Bipolar disorders are characterized by alternating episodes of mania, depression, and normal mood, each lasting for weeks to months at a time in bipolar I disorder. Major depression and hypomania (but never mania) occur in bipolar II disorder, while mild depression and hypomania occur in cyclothymia. The etiology is suspected to be due heredity and changes in the level of brain neurotransmitters; psychosocial factors may also be involved. Diagnosis is based on history. Treatment consists of mood-stabilizing medications, sometimes with psychotherapy.
Bipolar disorder is characterized by significant mood disturbances, which include episodes of mania (or hypomania) and major depression, interspersed with periods of normal mood. Episodes of bipolar disorder can vary in symptoms (ie, depression, mania or both), intensity, and duration. Bipolar disorder has a peak age of onset at around age 15, with 10% of cases starting by age 10, 31% by age 18, and 69% by age 25 (1). In many children, the initial manifestation is 1 or more episodes of depression. (See also Bipolar Disorders in adults.)
Early onset of bipolar disorder in childhood and adolescence has been associated with greater symptom severity of depression, anxiety, delays to treatment (2), and substance use (3). Longitudinal studies indicate a continuum between the juvenile and adult onset forms of bipolar disorder (4), with similar neurological findings (5, 6) and comorbidities.
In the past, bipolar disorder was diagnosed in prepubertal children who were disabled by intense, unstable moods. However, because such children typically progress to a depressive rather than bipolar disorder, they are now classified as having disruptive mood dysregulation disorder.
General references
1. Solmi M, Radua J, Olivola M, et al. Age at onset of mental disorders worldwide: large-scale meta-analysis of 192 epidemiological studies. Mol Psychiatry. 2022;27(1):281-295. doi:10.1038/s41380-021-01161-7
2. Joslyn C, Hawes DJ, Hunt C, Mitchell PB. Is age of onset associated with severity, prognosis, and clinical features in bipolar disorder? A meta-analytic review. Bipolar Disord. 2016;18(5):389-403. doi:10.1111/bdi.12419
3. Hunt GE, Malhi GS, Cleary M, Lai HM, Sitharthan T. Comorbidity of bipolar and substance use disorders in national surveys of general populations, 1990-2015: Systematic review and meta-analysis. J Affect Disord. 2016;206:321-330. doi:10.1016/j.jad.2016.06.051
4. Hafeman DM, Goldstein TR, Strober M, et al. Prospectively ascertained mania and hypomania among young adults with child- and adolescent-onset bipolar disorder. Bipolar Disord. 2021;23(5):463-473. doi:10.1111/bdi.13034
5. Phillips ML, Swartz HA. A critical appraisal of neuroimaging studies of bipolar disorder: toward a new conceptualization of underlying neural circuitry and a road map for future research. Am J Psychiatry. 2014;171(8):829-843. doi:10.1176/appi.ajp.2014.13081008
6. Adler CM, Adams J, DelBello MP, et al. Evidence of white matter pathology in bipolar disorder adolescents experiencing their first episode of mania: a diffusion tensor imaging study. Am J Psychiatry. 2006;163(2):322-324. doi:10.1176/appi.ajp.163.2.322
Etiology of Bipolar Disorder
Environmental, social, genetic (familial bipolar disorder), and perinatal factors (low birth weight, maternal infections), and mitochondrial dysfunction (1, 2) have been implicated in the etiopathogenesis of bipolar disorder. The "kindling" hypothesis suggests that environmental stressors and early life adversities can interact with preexisting genetic predispositions to trigger the onset of bipolar disorder. In twin studies, bipolar disorder was characterized by a high heritability of >70% (3, 4). Several genetic variants have been associated with bipolar disorder (5), although there are currently no markers useful for diagnosing bipolar disorder. However, neuroimaging studies in youths report smaller volumes in the amygdala (6–8) and prefrontal cortex (9), as well as lack of the normal increase in volume of the amygdala (10) and anterior white matter that occurs in normal controls during adolescence. Relative hyperactivation of the amygdala may contribute. Research also indicates that there is an increased risk of developing certain psychotic disorders (namely, bipolar disorder and schizophrenia) among adolescents who use cannabis products. Additional factors may include defects in the pathways involved in insulin secretion and endocannabinoid signaling () and anterior white matter that occurs in normal controls during adolescence. Relative hyperactivation of the amygdala may contribute. Research also indicates that there is an increased risk of developing certain psychotic disorders (namely, bipolar disorder and schizophrenia) among adolescents who use cannabis products. Additional factors may include defects in the pathways involved in insulin secretion and endocannabinoid signaling (11).
