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). 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.