Sleep, illness course, and concurrent symptoms in inter-episode bipolar disorder

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Abstract

We investigated associations between sleep, illness course, and concurrent symptoms in 21 participants with bipolar disorder who were inter-episode. Sleep was assessed using a week-long diary. Illness course and symptoms were assessed via validated semi-structured interviews. Lower and more variable sleep efficiency and more variable total wake time were associated with more lifetime depressive episodes. Variability in falling asleep time was positively correlated with concurrent depressive symptoms. Sleep efficiency was positively correlated with concurrent manic symptoms. These findings suggest that inter-episode sleep disturbance is associated with illness course and that sleep may be an important intervention target in bipolar disorder.

Introduction

Sleep disturbance is a hallmark feature of bipolar disorder, occurring in both mania and depression. Sleep disturbance found in the inter-episode period has also been reported to be equivalent to that experienced by patients with chronic insomnia (Harvey, Schmidt, Scarna, Neitzert Semler, & Goodwin, 2005). A complex and varied presentation of sleep disturbances in bipolar disorder has been reported and includes a relatively high prevalence of insomnia (Harvey et al., 2005), hypersomnia (Kaplan & Harvey, 2009), reduced sleep need, and delayed phase sleep disorders (Staton, 2008). Thus, sleep variables of interest include total wake time (the total duration of sleep onset latency, duration of wake after sleep onset, and duration of early morning awakening; TWT), total sleep time (total duration of sleep over the course of the night; TST), sleep efficiency (the ratio of total sleep time to time spent in bed; SE), and variability in the timing of sleep.

Even with optimal psychiatric care, approximately 50% of recovered bipolar individuals relapse within 1 year (Perlis, et al., 2006) and almost all relapse within 4 years (Tohen, Waternaux, & Tsuang, 1990), most commonly into a depressive episode. Hence, focusing on potential predictors of illness course is a critical domain for research. Several lines of evidence suggest that sleep disturbance may be one such key predictor. First, disturbed sleep appears to be a predictor of increased symptoms in bipolar disorder (see Harvey, 2008 for review). Second, one night of sleep deprivation causes mania or hypomania in a proportion of bipolar individuals, with manic/hypomanic symptoms reported in as many as 75% of the sample in one study (e.g., Wehr, Sack, & Rosenthal, 1987). Third, sleep deprivation contributes to mood dysregulation and hypersensitive emotional responses in healthy controls as indexed by overactive amygdala response (Yoo, Gujar, Hu, Jolesz, & Walker, 2007). In addition to serving as a potential predictor of illness course, sleep disturbance in bipolar disorder is a particularly important research focus given the potential clinical implications of such research for treating this chronic and impairing disorder.

While several psychological therapies for bipolar disorder target sleep disturbance (see Harvey, 2008 for review), there remains significant room for improvement in treatment outcome (Miklowitz et al., 2007) and a need for basing treatments in empirical research (Salkovskis, 2002). Furthermore, bipolar disorder treatments have not yet taken advantage of advances made in the treatment of chronic insomnia, and several investigators (e.g., Harvey, 2008, Plante and Winkelman, 2008) have called for an empirical approach to integrating insomnia treatments into therapies for bipolar disorder. The treatment of sleep disturbance in bipolar disorder is often approached pharmacologically. However, there may be advantages to using psychological interventions to manage sleep disturbance in bipolar disorder, including the relative lack of side effects and the absence of adverse drug interactions with mood stabilizing medications. There is evidence that managing sleep disturbance psychologically has been a promising approach in unipolar depression. For instance, the use of cognitive behavioral therapy for insomnia in combination with antidepressant medication is associated with higher rates of remission than antidepressants alone in unipolar depressed individuals (Manber et al., 2008).

With the dual goals of further clarifying the role of sleep in bipolar disorder as well as developing an empirical basis for adapting current psychological treatments for sleep disturbance specifically for patients with bipolar disorder, the present study aimed to determine if inter-episode sleep/circadian variables in adult bipolar disorder are associated with illness course and concurrent symptoms. The first hypothesis was that greater inter-episode sleep disturbance would be correlated with a more severe and chronic illness course (i.e., earlier age at illness onset and more lifetime manic and depressive episodes). This was of interest as previous studies have indicated the importance of illness course as a predictor of future symptoms and impairment in bipolar disorder (Judd et al., 2002, Robinson and Ferrier, 2006) and have suggested that an earlier age at illness onset predicts more severe sleep disturbance in pediatric bipolar disorder (Mehl et al., 2006). The second hypothesis was that inter-episode sleep disturbance would be positively correlated with concurrent manic and depressive symptoms, based on evidence that sleep is critical for effective mood regulation (e.g., Harvey, 2008, Wehr et al., 1987, Yoo et al., 2007). For both the first and second hypotheses we sought to determine which specific sleep parameters were most important (e.g., TWT, TST, sleep efficiency, and variability in sleep), with an eye to identifying variables that might be targeted in intervention development. Following recent theories in pediatric bipolar disorder (Staton, 2008), the third hypothesis was that a tendency toward delayed phase sleep (measured via bedtime and falling asleep time) would be associated with a more chronic and severe illness course and more concurrent manic and depressive symptoms. We aimed to test these hypotheses in a diverse and representative sample. Given that bipolar disorder is typically associated with the presence of comorbid psychiatric diagnoses (Kessler, Chiu, Demler, & Walters, 2005), we enrolled participants with comorbid psychiatric illnesses.

Section snippets

Participants

The majority of participants were recruited through advertisements, and several participants were also recruited via referrals. Of the 119 individuals screened, 21 chose not to enroll or were unable to be reached subsequently and 77 fell outside the inclusion criteria (specific details on the 77 excluded participants are presented below). Our final sample consisted of 21 participants diagnosed with bipolar disorder Type I (n = 19) or Type II (n = 2) according to the Structured Clinical Interview

Results

The average age of the sample was 37.0 years old (SD = 10.65). The majority of the sample was female (85.7%), single (47.6%), college educated (66.7%), Caucasian (71.4%), and employed (81%). Average TWT ranged from 12.83 to 193.00 min (M = 72.79) with a standard deviation of 48.88, average TST ranged from 264.67 to 546.86 min (M = 414.36) with a standard deviation of 68.28, and average SE ranged from 61% to 96% (M = 85.35%) with a standard deviation of 9.29. Mean bedtime was 11:37PM (SD = 71.40 min) and

Discussion

This study investigated whether inter-episode sleep/circadian variables are associated with illness course and concurrent symptoms in bipolar disorder. Our hypothesis that greater inter-episode sleep disturbance would correlate with a more chronic and severe illness course was partially supported. Specifically, having experienced a greater number of depressive episodes was associated with poorer and more variable sleep efficiency and with more variable TWT. Additionally, although the

Acknowledgements

Thank you to Dr. Ilana Hairston and the research assistants who were an instrumental and essential part of this research.

Disclosure: Dr. Harvey is a consultant to Actelion Pharmaceuticals and a speaker for Sanofi-aventis and the Sleep Medicine Education Institute. All other authors declare that they have no conflicts of interest. This project was supported by National Institute of Mental Health Grant No. R34 MH080958 awarded to AGH.

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