Bipolar disorder (BD), previously known as manic depression, is a mental disorder characterized by periods of depression and abnormally elevated mood, lasting days to weeks, and in some cases months. If the elevated mood is severe or associated with psychosis, it is called mania; if it does not significantly affect functioning, it is called hypomania. During mania, an individual behaves or feels abnormally energetic, happy, or irritable, and often makes impulsive and reckless decisions. There is usually sleep disturbance during manic phases. During periods of depression, the individual may experience crying, have a negative outlook, and demonstrate poor eye contact. People with BD are at 11.7 times greater risk of dying by suicide than the general population. Approximately 34% attempt suicide during their lifetime. Among adolescents with BD, 78% engaged in self-harm. The mechanisms of this mood disorder are not clearly understood, although some studies suggest areas for future clinical research. Structural and functional MRI studies have shown differences in brain regions in BD, such as regions involved in perceiving risk-reward and regulating emotions. A systematic review and meta-analysis by Murri and others found that cortisol levels are "associated with the manic phase" of BD. Likewise, various other studies support an important role for hypothalamic-pituitary-adrenal axis (HPA axis). Risk for BD is thought to be influenced by genetics, environment, and ADHD. In one respect (heritability), genetic factors may account for up to 70–90% of the risk of developing BD. In another respect (concordance rate), identical twins both have bipolar disorder (or both do not) at a rate of ~40%, in contrast to dizygotic twins' ~5%. Environmental risks include a history of child abuse and long-term stress. A meta-analysis and a separate critical literature review have found worse prognosis and earlier onset of BD in people with childhood maltreatment and "early emotional trauma" respectively. Likewise, traumatic bonding increases risk of BD. ADHD increases the risk of developing bipolar disorder. More research is needed to understand the nature of this association. The condition is classified as bipolar I disorder if there has been at least one manic episode, with or without depressive episodes, and as bipolar II disorder if there has been at least one hypomanic episode (but no full manic episodes) and one major depressive episode. It is classified as cyclothymia if there are hypomanic episodes with periods of depression that do not meet the criteria for major depressive episodes. If these symptoms are due to drugs or medical problems, they are not diagnosed as BD. Mood stabilizers, particularly lithium, and anticonvulsants, such as lamotrigine and valproate, as well as atypical antipsychotics are used for treatment. Atypical antipsychotics are used for acute manic episodes or when mood stabilizers are ineffective or not tolerated, with long-acting injectables available for patients who struggle to maintain a medication regimen. There is evidence that psychotherapy improves the course of BD. Use of antidepressants in depressive episodes is controversial: they can be effective, but certain classes of antidepressants increase the risk of mania. The treatment of depressive episodes, therefore, is often difficult. Past studies have found that electroconvulsive therapy (ECT) is effective in acute manic and depressive episodes, particularly with psychosis or catatonia; likewise, past guidelines have recommended admission to a psychiatric hospital if someone is a risk to themselves or others, and/or involuntary treatment if someone refuses treatment. However, the Committee on Rights of Persons with Disabilities (CRPD) of the United Nations has recommended the abolition of institutionalization and forced treatments "such as sedatives, mood stabilizers, electro-convulsive treatment, and conversion therapy". The 6-12 month prevalence of bipolar disorder is 1%, while the lifetime prevalence is between 1 and 3%. The prevalence of pediatric bipolar disorder is 3.9%, although study estimates are higher with "broad bipolar criteria" and "older minimum age". The most frequent ages of onset are 24 or 46; the distribution of onset age is bimodal. An earlier onset is associated with worse depression and more frequent co-diagnosis of anxiety and substance use. Around 40-60% of people with BD are employed and over 80% "may take time off work for psychiatric reasons in a five year period." Occupational therapies appear cost-effective at returning people with BD to work. Social cognition is moderately impaired in people with BD, regardless of mood state. 16% of people with BD are high functioning. As of 2021, people with BD accounted for 183 Years Lived with Disability (YLDs) per 100,000 people in the Americas (ranking 20th out of all conditions). Risk of death due to unnatural and natural causes is 7.3 and 1.9 times higher respectively. On average, life expectancy is 12.9 years shorter.
