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Bipolar Disorder

  1. Tina R. Goldstein

Published Online: 30 JAN 2010

DOI: 10.1002/9780470479216.corpsy0134

Corsini Encyclopedia of Psychology

Corsini Encyclopedia of Psychology

How to Cite

Goldstein, T. R. 2010. Bipolar Disorder. Corsini Encyclopedia of Psychology. 1–4.

Author Information

  1. University of Pittsburgh

Publication History

  1. Published Online: 30 JAN 2010

Bipolar disorder, previously referred to as manic-depressive illness, is a disorder affecting mood, behavior, and cognition. Individuals with bipolar disorder experience symptoms from two “poles”: (1) depression, characterized by low mood, sadness, anhedonia, sleep and appetite disturbance, poor concentration, fatigue, feelings of guilt and worthlessness, and psychomotor slowing; and (2) mania, distinguished by euphoric, elevated and/or irritable mood, decreased need for sleep, increased energy and activity, hypersexuality, pressured speech, racing thoughts, grandiosity, and increased risk-taking.

Subtypes of bipolar disorder include bipolar I disorder, in which the individual experiences depressive episodes alternating with manic episodes. DSM-IV criteria for mania require elevated, expansive, or irritable mood lasting at least one week, or any period of time if hospitalization is required. Some individuals simultaneously experience symptoms of mania and depression, which is referred to as a mixed state. Bipolar II disorder is characterized by depressive episodes alternating with hypomanic episodes—that is, a less severe manic state that is not associated with psychosis, need for hospitalization, or marked functional impairment, yet is still noticeable by others and uncharacteristic of the individual when euthymic (in a stable mood). DSM-IV criteria for hypomania require elevated, expansive, or irritable mood lasting at least four days.

1 Epidemiology

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings

Bipolar disorder is estimated to affect between 0.5% and 1.3% of the population. Bipolar I disorder is equally common among men and women, whereas rates of bipolar II disorder are higher among women. The disorder appears to be similarly distributed among social classes and education levels, although recent studies indicate that bipolar disorder is associated with lower family income—possibly as a consequence of illness. No associations with race or ethnicity have been supported.

2 Course and Outcome

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings

There exists great interindividual variability in the course of bipolar illness. Three basic mood-cycling patterns have been identified among individuals with bipolar disorder: mania followed by depression followed by euthymia; depression followed by mania followed by euthymia; and continuous cycling between mood episodes. Individuals who experience four or more mood episodes within a one-year period are labeled “rapid cycling.” Rapid cycling is equally common in bipolar I and II disorders and more common among women, and it is generally considered to be a more treatment-refractory variant of illness. Recent research indicates that more than half of individuals with bipolar disorder continue to experience subsyndromal symptoms that interfere with functioning during the interepisode period.

Depressive episodes and mixed episodes tend to last longer than pure manic episodes, with an overall mean episode length of approximately four months (Goodwin & Jamison, 2007a). Improvements in pharmacotherapy have resulted in a significant decrease in the duration of affective episodes in bipolar disorder. However, nearly three-fourths of individuals with bipolar disorder experience affective episode recurrences over five years even with adequate pharmacotherapy. Furthermore, treatment adherence is a significant clinical problem associated with bipolar disorder, with up to 50% of patients reporting nonadherence to their treatment regimen at any point in time.

Recent research indicates that the average age of bipolar illness onset is 22. This figure has steadily decreased since the 1990s, with various hypotheses having been set forth to account for this phenomenon. These hypotheses include genetic anticipation, improved diagnostic specificity, increased use of antidepressants and stimulants among youth (possibly hastening a bipolar diathesis in vulnerable individuals), and increasing recognition of bipolar disorder in children and teens. Studies consistently indicate that earlier age of onset is associated with poorer outcomes. A significant gap (on average, 6–8 years) between time of illness onset and time to first diagnosis and treatment is commonly reported.

Bipolar disorder currently ranks among the top 10 most disabling disorders. The illness can have an enduring negative impact on an individual's ability to function in occupational, interpersonal, and recreational domains. Up to 30% of patients with bipolar disorder cannot work, and nearly 75% fail to recover premorbid levels of functioning. Depressive, rather than manic, symptoms appear to be associated with the majority of the functional impairment in bipolar disorder. The illness is associated with high rates of divorce, legal problems, and substance use, and it is associated with annual direct health care costs exceeding $15,000 per individual (Dardennes, Thuile, Even, Friedman, & Guelfi, 2006).

Mortality rates up to six times the expected rate in the general population have been documented among individuals with bipolar disorder. Suicide accounts for a great burden of the mortality; up to 15% of individuals with bipolar disorder will die from suicide. However, other illness-related factors contribute to morbidity rates in this population, including increased burden of medical illness (particularly cardiovascular disease), substance abuse, and accidents.

