Biological correlates of direct exposure to terrorism several years postdisaster.

Background: It is important to understand long-term biological and psychiatric correlates of intense exposure to terrorism.

Methods: We assessed psychiatric diagnoses and biological stress measures in 50 healthy, highly exposed Oklahoma City bombing survivors recruited from a bombing registry 6 1/2 to 7 years postdisaster, comparing them with demographically matched, nonexposed community members. The Diagnostic Interview Schedule (DIS) determined Axis I psychiatric diagnoses.

Physiologic reactivity despite emotional resilience several years after direct exposure to terrorism.

Objective: Six and a half to 7 years after the 1995 terrorist bombing in Oklahoma City, the authors assessed autonomic reactivity to trauma reminders and psychiatric symptoms in adults who had some degree of direct exposure to the blast.

Method: Sixty survivors who were listed in a state health department registry of persons exposed to the bombing and 60 age- and gender-matched members of the Oklahoma City metropolitan area community were assessed for symptoms of PTSD and depression and for axis I diagnoses. Heart rate and systolic, diastolic, and mean arterial blood pressures were measured before, during, and after bombing-related interviews.

Neuroimmune and cortisol changes in selective serotonin reuptake inhibitor and placebo treatment of chronic posttraumatic stress disorder.

Background: To explore relations between neuroimmune and neuroendocrine systems relative to posttraumatic stress disorder (PTSD) treatment, cortisol and cytokine changes in response to selective serotonin reuptake inhibitor (SSRI) and placebo treatment of chronic PTSD were assessed prospectively.

Methods: Baseline measures of PTSD, depression, salivary 8 am and 4 pm cortisol, and serum interleukin-1beta (IL-1beta; pro-inflammatory) and soluble interleukin-2 receptors (IL-2R; cell-mediated immunity) were obtained for 58 PTSD and 21 control subjects. The PTSD subjects participated in a 10-week, double-blind treatment with citalopram (n = 19), sertraline (n = 18), or placebo (n = 7).

Paroxetine treatment of depression with posttraumatic stress disorder: effects on autonomic reactivity and cortisol secretion.

Effects of paroxetine treatment of comorbid depression and posttraumatic stress disorder (PTSD) on subjective symptoms, autonomic reactivity, and diurnal salivary cortisols were assessed prospectively. Cross-sectional baseline psychophysiologic assessments of 22 patients with depression + PTSD, 21 with depression alone, and 20 asymptomatic, previously traumatized controls found that comorbid patients had higher blood pressure and heart rate reactivity to individualized trauma scripts than purely depressed and control groups. On discriminant analyses comparing comorbid patients with each other group, combined autonomic variables correctly classified 55% of comorbid patients (sensitivity) and 75% of traumatized, healthy subjects (specificity) as well as 55% of comorbid patients (sensitivity) and 86% of purely depressed patients (specificity).

Can physiologic assessment and side effects tease out differences in PTSD trials? A double-blind comparison of citalopram, sertraline, and placebo.

Effects of double-blind treatment of chronic posttraumatic stress disorder (PTSD) with 2 SSRIs and placebo on emotional symptoms and autonomic reactivity were assessed prospectively. PTSD subjects received citalopram (n=25), sertraline (n=23), or placebo (n=10) for 10 weeks, with psychophysiologic assessments performed before and after treatment. Intent-to-treat analysis showed that all treatment groups improved significantly in total symptoms of PTSD (as measured by the Clinician Administered PTSD Scale), all 3 PTSD symptom clusters, and sleep time.