Signs and symptoms Bipolar symptoms usually begin in adolescence or early adulthood. The condition is characterized by intermittent episodes of mania, commonly (but not in everyone) alternating with bouts of depression, with an absence of symptoms in between. During these episodes, people with bipolar disorder exhibit disruptions in normal mood, psychomotor activity (the level of physical activity that is influenced by mood)—such as constant fidgeting during mania or slowed movements during depression—circadian rhythm and cognition. Mania can present with varying levels of mood disturbance, ranging from euphoria, which is associated with "classic mania", to dysphoria and irritability. Psychotic symptoms such as delusions or hallucinations may occur in both manic and depressive episodes; their content and nature are consistent with the person's mood. Of people with bipolar I disorder, 58–68% have experienced psychosis. For context, co-diagnosis of schizophrenia is "low" in bipolar disorder (8%). For further context, psychotic symptoms are more common in bipolar type I than in bipolar type II. In some people with bipolar disorder, depressive symptoms predominate, and the episodes of mania are always the more subdued hypomania type. According to the DSM-5 criteria, mania is distinguished from hypomania by the duration: hypomania is present if elevated mood symptoms persist for at least four consecutive days, while mania is present if such symptoms persist for more than a week. Unlike mania, hypomania is not always associated with impaired functioning.
Manic episodes
Also known as mania, a manic episode is a period of at least one week of elevated or irritable mood, which can range from euphoria to delirium. The core symptom of mania involves an increase in energy of psychomotor activity. Mania can also present with increased self-esteem or grandiosity, racing thoughts, pressured speech that is difficult to interrupt, decreased need for sleep, disinhibited social behavior, increased goal-oriented activities and impaired judgement, which can lead to impulsive or high-risk behaviors, such as excessive spending. To fit the definition of a manic episode, these behaviors must impair the individual's ability to socialize or work. If untreated, a manic episode usually lasts three to six months. In severe manic episodes, a person can experience psychotic symptoms, where thought content is affected along with mood. They may feel unstoppable, persecuted, or as if they have a special relationship with God, a great mission to accomplish, or other grandiose or delusional ideas. This occasionally results in hospitalization in an inpatient psychiatric hospital, but a systematic review and meta-analysis showed that bipolar disorder, by itself, does not increase criminally violent behavior. The severity of manic symptoms can be measured by rating scales such as the Young Mania Rating Scale, though questions remain about the reliability of these scales. Authors of a chapter for a "clinical textbook" posit that mania is a medical emergency. Two other authors (Kane and Director) in the Journal of Medical Ethics have debated the medical decision-making capacity of people with mania. In a study of fifty inpatients with mania, 38% were found to have capacity to make their own treatment choices. The onset of a manic or depressive episode is often foreshadowed by sleep disturbance. Manic individuals often have a history of substance use disorder developed over years as a form of "self-medication".
Hypomanic episodes
Hypomania is the milder form of mania, defined as at least four days of the same criteria as mania, but does not cause a significant decrease in the individual's ability to socialize or work, lacks psychotic features, and does not require psychiatric hospitalization. Overall functioning may increase during episodes of hypomania and is thought to serve as a defense mechanism against depression by some. Hypomanic episodes rarely progress to full-blown manic episodes. Some people who experience hypomania show increased creativity, while others are irritable or demonstrate poor judgment. Hypomania may feel good to some individuals who experience it, though most people who experience hypomania state that the stress of the experience is very painful. People with bipolar disorder who experience hypomania tend to forget the effects of their actions on those around them. Even when family and friends recognize mood swings, the individual will often deny that anything is wrong. If not accompanied by depressive episodes, hypomanic episodes are often not deemed problematic unless the mood changes are uncontrollable or volatile. In individuals with bipolar II disorder, depressive symptoms typically overlap with hypomania symptoms. These individuals may not be able to identify these specific symptoms as hypomania, rather they view them as typical depression with slight alterations in mood. Most commonly, symptoms continue for time periods from a few weeks to a few months.
