A randomized clinical trial of eye movement desensitization and reprocessing (EMDR), fluoxetine, and pill placebo in the treatment of posttraumatic stress disorder: treatment effects and long-term maintenance.

OBJECTIVE: The relative short-term efficacy and long-term benefits of pharmacologic versus psychotherapeutic interventions have not been studied for posttraumatic stress disorder (PTSD). This study compared the efficacy of a selective serotonin reup-take inhibitor (SSRI), fluoxetine, with a psychotherapeutic treatment, eye movement desensitization and reprocessing (EMDR), and pill placebo and measured maintenance of treatment gains at 6-month follow-up. METHOD: Eighty-eight PTSD subjects diagnosed according to DSM-IV criteria were randomly assigned to EMDR, fluoxetine, or pill placebo. They received 8 weeks of treatment and were assessed by blind raters posttreatment and at 6-month follow-up. The primary outcome measure was the Clinician-Administered PTSD Scale, DSM-IV version, and the secondary outcome measure was the Beck Depression Inventory-II. The study ran from July 2000 through July 2003. RESULTS: The psychotherapy intervention was more successful than pharmacotherapy in achieving sustained reductions in PTSD and depression symptoms, but this benefit accrued primarily for adult-onset trauma survivors. At 6-month follow-up, 75.0% of adult-onset versus 33.3% of child-onset trauma subjects receiving EMDR achieved asymptomatic end-state functioning compared with none in the fluoxetine group. For most childhood-onset trauma patients, neither treatment produced complete symptom remission. CONCLUSIONS: This study supports the efficacy of brief EMDR treatment to produce substantial and sustained reduction of PTSD and depression in most victims of adult-onset trauma. It suggests a role for SSRIs as a reliable first-line intervention to achieve moderate symptom relief for adult victims of childhood-onset trauma. Future research should assess the impact of lengthier intervention, combination treatments, and treatment sequencing on the resolution of PTSD in adults with childhood-onset trauma.

Preliminary evidence of parasympathetic influence on basal heart rate in posttraumatic stress disorder.

OBJECTIVE: Evidence of elevated basal heart rate (HR) in posttraumatic stress disorder (PTSD) has been interpreted in terms of elevated sympathetic cardiac activity, as have possible increased cardiovascular disease risks and outcomes associated with elevated HR. Yet it is well-established that the parasympathetic branch of the autonomic nervous system not only influences HR independently of the sympathetic branch, but makes a greater contribution to HR, including resting HR. Additionally, abnormally low tonic parasympathetic activity on the heart has been implicated in cardiovascular disease and hypertension. This study addressed a potential parasympathetic contribution to elevated basal HR in PTSD. METHODS: We used a descriptive and subgroup differences approach to investigate relationships between parasympathetic activity and basal HR in 59 adults (50 females) with PTSD, all of whom were participants in a treatment outcome study and assessed prior to exposure to trauma-related script-driven imagery. Consistent with the well-known relationship between parasympathetic activity and HR, we hypothesized that basal respiratory sinus arrhythmia (RSA), a measure of parasympathetic cardiac activity, would be negatively correlated with basal HR. More important, we predicted that pathologically elevated HRs previously associated with PTSD would only characterize a low-RSA subgroup. Potential confounds of age, respiration rate, and aerobic fitness were addressed. RESULTS: As predicted, mean HR was 80.5 bpm in the low-RSA tercile group, similar to mean HRs of PTSD groups in prior research and significantly higher than 69 and 65 bpm in the middle- and high-RSA groups, respectively, which are typical of non-PTSD controls. CONCLUSION: These findings suggest that a substantial proportion of those with PTSD may not have elevated basal HRs. Furthermore, among those who do exhibit elevated HR, there may be a parasympathetic contribution that is independent of any sympathetic one. Only measuring both branches at once, ideally with autonomic blockades, can definitively address these issues.

Prevalence and incidence of androgen deficiency in middle-aged and older men: estimates from the Massachusetts Male Aging Study.

Little is known about the descriptive epidemiology of androgen deficiency. In this study, we sought to address this issue by providing estimates of the crude and age-specific prevalence and incidence rates of androgen deficiency in a randomly sampled population-based cohort of middle-aged and older men. Data on androgen deficiency (defined using both signs/symptoms plus total and calculated free testosterone) were available for n = 1691 (baseline) and n = 1087 (follow-up) men from the Massachusetts Male Aging Study. Crude and age-specific prevalence and incidence rates were calculated. Based on these estimates, projections for the number of cases of androgen deficiency in the 40- to 69-yr-old U.S. male population were computed. Estimates of the crude prevalence of androgen deficiency at baseline and follow-up were 6.0 and 12.3%, respectively. Prevalence increased significantly with age. From baseline age-specific prevalence data, it is estimated that there are approximately 2.4 million 40- to 69-yr-old U.S. males with androgen deficiency. The crude incidence rate of androgen deficiency was 12.3 per 1,000 person-years, and the rate increased significantly (P < 0.0001) with age. Based on these incidence data, we can expect approximately 481,000 new cases of androgen deficiency per year in U.S. men 40-69 yr old.