Pharmacotherapy is an effective treatment for generalized anxiety disorder (GAD), but few studies have examined the nature of decline of anxiety and depression during pharmacotherapy for GAD and even fewer studies have examined predictors of symptom decline. This study examined the decline in symptoms of anxiety and depression in patients with GAD during a 6-week open trial of fluoxetine. Growth curve analyses indicated that pharmacotherapy with fluoxetine led to significant declines in symptoms of anxiety and depression over the 6 weeks of treatment. However, the decay slope observed for anxiety symptoms was significantly greater than that for depressive symptoms. Further analyses revealed that the decline in anxiety remained significant after accounting for the changes in symptoms of depression. However, the effect of treatment on depression was no longer significant after controlling for the reduction in anxiety symptoms. Overall anxiety sensitivity (AS) did not moderate the level of reduction in symptoms of anxiety or depression during pharmacotherapy. However, AS specific to physical concerns demonstated a marginal negative association with decline in anxiety and depression. AS specific to social concerns also demonstrated a marginal negative association with decline in anxiety symptoms. These findings suggest that the decline in anxiety symptoms is independent of the decline in symptoms of depression during pharmacotherapy for GAD and specific AS dimensions may predict symptom change in GAD.

Background

Sleep quality may be an important, yet relatively neglected, predictor of treatment outcome in cognitive-behavioral therapy (CBT) for anxiety disorders. Specifically, poor sleep quality may impair memory consolidation of in-session extinction learning. We therefore examined sleep quality as a predictor of treatment outcome in CBT for social anxiety disorder and the impact of d-cycloserine (DCS) on this relationship.

Methods

One hundred sixty-nine participants with a primary diagnosis of DSM-IV generalized social anxiety disorder were recruited across three sites. Participants were enrolled in 12 weeks of group CBT. Participants randomly received 50 mg of DCS (n = 87) or pill placebo (n = 82) 1 hr prior to sessions 3-7. Participants completed a baseline measure of self-reported sleep quality and daily diaries recording subjective feelings of being rested upon wakening. Outcome measures including social anxiety symptoms and global severity scores were assessed at each session.

Results

Poorer baseline sleep quality was associated with slower improvement and higher posttreatment social anxiety symptom and severity scores. Moreover, patients who felt more "rested" after sleeping the night following a treatment session had lower levels of symptoms and global severity at the next session, controlling for their symptoms and severity scores the previous session. Neither of these effects were moderated by DCS condition.

Conclusions

Our findings suggest that poor sleep quality diminishes the effects of CBT for social anxiety disorder and this relation is not attenuated by DCS administration. Therapeutic attention to sleep quality prior to initiation of CBT and during the acute treatment phase may be clinically indicated.

Introduction

Poor sleep is prevalent among individuals with social anxiety disorder (SAD) and may negatively affect exposure therapy outcomes. Poor sleep may impair memory and learning, and thus compromise fear extinction learning thought to take place in exposure therapy. We examined poor sleep as a predictor of exposure therapy outcomes for SAD and the moderating role of d-cycloserine (DCS) on this relationship.

Methods

Participants were 152 individuals with a primary diagnosis of SAD. As part of a randomized clinical trial evaluating the efficacy of DCS for enhancing the effects of exposure therapy, they completed self-report baseline measure of sleep quality, and self-report sleep diaries assessing sleep duration (total sleep time [TST]) and sleep quality the nights before and after treatment sessions.

Results

Poorer baseline sleep quality was significantly associated with slower improvement over time and worse symptom outcomes at the end of treatment and follow-up after controlling for baseline symptoms of depression and social anxiety. Greater TST the night before treatment predicted lower SAD symptoms at the next session, after controlling for symptoms at the previous session. There was no relation between prior or subsequent night sleep quality on symptoms at the next session. No associations were moderated by DCS.

Conclusions

We replicated and extended findings indicating that poor sleep quality is associated with poorer exposure therapy outcomes for SAD. Assessing for sleep difficulties before treatment initiation and incorporating sleep interventions into treatment may enhance exposure therapy outcomes for SAD.