Depressive episodes
Symptoms of the depressive phase of bipolar disorder include persistent feelings of sadness, irritability or anger, loss of interest in previously enjoyed activities, excessive or inappropriate guilt, hopelessness, sleeping too much or not enough, changes in appetite or weight, fatigue, problems concentrating, self-loathing or feelings of worthlessness, and thoughts of death or suicide. Although the DSM-5 criteria for diagnosing unipolar and bipolar episodes are the same, some clinical features are more common in the latter, including increased sleep, sudden onset and resolution of symptoms, significant weight gain or loss, and severe episodes after childbirth. The earlier the age of onset, the more likely the first few episodes are to be depressive. For most people with bipolar types 1 and 2, the depressive episodes are much longer than the manic or hypomanic episodes. Since a diagnosis of bipolar disorder requires a manic or hypomanic episode, many affected individuals are initially misdiagnosed as having major depression and treated with prescribed antidepressants.
Mixed affective episodes
In bipolar disorder, a mixed state is an episode during which symptoms of both mania and depression occur simultaneously. Individuals experiencing a mixed state may have manic symptoms such as grandiose thoughts while simultaneously experiencing depressive symptoms such as excessive guilt or feeling suicidal. They are considered to have a higher risk for suicidal behavior as depressive emotions such as hopelessness are often paired with mood swings or difficulties with impulse control. Anxiety disorders occur more frequently as a comorbidity in mixed bipolar episodes than in non-mixed bipolar depression or mania. Substance (including alcohol) use also follows this trend, thereby appearing to depict bipolar symptoms as no more than a consequence of substance use.
Cycling
Predictable timing of mood switches is possible though uncommon in bipolar disorder. A systematic review by Geoffroy and others (2014) found seasonal pattern mania in 15% of patients.
Causes The causes of bipolar disorder likely vary between individuals and the exact mechanism underlying the disorder remains unclear. Genetic influences are believed to account for 73–93% of the risk of developing the disorder indicating a strong hereditary component. The overall heritability of the bipolar spectrum has been estimated at 0.71. Twin studies have been limited by relatively small sample sizes but have indicated a substantial genetic contribution, as well as environmental influence. For bipolar I disorder, the rate at which identical twins (same genes) will both have bipolar I disorder (concordance) is around 40%, compared to about 5% in fraternal twins. A combination of bipolar I, II, and cyclothymia similarly produced rates of 42% and 11% (identical and fraternal twins, respectively). The rates of bipolar II combinations without bipolar I are lower—bipolar II at 23 and 17%, and bipolar II combining with cyclothymia at 33 and 14%—which may reflect relatively higher genetic heterogeneity. The cause of bipolar disorders overlaps with major depressive disorder. When defining concordance as the co-twins having either bipolar disorder or major depression, then the concordance rate rises to 67% in identical twins and 19% in fraternal twins. The relatively low concordance between fraternal twins brought up together suggests that shared family environmental effects are limited, although the ability to detect them has been limited by small sample sizes.
