No abstract

Children and adults exposed to chronic interpersonal trauma consistently demonstrate psychological disturbances that are not captured in the posttraumatic stress disorder (PTSD) diagnosis. The DSM-IV (American Psychiatric Association, 1994) Field Trial studied 400 treatment-seeking traumatized individuals and 128 community residents and found that victims of prolonged interpersonal trauma, particularly trauma early in the life cycle, had a high incidence of problems with (a) regulation of affect and impulses, (b) memory and attention, (c) self-perception, (d) interpersonal relations, (e) somatization, and (f) systems of meaning. This raises important issues about the categorical versus the dimensional nature of posttraumatic stress, as well as the issue of comorbidity in PTSD. These data invite further exploration of what constitutes effective treatment of the full spectrum of posttraumatic psychopathology.

Ever since people's responses to overwhelming experiences have been systematically explored, researchers have noted that a trauma is stored in somatic memory and expressed as changes in the biological stress response. Intense emotions at the time of the trauma initiate the long-term conditional responses to reminders of the event, which are associated both with chronic alterations in the physiological stress response and with the amnesias and hypermnesias characteristic of posttraumatic stress disorder (PTSD). Continued physiological hyperarousal and altered stress hormone secretion affect the ongoing evaluation of sensory stimuli as well. Although memory is ordinarily an active and constructive process, in PTSD failure of declarative memory may lead to organization of the trauma on a somatosensory level (as visual images or physical sensations) that is relatively impervious to change. The inability of people with PTSD to integrate traumatic experiences and their tendency, instead, to continuously relieve the past are mirrored physiologically and hormonally in the misinterpretation of innocuous stimuli as potential threats. Animal research suggests that intense emotional memories are processed outside of the hippocampally mediated memory system and are difficult to extinguish. Cortical activity can inhibit the expression of these subcortically based emotional memories. The effectiveness of this inhibition depends, in part, on physiological arousal and neurohormonal activity. These formulations have implications for both the psychotherapy and the pharmacotherapy of PTSD.

Since trauma arises from an inescapable stressful event that overwhelms people's coping mechanisms, it is uncertain to what degree the results of laboratory studies of ordinary events are relevant to the understanding of traumatic memories. This paper reviews the literature on differences between recollections of stressful and of traumatic events. It then reviews the evidence implicating dissociation as the central pathogenic mechanism that gives rise to posttraumatic stress disorder (PTSD). A systematic exploratory study of 46 subjects with PTSD indicated that traumatic memories were retrieved, at least initially, in the form of dissociated mental imprints of sensory and affective elements of the traumatic experience: as visual, olfactory, affective, auditory, and kinesthetic experiences. Over time, subjects reported the gradual emergence of a personal narrative that can be properly referred to as "explicit memory." The implications of these findings for understanding the nature of traumatic memories are discussed.

The results suggest that emotions associated with the PTSD symptomatic state are mediated by the limbic and paralimbic systems within the right hemisphere. Activation of visual cortex may correspond to the visual component of PTSD reexperiencing phenomena.

Childhood exposure to victimization is prevalent and has been shown to contribute to significant immediate and long-term psychological distress and functional impairment. Children exposed to interpersonal victimization often meet criteria for psychiatric disorders other than posttraumatic stress disorder (PTSD). Therefore, this article summarizes research that suggests directions for broadening current diagnostic conceptualizations for victimized children, focusing on findings regarding victimization, the prevalence of a variety of psychiatric symptoms related to affect and behavior dysregulation, disturbances of consciousness and cognition, alterations in attribution and schema, and interpersonal impairment. A wide range of symptoms is common in victimized children. As a result, in the current psychiatric nosology, multiple comorbid diagnoses are necessary-but not necessarily accurate-to describe many victimized children, potentially leading to both undertreatment and overtreatment. Related findings regarding biological correlates of childhood victimization and the treatment outcome literature are also reviewed. Recommendations for future research aimed at enhancing diagnosis and treatment of victimized children are provided.

Research suggests that responses to script-driven trauma imagery in posttraumatic stress disorder (PTSD) include reexperiencing and dissociative symptom subtypes. This functional magnetic resonance imaging (fMRI) study employed a dimensional approach to characterizing script-driven imagery responses, using the Responses to Script-Driven Imagery Scale and correlational analyses of relationships between severity of state posttraumatic symptoms and neural activation. As predicted, state reexperiencing severity was associated positively with right anterior insula activity and negatively with right rostral anterior cingulate cortex (rACC). Avoidance correlated negatively with rACC and subcallosal anterior cingulate activity. In addition, as predicted, dissociation correlated positively with activity in the left medial prefrontal and right superior temporal cortices, and negatively with the left superior temporal cortex. Theoretical and clinical implications are discussed, particularly with respect to an emotion-dysregulation account of PTSD.

ClinicalTrials.gov identifier: NCT00839813.