Elaine M. Boland

Cognitive vulnerabilities and depression versus other psychopathology symptoms and diagnoses in early adolescence.

We examined the concurrent associations between multiple cognitive vulnerabilities to depression featured in hopelessness theory, Becks theory, and response styles theory and depressive symptoms and diagnoses in a sample of early adolescents. We also examined the specificity of these cognitive vulnerabilities to depression versus anxiety and externalizing psychopathology, controlling for co-occurring symptoms and diagnoses. Male and female, Caucasian and African American, 12- to 13-year-old adolescents were assessed in a cross-sectional design. Cognitive vulnerabilities of hopelessness, inferential style, rumination, and self-referent information processing were assessed with self-reports and behavioral tasks. Symptoms and diagnoses of depressive, anxiety, and externalizing disorders were assessed with self-report questionnaires and diagnostic interviews. Hopelessness exhibited the greatest specificity to depressive symptoms and diagnoses, whereas negative inferential styles, rumination, and negative self-referent information processing were associated with both depressive and anxiety symptoms and diagnoses and, in some cases, with externalizing disorders. Consistent with cognitive theories of depression, hopelessness, negative inferential styles, rumination, and negative self-referent information processing were associated with depressive symptoms and diagnoses. However, with the exception of hopelessness, most of the remaining cognitive vulnerabilities were not specific to depression. With further maturation of our sample, these cognitive vulnerabilities may become more specific to depression as cognitive styles further develop and consolidate, the rates of depression increase, and individuals’ presentations of psychopathology become more differentiated.

Sleep disturbance and cognitive deficits in bipolar disorder: toward an integrated examination of disorder maintenance and functional impairment.

Bipolar disorder is frequently associated with a number of poor outcomes including, but not limited to, a significant impairment in the ability to return to premorbid levels of occupational and psychosocial functioning, often despite the remission of mood symptoms. Sleep disturbance is an oft-reported residual symptom of manic and depressive episodes that has likewise been associated with the onset of manic episodes. Also present during affective episodes as well as the inter-episode periods are reports of deficits in cognitive functioning, which many reports have shown to play an important role in this persistent disability. Despite the presence of deficits in these two domains of functioning during affective episodes as well as the inter-episode phase, there has been no evaluation of the degree to which these systems may interact to maintain such high rates of functional disability. The aim of this review is to examine evidence for the study of the relationship between sleep disturbance and cognitive impairments in bipolar disorder as well as the ways in which deficits in these domains may work together to maintain functional impairment.

The Development and Course of Bipolar Spectrum Disorders: An Integrated Reward and Circadian Rhythm Dysregulation Model

In this article, we present and review the evidence for two major biopsychosocial theories of the onset and course of bipolar spectrum disorders (BSDs) that integrate behavioral, environmental, and neurobiological mechanisms: the reward hypersensitivity and the social/circadian rhythm disruption models. We describe the clinical features, spectrum, age of onset, and course of BSDs. We then discuss research designs relevant to demonstrating whether a hypothesized mechanism represents a correlate, vulnerability, or predictor of the course of BSDs, as well as important methodological issues. We next present the reward hypersensitivity model of BSD, followed by the social/circadian rhythm disruption model of BSD. For each model, we review evidence regarding whether the proposed underlying mechanism is associated with BSDs, provides vulnerability to the onset of BSDs, and predicts the course of BSDs. We then present a new integrated reward/circadian rhythm (RCR) dysregulation model of BSD and discuss how the RCR model explains the symptoms, onset, and course of BSDs. We end with recommendations for future research directions.

Life events and social rhythms in bipolar spectrum disorders: an examination of social rhythm sensitivity.

OBJECTIVES To examine the presence of an underlying social rhythm sensitivity in individuals with bipolar spectrum disorders. METHODS The present study examined the impact of life events on sleep loss and social rhythm disruption in 184 individuals with bipolar spectrum disorders (BSD) compared to 197 demographically similar normal controls (NC) drawn from the Longitudinal Investigation of Bipolar Spectrum Disorders (LIBS) project. Life events data were obtained at three time points, each spaced four months apart, and included information on the intensity of the event (high or low), valence (negative or positive), and levels of sleep loss and social rhythm disruption brought about the event. We hypothesized that BSD participants would exhibit higher levels of social rhythm disruption and sleep loss than normal controls as a consequence of the same life events. RESULTS BSD participants experienced significantly more social rhythm disruption and sleep loss following all classes of life events. LIMITATIONS The cross-sectional design of this study limits the strength of the conclusions that can be drawn, primarily cause and effect relationships between social rhythms and symptoms. CONCLUSIONS Findings support the presence of an underlying social rhythm sensitivity in individuals with bipolar spectrum disorders. An additive effect of sleep loss and social rhythm disruption may contribute to subsequent mood symptomatology. Results from this study may inform early psychosocial interventions for at-risk individuals.

Kindling of Life Stress in Bipolar Disorder: Comparison of Sensitization and Autonomy Models

Research on life stress in bipolar disorder largely fails to account for the possibility of a dynamic relationship between psychosocial stress and episode initiation. The kindling hypothesis (Post, 1992) states that over the course of recurrent affective disorders, there is a weakening temporal relationship between major life stress and episode initiation that could reflect either a progressive sensitization or progressive autonomy to life stress. The present study involved a comprehensive and precise examination of the kindling hypothesis in 102 participants with bipolar II disorder that allowed for a direct comparison of sensitization and autonomy models. Polarity-specific tests were conducted across the continuum of event severity with respect to impact and frequency of life events. Hypotheses were polarity- and event-valence specific and were based on the stress sensitization model. Results were only partially consistent with the sensitization model: Individuals with more prior mood episodes had an increased frequency of minor negative events before depression and of minor positive events before hypomania. However, the number of past episodes did not moderate relationships between life events and time until prospective onset of mood episodes. These results are more consistent with a sensitization than an autonomy model, but several predictions of the sensitization model were not supported. Methodological strengths, limitations, and implications are discussed regarding putative changes in stress reactivity that may occur with repeated exposure to mood episodes in bipolar II disorder.