Certain drugs (eg, cocaine, amphetamines, phencyclidine, certain antidepressants) and environmental toxins (eg, lead) can exacerbate or mimic the disorder. Certain disorders (eg, thyroid disorders) can also cause similar symptoms. Infections may also contribute; mania has been associated with COVID-19 infections in youths12.
Etiology references
1. Lam XJ, Xu B, Yeo PL, Cheah PS, Ling KH. Mitochondria dysfunction and bipolar disorder: From pathology to therapy. IBRO Neurosci Rep. 2023;14:407-418. Published 2023 Apr 11. doi:10.1016/j.ibneur.2023.04.002
2. Freyberg Z, Andreazza AC, McClung CA, Phillips ML. Linking Mitochondrial Dysfunction, Neurotransmitter, and Neural Network Abnormalities and Mania: Elucidating Neurobiological Mechanisms of the Therapeutic Effect of the Ketogenic Diet in Bipolar Disorder. Biol Psychiatry Cogn Neurosci Neuroimaging. 2025;10(3):267-277. doi:10.1016/j.bpsc.2024.07.011
3. Gordovez FJA, McMahon FJ. The genetics of bipolar disorder. Mol Psychiatry. 2020;25(3):544-559. doi:10.1038/s41380-019-0634-7
4. Smoller JW, Finn CT. Family, twin, and adoption studies of bipolar disorder. Am J Med Genet C Semin Med Genet. 2003;123C(1):48-58. doi:10.1002/ajmg.c.20013
5. Craddock N, Sklar P. Genetics of bipolar disorder. Lancet. 2013;381(9878):1654-1662. doi:10.1016/S0140-6736(13)60855-7
6. Phillips ML, Swartz HA. A critical appraisal of neuroimaging studies of bipolar disorder: Toward a new conceptualization of underlying neural circuitry and a road map for future research. Am J Psychiatry. 171(8):829-843, 2014. doi: 10.1176/appi.ajp.2014.13081008
7. Hafeman D, Bebko G, Bertocci MA, et al. Amygdala-prefrontal cortical functional connectivity during implicit emotion processing differentiates youth with bipolar spectrum from youth with externalizing disorders. J Affect Disord. 208:94-100, 2017. doi: 10.1016/j.jad.2016.09.064
8. Mwangi B, Spiker D, Zunta-Soares JC, et al. Prediction of pediatric bipolar disorder using neuroanatomical signatures of the amygdala. Bipolar Disord.16(7):713-721, 2014.
9. Najt P, Wang F, Spencer L, et al. Anterior cortical development during adolescence in bipolar disorder. Biol Psychiatry. 79(4):303-310, 2016.
10. Bitter SM, Mills NP, Adler CM, et al. Progression of amygdala volumetric abnormalities in adolescents following their first manic episode. J Am Acad Child Adolesc Psychiatry. 50(10):1017-1026, 2011.
