928 resultados para Posttraumatic stress disorder


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High rates of posttraumatic stress disorder (PTSD) have been reported among people seeking treatment for substance use disorders (SUDs), although few studies have examined the relationship between PTSD and substance use in young drug users. This study compared levels of substance use, coping styles, and high-risk triggers for substance use among 66 young adults with SUD, with or without comorbid PTSD. Young people with current SUD–PTSD (n = 36) reported significantly higher levels of substance use in negative situations, as well as emotion-focused coping, compared to the current SUD-only group (n = 30). Severity of PTSD was a significant predictor of negative situational drug use, and emotion-focused coping was found to mediate this relationship. The findings underscore the need for youth substance abuse treatment programs to include coping skills training and management of affect regulation for those individuals with comorbid SUD–PTSD.

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Posttraumatic stress disorder (PTSD) is a debilitating mental health condition frequently associated with psychiatric comorbidity and diminished quality of life, and it typically follows a chronic, often lifelong, course. Previous research has shown that trauma‐related psychopathology (but not necessarily clinical PTSD) can be effectively treated via the Internet. This study is the first of its kind to report on the online treatment of patients with a Diagnostic and Statistical Manual of Mental Disorders (fourth edition) clinical diagnosis of PTSD with therapist support by e‐mail only. Preliminary findings are presented of an open trial involving a 10‐week Internet‐based therapist‐assisted cognitive behavioural treatment for PTSD (PTSD Online). Pre and posttreatment measures of PTSD and related symptomatology were compared for 16 participants with a variety of trauma experiences. Participants showed clinically significant reductions in PTSD severity and symptomatology, moderate tolerance of the program content, and high therapeutic alliance ratings. No significant change was found on measures of more general psychological symptoms. The results suggest that PTSD Online appears to be an effective and accessible clinical treatment for people with a confirmed PTSD diagnosis.

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To assess, from a health sector perspective, the incremental cost-effectiveness of three treatment recommendations in the most recent Australian Clinical Practice Guidelines for posttraumatic stress disorder (PTSD). The interventions assessed are trauma-focused cognitive behavioural therapy (TF-CBT) and selective serotonin reuptake inhibitors (SSRIs) for the treatment of PTSD in adults and TF-CBT in children, compared to current practice in Australia.

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Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart disease.

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Inflammation might link posttraumatic stress disorder (PTSD) with an increased risk of cardiovascular events. We explored the association between PTSD and inflammatory biomarkers related to cardiovascular morbidity and the role of co-morbid depressive symptoms in this relationship.

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Chronic posttraumatic stress disorder (PTSD) has been associated with perturbed hypothalamic-pituitary-adrenal (HPA) axis function and a hyperadrenergic state. We hypothesized that patients with PTSD attributable to myocardial infarction (MI) would show peripheral hypocortisolemia and increased norepinephrine levels, whereby taking into account that depressive symptoms would affect this relationship.

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Posttraumatic stress disorder (PTSD) and circulating cellular adhesion molecules (CAMs) predict cardiovascular risk. We hypothesized a positive relationship between PTSD caused by myocardial infarction (MI) and soluble CAMs. We enrolled 22 post-MI patients with interviewer-rated PTSD and 22 post-MI patients with no PTSD. At 32±6months after index MI, all patients were re-scheduled to undergo the Clinician-Administered PTSD Scale (CAPS) interview and had blood collected to assess soluble CAMs at rest and after the CAPS interview. Relative to patients with no PTSD, those with PTSD had significantly higher levels of soluble vascular cellular adhesion molecule (sVCAM)-1 and intercellular adhesion molecule (sICAM)-1 at rest and, controlling for resting CAM levels, significantly higher sVCAM-1 and sICAM-1 after the interview. Greater severity of PTSD predicted significantly higher resting levels of sVCAM-1 and soluble P-selectin in patients with PTSD. At follow-up, patients with persistent PTSD (n=15) and those who had remitted (n=7) did not significantly differ in CAM levels at rest and after the interview; however, both these groups had significantly higher sVCAM-1 and sICAM-1 at rest and also after the interview compared to patients with no PTSD. Elevated levels of circulating CAMs might help explain the psychophysiologic link of PTSD with cardiovascular risk.

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Hypercoagulability of the blood might partially explain the increased cardiovascular disease risk in posttraumatic stress disorder (PTSD) and is also triggered by anticipatory stress. We hypothesized exaggerated procoagulant reactivity in patients with PTSD in response to a trauma-specific interview that would be moderated by momentary stress levels. We examined 23 patients with interviewer-diagnosed PTSD caused by myocardial infarction (MI) and 21 post-MI patients without PTSD. A second diagnostic (i.e., trauma-specific) interview to assess posttraumatic stress severity was performed after a median follow-up of 26 months (range 12-36). Before that interview patients rated levels of momentary stress (Likert scale 0-10) and had blood collected before and after the interview. The interaction between PTSD diagnostic status at study entry and level of momentary stress before the follow-up interview predicted reactivity of fibrinogen (P=0.036) and d-dimer (P=0.002) to the PTSD interview. Among patients with high momentary stress levels, PTSD patients had greater fibrinogen (P=0.023) and d-dimer (P=0.035) reactivity than non-PTSD patients. Among patients with low momentary stress levels, PTSD patients had less d-dimer reactivity than non-PTSD patients (P=0.024); fibrinogen reactivity did not significantly differ between groups. Momentary stress levels, but not severity of posttraumatic stress, correlated with d-dimer reactivity in PTSD patients (r=0.46, P=0.029). We conclude that momentary stress levels moderated the relationship between PTSD and procoagulant reactivity to a trauma-specific interview. Procoagulant reactivity in post-MI patients with PTSD confronted with their traumatically experienced MI was observed if patients perceived high levels of momentary stress before the interview.

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Based on a brief systematic review suggesting dyslipidemia in posttraumatic stress disorder (PTSD), we studied, for the first time, levels of blood lipids in patients with a DSM-IV diagnosis of PTSD caused by myocardial infarction (MI).