3 Comorbid Conditions

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings

Comorbid psychiatric conditions are the rule rather than the exception in bipolar disorder, wherein upward of 60% of patients meet criteria for at least one comorbid Axis I disorder (Bauer et al., 2005). The most common comorbid classes of psychiatric disorder include substance use disorders (42%) and anxiety disorders (42%; most commonly panic disorder) (Sasson, Chopra, Harrari, Amitai, & Zohar, 2003).

Bipolar patients also experience general medical conditions at a higher rate than the general public. The metabolic syndrome, characterized by obesity, glucose dysregulation, and dyslipidemia, is present among 30% of adult patients with bipolar disorder, placing bipolar patients at increased risk for cardiovascular disease (Fagiolini, Frank, Scott, Turkin, & Kupfer, 2005). Biological, behavioral, and treatment-related factors, including sedentary lifestyle, unhealthy eating habits, suboptimal medical care, and negative effects of psychotropic medications are believed to contribute to the development of comorbid medical illness in individuals with bipolar disorder.

4 Models of Bipolar Disorder

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings

4.1 Biological Factors

Bipolar disorder is among the most heritable of psychiatric conditions. The most powerful evidence for the contribution of genetics to susceptibility for bipolar disorder is evidence from twin studies. Recent studies report a 63% concordance rate among monozygotic twins and a 13% rate among dizygotic twins, with an overall heritability of 0.78 (where 1.0 is complete heritability) (Goodwin & Jamison, 2007b). Genetic linkage studies have identified multiple regions of potential interest on several chromosomes, including 4 and 18. More recently, results from genetic association studies implicate the role of the serotonin transporter gene and the brain-derived neurotrophic factor (BDNF) (Neves-Pereira et al., 2002), although attempts to replicate these findings have been mixed. Taken together, these findings overwhelmingly indicate that bipolar disorder is a complex disorder characterized by genetic heterogeneity, such that several genes differentially contribute to risk for bipolar disorder across families.

Research has also focused on understanding the physiological mechanisms underlying bipolar disorder. Alterations in three primary neurotransmitter systems—serotonin, dopamine, and norepinephrine— have been widely studied, and attempts have been made to link these neurotransmitter deficits to drug mechanisms of action. Structural neuroimaging studies have identified decreased volume in multiple brain areas of individuals with bipolar disorder including the prefrontal cortex, basal ganglia, hippocampus, and anterior cingulate; functional neuroimaging studies show hypoactivity in the prefrontal cortex and hippocampus, and hyperactivity in the amygdala (Phillips, Drevets, Rauch, & Lane, 2003). These findings converge on a model in which brain dysfunction in bipolar disorder is characterized by dysregulation in those brain regions associated with emotion and reward sensitivity. As technology continues to advance, the clinical relevance of these findings may contribute to improved methods for diagnosis and treatment.

4.2 Psychosocial Factors

The lack of complete (i.e., 100%) concordance for bipolar disorder among monozygotic twins, as well as the wide-ranging heterogeneity observed in the course and presentation of bipolar disorder, have been cited as evidence for a contribution of environmental factors to bipolar disorder. Research has identified several psychosocial factors that contribute to risk, primarily involving the family environment and stressful life events. It is believed that these environmental stressors interact with biology in individuals with a biological diathesis for the disorder. Specifically, research indicates that individuals with bipolar disorder who return to stressful family environments characterized by criticism, hostility, and/or emotional overinvolvement (operationalized as Expressed Emotion) following hospitalization for an acute affective episode have been shown to be at increased risk for relapse over one-year follow-up (Butzlaff & Hooley, 1998). However, the directionality of this relationship is not yet well understood. It is possible that the stress of the family environment evokes symptoms in vulnerable individuals, that the strain of caring for a psychiatrically ill relative contributes to increased tension in the family, or alternatively, the relationship may be mediated by a third variable.

Retrospective studies also link life stress to episode onset and course in bipolar disorder. More stressful life events have consistently been described in the month preceding affective relapse among bipolar patients (Hunt, Bruce-Jones, & Silverstone, 1992). Furthermore, recovery from mood episodes triggered by stressful life events is prolonged, up to threefold, over those episodes not associated with life events (Johnson & Miller, 1997). Substantial evidence indicates that bipolar disorder is strongly linked to circadian functioning; thus, those life events with a disruptive effect on sleep/wake cycles, including pregnancy and childbirth, are associated with a particularly elevated risk for relapse.

Research suggests that life events are more strongly associated with relapse early in the course of illness (Swann et al., 1990). Some studies suggest the mechanism whereby this occurs is through activating a preexisting biological vulnerability. This is in accord with the kindling hypothesis (Post, 1992), which posits that episodes increase in frequency and duration over time, with diminishing importance of psychosocial stressors in the onset and course of the illness.