Genetic
Behavioral genetic studies have suggested that many chromosomal regions and candidate genes are related to bipolar disorder susceptibility with each gene exerting a mild to moderate effect. The risk of bipolar disorder is nearly ten-fold higher in first-degree relatives of those with bipolar disorder than in the general population; similarly, the risk of major depressive disorder is three times higher in relatives of those with bipolar disorder than in the general population. Although the first genetic linkage finding for mania was in 1969, linkage studies have been inconsistent. Findings point strongly to heterogeneity, with different genes implicated in different families. Robust and replicable genome-wide significant associations showed several common single-nucleotide polymorphisms (SNPs) are associated with bipolar disorder, including variants within the genes CACNA1C, ODZ4, and NCAN. The largest and most recent genome-wide association study failed to find any locus that exerts a large effect, reinforcing the idea that no single gene is responsible for bipolar disorder in most cases. Polymorphisms in BDNF, DRD4, DAO, and TPH1 have been frequently associated with bipolar disorder and were initially associated in a meta-analysis, but this association disappeared after correction for multiple testing. On the other hand, two polymorphisms in TPH2 were identified as being associated with bipolar disorder. Due to the inconsistent findings in a genome-wide association study, multiple studies have undertaken the approach of analyzing SNPs in biological pathways. Signaling pathways traditionally associated with bipolar disorder that have been supported by these studies include corticotropin-releasing hormone signaling, cardiac β-adrenergic signaling, phospholipase C signaling, glutamate receptor signaling, cardiac hypertrophy signaling, Wnt signaling, Notch signaling, and endothelin 1 signaling. Of the 16 genes identified in these pathways, three were found to be dysregulated in the dorsolateral prefrontal cortex portion of the brain in post-mortem studies: CACNA1C, GNG2, and ITPR2. Bipolar disorder is associated with reduced expression of specific DNA repair enzymes and increased levels of oxidative DNA damages. The AKAP11 gene was discovered in 2022 as the first gene linked to bipolar disorder. The exomes of around 14,000 individuals with bipolar disorder were analyzed and compared to those without the condition. The findings were combined with data from another study in the Schizophrenia Exome Sequencing Meta-Analysis (SCHEMA), examining the genome sequences of 24,000 people alongside the original 14,000 bipolar disorder cases. This study identified genetic variants, including the AKAP11 gene, associated with an increased risk of bipolar disorder. The AKAP11 gene's interaction with the GSK3B protein, a molecular target of lithium, points to a possible mechanism behind the medication's therapeutic effects.
Environmental Psychosocial factors play a significant role in the development and course of bipolar disorder, and individual psychosocial variables may interact with genetic dispositions. Recent life events and interpersonal relationships likely contribute to the onset and recurrence of bipolar mood episodes, just as they do for unipolar depression. In surveys, 30–50% of adults diagnosed with bipolar disorder report traumatic/abusive experiences in childhood, which is associated with earlier onset, a higher rate of suicide attempts, and more co-occurring disorders such as post-traumatic stress disorder. Subtypes of abuse, such as sexual and emotional abuse, also contribute to violent behaviors seen in patients with bipolar disorder. The number of reported stressful events in childhood is higher in those with an adult diagnosis of bipolar spectrum disorder than in those without, particularly events stemming from a harsh environment rather than from the child's own behavior. Acutely, mania can be induced by sleep deprivation in around 30% of people with bipolar disorder.
Gene-environment interaction According to the "kindling" hypothesis, when people who are genetically predisposed toward bipolar disorder experience stressful events, the stress threshold at which mood changes occur becomes progressively lower, until the episodes eventually start (and recur) spontaneously. There is evidence supporting an association between early-life stress (such as childhood trauma) and dysfunction of the hypothalamic-pituitary-adrenal axis leading to its overactivation, which may play a role in the pathogenesis of bipolar disorder.
Neurological Less commonly, bipolar disorder or a bipolar-like disorder may occur as a result of or in association with a neurological condition or injury including stroke, traumatic brain injury, HIV infection, multiple sclerosis, porphyria, and rarely temporal lobe epilepsy.
Mechanisms
Psychosocial hypotheses
Childhood trauma According to Quide and others (2020), childhood trauma is associated with "earlier onset and greater severity of bipolar disorder (BD) in adulthood". A systematic review and meta-analysis by Murri and others (2016) found that cortisol levels are "associated with the manic phase of BD" and that "HPA axis dysregulation is not an endophenotype of BD, but seems related to environmental risk factors, such as childhood trauma".
Stigmatization According to Latifian and others (2023),
Stigma has considerable consequences for people living with bipolar disorders and their families and causes them to suffer from severe psychological distress in addition to the pain and agony inflicted by the disease. From Table 5 of the same systematic review, examples of 'severe psychological distress' include lower self-esteem, 'social deprivation', and lower quality of life.
Biological hypotheses
The biological mechanism responsible for switching from a manic or hypomanic episode to a depressive episode, or vice versa, "remains poorly understood".
Vigilance regulation Hegerl and Hensch (2014) proposed a "common pathophysiology" between ADHD and bipolar disorder composed of a three-part cycle:
"Unstable vigilance regulation", as measured by electroencephalography (EEG). Efforts at "Vigilance stabilization", such as "hyperactivity, sensation seeking". "Sleep deficits", which have already been found to be associated with mania. Further development of this hypothesis was undertaken by Strauß and others, including Hegerl (March 2018).