11. Carvalho AF, Firth J, Vieta E. Bipolar Disorder. N Engl J Med. 2020;383(1):58-66. doi:10.1056/NEJMra1906193
12. Meeder R, Adhikari S, Sierra-Cintron, et al. New-onset mania and psychosis in adolescents in the context of COVID-19 infection. Cureus14(4):e24322, 2022. doi: 10.7759/cureus.24322
Symptoms and Signs of Bipolar Disorder
Bipolar disorder is characterized by recurrent episodes of elevated mood (mania or hypomania). Manic episodes usually alternate with depressive episodes, which can be more frequent. During a manic episode in adolescents, mood may be very positive or hyperirritable and often alternate depending on social circumstances. Speech in manic episodes is rapid and pressured, sleep is decreased, and self-esteem is inflated. Mania may reach psychotic proportions (eg, “I have become one with God”). Judgment may be severely impaired, and adolescents may engage in risky behaviors (eg, promiscuous sex, reckless driving). Increased energy or irritability, elation, and even euphoria may also be present.
Prepubertal children may experience dramatic moods, but the duration of these moods is much shorter (often lasting only a few moments) than that in adolescents.
Onset is characteristically insidious, and children typically have a history of being very temperamental and difficult to manage.
Depressive symptoms such as pervasive depressed mood or irritability, marked loss of interest in activities, significant changes in weight or appetite, sleep disturbances, psychomotor agitation or retardation, fatigue, feelings of worthlessness or excessive guilt, difficulty concentrating, recurrent thoughts of death or suicidal ideation, and clinically significant distress or impairment in daily functioning may occur. If these are the initial presenting symptoms, substance use or other medical conditions should be excluded.
Diagnosis of Bipolar Disorder
Psychiatric assessment
Diagnostic and Statistical Manual of Mental Disorders, Fifth edition, Text Revision (DSM-5-TR) criteria
Testing for toxicologic causes
The diagnosis of bipolar disorder is based on identification of symptoms of mania as described above, plus a history of remission and relapse (1).
A number of medical disorders (eg, thyroid disorders, brain infections or tumors) and drug intoxication must be excluded with appropriate medical assessment, including a toxicology screen for drugs of abuse and environmental toxins. The interviewer should also search for precipitating events, such as severe psychological stress, including child maltreatment.
Bipolar I disorder is defined by the occurrence of at least one manic episode, which may be accompanied by major depressive episodes but does not require them; mania is characterized by abnormally elevated or irritable mood and increased activity or energy lasting at least 1 week, often with marked impairment and sometimes with need for hospitalization.
Bipolar II disorder requires episodes of major depression but never a manic episode. There may be periods of less severe mood elevations (ie, hypomania) which may include increased energy, decreased sleep, racing thoughts, and heightened distractibility.
Cyclothymia includes prolonged (> 2-year) periods with both hypomanic and depressive episodes; however, these episodes do not meet the specific criteria for a bipolar or major depressive disorder.
Unspecified bipolar disorder not otherwise specified includes sub-threshold symptoms that do not meet criteria for any of the above disorders. Unspecified bipolar disorder may convert to bipolar I or II disorders in approximately 50 to 75% of youth (2).
Diagnosis references
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), Washington: American Psychiatric Association, 2022.
2. Birmaher B, Merranko JA, Goldstein TR, et al. A Risk Calculator to Predict the Individual Risk of Conversion From Subthreshold Bipolar Symptoms to Bipolar Disorder I or II in Youth. J Am Acad Child Adolesc Psychiatry. 2018;57(10):755-763.e4. doi:10.1016/j.jaac.2018.05.023
Treatment of Bipolar Disorders
Psychotherapy
Mania: second-generation antipsychotics, sometimes adding mood stabilizers
Depression: second-generation antipsychotics plus an SSRI, sometimes lithiumDepression: second-generation antipsychotics plus an SSRI, sometimes lithium
Psychotherapy that is family focused can help children and their families cope with the consequences of the disorder and reduce the frequency of mood-related episodes (1). Individual psychotherapy can also support and reassure adolescents and reinforce medication adherence.