5 Treatment

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings

Guidelines for the treatment of bipolar disorder recognize pharmacotherapy as an essential cornerstone of optimal treatment. Psychotherapy is also strongly recommended as an adjunct to medication management for the illness.

5.1 Pharmacotherapy

Mood-stabilizing medications serve as the foundation of pharmacotherapy for individuals with bipolar disorder. Such medications moderate acute affective symptoms and prevent future mood episodes of both mania and depression. For many years, lithium was the only FDA-approved option for the treatment of bipolar disorder. Effective for approximately 50% of patients, lithium can also be associated with undesirable side effects, including problems with the kidney and thyroid, and lithium treatment therefore warrants regular blood tests. In the 1990s, anticonvulsants including divalproex (Depakote) and carbamazepine (Tegretol) were found to have mood-stabilizing properties and began to be widely used for individuals with bipolar disorder who had difficulty tolerating lithium, were lithium nonresponsive, or had certain illness profiles deemed to be less lithium responsive (e.g., rapid cycling). More recently, the atypical neuroleptics, including olanzapine (Zyprexa), aripiprazole (Abilify), and quetiapine (Seroquel) have become widely used as first-line mood-stabilizing agents in bipolar disorder.

Unfortunately, mood-stabilizing medications appear to be more efficacious in the treatment and prevention of mania than depression. Thus, adjunctive antidepressants, most often selective serotonin reuptake inhibitors (SSRIs) are added to a mood stabilizer as a means of treating depressive symptoms. Antidepressant treatment in bipolar disorder should be undertaken with caution, as antidepressants can precipitate manic symptoms as well as accelerate mood cycling in up to half of bipolar patients (Ghaemi, Boiman, & Goodwin, 2000). There is also evidence to support the use of electroconvulsive therapy (ECT) in bipolar depression for patients with treatment refractory depression. Experimental procedures including transcranial magnetic stimulation (tms) and vagus nerve stimulation (vns) also may hold promise for treatment-resistant bipolar depression, but further research is needed to understand the appropriate parameters for these treatments. Other common adjunctive medications include antipsychotics for the treatment of psychosis, agitation, and sleep difficulties and anxiolytics for the treatment of comorbid anxiety.

Treatment adherence has long been identified as a major clinical problem associated with bipolar disorder—in fact, among psychiatric populations, individuals being treated for bipolar illness rank among the least treatment adherent of all diagnostic groups. Studies examining nonadherence rates in bipolar illness report poor adherence in nearly 60% of patients. A substantive body of work has identified risk factors for nonadherence in bipolar illness, with four categories of adherence-related factors (Jamison, Gerner, & Goodwin, 1979): (1) illness-specific factors including comorbid substance abuse; (2) patient factors like negative feelings about having mood controlled by medicine and missing the “highs” of mania; (3) treatment factors consisting largely of unpleasant medication side effects like weight gain, cognitive dulling, and gastrointestinal upset; and (4) physician factors, in particular the extent to which the patient feels his/her treatment is a collaborative effort with the treatment team.

5.2 Psychotherapy

Bipolar disorder can be a debilitating, unpredictable disorder with symptoms that can wreak havoc on the lives of those afflicted and those close to them. Symptoms can profoundly affect relationships, occupational functioning, and financial well-being. Psychotherapy can be a valuable means of aiding bipolar patients to monitor symptoms and triggers, manage stressors, improve relationships, and work toward acceptance of the illness. It is through these avenues that psychotherapy is believed to help delay manic and depressive relapses, improve psychosocial functioning, and enhance medication adherence.

Recent data from the large multisite Systematic Treatment Enhancement for Bipolar Disorder (STEP-BD) trial indicate that three empirically validated intensive psychotherapy approaches for bipolar disorder are equally effective in hastening recovery from depression, increasing amount of time well, and enhancing overall psychosocial functioning, relationship functioning, and life satisfaction over a brief (three-session) psychoeducational intervention. These approaches include Family-Focused Therapy (FFT) (Miklowitz, George, Richards, Simoneau, & Suddath, 2003), which is a treatment model delivered with the family unit that includes psychoeducation, communication, and problem-solving skills; Interpersonal and Social Rhythm Therapy (IPSRT) (Frank, 2005), primarily an individual treatment approach in which the aim is to help patients achieve stability in daily social routines and sleep/wake cycles, as well as improve interpersonal functioning; and Cognitive Behavioral Therapy (CBT), in which the focus is on the interrelationship between thoughts, feelings, and behaviors (Otto & Reilly-Harrington, 2002).

In summary, bipolar disorder is a severe mental disturbance affecting mood, cognition, and behavior. The illness can have a profound deleterious effect on occupational, economic, interpersonal, and social functioning. Psychosocial stress impacts the course of the illness. Treatments, both pharmacological and psychotherapeutic, have been shown to ameliorate the negative outcomes associated with this condition.

