According to the Diagnostic and Statistical Manual-IV-TR, Bipolar Disorder can be divided into three types:
Bipolar 1 Disorder – when the primary symptom is rapid cycling episodes of mania and depression.
Bipolar 2 Disorder – when the primary symptom is depression accompanied by mild manic episodes that are not severe enough to cause markedly impaired functioning.
Cyclothymic Disorder – when there is a chronic state of cycling between episodes of mania and depression but that do not meet the diagnostic criteria for Bipolar Disorder.
The lifetime prevalence of Bipolar Disorder is approximately 1.3% in adults (Kleinman et al., 2003).
Signs of Bipolar Disorder often manifest in the adolescent years or early adulthood.
Bipolar Disorder is highly genetic:
One study assessing the genetic and environmental contributions to the development of Bipolar Disorder found that first-degree relatives of people with Bipolar Disorder (n=40) were at significantly increased risk of developing the disorder (Lichtenstein et al., 2009).
Heritability has been estimated to range from 59-80%, the higher percentage being obtained from studies of genetic twins (Lichtenstein et al., 2009).
Despite the strong genetic aspect of Bipolar Disorder, the evidence shows that a number of other factors also contribute to the symptoms, including:
Treatment is usually a combination of psychological input and pharmacotherapy (medication).
The aim of treatment is to reduce the frequency, acuteness, and duration of episodes of mania and depression.
In some instances, hospitalisation with intensive pharmacological treatment is required to stabilise moods.
Treatments are also often aimed at treating co-morbidities, which are frequently found in people with Bipolar Disorder, where excess behaviours such as binge eating, drinking or drug taking can lead to obesity, heart disease, diabetes, and drug addiction (Morriss & Mohammed, 2005).
In one study, 81% of people with Bipolar Disorder also had co-morbidity.
Psychological treatments with scientific evidence supporting their efficacy include:
Interpersonal Social Rhythm Therapy (IPSRT)
Cognitive-Behavioural Therapy (CBT)
All of these approaches encourage the use of medication alongside the psychological treatment (Mansell et al., 2007).
IPSRT focuses on training people with Bipolar Disorder to regulate disruptive sleep patterns, which can cause more frequent mood cycling. It also targets issues around daily routines, stress, and interpersonal relationships.
CBT targets the cognitive issues associated with cycling moods, such as over-optimism, feelings of grandiosity, and goal-oriented thinking, all of which can contribute to risky behaviours.
Family-focused therapy provides a combination of psycho-education, where the main goal is to teach people with Bipolar Disorder and their families about the nature of the illness and how family dynamics can help or hinder life with Bipolar Disorder.
First line medication is usually lithium, anticonvulsants, or atypical antipsychotics, but it has been found that some people benefit from:
calcium channel blockers
The combination of psychological treatment and medication is designed to treat the specific episode of mania or depression, but the objective also needs to be to produce a treatment plan that assists in managing the condition long-term.
DSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders/APA 2000. 4th edition.
Kleinman, L.S., Lowin, A., Flood, E., Gandhi, G., Edgell, E., Revicki D.A. Costs of Bipolar Disorder. PharmacoEconomics, 21 (9), 601-622(22).
Lichtenstein, P., Yip, B.H., Björk, C., Pawitan, Y., Cannon, T.D., Sullivan, P.F., et al. (2009). Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study. Lancet, 17 (373), 234-9.
Mansell, W., Colom, & Scott, J., (2005).The nature and treatment of depression in bipolar disorder: a review and implications for future psychological investigation, Clinical Psychology Review, 25, 1076–1100.
Morriss, R. & Mohammed, F.A. (2005) Metabolism, lifestyle and bipolar affective disorder. Journal of Psychopharmacology, 19, 94–101.