Dopamine A review by Ashok and others (2017) proposed that mania is caused by "elevations in D2/3 receptor availability and a hyperactive reward processing network", though they conceded that their model "[relies] on pharmacological evidence". Wu and others (2024) proposed that 'sleep loss' underlies changes in dopaminergic activity and subsequent mood change. Alloy and others (2015) proposed a similar model.
Neuroimmunology Barbosa and others (2014) note the elevated rate of autoimmune diseases and other immunological aberrations in bipolar disorder. They propose that pro-inflammatory cytokines alter "neural processes" such as neurogenesis and memory, causing neurodegeneration. Rosenblat and McIntyre (2017) propose a "bidirectional relationship between BD and immune dysfunction," with a variety of possible mechanisms connecting cytokine levels to mood changes. They conjecture that immune dysfunction is relevant to some but not all bipolar disorder patients.
Diagnosis Bipolar disorder is commonly diagnosed during adolescence or early adulthood, but onset can occur throughout life. Its diagnosis is based on the self-reported experiences of the individual, abnormal behavior reported by family members, friends or co-workers, observable signs of illness as assessed by a clinician, and ideally a medical work-up to rule out other causes. Caregiver-scored rating scales, specifically from the mother, have shown to be more accurate than teacher and youth-scored reports in identifying youths with bipolar disorder. Assessment is usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to oneself or others. The most widely used criteria for diagnosing bipolar disorder are from the American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the World Health Organization's (WHO) International Statistical Classification of Diseases and Related Health Problems, 10th Edition (ICD-10). The ICD-10 criteria are used more often in clinical settings outside of the U.S. while the DSM criteria are used within the U.S. and are the prevailing criteria used internationally in research studies. The DSM-5, published in 2013, includes further and more accurate specifiers compared to its predecessor, the DSM-IV-TR. This work has influenced the eleventh revision of the ICD (ICD-11), which includes the various diagnoses within the bipolar spectrum of the DSM-5. Several rating scales for the screening and evaluation of bipolar disorder exist, including the Bipolar Spectrum Diagnostic Scale, Mood Disorder Questionnaire, the General Behavior Inventory and the Hypomania Checklist. The use of evaluation scales cannot substitute for a full clinical interview, but they serve to systematize the recollection of symptoms. On the other hand, instruments for screening bipolar disorder tend to have lower sensitivity.
Differential diagnosis Mental disorders that can mimic bipolar disorder include schizophrenia, major depressive disorder, attention deficit hyperactivity disorder (ADHD), and certain personality disorders, such as borderline personality disorder. A key difference between bipolar disorder and borderline personality disorder is the nature of the mood swings; in contrast to the sustained changes to mood over days to weeks or longer seen in bipolar disorder, those experienced in borderline personality disorder (more accurately called emotional dysregulation) are sudden and often short-lived, and secondary to social stressors. Although there are no biological tests that are diagnostic of bipolar disorder, blood tests and/or imaging are carried out to investigate whether medical illnesses with clinical presentations similar to that of bipolar disorder are present before making a definitive diagnosis. Neurologic diseases such as multiple sclerosis, complex partial seizures, strokes, brain tumors, Wilson's disease, traumatic brain injury, Huntington's disease, and complex migraines can mimic features of bipolar disorder. An EEG may be used to exclude neurological disorders such as epilepsy, and a CT scan or MRI of the head may be used to exclude brain lesions. Additionally, disorders of the endocrine system such as hypothyroidism, hyperthyroidism, and Cushing's disease are in the differential as is the connective tissue disease systemic lupus erythematosus. Infectious causes of mania that may appear similar to bipolar mania include herpes encephalitis, HIV, influenza, or neurosyphilis. Certain vitamin deficiencies such as pellagra (niacin deficiency), vitamin B12 deficiency, folate deficiency, and Wernicke–Korsakoff syndrome (thiamine deficiency) can also lead to mania. Common medications that can cause manic symptoms include antidepressants, prednisone, Parkinson's disease medications, thyroid hormone, stimulants (including cocaine and methamphetamine), and certain antibiotics.
