Search

Background: In patients with post-traumatic stress disorder (PTSD) two open pilot studies about the effects of 35% carbon dioxide (CO 2 ) exist. One shows an augmented panicogenic and anxiogenic response (Muhtz et al., 2011), the other does not (Talesnik et al. 2007). We further characterized the CO 2 reactivity in PTSD using for the first time placebo-controlled and double-blind conditions., Methods: In 20 patients with PTSD we assessed panic, anxiety, dissociative and PTSD symptoms after a single vital capacity inhalation of 35% CO 2 compared to a placebo gas condition in a within-participant cross-over, placebo-controlled, double-blind and randomized design., Results: Inhalation of 35% CO 2 versus placebo provoked significantly increased panic, anxiety, dissociative and PTSD symptoms. The reaction to placebo gas was minimal. Order of inhalation, patients' sex or age did not influence the results. The panic and anxiety response under CO 2 was considerably higher in the PTSD patients than in healthy controls from our previous open study., Conclusions: The results corroborate that our preceding findings of an increased CO 2 reactivity in patients with PTSD are not false positive due to the open design or the lack of placebo control. Replication in a larger number of PTSD patients and matched control subjects is needed. The potential role of childhood traumatisation, psychiatric comorbidity, psychotropic medication and trait dissociation in prior contradictory reports should be clarified., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Intimate partner violence (IPV) is often a chronic form of trauma with deleterious mental health problems. Furthermore, IPV survivors have also often experienced trauma in childhood. Consequently, by examining a sample of IPV survivors, this study sought to assess typical trauma sequelae--Posttraumatic Stress Disorder (PTSD), Major Depressive Disorder (MDD), or dissociative symptoms-and trauma-related characteristics consistent with Herman's Trauma theory (1992; i.e., chronicity of trauma, age of first trauma exposure, and social support), in relation to hypothalamic-pituitary-adrenal axis function. The study compared basal and diurnal cortisol in women (n = 88) based on diagnostic status and symptom severity (PTSD [n = 14], PTSD and comorbid MDD [n = 43], subthreshold symptoms of PTSD and MDD [n = 19]), dissociative symptoms, and the aforementioned trauma-related characteristics to a matched control group (n = 12) without any lifetime history of mental health diagnoses or exposure to interpersonal trauma. Regardless of their diagnostic status and trauma-related characteristics, trauma-exposed women had higher levels of dissociative symptoms relative to women in the control group, and these dissociative symptoms were inversely related to awakening cortisol levels. Findings suggest that low cortisol levels may not be a diagnostic marker, but instead may be associated with a dissociative coping style developed in the context of trauma exposure, consistent with mechanisms posited by Trauma theory.

This article explicates a theory that oxytocin, a sexually dimorphic neurotransmitter and paracrine hormone, is a plausible mechanism linking early relational trauma with posttraumatic self disorders (e.g., dissociation, somatization, and interpersonal sensitivity), posttraumatic stress disorder, and pelvic visceral dysregulation disorders (e.g., irritable bowel syndrome, chronic pelvic pain, interstitial cystitis, and hyperemesis gravidarum). This posttraumatic oxytocin dysregulation disorders theory is consistent with the historical and contemporary literature. It integrates attention to psychological and physical comorbidities and could account for the increased incidence of these disorders among females. Specific propositions are explored in data from studies of traumatic stress and women's health.

Dissociation is defined as the disruption of the usually integrated functions of consciousness, such as memory, identity, and perceptions of the environment. Causes include various psychological, neurological and neurobiological mechanisms, none of which have been consistently supported. To our knowledge, the role of gene-environment interactions in dissociative experiences in obsessive-compulsive disorder (OCD) has not previously been investigated. Eighty-three Caucasian patients (29 male, 54 female) with a principal diagnosis of OCD were included. The Dissociative Experiences Scale was used to assess dissociation. The role of childhood trauma (assessed with the Childhood Trauma Questionnaire), and a functional 44-bp insertion/deletion polymorphism in the promoter region of the serotonin transporter, or 5-HTT, in mediating dissociation, was investigated using multiple regression analysis and path analysis using the partial least squares model. Both analyses indicated that an interaction between physical neglect and the S/S genotype of the 5-HTT gene significantly predicted dissociation in patients with OCD. Dissociation may be a predictor of poorer treatment outcome in patients with OCD; therefore, a better understanding of the mechanisms that underlie this phenomenon may be useful. Here, two different but related statistical techniques (multiple regression and partial least squares), confirmed that physical neglect and the 5-HTT genotype jointly play a role in predicting dissociation in OCD., ((c) 2007 S. Karger AG, Basel.)