The course of BD can be understood from a lifespan/developmental psychopathology perspective. Episodes of the illness result from a complex interplay between genes, neurobiology, stress, and psychological vulnerabilities at various points in development (Miklowitz & Cicchetti, 2006). Findings from twin, family, and adoption studies make a compelling case for genetic transmission in the onset of the disorder (Smoller & Finn, 2003). Functional and structural changes in the brain – notably cortico-limbic circuitry - distinguish BD from other disorders (Mayberg, Keightley, Mahurin, & Brannan, 2004). However, interpersonal variables play risk or protective roles in the onset and course of the disorder. Childhood adversity (i.e., sexual or physical abuse, neglect), life events, and high familial expressed emotion and discord appear to evoke or at least exacerbate certain preexisting vulnerabilities, resulting in more debilitating courses of illness for some patients (Leverich et al., 2002; Miklowitz & Johnson, 2006).

Although pharmacotherapy is the first-line treatment for stabilizing episodes of bipolar disorder, psychosocial treatments that accompany pharmacotherapy and address stress variables, cognitive, interpersonal, or emotional vulnerabilities, and their interactions will be more effective in preventing recurrences and enhancing functioning than pharmacotherapy alone. There is now considerable evidence that psychosocial interventions are effective adjuncts to pharmacotherapy in illness stabilization and maintenance (Miklowitz, in press).

In this article, we review evidence for the role of social variables - notably life events and family discord – in the longitudinal course of BD. We also examine several key personality or psychological variables (neuroticism, positive affectivity, reward sensitivity, and deficits in sensitivity to facial displays of emotions) that may influence the vulnerability of patients to social and family problems, or help explain their associations with illness outcomes. Then, we briefly review randomized controlled trials indicating that psychosocial interventions are effective adjuncts to pharmacotherapy in improving symptomatic and interpersonal functioning in BD. A final section offers recommendations for future research and clinical practice.

In describing this literature, we consider an important methodological and conceptual issue. Current symptoms exacerbate social and psychological impairments. Depressive symptoms may increase the reactivity of patients to social concerns, and subjective reports of the social environment may become more negative. Likewise, manic symptoms can positively distort patients’ perceptions of the quality of their family or social supports. The best longitudinal studies, then, examine whether a given psychological variable predicts increases in symptoms over time after controlling for baseline symptoms. Hence, we focus our review on prospective research, and make clear when current symptoms have been statistically controlled in examining predictor/outcome relationships. Where such evidence is not available, we describe cross-sectional research on social variables during periods of illness remission, to clarify directions for future prospective research.

Bipolar youth make more errors on facial emotion recognition tasks than healthy controls or youth with MDD or ADHD. These errors occur across a variety of facial emotions and types of tasks (Brotman et al., 2008; McClure et al., 2005; Rich et al., 2006; Rich et al., 2008; Guyer et al., 2007). Similar to children who have experienced trauma or abuse (e.g., Pollak & Tolley-Schell, 2003), children with BD are especially likely to misclassify neutral facial expressions as hostile and threatening, even though they do not rate angry faces as more angry than healthy children do (Rich et al., 2006).

Rich et al. (2008) compared “narrow spectrum” (i.e., bipolar I or II with elation or grandiosity) bipolar youth, youth with severe mood dysregulation (chronic irritability and hyperarousal), and healthy control participants on an experimental task involving rating gradations of facial emotions (happiness, surprise, fear, sadness, anger, and disgust). The task required that participants indicate when they were certain of the emotion being expressed as the faces “morphed” from neutral to full expressions of emotion. Regardless of the emotion purveyed on the facial stimuli, BD youth who were in a hypomanic or mixed state required more intense facial expressions before they were able to accurately identify the emotion. The euthymic bipolar youth also required more intense facial stimuli than the healthy controls, but only for faces that expressed disgust or happiness. Interestingly, the youth with severe mood dysregulation also showed emotion recognition deficits. Impaired face emotion labeling predicted the degree to which the bipolar youth showed social reciprocity skill deficits – the capacity to process social information and enact responses that fit the situation.