Bipolar spectrum
Bipolar spectrum disorders include bipolar I disorder, bipolar II disorder, cyclothymic disorder, and cases where subthreshold symptoms are found to cause clinically significant impairment or distress. These disorders involve major depressive episodes that alternate with manic or hypomanic episodes, or with mixed episodes that feature symptoms of both mood states. The concept of the bipolar spectrum is similar to that of Emil Kraepelin's original concept of manic depressive illness. Bipolar II disorder was established as a diagnosis in 1994 within DSM IV; though debate continues over whether it is a distinct entity, part of a spectrum, or is the very same condition as bipolar I disorder.
Criteria and subtypes
The DSM and the ICD characterize bipolar disorder as a spectrum of disorders occurring on a continuum. The DSM-5 and ICD-11 lists three specific subtypes:
Bipolar I disorder: At least one manic episode is necessary to make the diagnosis; depressive episodes are common in the vast majority of cases with bipolar disorder I, but are unnecessary for the diagnosis. Specifiers such as "mild, moderate, moderate-severe, severe" and "with psychotic features" should be added as applicable to indicate the presentation and course of the disorder. Bipolar II disorder: No manic episodes and one or more hypomanic episodes and one or more major depressive episodes. Hypomanic episodes do not go to the full extremes of mania (i.e., do not usually cause severe social or occupational impairment, and are without psychosis), and this can make bipolar II more difficult to diagnose, since the hypomanic episodes may simply appear as periods of successful high productivity and are reported less frequently than a distressing, crippling depression. Cyclothymia: A history of hypomanic episodes with periods of depression that do not meet criteria for major depressive episodes. In cyclothymia, hypomanic and depressive episodes alternate for at least two years in adults and at least one year in children and adolescents. When relevant, specifiers for peripartum onset and with rapid cycling should be used with any subtype. Individuals who have subthreshold symptoms that cause clinically significant distress or impairment, but do not meet full criteria for one of the three subtypes may be diagnosed with other specified or unspecified bipolar disorder. Other specified bipolar disorder is used when a clinician chooses to explain why the full criteria were not met (e.g., hypomania without a prior major depressive episode). If the condition is thought to have a non-psychiatric medical cause, the diagnosis of bipolar and related disorder due to another medical condition is made, while substance/medication-induced bipolar and related disorder is used if a medication is thought to have triggered the condition. While hyperthymic temperament is not considered a pathological disorder, it is genetically associated with bipolar I and may predispose affected individuals to a manic-depressive episode. Hyperthymic temperament has been described as subsyndromal manifestation within the broader bipolar spectrum.
Rapid cycling Most people who meet criteria for bipolar disorder experience a number of episodes, on average 0.4 to 0.7 per year, lasting three to six months. Rapid cycling, however, is a course specifier that may be applied to any bipolar subtype. It is defined as having four or more mood disturbance episodes within a one-year span. Rapid cycling is usually temporary but is common amongst people with bipolar disorder and affects 25.8–45.3% of them at some point in their life. These episodes are separated from each other by a remission (partial or full) for at least two months or a switch in mood polarity (i.e., from a depressive episode to a manic episode or vice versa). The definition of rapid cycling most frequently cited in the literature (including the DSM-5 and ICD-11) is that of Dunner and Fieve: at least four major depressive, manic, hypomanic or mixed episodes during a 12-month period. The literature examining the pharmacological treatment of rapid cycling is sparse and there is no clear consensus with respect to its optimal pharmacological management. "Ultra rapid" and "ultradian" have been applied to faster-cycling types of bipolar disorder. People with the rapid cycling or faster-cycling subtypes of bipolar disorder tend to be more difficult to treat and less responsive to medications than other people with bipolar disorder. There is evidence that rapid cycling may be iatrogenic and caused by antidepressant use. In contrast, atypical antipsychotics and mood stabilizers do not worsen rapid cycling.