For acute mania, second-generation antipsychotics are the first line of treatment (2–5). A meta-analysis reporting efficacy and response to risperidone, olanzapine, aripiprazole, quetiapine, and asenapine supports a trial of these agents in that order. Lithium can also be initiated in the acute phase of disease to achieve therapeutic efficacy for maintenance. Other mood stabilizers (divalproex, lamotrigine, carbamazepine) may be used for patients who fail 2 or 3 trials of antipsychotics (). A meta-analysis reporting efficacy and response to risperidone, olanzapine, aripiprazole, quetiapine, and asenapine supports a trial of these agents in that order. Lithium can also be initiated in the acute phase of disease to achieve therapeutic efficacy for maintenance. Other mood stabilizers (divalproex, lamotrigine, carbamazepine) may be used for patients who fail 2 or 3 trials of antipsychotics (6).
For acute depression, second-generation antipsychotics (eg, quetiapine, lurasidone) alone or combined with a selective serotonin reuptake inhibitor (SSRI) are the first line of treatment. An olanzapine-fluoxetine combination has also been used to treat bipolar depression, but there are no comparative data to show that fluoxetine is more effective than the shorter-acting SSRIs. Lithium is an alternative and may also be combined with an SSRI. Compared to other mood stabilizers and antipsychotics, lithium results in decreased suicidality, less depression and better psychosocial function. These findings mimic those found in adults (, second-generation antipsychotics (eg, quetiapine, lurasidone) alone or combined with a selective serotonin reuptake inhibitor (SSRI) are the first line of treatment. An olanzapine-fluoxetine combination has also been used to treat bipolar depression, but there are no comparative data to show that fluoxetine is more effective than the shorter-acting SSRIs. Lithium is an alternative and may also be combined with an SSRI. Compared to other mood stabilizers and antipsychotics, lithium results in decreased suicidality, less depression and better psychosocial function. These findings mimic those found in adults (7). Antidepressants should not be used alone but in combination with the antipsychotics or lithium. Antidepressants do not increase the risk of treatment-resistant mania (as was thought in the past) but may destabilize mood in children and adolescents with a bipolar disorder (). Antidepressants should not be used alone but in combination with the antipsychotics or lithium. Antidepressants do not increase the risk of treatment-resistant mania (as was thought in the past) but may destabilize mood in children and adolescents with a bipolar disorder (8, 9). Psychotherapy is also important.
Maintenance treatment includes continuing the medications that were effective in the acute phase. Treatment with second-generation antipsychotics alone or in combination with lithium lower the risk of recurrence. Lithium remains one of the most effective medications used for the prevention of both depressive and manic recurrences in bipolar disorder.includes continuing the medications that were effective in the acute phase. Treatment with second-generation antipsychotics alone or in combination with lithium lower the risk of recurrence. Lithium remains one of the most effective medications used for the prevention of both depressive and manic recurrences in bipolar disorder.
All of these medications pose a small but serious risk for a variety of adverse effects. (See table Selected Medications for Bipolar Disorder/Psychoses.) Therefore, benefits must be carefully weighed against potential risks. For the second-generation antipsychotics, there is a concern for weight gain and metabolic syndrome. Ziprasidone is reported to have fewer metabolic adverse effects but is associated with greater QTc prolongation than most other antipsychotics (.) Therefore, benefits must be carefully weighed against potential risks. For the second-generation antipsychotics, there is a concern for weight gain and metabolic syndrome. Ziprasidone is reported to have fewer metabolic adverse effects but is associated with greater QTc prolongation than most other antipsychotics (5,10).
Cytochrome P450 (CYP) enzyme metabolism has important implications for dosing and safety of medications used in the treatment of bipolar disorder (see genetic testing panels). Poor metabolizers of CYP2D6 require half the usual dose because of an increased risk of adverse effects (eg, weight gain, sedation, movement disorder) (11).
