Paroxetine Treatment of Depression With Posttraumatic Stress Disorder

Abstract

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). Although baseline AM and PM salivary cortisol levels were within reference range and did not differ significantly across groups, depression + PTSD patients differed from the other 2 groups in having a flattened diurnal pattern. After 10 weeks of open-label paroxetine, comorbid patients significantly improved in all PTSD symptom evaluations and physiologic reactivity measures but did not change cortisol levels or acquire a robust diurnal cortisol pattern. Ten treated depressed patients did not change in physiologic or cortisol measures. Results demonstrate that sampled comorbid patients had autonomic reactivity patterns similar to PTSD that responded to selective serotonin reuptake inhibitor treatment but had diurnal cortisol secretion patterns different from depression or that expected for PTSD, which did not change with treatment. Results suggest a complexity in the neurobiology of comorbid PTSD and major depression and its response to treatment.

Differential Patterns of HPA Activity and Reactivity in Adult Posttraumatic Stress Disorder and Major Depressive Disorder

“…45 Preliminary research has begun to address this HPA in PTSD & MDD 195 question, with a recent study revealing consistency in HPA activity despite significant improvement in clinical profile after a ten-week treatment with paroxetine. 63 This finding is consistent with the suggestion that an altered HPA profile may represent a preexisting risk factor for developing PTSD-and one that remains unchanged with pharmacotherapy. It should be noted, however, that this study was conducted in individuals with PTSD and comorbid depression; future research should target those with PTSD alone.…”

Impact of the selective serotonin reuptake inhibitor citalopram on insulin sensitivity, leptin and basal cortisol secretion in depressed and non-depressed euglycemic women of reproductive age

“…However, there is little information in the published literature addressing the effect of long-term administration of SSRIs on HPA axis functioning in depressed populations. Tucker and associates found no longitudinal difference in cortisol production in ten depressed women treated for 10 weeks with paroxetine [38]. In a similar study, a mixed gender group of depressed individuals treated with paroxetine for 35 days also failed to demonstrate modulation of HPA activity [6].…”

Impact of PTSD comorbidity on one-year outcomes in a depression trial

“…In the medication condition, this may have occurred because paroxetine is an approved treatment for PTSD as well as for depression. It has been shown to be effective for PTSD and its associated features in mixed samples of men and women, civilian and military populations (Davidson, 2003;Stein, Davidson, Seedat, & Beebe, 2003;Tucker et al, 2004). Indeed, studies that compared medication treatment of depression with and without PTSD did not find differences (Papakostas et al, 2003;Tucker et al, 2004).…”

“…That is, it was hypothesized that there would be a significant interaction between comorbid PTSD and treatment condition. The interaction hypothesis was based on the fact that paroxetine is an FDA-approved treatment for PTSD as well as depression; thus, it would be expected to have similar effects in the two diagnostic groups (Tucker et al, 2004). Functional outcomes were expected to follow the same pattern because these outcomes have been shown to improve with treatment for depression (Coulehan et al, 1997;Kocsis et al, 2002;Miller et al, 1998;Simon, Revicki, Grothaus, & Von Korff, 1998;Simon et al, 1996;Wells et al, 2000), and treatment for PTSD (Drake et al, 2003;Ehlers et al, 2003;Falsetti et al, 2003;Power et al, 2002).…”