Coexisting psychiatric conditions The diagnosis of bipolar disorder can be complicated by coexisting (comorbid) psychiatric conditions including obsessive–compulsive disorder, substance-use disorder, eating disorders, attention deficit hyperactivity disorder, social phobia, premenstrual syndrome (including premenstrual dysphoric disorder), or panic disorder. A thorough longitudinal analysis of symptoms and episodes, assisted if possible by discussions with friends and family members, is crucial to establishing a treatment plan where these comorbidities exist. Children of parents with bipolar disorder more frequently have other mental health problems.
Prevention Attempts at prevention of bipolar disorder have focused on stress (such as childhood adversity or highly conflictual families) which, although not a diagnostically specific causal agent for bipolar, does place genetically and biologically vulnerable individuals at risk for a more severe course of illness. Longitudinal studies have indicated that full-blown manic stages are often preceded by a variety of prodromal clinical features, providing support for the occurrence of an at-risk state of the disorder when an early intervention might prevent its further development and/or improve its outcome. Circadian rhythm disruptions such as traveling across many time zones (jet lag) can destabilize bipolar disorder and lead to manic or psychotic episodes.
Management
The aim of management is to treat acute episodes safely with medication and work with the patient in long-term maintenance to prevent further episodes and optimise function using a combination of pharmacological and psychotherapeutic techniques. Involuntary hospitalization and institutionalization were once acceptable practice, but new recommendations to advance human rights instead call for the abolition of institutionalization and forced treatment. In lieu of a hospital admission, support services available can include drop-in centers, visits from members of a community mental health team or an Assertive Community Treatment team, supported employment, patient-led support groups, and intensive outpatient programs. These are sometimes referred to as partial-inpatient programs. Compared to the general population, people with bipolar disorder are less likely to frequently engage in physical exercise. Exercise may have physical and mental benefits for people with bipolar disorder, but there is a lack of research.
Psychosocial Psychotherapy aims to assist a person with bipolar disorder in accepting and understanding their diagnosis, coping with various types of stress, improving their interpersonal relationships, and recognizing prodromal symptoms before full-blown recurrence. Cognitive behavioral therapy (CBT), family-focused therapy, psychoeducation, as well as interpersonal and social rhythm therapy appear to be effective. Further, recent research indicates that mindfulness and mindfulness-based therapies show considerable potential to alleviate depression and anxiety as well as to improve mood regulation and executive control in bipolar patients. Most studies have been based only on bipolar I, however, and treatment during the acute phase can be a particular challenge. Some clinicians emphasize the need to talk with individuals experiencing mania, to develop a therapeutic alliance in support of recovery.
Medication
Medications are often prescribed to help improve symptoms of bipolar disorder. Medications approved for treating bipolar disorder including mood stabilizers and atypical antipsychotics. Sometimes a combination of medications may also be suggested. The choice of medications may differ depending on the bipolar disorder episode type or if the person is experiencing unipolar or bipolar depression. Other factors to consider when deciding on an appropriate treatment approach includes if the person has any comorbidities, their response to previous therapies, adverse effects, and the desire of the person to be treated.
Mood stabilizers Lithium and the anticonvulsants carbamazepine, lamotrigine, and valproic acid are classed as mood stabilizers due to their effect on the mood states in bipolar disorder.
Lithium has the best overall evidence and is considered an effective treatment for acute manic episodes, preventing relapses, and bipolar depression. Lithium reduces the risk of suicide, self-harm, and death in people with bipolar disorder. Lithium is preferred for long-term mood stabilization. Lithium treatment is also associated with adverse effects and it has been shown to erode kidney and thyroid function over extended periods. Valproate has become a commonly prescribed treatment and effectively treats manic episodes. Carbamazepine is less effective in preventing relapse than lithium or valproate. Carbamazepine effectively treats manic episodes, with some evidence it has greater benefit in rapid-cycling bipolar disorder, or those with more psychotic symptoms or more symptoms similar to that of schizoaffective disorder. Lamotrigine has some efficacy in treating depression, and this benefit is greatest in more severe depression. Lamotrigine may have a similar effectiveness to lithium for treating bipolar disorder, however, there is evidence to suggest that lamotrigine is less effective at preventing recurrent mania episodes. Lamotrigine treatment has been shown to be safer compared to lithium treatment, with less adverse effects. Valproate and carbamazepine are teratogenic and should be avoided as a treatment in women of childbearing age, but discontinuation of these medications during pregnancy is associated with a high risk of relapse. Lithium is also teratogenic in the first trimester, though it can be acceptable during this period after careful weighing of benefits and risks. The effectiveness of topiramate is unknown. Mood stabilizers are used for long-term maintenance but have not demonstrated the ability to quickly treat acute bipolar depression. However, several atypical antipsychotics are FDA approved to treat bipolar depression.