For medications metabolized primarily by CYP1A2, strong inhibitors (eg, fluvoxamine, ciproflaxin) can increase plasma levels. For medications metabolized by CYP3A4, strong inhibitors (eg, ketoconazole, clarithromycin, erythromycin, grapefruit juice) will increase plasma levels, and inducers (eg, carbamazepine, rifampin, phenytoin) will decrease plasma levels. For medications metabolized by 2D6, strong inhibitors (eg, fluoxetine, paroxetine) can increase plasma levels. Paliperidone is typically cleared without metabolic modification through the kidneys and with minimal involvement of CYP2D6 and 3A4.For medications metabolized primarily by CYP1A2, strong inhibitors (eg, fluvoxamine, ciproflaxin) can increase plasma levels. For medications metabolized by CYP3A4, strong inhibitors (eg, ketoconazole, clarithromycin, erythromycin, grapefruit juice) will increase plasma levels, and inducers (eg, carbamazepine, rifampin, phenytoin) will decrease plasma levels. For medications metabolized by 2D6, strong inhibitors (eg, fluoxetine, paroxetine) can increase plasma levels. Paliperidone is typically cleared without metabolic modification through the kidneys and with minimal involvement of CYP2D6 and 3A4.
Preliminary data on the ketogenic diet in adults have shown improvement in bipolar symptoms as well as metabolic outcomes (12, 13). The proposed mechanism of action of this diet is that reduced carbohydrate intake results in the production of ketones from fat sources that serve as an alternate fuel source for the brain. More research is needed on the critical role of early preventive interventions in mitigating disease progression (14).
Pearls & Pitfalls
|
Selected Medications for Bipolar Disorder and Schizophrenia*†
Medication | Indication | CYP Substrates | Comments |
|---|---|---|---|
LithiumLithium | |||
Lithium extended-release in childrenLithium extended-release in children ≥ 12 years‡ | Acute mania and maintenance | — | Dose titrated to a blood level of 0.8–1.2 mEq/L (or mmol/L) Associated with decreased suicidality, decreased depression, and better psychosocial functioning in children with bipolar disorder Monitor kidney function, thyroid function, serum calcium levels |
Lithium, immediate-release in childrenLithium, immediate-release in children ≥ 7 years‡,§ | Acute mania and maintenance | — | Dose titrated to a blood level of 0.8–1.2 mEq/L (or mmol/L) Maximum daily dose is 40 mg/kg Associated with decreased suicidality, decreased depression, and better psychosocial functioning in children with bipolar disorder Monitor kidney function, thyroid function, serum calcium levels |
Antipsychotics | |||
Aripiprazole in children (for bipolar IAripiprazole in children (for bipolar I≥ 10 years; for schizophrenia, ≥ 13 years)‡ | Bipolar Schizophrenia | 2D6, 3A4 | The only antipsychotic that does not increase prolactin level |
Asenapine in childrenAsenapine in children≥10 years | Bipolar I | 1A2 | Sublingual administration allows rapid entry into systemic circulation Sedation and somnolence, transient tongue numbness and tingling |
Lurasidone in children (for bipolar I Lurasidone in children (for bipolar I≥ 10 years; for schizophrenia ≥ 13 years) | Bipolar I Schizophrenia | 3A4 | Greater improvement in bipolar I depression with elevated CRP in adults and ages 10-17 years¶ |
Olanzapine in childrenOlanzapine in children≥13 years‡ | Bipolar I Schizophrenia | IA2, 2D6, 3A4 | Causes weight gain, which may limit use in some patients Can increase liver transaminases |
