpleasant memories roughly the same. Presence of the dissociative subtype of PTSD does not moderate the outcome of intensive trauma-focused treatment for PTSD - Zoet article (2018) Introduction Dissociation is thought to be negatively associated with worse treatment outcomes in PTSD. The proposed mechanism is that dissociation hinders fear activation, which is needed for a successful PTSD treatment. Study: among 137 individuals who had just recently been exposed to a traumatic event, those that showed dissociation prior to the first session of an early intervention responded less to treatment. Study: among 244 veterans who receive trauma-focused CBT & group therapy, higher levels of baseline dissociation were associated with worse post- treatment PTSD outcomes. Study: in 69 PTSD patients receiving EMDR, dissociation was a significant predictor of non-response. Other authors refer to opposite findings, e.g. that patients with dissociative symptoms benefit similarly from trauma-focused therapy compared to patients without these symptoms. In most studies, however, the samples are limited to specific trauma populations (e.g. female veterans, refugees, psychotic patients etc.). The purpose of this study is to determine the impact of dissociation on PTSD treatment outcome using a sample of both women & men with PTSD as a result of a wide variety of traumatic events and suffering from multiple comorbidities. Psychopathology Page 11 result of a wide variety of traumatic events and suffering from multiple comorbidities. Patients undergo a short, highly intensive treatment program consisting of prolonged exposure & EMDR therapy, which were applied without explicitly addressing dissociation during treatment. Based on the assumptions underlying the decision to include the dissociative subtype of PTSD (DS) into the DSM-5 (namely, that DS individuals show certain neural activation patterns that suggest emotional overmodulation, thereby preventing emotional engagement with trauma-related material), it is hypothesized that patients who meet the criteria for DS will respond more poorly than those who don't. Another goal is to determine the degree of loss of DS diagnostic criteria following trauma-focused treatment. Discussion Even though most patients in the study suffered from severe PTSD and multiple comorbidities, a large & significant reduction in PTSD symptoms was achieved after treatment. The severity scores of both DS and non-DS groups decreased from severe PTSD to mild/no PTSD. The decline in PTSD symptom severity was similar for individuals with DS and for those without DS. Therefore, the results do not provide support for the idea that presence of DS has a negative impact on the outcome of first-line, trauma- focused treatments for PTSD. These findings are at odds with the prevalent assumptions in the trauma field that high-dissociation individuals do worse in trauma-focused treatments than other groups of patients. Still, individuals with DS reported significantly higher PTSD symptom severity at the beginning. This difference remained constant throughout treatment. Therefore, DS may demand a longer treatment duration or other approaches to compensate for a higher initial PTSD severity. After treatment, most of the DS patients did not meet the criteria of DS anymore, even though the dissociative symptoms were not explicitly addressed during treatment. This fact, and the fact that DS and non-DS patients improved similarly after treatment, may have implications for both reliability & validity of the DS subtype, which may be a trait, rather than a state-dependent PTSD subtype. Dissociative disorders - Kihlstrom article (2005) Dissociative disorders Dissociative disorders - a wide variety of syndromes whose common core is an alteration in consciousness that affects memory & identity. Dissociative amnesia - patients suffer a loss of autobiographical memory for certain past experiences. Dissociative fugue - the amnesia covers the whole (or at least a large part) of the patient's life. It is also accompanied by a loss of personal identity, and, often, physical relocation. Dissociative identity disorder (DID) - patients seems to have & manifest 2 or more distinct identities (a "host personality" and 1 or more "alter egos"/"ego states") that alternate in control over conscious experience, thought, and action, and are typically separated by some degree of amnesia. It was renamed from multiple personality disorder in DSM-IV, in order to emphasize the importance of changes in consciousness & identity, rather than personality. Depersonalization disorder - patients believe that they have changed in some way, or are in some way no longer real (in derealization, the same beliefs are held about the patient's surrounding environment). Dissociative disorders not otherwise specified - patients display some dissociative symptoms, but not to the extent that they quality for 1 of the major categories. This category includes certain culturally specific “spirit-possession” states, such as amok (in Indonesia), latah (Malaysia), and ataque de nervios (Latin America). Diagnosis, assessment, and epidemiology The diagnosis of dissociative disorders is to an extent subjective: it is easy to mistake them with bipolar disorder, borderline personality disorder and schizophrenia. Clinicians that are looking to diagnose someone with DID can do it even due to normal behavior variability (e.g. because an otherwise "normal" person just "doesn't feel like himself" at some point). The "gold standard" for diagnosis of dissociative disorders is the Structured Clinical Interview for Diagnosis' protocol for dissociative disorders (SCID-D). Clinician-Administered Dissociative States Scale - used to measure episodic dissociative states, focuses on symptoms of depersonalization & derealization, and not the disruptions of memory & identity that lie at the core of the dissociative