Cognitive behavioral therapy for insomnia enhances depression outcome in patients with comorbid major depressive disorder and insomnia.

DIFFICULTY INITIATING AND/OR MAINTAINING SLEEP IS COMMON IN MAJOR DEPRESSIVE DISORDER (MDD) BUT IS OFTEN INADEQUATELY ADDRESSED. Subjective and objective (electroencephalographic) sleep disturbances are associated with slower and lower rates of remission from depression.1–3 Depressed patients with abnormal sleep profiles have significantly poorer clinical outcomes with respect to symptom ratings, attrition and remission rates, and the stability of response to treatment than those with more normal sleep profiles.2,4 Patients with MDD who experience sleep continuity disturbance and early morning awakening are also more likely to have suicidal ideation than those without such disturbances.5 Collectively, these findings indicate that insomnia symptoms hinder response to antidepressant treatment. Sleep disturbance does not always resolve with antidepressant treatment. Sleep difficulties are also common residual symptoms in individuals who have responded to depression treatment.6–10 Continued insomnia following the acute phase of antidepressant therapy poses a significant risk for relapse. For example, two-thirds of patients with persistent insomnia at the end of treatment with nortriptyline and interpersonal psychotherapy relapsed within one year after switching to pill placebo. In contrast, 90% of patients with good sleep at the end of the acute treatment remained well during the first year after discontinuing antidepressants.11 Additionally, there are indications that insomnia may be a first-occurring prodromal symptom in previously depression-remitted persons.12 Thus, insomnia is often more than merely a correlate or symptom of the depressive illness; it also affects the course of the illness, response to treatment, and when unresolved, it is a risk factor for relapse. The prevailing model for the development of insomnia is based on the diathesis-stress model whereby a “stressor” precipitates insomnia in predisposed individuals. This model posits that, with time, conditioned insomnia develops and persists even after the stressor is removed. Specifically, as anxiety about not being able to sleep grows, it can lead to cognitive and/or somatic arousal that further interferes with sleep and perpetuates the sleep problem.13 When these sleep difficulties become associated with significant distress or impairment of function in significant domains, all criteria for a diagnosis of insomnia are met and the individual experiences comorbid MDD and insomnia. Thus, insomnia is no longer simply a symptom of depression, but has become an independent disease process and a comorbid disorder that can subsequently hinder antidepressant response. Cognitive-behavioral therapy for insomnia (CBTI) is a skill-based, nonpharmacological intervention with many attributes that make it appealing for addressing insomnia in the context of MDD. Extensive research summarized in several meta-analyses14–17 has shown that CBTI produces improvements in primary insomnia equivalent to those achieved during acute treatment with hypnotic medications18,19 in terms of reducing nocturnal wakefulness, increasing sleep efficiency, and improving subjective sleep quality.14,20 There is also some evidence that CBTI is effective for insomnia that is comorbid with depression.21–25 Most important, sleep improvements achieved during CBTI endure up to 2 years after the course of CBTI is completed.26 This attribute of CBTI is particularly important in the context of depression, as patients who remain insomnia free are likely to remain depression free for longer periods of time than those whose insomnia recurs.12,27 The aim of the present randomized controlled pilot study was to evaluate the feasibility, acceptability, and indications of efficacy of combining an antidepressant medication (escitalopram) with CBTI in people with MDD and insomnia. The main outcome measure was remission from MDD, which is considered the ultimate goal of depression treatment.28