Olanzapine/fluoxetine fixed combination in children Olanzapine/fluoxetine fixed combination in children> 10 years‡,§ | Bipolar I | IA2, 2D6, 3A4 | Limited experience in children |
Paliperidone in children Paliperidone in children≥12 years ‡,§ | Schizophrenia | Cleared unchanged through kidneys 2D6, 3A4 | Closely related to risperidoneClosely related to risperidone Very limited experience in children |
Quetiapine, immediate-release, in children (for bipolar I Quetiapine, immediate-release, in children (for bipolar I≥ 10 years; for schizophrenia ≥ 13 years)‡ | Bipolar Schizophrenia | 3A4 | Causes sedation that may limit dose increases |
Risperidone in children (for bipolar I Risperidone in children (for bipolar I≥ 10 years; for schizophrenia ≥ 13 years) ‡ | Bipolar Schizophrenia | 2D6 | Associated with risk of irreversible gynecomastia Maintenance dose highly variable Doses up to 6 mg/day have been studied, but they provide no additional benefit and increase risk of neurologic adverse effects |
Ziprasidone in children Ziprasidone in children≥10 years‡ | Acute mania Psychosis | — | Very limited experience in children QTc interval prolongation |
Antiseizure medications | |||
CarbamazepineCarbamazepine | Bipolar | — | Metabolic enzyme induction, possibly requiring dose adjustments May cause Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) especially in patients with HLA-B*15:02 genotype (more common in East Asian populations) and maculopapular exanthema (MPE), drug reaction with eosinophilia (DRESS) and SJS/TEN in patients with HLA-A*31:01 genotype (more common in European and Hispanic populations) |
Divalproex | Bipolar I | — | Dose titrated to a blood level of 50–125 mcg/mL Avoid in people in the reproductive age group |
LamotrigineLamotrigine | Bipolar | — | Requires that dosing guidelines in the package insert be followed closely |
* These medications pose a small but serious risk for a wide variety of major adverse effects. Therefore, benefits must be carefully weighed against potential risks. | |||
† This table is not a substitute for the full prescribing information. | |||
‡ These medications increase the risk of weight gain, negative effects on the lipid profile, increases in glucose and prolactin levels, and QT prolongation. | |||
§ These medications have not been studied in children. | |||
¶ Bipolar I disorder is one presentation of bipolar disorder and is characterized always by mania, that may sometimes also be accompanied by depression. CRP = C-reactive protein; CYP = cytochrome P450. | |||
Treatment references
1. Miklowitz DJ, Schneck CD, Walshaw PD, et al. Effects of Family-Focused Therapy vs Enhanced Usual Care for Symptomatic Youths at High Risk for Bipolar Disorder: A Randomized Clinical Trial. JAMA Psychiatry. 2020;77(5):455-463. doi:10.1001/jamapsychiatry.2019.4520
2. Kendall T, Morriss R, Mayo-Wilson E, et al. Assessment and management of bipolar disorder: Summary of updated NICE guidance. BMJ. 349:g5673, 2014. doi: https://doi.org/10.1136/bmj.g5673
3. Yatham LN, Kennedy SH, Parikh SV, et al. Canadian Network for mood and anxiety treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) collaborative update of CANMAT guidelines for the management of patients with bipolar disorder: Update 2013. Bipolar Disord.15(1):1-44, 2013. doi: 10.1111/bdi.12025
4. Walkup JT, Wagner KD, Miller L. Treatment of early-age mania: Outcomes for partial and nonresponders to initial treatment. J Am Acad Child Adolesc Psychiatry 54(12):10081019, 2015.
