The diagnostic status of ‘complex’ post-traumatic stress disorder (PTSD) remains controversial. The revisions to PTSD diagnostic criteria in ICD-11 and DSM-5 take opposing positions on how best to conceptualise post-traumatic presentations that include affect dysregulation, interpersonal difficulties and negative self-concept. ICD-11 carved out a separate category of complex PTSD (CPTSD) that is distinct from PTSD, whereas DSM-5 expanded PTSD to encompass such symptoms. Each approach carries problematic implications for clinical care. ICD-11 creates a dichotomy but the criteria themselves suggest a difference in severity rather than category. Furthermore, separating CPTSD perpetuates expectations that a ‘simple’ PTSD can be easily treated with brief trauma-focused therapy. DSM-5 complicates the PTSD diagnosis, but does not revise treatment recommendations. Both ICD and DSM need to recognise that most patients with PTSD do not reflect the clinical trial samples and do not fully recover with brief manualised therapies. Treatment guidelines should be developed that address the multiple needs and challenges of all patients with PTSD.

The question of whether and how the effects of cultural trauma can be transmitted intergenerationally from parents to offspring, or even to later generations, has evoked interest and controversy in academic and popular forums. Recent methodological advances have spurred investigations of potential epigenetic mechanisms for this inheritance, representing an exciting area of emergent research. Epigenetics has been described as the means through which environmental influences “get under the skin,” directing transcriptional activity and influencing the expression or suppression of genes. Over the past decade, this complex environment–biology interface has shown increasing promise as a potential pathway for the intergenerational transmission of the effects of trauma. This article reviews challenges facing research on cultural trauma, biological findings in trauma and posttraumatic stress disorder, and putative epigenetic mechanisms for transmission of trauma effects, including through social, intrauterine, and gametic pathways. Implications for transmission of cultural trauma effects are discussed, focused on the relevance of cultural narratives and the possibilities of resilience and adaptivity.

Mexican Americans (MAs) and American Indians (AIs) constitute conspicuously understudied groups with respect to risk for post-traumatic stress disorder (PTSD), especially in light of findings showing racial/ethnic differences in trauma exposure and risk for PTSD. The purpose of this study was to examine genetic influences on PTSD in two minority cohorts. A genome-wide association study (GWAS) with sum PTSD symptoms for trauma-exposed subjects was run in each cohort. Six highly correlated variants in olfactory receptor family 11 subfamily L member 1 (OR11L1) were suggestively associated with PTSD in the MA cohort. These associations remained suggestively significant after permutation testing. A signal in a nearby olfactory receptor on chromosome 1, olfactory receptor family 2 subfamily L member 13 (OR2L13), tagged by rs151319968, was nominally associated with PTSD in the AI sample. Although no variants were significantly associated after correction for multiple testing in a meta-analysis of the two cohorts, pathway analysis of the top hits showed an enrichment cluster of terms related to sensory transduction, olfactory receptor activity, G-protein coupled receptors, and membrane. As previous studies have proposed a role for olfaction in PTSD, our results indicate this influence may be partially driven by genetic variation in the olfactory system.

The aim of this meeting was to obtain a consensus on what constitutes good research practice in posttraumatic stress disorder (PTSD). Objectives were to review relevant parameters of trials, such as the patients recruited, the means of assessing PTSD at baseline, and the change in symptomatology in response to treatment, and to reach a consensus on the most appropriate parameters to use in future research. The bases for the discussion were the 1995 National Institute of Mental Health (NIMH) and the National Center for PTSD consensus on the assessment of PTSD, results of drug treatment trials, and information on the assessment scales used in PTSD research.

In 1980, the diagnosis of posttraumatic stress disorder (PTSD) was established to recognize that exposure to events such as rape, physical assault, torture, or combat can leave long-lasting psychological scars in persons who undergo these experiences. The intention of the diagnosis was to acknowledge that exposure to a traumatic event was a sufficient explanation for the occurrence of longterm psychological problems. Prior to this formulation, stressful events were thought to precipitate symptoms that would resolve over time. The symptoms manifested by persons following adverse events were characterized as transient adjustment reactions. Longerterm symptoms were considered to be a reflection of underlying neurosis, rather than stress exposure per se.

