Mania

Mania (/ˈmeɪniːə/ (Audio file "LL-Q1860 (eng)-Vealhurl-mania.wav" not found) MAY-nee-ə; also known as manic syndrome) is a psychiatric behavioral syndrome[1][2] defined as a state of abnormally elevated mood and unusually high energy.[3] During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived of as a "mirror image" to depression, the heightened mood can be euphoric as well as dysphoric.[4]

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas, pressure of speech, increased energy, decreased need for sleep, and hyperactivity. Persistent irritability is a symptom of both mania and depression.[5] In severe manic episodes (characteristic of bipolar I disorder), psychotic symptoms may manifest, including delusions (such as grandiose delusions and paranoid delusions[6]) or hallucinations. The prevalence of psychosis in manic episodes is 57%; the rate in depressive episodes is 13%.[7] Other psychotic symptoms include fragmentation of behavior and catatonia.{{Citation needed|date=July 2026} hrenia in bipolar disorder is 8%.[8] More than 5% of the general human population has experienced mania or hypomania in some degree.[9]

## Contents

* 1 Classification
* 1.1 Mixed states
* 1.2 Hypomania
* 1.3 Associated disorders
* 2 Signs and symptoms
* 3 Causes
* 4 Mechanism
* 5 Diagnosis
* 5.1 Diagnostic codes
* 5.2 Differential diagnosis
* 6 Treatment
* 6.1 Debate over decision-making capacity
* 6.2 Acute treatment
* 6.3 Prophylaxis following acute treatment
* 6.4 Contraindication of antidepressants
* 7 Society and culture
* 8 Etymology
* 9 See also
* 10 References
* 11 Further reading
* 12 External links

## Classification

### Mixed states

Main article: Medicine:Mixed affective state

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians[who?], that mania and depression, rather than constituting "true" polar opposites, are, rather, two independent axes in a unipolar—bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act on suicidal impulses.

### Hypomania

Main article: Medicine:Hypomania

Hypomania, which means "less than mania",[10] is a lowered state of mania that does not always impair function or decrease quality of life.[11] Although creativity and hypomania have been historically linked, a review and meta-analysis exploring this relationship found that this assumption may be too general and empirical research evidence is lacking.[12]

In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, others failed to detect differences.[13] Though the elevated mood and energy level typical of hypomania could be seen positively, mania itself generally has many undesirable consequences, including suicidal tendencies. Hypomania can also have these effects, if the prominent mood is irritable as opposed to euphoric. In addition, the intense cases of hypomania can lead to problems. Where trait-based positivity for a person could make them more engaging, outgoing, and cause them to have a positive outlook in life,[14] exaggerated in hypomania, such a person can display excessive optimism, grandiosity, and poor decision-making, often with little regard to the consequences.[14]

### Associated disorders

A single manic episode, in the absence of secondary causes, (i.e., substance use disorders, certain medications, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate.

Certain obsessive–compulsive spectrum disorders as well as impulse-control disorders share the suffix "-mania", namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders.

Evidence indicates a vitamin B12 deficiency can also cause symptoms characteristic of mania and psychosis.[15] Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.[16][17] Postpartum psychosis can also cause manic episodes (unipolar mania).

## Signs and symptoms

A manic episode is defined in the American Psychiatric Association's diagnostic manual (DSM) as a "distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalization is necessary)",[18] where the mood is not caused by drugs/medication or a non-mental medical illness (e.g., hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person has psychosis.[19]

To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep.
3. More talkative than usual or pressure of speech.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Increase in goal-directed activity, or psychomotor agitation.
6. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli).
7. Excessive involvement in activities with a high likelihood of painful consequences. (e.g., overspending, improbable commercial schemes, hypersexuality).[19]

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are more common.

If the person is concurrently depressed, they are said to be having a mixed episode.[19]

The World Health Organization defines a manic episode as one where "a person experiences an extremely high mood". It is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed.[5]

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after.[20] Hypomania is different, as it may cause little or no impairment in function. The hypomanic person's connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those with prolonged unresolved hypomania do run the risk of developing full mania, and may do so without even realizing they have.[21]

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli.[22] This experience creates an absent-mindedness where the manic individual's thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the affected individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly "genius" characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a thus far clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or "over-happy".

Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally "wide open", rarely blinking, and may contribute to some clinicians' erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug.

Individuals may also engage in out-of-character behavior during the episode, such as questionable business transactions, wasteful expenditures of money (e.g., spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behavior (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g., over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.[23][24]

The experience of mania is often quite unpleasant and sometimes frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the individual's lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients may frequently deny anything is wrong with them.[25] Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly.

Mania may also, as earlier mentioned, be divided into three "stages". Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as hypersociality and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell's), respectively.

## Causes

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies give widely varying estimates of the switching while on an antidepressant, with tricyclic antidepressants generally showing higher risk. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medications possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.[26]

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.[27]

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.[28][29]

Deep brain stimulation of the subthalamic nucleus in Parkinson's disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.[30]

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.[31] In some individuals, manic symptoms are also correlated with the season of spring.[32][33]

In "bipolar I or genetically vulnerable individuals", non-clinical use of psychedelics elevates risk for mania.[34]

## Mechanism

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies.[35][36] Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3,[37] dopamine, Protein kinase C, and Inositol monophosphatase.[38]

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation.[39] Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex.[40] A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania.[41] Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.[42]

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC).[43] While limited, some studies demonstrate manipulation of PKC in animals produces behavioral changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-estrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.[36]

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.[44]

Limited evidence suggests that mania is associated with behavioral reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioral activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss.

Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania.[45] Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.[46]

## Diagnosis

### Diagnostic codes

In the ICD-10, there are several disorders with the manic syndrome: organic manic disorder (F06.30), mania without psychotic symptoms (F30.1), mania with psychotic symptoms (F30.2), other manic episodes (F30.8), unspecified manic episode (F30.9), manic type of schizoaffective disorder (F25.0), bipolar disorder, current episode manic without psychotic symptoms (F31.1), bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).[47]

### Differential diagnosis

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out other conditions. Conditions whose symptoms may resemble mania include substance use, various physical conditions such as hyperthyroidism, and various mental health conditions such as "severe anxiety" or "major depressive disorder with psychotic features".[48]

## Treatment

### Debate over decision-making capacity

Writing a chapter for the Clinical Textbook of Mood Disorders, Jauhar and Wong (2024) assert that acute mania is a medical emergency.[49] It is currently debated in the Journal of Medical Ethics whether (or to what extent) patients with acute mania have the capacity to make their own medical decisions.[50][51] Beckett and Chaplin (2006) conducted clinical interviews of 50 inpatients and found that 38% "had overall capacity".[52]

From the United Nations Handbook for Parliamentarians on the Convention on the Rights of Persons with Disabilities[53]:

> When individuals lack the legal capacity to act, they are not only robbed of their right to equal recognition before the law, they are also robbed of their ability to defend and enjoy other human rights. Guardians and tutors acting on behalf of persons with disabilities sometimes fail to act in the interests of the individual they are representing; worse, they sometimes abuse their positions of authority, violating the rights of others. Article 12 of the Convention recognizes that persons with disabilities have legal capacity on an equal basis with others. In other words, an individual cannot lose his/her legal capacity to act simply because of a disability. (However, legal capacity can still be lost in situations that apply to everyone, such as if someone is convicted of a crime.)

### Acute treatment

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (e.g., carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (e.g., olanzapine, quetiapine, asenapine, risperidone, aripiprazole, or cariprazine).[54] In 2024, iloperidone was approved by the FDA for the acute treatment of manic episodes related to bipolar I disorder.[55] The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.[56]

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.{{citation needed|date=March 2026}

### Prophylaxis following acute treatment

Sources differ on the significance of relapse risk following discontinuation of medication.[57][58]

With the former disagreement noted, long-term treatment focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy.[25] While medication for bipolar disorder can help to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.[59]

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment reduces the relative risk of bipolar manic relapse by 38%, "relative risk=0.62".[60] Anticonvulsants such as valproate, oxcarbazepine, and carbamazepine are also used for prophylaxis; more recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.