disorders. There are a number of questionnaires used for the assessment of dissociative tendencies, but they (expect for the mini SCID-D) are heavily loaded on absorption - a feature of normal personality reflecting the individual's tendency to alter consciousness by markedly narrowing/expanding his attention and blurring the boundary between self and world. Absorption is related to Big 5 Openness. There aren't many epidemiological studies of dissociative disorders because they are quite rare and diagnostic criteria are not very reliable. Etiology of dissociative disorder Historically, dissociative disorders have been attributed to pathological psychological stress levels, which causes some aspects of experience, thought, and action to split off from consciousness (to dissociate). Trauma-memory argument - trauma victims typically deploy psychological defenses such as repression/dissociation to block their awareness of the trauma. A plausible traumatic origin can be identified in most cases of amnesia and fugue. On the other hand, trauma history is sometime absent. Moreover, it is not hard to find if one searches for it with a broad definition of the concept. Even when trauma is there, it is not guaranteed that it is the cause of the amnesia. Psychopathology Page 12  Even when trauma is there, it is not guaranteed that it is the cause of the amnesia. In summary, even though it's plausible that dissociative disorders are caused by trauma, the current evidence for that is not convincing. The trauma-memory argument Theories that attempt to describe the psychological/biological processes by which trauma induces amnesia are rejected by the fact that trauma-induced psychogenic amnesia occurs rarely, if at all. Treatment of dissociative disorders Apart from individual case reports, there is little systematic outcome studies of dissociative amnesia or fugue. There is more extensive literature on the treatment of DID. Although some CBT examples exist, most treatment approaches to DID are based on the idea that it's caused by childhood trauma. The therapy is typically psychodynamic and insight-oriented, focused on uncovering, releasing and working through trauma and other conflicting issues underlying the disorder, and getting the patient to abandon dissociative defenses. The therapist also seeks to integrate the patient's alter ego in a single, coherent identity. The lack of standardized treatment protocols for DID makes it hard to estimate effectiveness of therapy. Experimental psychopathology of dissociation Fugue patients' amnesia is retrograde, not anterograde (they are amnesic for events that occurred prior to the onset of the fugue state). After the fugue has remitted, memory for premorbid events is restored. During the fugue state, access to semantic memory is generally preserved, except for semantic knowledge about the patient's own identity. Study: in DID, one's alter egos are typically unable to recall/recognize words/pictures that had been studied by another. Study: directed forgetting effects are stronger between alter egos than within a single one. However, there were no differences between emotional & neutral stimulus materials. While explicit memories do not transfer between personalities, some implicit memories do. It is not clear which types of implicit memories transfer between personalities, that most likely depends on the nature of the implicit memory test. Case study of fugue: the patient lost use of his native language (German) and his identity and part of his autobiographical memory. In one experiment, the patient showed enhanced SCR to personally relevant material (e.g. names of family and friends). In another, he performed perfectly on a task involving learning pairs of semantically related German & English words, compared to unrelated word pairs and pairs including German nonwords. He also showed faster responses in a lexical decision task with German words, compared with English & German nonwords, while fMRI showed a shift from frontal to parietal activity. Amnesias in the dissociative disorders are retrograde, indicating that the issues are related to retrieval, not to encoding & storage of memories. The encoding & retrieval of episodic memories preferentially activates the left & right PFC, respectively. Study: cases of psychogenic amnesia fugue have lower activity in right frontal & temporal structures during autobiographical memory tasks. Subclinical dissociation Dissociative Experiences Scale (DES) - used to measure dissociative tendencies. Twin study: 45% of variance in DES is due to the shared environment and 55% due to the unique environment. There is a small correlation between DES and self-reported trauma in student & community samples. Association between self-reported dissociative symptoms and self-reported child sexual abuse is statistically significant, but weak (r = 0.07). However, the difference between high and low dissociators is greater for low-betrayal experiences (e.g. natural disasters), than it is for high- betrayal experiences (e.g. incest). DES scores are also correlated with fantasy proneness, false positives in recognition tests of memory, interrogative suggestibility, imagination inflation, source-monitoring problems, and the creation of pseudo-memories. DES scores are related to interference on Stroop task under selective-attention conditions, which suggests that individuals who have a tendency toward dissociation also have difficulties in deploying attention. Expanding the dissociative spectrum? A proposal for the DSM-5 is to classify dissociative disorders as forms of PTSD or to classify PTSD as essentially dissociative in nature. While PTSD includes vivid, intrusive memories of the traumatic event, dissociative disorders would represent a special case involving the absence of conscious recollection of the trauma. Appendix: DSM-5 Criteria for PTSD Psychopathology Page 13 Psychopathology Page 14