The diagnosis of PTSD provided a paradigm for acknowledging that exposure to devastating trauma can produce symptoms that can be quite severe and chronic in nature. Although many of the symptoms of PTSD were similar to those that occur in other anxiety or mood disorders, the hallmark of PTSD appeared to be a preoccupation with the traumatic event and a resultant set of behavioral changes that occurred because of attempts to avoid reminders of the event.

As part of an established traumatic stress research and treatment program located in New York City, we experienced the September 11, 2001, terrorist attacks on the World Trade Center first as New Yorkers, but also as professionals with an interest in both treating the survivors and furthering scientific knowledge regarding the neurobiology and treatment of traumatic stress. This paper gives vignettes of calls to our program and the treatment of World Trade Center terrorist attack survivors.

Anabolic–androgenic steroids (AASs) are synthetic hormones used by individuals who want to look better or perform better in athletics and at the gym. Their use raises an interesting paradox in which drug use is associated with a number of health benefits, but also the possibility of negative health consequences. Existing models of AAS addiction follow the traditional framework of drug abuse and dependence, which suggest that harmful use occurs as a result of the drug's ability to hijack the motivation–reward system. However, AASs, unlike typical drugs of abuse, are not used for acute intoxication effects or euphoria. Rather, AASs are used to affect the body through changes to the musculoskeletal system and the hypothalamic–pituitary–gonadal axis as opposed to stimulating the reward system. We offer an allostatic model of AAS addiction to resolve this inconsistency between traditional drug addiction and AAS addiction. This allostatic framework provides a way to (a) incorporate exercise into AAS misuse, (b) identify where AAS use transitions from recreational use into a drug problem, and (c) describe individual differences in vulnerability or resilience to AASs. Implications for this model of AAS addiction are discussed.

The effects of childhood abuse are diverse, and although pathology is not the only outcome, psychiatric illness, including posttraumatic stress disorder (PTSD), can develop. However, adult PTSD is less common among those who experienced single-event traumas as children than it is among those who experienced childhood abuse. In addition, PTSD is more common among adults than children who experienced childhood abuse. Such evidence raises doubt about the direct, causal link between childhood trauma and adult PTSD. The experience of childhood trauma, and in particular abuse, has been identified as a risk factor for subsequent development of PTSD following exposure to adult trauma, and a substantial literature identifies revictimization as a factor that plays a pivotal role in this trajectory. The literature on the developmental effects of childhood abuse and pathways to revictimization, when considered in tandem with the biological effects of early stress in animal models, may provide some explanations for this. Specifically, it seems possible that permanent sensitization of the hypothalamic–pituitary–adrenal axis and behavioral outcomes are a consequence of childhood abuse, and these combine with the impact of retraumatization to sustain, perpetuate, and amplify symptomatology of those exposed to maltreatment in childhood.

Given the personal and societal costs associated with acute impairment and enduring post-traumatic stress disorder (PTSD), the mental health response to disasters is an integral component of disaster response planning. The purpose of this paper is to explore the compatibility between cognitive-behavioral psychology and the disaster mental health model, and explicate how cognitivebehavioral perspectives and intervention methods can enhance the effectiveness of disaster mental health services. It is argued that cognitive-behavioral methods, if matched to the contexts of the disaster and the needs of individuals, will improve efforts to prevent the development of PTSD and other trauma-related problems in survivors of disaster or terrorist events. First, the similarities between models of care underlying both disaster mental health services and cognitive-behavioral therapies are described. Second, examples of prior cognitive-behavioral therapy-informed work with persons exposed to disaster and terrorism are provided, potential cognitive-behavioral therapy applications to disaster and terrorism are explored, and implications of cognitive-behavioral therapy for common challenges in disaster mental health is discussed. Finally, steps that can be taken to integrate cognitive-behavioral therapy into disaster mental health are outlined. The aim is to prompt disaster mental health agencies and workers to consider using cognitive-behavioral therapy to improve services and training, and to motivate cognitive-behavioral researchers and practitioners to develop and support disaster mental health response.

