Urinary 17-OHCS levels. Data on seven helicopter ambulance medics in combat.

Archives of General Psychiatry (Impact Factor: 13.77). 08/1967; 17(1):104-10.
Source: PubMed
  • [Show abstract] [Hide abstract]
    ABSTRACT: Post-traumatic stress disorder (PTSD) is a syndrome of psychophysiological sequelae occurring in the aftermath of severe emotional trauma. Phenomenologically, symptoms occur in 3 clusters: re-experiencing, avoidance and hyperarousal. Other psychiatric disorders such as depression, panic disorder and substance abuse frequently co-occur with PTSD. Treatment strategies for PTSD are often multimodal and attempt to integrate biological, behavioural, cognitive, psychodynamic and social formulations. Pharmacotherapy must target specific symptoms in all 3 clusters, and address the presence of comorbid psychiatric disorders. Psychotropic medication can facilitate psychotherapeutic work, or serve as the primary modality in a biologically based approach to treatment. Specific medications used in the treatment of PTSD span a broad spectrum of pharmacological agents. The most empirically studied agents, tricyclic antidepressants and monoamine oxidase inhibitors, demonstrate a definite but limited impact on specific PTSD symptoms. For the patient who presents in an acute symptomatic state, benzodiazepine anxiolytics may be appropriate. For longer term treatment, selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs), particularly fluoxetine, appear to have broader spectrum therapeutic effects on specific PTSD symptom clusters. Both antidepressants and anxiolytics have, in some studies, shown beneficial effects on depressive symptoms and anxiety, without measurable impact on the symptoms more specific to PTSD. Maintenance pharmacotherapy frequently requires a multidrug regimen; an SSRI may serve as the primary agent, with adjunctive agents targeting residual hyperarousal and re-experiencing symptoms. Benzodiazepines, sedating tricyclic or antihistamine compounds, and the noradrenergic drugs Clonidine and propranolol are used in this way. Buspirone, a serotonergic anxiolytic, may serve a similar role for some patients, and cyproheptadine in particular appears to be helpful for nightmares. The antikindling agents carbamazepine and valproic acid (sodium valproate) have also been reported to be beneficial, and may provide an alternative for patients with persistent hyper-reactivity and explosiveness that have not responded to other treatments.
    CNS Drugs 10/1997; 8(4). · 4.38 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Determine the association between prenatal cocaine exposure and postnatal environmental adversity on salivary cortisol stress reactivity in school-aged children. Subjects included 743 11-year-old children (n = 320 cocaine-exposed; 423 comparison) followed since birth in a longitudinal prospective multisite study. Saliva samples were collected to measure cortisol at baseline and after a standardized procedure to induce psychological stress. Children were divided into those who showed an increase in cortisol from baseline to post stress and those who showed a decrease or blunted cortisol response. Covariates measured included site, birthweight, maternal pre and postnatal use of alcohol, tobacco or marijuana, social class, changes in caretakers, maternal depression and psychological symptoms, domestic and community violence, child abuse, and quality of the home. With adjustment for confounding variables, cortisol reactivity to stress was more likely to be blunted in children with prenatal cocaine exposure. Children exposed to cocaine and who experienced domestic violence showed the strongest effects. The combination of prenatal cocaine exposure and an adverse postnatal environment could downregulate the hypothalamic-pituitary-adrenal axis resulting in the blunted cortisol response to stress possibly increasing risk for later psychopathology and adult disease.
    The Journal of pediatrics 08/2010; 157(2):288-295.e1. · 4.02 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Neuroendocrine studies examining the hypothalamic-pituitary-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore, in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiology of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to different mechanisms of action for cortisol and its regulatory factors.
    Biological Psychiatry 12/1991; · 9.25 Impact Factor