Low Social Rhythm Regularity Predicts First Onset of Bipolar Spectrum Disorders Among At Risk Individuals with Reward Hypersensitivity

The social zeitgeber model (Ehlers, Frank, & Kupfer, 1988) suggests that irregular daily schedules or social rhythms provide vulnerability to bipolar spectrum disorders. This study tested whether social rhythm regularity prospectively predicted first lifetime onset of bipolar spectrum disorders in adolescents already at risk for bipolar disorder based on exhibiting reward hypersensitivity. Adolescents (ages 14-19 years) previously screened to have high (n = 138) or moderate (n = 95) reward sensitivity, but no lifetime history of bipolar spectrum disorder, completed measures of depressive and manic symptoms, family history of bipolar disorder, and the Social Rhythm Metric. They were followed prospectively with semistructured diagnostic interviews every 6 months for an average of 31.7 (SD = 20.1) months. Hierarchical logistic regression indicated that low social rhythm regularity at baseline predicted greater likelihood of first onset of bipolar spectrum disorder over follow-up among high-reward-sensitivity adolescents but not moderate-reward-sensitivity adolescents, controlling for follow-up time, gender, age, family history of bipolar disorder, and initial manic and depressive symptoms (β = -.150, Wald = 4.365, p = .037, odds ratio = .861, 95% confidence interval [.748, .991]). Consistent with the social zeitgeber theory, low social rhythm regularity provides vulnerability to first onset of bipolar spectrum disorder among at-risk adolescents. It may be possible to identify adolescents at risk for developing a bipolar spectrum disorder based on exhibiting both reward hypersensitivity and social rhythm irregularity before onset occurs.

Circadian Rhythm Dysregulation in Bipolar Spectrum Disorders

Purpose of ReviewWe review recent evidence for circadian rhythm dysregulation in bipolar spectrum disorders (BSDs). We examine evidence for endogenous abnormalities in the biological clock and disruptions in the external entrainment of circadian rhythms in BSDs. We also address whether circadian dysregulation provides vulnerability to onset of BSD and evidence for a new integration of reward and circadian dysregulation in BSD.Recent FindingsRelative circadian phase delay (e.g., later melatonin peak, evening chronotype) is associated with BSD, particularly in the depressive phase. More consistent evidence supports irregularity of social rhythms, sleep/wake and activity patterns, and disruptions of social rhythms by life events, as stable trait markers of BSD and potential vulnerabilities for BSD onset. Growing research supports an integrative reward/circadian model.SummaryBoth endogenous abnormalities in the biological clock pacemaking function and disruptions in the external entrainment of circadian rhythms by physical and social cues are involved in BSDs. Circadian dysregulation may provide vulnerability to BSD onset.

Associations between sleep disturbance, cognitive functioning and work disability in Bipolar Disorder

Bipolar Disorder (BD) is associated with impairment in a number of areas including poor work functioning, often despite the remission of mood symptoms. The present study aimed to examine the role of sleep disturbance and cognitive functioning in occupational impairment in BD. Twenty-four euthymic BD participants and 24 healthy control participants completed a week of prospective assessment of sleep disruption via self-report and actigraphy, a battery of neuropsychological tests of executive functioning, working memory, and verbal learning, and assessments of work functioning. BD participants experienced significantly poorer cognitive functioning as well as greater months of unemployment and greater incidence of being fired than controls. Moderation analyses revealed that both poor sleep and cognitive functioning were associated with poor work performance in BD participants, but not control participants. Sleep and cognitive functioning may be impaired in euthymic BD and are associated with poor work functioning in this population. More research should be conducted to better understand how sleep and cognitive functioning may interact in BD.

Recent Advances in the Study of Sleep in the Anxiety Disorders, Obsessive-Compulsive Disorder, and Posttraumatic Stress Disorder

Sleep disturbance is frequently associated with generalized anxiety disorder, panic disorder, obsessive-compulsive disorder, and posttraumatic stress disorder. This article reviews recent advances in understanding the mechanisms of the sleep disturbances in these disorders and discusses the implications for developing improved treatments.

Affective Disruption From Social Rhythm and Behavioral Approach System (BAS) Sensitivities A Test of the Integration of the Social Zeitgeber and BAS Theories of Bipolar Disorder

The behavioral approach system (BAS)/reward hypersensitivity theory and the social zeitgeber theory are two biopsychosocial theories of bipolar spectrum disorders (BSDs) that may work together to explain affective dysregulation. The present study examined whether BAS sensitivity is associated with affective symptoms via (a) increased social rhythm disruption in response to BAS-relevant life events or (b) greater exposure to BAS events leading to social rhythm disruption and subsequent symptoms. Results indicated that high BAS individuals were more likely to experience social rhythm disruption following BAS-relevant events. Social rhythm disruption mediated the association between BAS-relevant events and symptoms (Hypothesis a). High BAS individuals experienced significantly more BAS-relevant events, which predicted greater social rhythm disruption, which predicted greater levels of affective symptoms (Hypothesis b). Individuals at risk for BSD may be sensitive to BAS-relevant stimuli, experience more BAS-relevant events, and experience affective dysregulation due to the interplay of the BAS and circadian rhythms.