The aim of the study was to prospectively evaluate the association between the occurrence of post-traumatic stress disorder (PTSD) and the adrenergic response to the traumatic event, and additionally, to explore the link between PTSD and the initial norepinephrine:cortisol ratio. Plasma levels and urinary excretion of norepinephrine (NE) were measured in 155 survivors of traumatic events during their admission to a general hospital emergency room (ER) and at 10 d, 1 month and 5 months later. Symptoms of peri-traumatic dissociation, PTSD and depression were assessed in each follow-up session. The Clinician-Administered PTSD Scale (CAPS) conferred a diagnosis of PTSD at 5 months. Trauma survivors with (n=31) and without (n=124) PTSD had similar levels of plasma NE, urinary NE excretion, and NE:cortisol ratio in the ER. Plasma NE levels were lower in subjects with PTSD at 10 d, 1 month, and 5 months. There was a weak but significant positive correlation between plasma levels of NE in the ER and concurrent heart rate, and a negative correlation between NE in the ER and dissociation symptoms. Peripheral levels of NE, shortly after traumatic events, are poor risk indicators of subsequent PTSD among civilian trauma victims. Simplified biological models may not properly capture the complex aetiology of PTSD.

The aim of the study was to evaluate the association between post-traumatic disorder (PTSD) and hypothalamic–pituitary–adrenal (HPA) axis responses to the triggering trauma. A companion paper evaluates the adrenergic response and interactions between the two. We measured plasma and saliva cortisol, hourly urinary excretion of cortisol, plasma levels of adrenocorticotropin (ACTH), and the leukocyte glucocorticoid receptor (GR) density of 155 non-injured survivors of traumatic events (91 males and 64 females; 125 road traffic accidents, 19 terrorist attacks, 11 others). Measurements were taken during survivors' admissions to an emergency room (ER) of a general hospital, and in the mornings, 10 d, 1 month, and 5 months later. Symptoms of peri-traumatic dissociation, PTSD, and depression were assessed on each follow-up session. The clinician-administered PTSD scale (CAPS) conferred a diagnosis of PTSD at 5 months. Survivors with (n=31) and without (n=124) PTSD at 5 months had similar levels of hormones at all times. Plasma cortisol levels decreased with time in both groups. Female subjects had lower ACTH levels than males. PTSD in females was associated with higher levels of ACTH. In unselected cohorts of trauma survivors, PTSD is not preceded by a detectable abnormality of peripheral HPA axis hormones.

Among the adverse mental health consequences of childhood trauma is the risk related to the development of posttraumatic stress disorder (PTSD) in adulthood. Other risk factors for PTSD, including parental trauma exposure and parental PTSD, can also contribute to the experience of child trauma. We examined associations between childhood trauma and PTSD in 51 adult children of Holocaust survivors and 41 comparison subjects, in consideration of parental trauma exposure and parental PTSD. We also examined these variables in relation to 24-hr urinary cortisol levels. Adult offspring of Holocaust survivors showed significantly higher levels of self-reported childhood trauma, particularly emotional abuse and neglect, relative to comparison subjects. The difference was largely attributable to parental PTSD. Self-reported childhood trauma was also related to severity of PTSD in subjects, and emotional abuse was significantly associated with 24-hr mean urinary cortisol secretion. We conclude that the experience of childhood trauma may be an important factor in the transmission of PTSD from parent to child.

This article reviews memory-related impairments in trauma survivors with posttraumatic stress disorder and their possible association to neuroendocrine alterations seen in this disorder. The neuroendocrine profile in PTSD first described in chronically ill combat veterans is characterized by lower basal cortisol levels, higher glucocorticoid receptor number, enhanced sensitivity to exogenous steroids, and increased variation in basal cortisol levels over the diurnal cycle. The generalizability and time course of these neuroendocrine alterations are explored in longitudinal studies and studies in other traumatized populations. These studies suggest that at least some aspects of this neuroendocrine profile can also be seen in other populations, including women, children, and victims of childhood trauma. Additionally, the alterations may be present early in the course of illness, perhaps even in the immediate aftermath of trauma, and may continue to be manifest in elderly trauma survivors. The mechanisms by which these neuroendocrine alterations may influence the formation and processing of traumatic memories are discussed.