5. Vita G, Nöhles VB, Ostuzzi G, et al. Systematic Review and Network Meta-Analysis: Efficacy and Safety of Antipsychotics vs Antiepileptics or Lithium for Acute Mania in Children and Adolescents. . Systematic Review and Network Meta-Analysis: Efficacy and Safety of Antipsychotics vs Antiepileptics or Lithium for Acute Mania in Children and Adolescents.J Am Acad Child Adolesc Psychiatry. 2025;64(2):143-157. doi:10.1016/j.jaac.2024.07.920
6. Kowatch RA, Suppes T, Carmody TJ, et al. Effect size of lithium, divalproex sodium, and carbamazepine in children and adolescents with bipolar disorder. . Effect size of lithium, divalproex sodium, and carbamazepine in children and adolescents with bipolar disorder.J Am Acad Child Adolesc Psychiatry.39(6):713-720, 2000. doi: 10.1097/00004583-200006000-00009
7. Hafeman DM, Rooks B, Merranko J, et al. Lithium versus other mood-stabilizing medications in a longitudinal study of youth diagnosed with bipolar disorder. . Lithium versus other mood-stabilizing medications in a longitudinal study of youth diagnosed with bipolar disorder.J Am Acad Child Adolesc Psychiatry. 59(10):1146-1155, 2020. doi: 10.1016/j.jaac.2019.06.013
8. Biederman J, Mick E, Spencer TJ, et al. Therapeutic dilemmas in the pharmacotherapy of bipolar depression in the young. J Child Adolesc Psychopharmacol. 10(3):185-192, 2000. doi: 10.1089/10445460050167296
9. Scheffer RE, Tripathi A, Kirkpatrick FG, et al. Guidelines for treatment-resistant mania in children with bipolar disorder. J Psychiatr Pract. 17(3):186-193, 2011. doi: 10.1097/01.pra.0000398411.59491.8c
10. Jensen KG, Juul K, Fink-Jensen A, Correll CU, Pagsberg AK. Corrected QT changes during antipsychotic treatment of children and adolescents: a systematic review and meta-analysis of clinical trials. J Am Acad Child Adolesc Psychiatry. 2015;54(1):25-36. doi:10.1016/j.jaac.2014.10.002
11. Oshikoya KA, Neely KM, Carroll RJ, et al. CYP2D6 genotype and adverse events to risperidone in children and adolescents. . CYP2D6 genotype and adverse events to risperidone in children and adolescents.Pediatr Res. 2019;85(5):602-606. doi:10.1038/s41390-019-0305-z
12. Sethi S, Wakeham D, Ketter T, et al. Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial. Psychiatry Res. 2024;335:115866. doi:10.1016/j.psychres.2024.115866
13. Campbell I, Campbell H. Mechanisms of insulin resistance, mitochondrial dysfunction and the action of the ketogenic diet in bipolar disorder. Focus on the PI3K/AKT/HIF1-a pathway. . Mechanisms of insulin resistance, mitochondrial dysfunction and the action of the ketogenic diet in bipolar disorder. Focus on the PI3K/AKT/HIF1-a pathway.Med Hypotheses. 2020;145:110299. doi:10.1016/j.mehy.2020.110299
14. Post RM, Goldstein BI, Birmaher B, et al. Toward prevention of bipolar disorder in at-risk children: Potential strategies ahead of the data. J Affect Disord. 2020;272:508-520. doi:10.1016/j.jad.2020.03.025
Prognosis for Bipolar Disorder
Prognosis for adolescents with bipolar disorder varies but tends to worsen with each recurrence. Factors that increase the risk of recurrence include early age of onset, severity of episodes, family psychopathology, and lack of and/or poor adherence to treatment (1). Those who have mild to moderate symptoms, who have a good response to treatment, and who remain adherent to treatment have an excellent prognosis. However, treatment response is often incomplete, and adolescents are notoriously nonadherent to drug regimens. For such adolescents, the long-term prognosis is not as good.
Little is known about the long-term prognosis of prepubertal children diagnosed with bipolar disorder based on highly unstable and intense moods.
Prognosis reference
1. Birmaher B, Merranko JA, Gill MK. Predicting personalized risk of mood recurrences in youths and young adults with bipolar spectrum disorder. J Am Acad Child Adolesc Psychiatry. 59(10):1156-1164, 2020. doi:https://doi.org/10.1016/j.jaac.2019.12.005
Key Points
Bipolar disorder is characterized by alternating periods of mania, depression, and normal mood, each lasting for weeks to months at a time.
Bipolar disorder typically begins during mid-adolescence through the mid-20s; it is rare in younger children.
Typically, onset is insidious; children have a history of being very temperamental and difficult to manage.
In adolescents and prepubertal children, treat manic or agitated episodes with antipsychotics first, since these medications work quickly, followed by mood stabilizers to prevent relapses, and SSRIs and psychotherapy to treat depressive episodes.
Drugs Mentioned In This Article