Progress has been made in clarifying the neural circuitry underlying facial affect labeling. Using functional magnetic resonance imaging, Rich et al. (2006) found that a subcortical limbic circuit was activated among bipolar youth during a face labeling task (judging facial emotions versus estimating nose width). When rating facial hostility, the BD youth had greater activation in the left amygdala, nucleus accumbens, putamen, and ventral prefrontal cortex; and when rating their fear of the face, greater activation in the left amygdala and bilateral accumbens, than age- and gender-matched controls.

Thus, most studies have found that BD youth misinterpret emotional faces, misidentify threat in neutral faces, and, when they accurately identify an emotion, require more intense displays of the emotion than are typical in real-life social situations. The literature is not consistent, however. One study found that undergraduates at risk for mania were more sensitive to positive facial expressions after small successes than controls (Trevisani et al., in press). Furthermore, facial emotion recognition deficits do not appear to be specific to pediatric BD; for example, they appear in children with post-traumatic stress disorder. No study to date has demonstrated that emotion labeling deficits predict the onset of BD among genetically at-risk youth, an important focus of future research.

A key area for future research is the overlap between emotion recognition deficits and family discord or EE. Theoretically, the degree to which bipolar youth have trouble labeling the emotions (or are biased toward the perception of negative emotions) of their parents may correlate with whether parents express highly critical attitudes toward the youth, or whether dyadic conflicts routinely escalate into “point-counterpoint” struggles (Simoneau et al., 1998). When both the parent and child suffer from BD, emotion labeling deficits may become bidirectional. It is not clear whether pediatric BD patients have difficulty reading the emotions of their parents– the emotion labeling tasks typically use standard stimuli rather than faces of adults known to the child, raising questions about the ecological validity of these measures. Videotape feedback studies, in which parents and children are asked to identify each others’ emotions following a direct interaction task could test these hypotheses, and also serve as an intervention strategy for teaching family members to correctly read each others’ more subtle emotional reactions.

This summary relies on a small number of prospective studies, and there is a need for replication of most of the findings. Beyond this, few studies have directly tested multivariate vulnerability/stress models of episode onset and occurrence, so this is a fertile area for future research. For example, goal-attainment life events may be especially potent in predicting mania when patients have heightened reward sensitivity, but calming, low-intensity, and supportive marital or family interactions may help protect against manic symptoms during those moments. Patients from families with high-EE attitudes may be especially relapse-prone when they show emotion labeling deficits, but these risk factors may be especially potent when the patient has had early experiences of adversity. Studies that take a developmental perspective, examining the interactions of risk and protective processes at different phases of the life cycle, are likely to be more informative than cross-sectional studies, especially given that mood cycling patterns are a “moving target” in this disorder.

The course of BD is characterized by a multifinality of outcomes, which can include recovery, remission, relapse, recurrence, ongoing symptoms, or psychosocial impairments (Frank et al., 1991; Martinez-Arán et al., 2008). It is rare for psychosocial studies to distinguish recovery from remission (i.e., lengthy versus brief asymptomatic periods) or recurrence from relapse (i.e., periods of symptom exacerbation that follow lengthy periods of recovery versus those that follow briefer periods of remission). These distinctions could help determine whether psychosocial predictors (or moderators of treatment outcome) are equally relevant to the short-term and long-term course of the disorder.

Adjunctive psychotherapy is a vital part of the effort to stabilize episodes of bipolar depression, prevent recurrences, and enhance functioning. This observation is beginning to be reflected in practice guidelines (e.g., Yatham et al., 2005; Goodwin & the Consensus Group of the British Association for Psychopharmacology, 2003). A major limitation of the existing psychosocial approaches, however, is their inaccessibility to most community clinicians. Future research should examine the most cost-effective methods for training clinicians and monitoring their adherence in practice settings.