### Contraindication of antidepressants

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients. Some atypical antidepressants, however, such as mirtazapine and trazodone, have been occasionally used after other options have failed.[61]

## Society and culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as "the most perfect prescription glasses with which to see the world... life appears in front of you like an oversized movie screen."[62] Behrman indicates early in his memoir that he sees himself not as a person with an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that there is a higher prevalence of bipolar disorder among people in the creative industries than in other occupations.[63] Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.[64]

English actor Stephen Fry, who has bipolar disorder,[65] recounts manic behaviour during his adolescence: "When I was about 17 ... going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails."[66] While he has experienced suicidal thoughts, he says the manic side of his condition has provided positive contributions in his life.[65]

## Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), "madness, frenzy"[67] and the verb μαίνομαι (maínomai), "to be mad, to rage, to be furious."[68]

## See also

* Antibiomania
* Cyclothymia
* Hyperthymic temperament
* Monomania
* Dancing mania
* Paranoia
* Abnormal psychology

## References

1. ↑ Sartorius, Norman; Henderson, A.S.; Strotzka, H.; Lipowski, Z.; Yu-cun, Shen; You-xin, Xu; Strömgren, E.; Glatzel, J. et al.. "The ICD-10 Classification of Mental and Behavioural Disorders Clinical descriptions and diagnostic guidelines". p. 30. https://www.who.int/classifications/icd/en/bluebook.pdf.
2. ↑ "Mania: Symptoms, diagnosis, treatments, and more" (in en). 2021-07-30. https://www.medicalnewstoday.com/articles/mania.
3. ↑ Berrios GE (2004). "Of mania". History of Psychiatry 15 (57 Pt 1): 105–124. doi:10.1177/0957154X04041829. PMID 15104084.
4. ↑ "Dysphoric mania: Symptoms, facts, and treatment". 29 November 2018. https://www.medicalnewstoday.com/articles/315016.
5. ↑ 5.0 5.1 "Bipolar disorder" (in en). https://www.who.int/news-room/fact-sheets/detail/bipolar-disorder.
6. ↑ Picardi, Angelo; Fonzi, Laura; Pallagrosi, Mauro; Gigantesco, Antonella; Biondi, Massimo (2018-04-05). "Delusional Themes Across Affective and Non-Affective Psychoses". Frontiers in Psychiatry 9. doi:10.3389/fpsyt.2018.00132. ISSN 1664-0640. PMID 29674982.
7. ↑ Aminoff, S. R.; Onyeka, I. N.; Ødegaard, M.; Simonsen, C.; Lagerberg, T. V.; Andreassen, O. A.; Romm, K. L.; Melle, I. (October 2022). "Lifetime and point prevalence of psychotic symptoms in adults with bipolar disorders: a systematic review and meta-analysis" (in en). Psychological Medicine 52 (13): 2413–2425. doi:10.1017/S003329172200201X. ISSN 0033-2917. PMID 36016504. PMC 9647517. https://www.cambridge.org/core/journals/psychological-medicine/article/lifetime-and-point-prevalence-of-psychotic-symptoms-in-adults-with-bipolar-disorders-a-systematic-review-and-metaanalysis/31492842FCD4D49E1FDE86B332F062AA.
8. ↑ Shao, Wen; Shao, Kangning; Bentall, Richard P. (2026). "Comorbid Schizophrenia and Psychotic Symptoms in Patients With Bipolar Disorder: A Meta-Analysis of the Global Literature" (in en). Bipolar Disorders 28 (3). doi:10.1111/bdi.70093. ISSN 1399-5618. PMID 41847966. PMC 12997143. https://onlinelibrary.wiley.com/doi/abs/10.1111/bdi.70093.
