Alterations in Stress Reactivity After Long‐Term Treatment with Paroxetine in Women with Posttraumatic Stress Disorder

Abstract

Posttraumatic stress disorder (PTSD) is typically accompanied by both acute and chronic alterations in the stress response. These alterations have mostly been described in individuals under baseline conditions, but studies have also used a challenge model to assess the role of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response. The purpose of this article was to assess the effect of long-term treatment with the selective reuptake inhibitor (SSRI), paroxetine, on stress reactivity in patients with PTSD. We assessed diurnal salivary cortisol and urinary cortisol as well as cortisol, heart rate, and behavioral responses to a standardized cognitive stress challenge, in 13 female patients with chronic PTSD before and after 12 months of paroxetine treatment. Treatment resulted in a significant decrease in PTSD symptoms. Twenty-four-hour urinary cortisol was lower compared to base line after successful treatment. Treatment resulted in a decrease of salivary cortisol levels on all time points on a diurnal curve. Despite similar stress perception, cortisol response to the cognitive stress challenge resulted in a 26.5% relative decrease in stress-induced salivary cortisol with treatment. These results suggest that successful treatment with SSRI in chronic PTSD is associated with a trend for a decrease in baseline diurnal cortisol and with reduced cortisol reactivity to stress.

Anxiolytic effects of a novel herbal treatment in mice models of anxiety

“…High levels of corticosterone, corticotropin-releasing hormone, stress or exposure to a new environment have been shown to impair the induction of long term potentiation (Kim and Diamond, 2002;Xu et al, 1998), proliferation and survival of neurons and dendritic spines in the hippocampus (Chen et al, 2008;Pham et al, 2003). Treatment with different SSRIs has been repeatedly found to reduce cortisol levels in patients with anxiety disorders (Lenze et al, 2011;Vermetten et al, 2006), as well as corticosterone levels in animal studies (Buhl et al, 2010;Schmidt et al, 2007). In light of these findings, it is assumed that a normalization of the HPA axis might be part of the mechanism by which SSRIs create their anxiolytic therapeutic effects.…”

Structural and functional plasticity of the human brain in posttraumatic stress disorder

“…In an open-label study we showed a 5% increase in hippocampal volume after 9 months of treatment with paroxetine, as well as a 30% improvement in verbal declarative memory function measured with neuropsychological testing . Paroxetine treatment was also associated with a decreased cortisol and heart rate response to a stressful task (Vermetten et al, 2006b). …”

Neuroimaging in Posttraumatic Stress Disorder and Other Stress-Related Disorders

“…These findings indicate that phenytoin has an effect on symptoms as well as brain structure in PTSD patients. In a second study, patients with PTSD were shown to have an increase in hippocampal volume and memory function with paroxetine [96], and a decrease in cortisol responsiveness to a stressful cognitive challenge [160]. One case report showed decreased inferior frontal, prefrontal, and insula blood flow measured with PET in response to war-related sounds.…”