References

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings
  • Bauer, M. S., Altshuler, L., Evans, D. R., Beresford, T., Williford, W., & Hauger, R. (2005). Prevalence and distinct correlates of anxiety, substance, and combined comorbidity in a multi-site public sector sample with bipolar disorder. Journal of Affective Disorders, 85, 301315.
  • Butzlaff, R. L., & Hooley, J. (1998). Expressed emotion and psychiatric relapse: A meta-analysis. Archives of General Psychiatry, 55, 547552.
  • Dardennes, R., Thuile, J., Even, C., Friedman, S., & Guelfi, J. (2006). The costs of bipolar disorder. L'Encephale, 32, 1825.
  • Fagiolini, A., Frank, E., Scott, J., Turkin, S., & Kupfer, D. J. (2005). Metabolic syndrome in bipolar disorder: findings from the Bipolar Disorder Center for Pennsylvanians. Bipolar Disorders, 7, 424430.
  • Frank, E. (2005). Treating bipolar disorder: A clinician's guide to interpersonal and social rhythm therapy. New York: Guilford Press.
  • Ghaemi, S. N., Boiman, E. E., & Goodwin, F. K. (2000). Diagnosing bipolar disorder and the effects of antidepressants: A naturalistic study. Journal of Clinical Psychiatry, 61, 804808.
  • Goodwin, F. K., & Jamison, K. R. (2007a). Course and outcome. In F. K. Goodwin & K. R. Jamison (Eds.), Manic-depressive illness (2nd ed., pp. 119154). New York: Oxford University Press.
  • Goodwin, F. K., & Jamison, K. R. (2007b). Genetics. In Manic-depressive illness (2nd ed., pp. 411462). New York: Oxford University Press.
  • Hunt, N., Bruce-Jones, W., & Silverstone, T. (1992). Life events and relapse in bipolar affective disorder. Journal of Affective Disorders, 25, 1320.
  • Jamison, K. R., Gerner, R. H., & Goodwin, F. K. (1979) Patient and physician attitudes toward lithium: Relationship to compliance. Archives of General Psychiatry, 36, 866869.
  • Johnson, S., & Miller, I. (1997). Negative life events and time to recovery from episodes of bipolar disorder. Journal of Abnormal Psychology, 106, 449457.
  • Miklowitz, D. J., George, E. L., Richards, J. A., Simoneau, T. L., & Suddath, R. L. (2003). A randomized study of family-focused psychoeducation and pharmacotherapy in the outpatient management of bipolar disorder. Archives of General Psychiatry, 60, 904912.
  • Neves-Pereira, M., Mundo, E., Muglia, P., King, N., Macciardi, F., & Kennedy, J. L. (2002). The brain-derived neurotrophic factor gene confers susceptibility to bipolar disorder. American Journal of Human Genetics, 71, 651655.
  • Otto, M. W., & Reilly-Harrington, N. A. (2002). Cognitive-behavioral therapy for the management of bipolar disorder. In S. G. Hoffman & M. Tompson (Eds.), Treating chronic and severe mental disorders: A handbook of empirically supported interventions (pp. 116130). New York: Guilford Press.
  • Phillips, M. L., Drevets, W. C., Rauch, S. L., & Lane, R. (2003). The neurobiology of emotion perception II: Implications for major psychiatric disorders. Biological Psychiatry, 54, 515528.
  • Post, R. M. (1992). Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. American Journal of Psychiatry, 149, 9991010.
  • Sasson, Y., Chopra, M., Harrari, E., Amitai, K., & Zohar, J. (2003). Bipolar comorbidity: From diagnostic dilemmas to therapeutic challenge. International Journal of Neuropsychopharmacology, 6, 139144.
  • Swann, A. C., Secunda, S. K., Stokes, P. E., Croughan, J., Davis, J. M., Koslow, S. H., et al. (1990). Stress, depression and mania: Relationship between perceived role of stressful events and clinical and biochemical characteristics. Acta Psychiatrica Scandinavica, 81, 389397.

Suggested Readings

  1. Top of page
  2. Epidemiology
  3. Course and Outcome
  4. Comorbid Conditions
  5. Models of Bipolar Disorder
  6. Treatment
  7. References
  8. Suggested Readings
  • Fawcett, J., Golden, B., & Rosenfeld, N. (2000). New hope for people with bipolar disorder. New York: Three Rivers Press.
  • Goodwin, F. K., & Jamison, K. R. (Eds.). (2007). Manic-depressive illness (2nd ed.). New York: Oxford University Press.
  • Jamison, K. R. (1995). An unquiet mind. New York: A.A. Knopf.