Antipsychotics Antipsychotic medications are effective for short-term treatment of bipolar manic episodes and appear to be superior to lithium and anticonvulsants for this purpose. Multiple atypical antipsychotics are FDA approved to treat bipolar depression: lurasidone, quetiapine, olanzapine-fluoxetine combination, cariprazine, and lumateperone are all FDA approved for depression in bipolar disorder. Atypical antipsychotics such as lurasidone and clozapine are also indicated for bipolar depression refractory to treatment with mood stabilizers. Olanzapine is effective in preventing relapses, although the supporting evidence is weaker than the evidence for lithium. A 2006 review found that haloperidol was an effective treatment for acute mania, limited data supported no difference in overall efficacy between haloperidol, olanzapine or risperidone, and that it could be less effective than aripiprazole.
Antidepressants Antidepressant monotherapy is not recommended in the treatment of bipolar disorder and does not provide any benefit over mood stabilizers. Atypical antipsychotic medications are preferred over antidepressants to augment the effects of mood stabilizers due to the lack of efficacy of antidepressants in bipolar disorder. The FDA has approved 5 atypical antipsychotic medications to specifically treat bipolar depression. Treatment of bipolar disorder using antidepressants may carry a risk of affective switches where a person switches from depression to manic or hypomanic phases or mixed states. There may also be a risk of accelerating cycling between phases when antidepressants are used in bipolar disorder, known as rapid cycling. The risk of affective switches is higher in bipolar I depression; antidepressants are generally avoided in bipolar I disorder or only used with mood stabilizers when they are deemed necessary. Whether modern antidepressants cause mania or rapid cycling in bipolar disorder is highly controversial, as is whether antidepressants provide any benefit over mood stabilizers alone. Selective serotonin reuptake inhibitors and bupropion still have a risk of rapid cycling and manic switch, but it is lower than other types of antidepressants. Serotonin-norepinephrine reuptake inhibitors, such as venlafaxine and duloxetine, tetracyclic antidepressants such as mirtazapine, and tricyclic antidepressants have higher rates of manic switch and rapid cycling.
Combined treatment approaches Atypical antipsychotics and mood stabilizers used together are quicker and more effective at treating mania than either class of drug used alone. According to the International Society for Bipolar Disorders (ISBD) and Canadian Network for Mood and Anxiety Treatments (CANMAT) guidelines, a first-line combination treatment for bipolar depression is the atypical antipsychotic lurasidone plus the mood stabilizers lithium or valproate.
Other drugs Short courses of benzodiazepines are used in addition to other medications for calming effect until mood stabilizing become effective. Electroconvulsive therapy (ECT) is an effective form of treatment for acute mood disturbances in those with bipolar disorder, especially when psychotic or catatonic features are displayed. ECT is also recommended for use in pregnant women with bipolar disorder. A single intravenous dose of ketamine may produce a rapid but transient antidepressant effect in bipolar depression, although the evidence is of low to very low certainty, and evidence for other glutamate receptor modulators or for sustained remission and safety remains inconclusive. Gabapentin and pregabalin are not proven to be effective for treating bipolar disorder.
Children Treating bipolar disorder in children involves medication and psychotherapy. The literature and research on the effects of psychosocial therapy on bipolar spectrum disorders are scarce, making it difficult to determine the efficacy of various therapies. Mood stabilizers and atypical antipsychotics are commonly prescribed. Among the former, lithium is the only compound approved by the FDA for children. Psychological treatment