9. ↑ Moreno, Ricardo Alberto; Moreno, Doris Hupfeld; Ratzke, Roberto (2005). "Diagnóstico, tratamento e prevenção da mania e da hipomania no transtorno bipolar" (in Portuguese). Archives of Clinical Psychiatry (São Paulo) 32: 39–48. doi:10.1590/S0101-60832005000700007. ISSN 1806-938X. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-60832005000700007&lng=pt&nrm=iso&tlng=en. Retrieved 2025-12-09.
10. ↑ Brondolo, Elizabeth; Amador, Xavier (2008). Break the Bipolar Cycle: A Day by Day Guide to Living with Bipolar Disorder. New York: McGraw Hill Professional. pp. 11. ISBN 978-0-07-148153-3. https://archive.org/details/breakbipolarcycl00bron/page/11.
11. ↑ NAMI (July 2007). "The many faces & facets of BP". http://www.nami.org/Content/ContentGroups/bp_and_Schizophrenia_Digest/The_Many_Faces_and_Facets_of_BP.htm.
12. ↑ Christa L. Taylor (September 2017). "Creativity and Mood Disorder: A Systematic Review and Meta-Analysis". Perspectives on Psychological Science 12 (6): 1040–1076. doi:10.1177/1745691617699653. PMID 28934560. https://journals.sagepub.com/doi/full/10.1177/1745691617699653. Retrieved 2022-02-25.
13. ↑ Soares, Jair; Walss-Bass, Consuelo; Brambilla, Paolo (2018). Bipolar Disorder Vulnerability: Perspectives from Pediatric and High-Risk Populations. London: Academic Press. p. 218. ISBN 978-0-12-812347-8.
14. ↑ 14.0 14.1 Doran, Christopher M. (2007). The Hypomania Handbook: The Challenge of Elevated Mood. Philadelphia. PA: Lippincott Williams & Wilkins. p. 75. ISBN 978-0-7817-7520-5.
15. ↑ "Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency". Israeli Medical Association Journal 3: 701–703. 2001. http://www.ima.org.il/imaj/dynamic/web/ArtFromPubmed.asp?year=2001&month=09&page=701. Retrieved 2009-09-12.
16. ↑ MedlinePlus Encyclopedia Hyperthyroidism
17. ↑ Hyperthyroidism at eMedicine
18. ↑ "DSM-5 Update: Supplement to Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition". American Psychiatric Association Publishing. September 2016. http://psychiatryonline.org/pb-assets/dsm/update/DSM5Update2016.pdf.
19. ↑ 19.0 19.1 19.2 "Manic Episode". https://www.behavenet.com/manic-episode.
20. ↑ DSM-IV
21. ↑ AJ Giannini. Biological Foundations of Clinical Psychiatry, NY Medical Examination Publishing Company, 1986.
22. ↑ Lakshmi N. Ytham, Vivek Kusumakar, Stanley P. Kutchar. (2002). Bipolar Disorder: A Clinician's Guide to Biological Treatments, page 3.
23. ↑ "High-risk behaviour in hypomanic states". J Affect Disord 150 (1): 50–6. 2013. doi:10.1016/j.jad.2013.02.018. PMID 23489397.
24. ↑ "Suicide attempts and psychological risk factors in patients with bipolar and unipolar affective disorder". Gen Hosp Psychiatry 35 (3): 309–13. 2013. doi:10.1016/j.genhosppsych.2012.11.010. PMID 23352318.
25. ↑ 25.0 25.1 Dailey, Mark W.; Saadabadi, Abdolreza (2023), "Mania", StatPearls (Treasure Island (FL): StatPearls Publishing), PMID 29630220, https://www.ncbi.nlm.nih.gov/books/NBK493168/, retrieved 2023-12-29
26. ↑ Salvadore, Giacomo; Quiroz, Jorge A.; Machado-Vieira, Rodrigo; Henter, Ioline D.; Manji, Husseini K.; Zarate, Carlos A. (Nov 2010). "The Neurobiology of the Switch Process in Bipolar Disorder: a Review". The Journal of Clinical Psychiatry 71 (11): 1488–1501. doi:10.4088/JCP.09r05259gre. ISSN 0160-6689. PMID 20492846.
27. ↑ Sharma, AN; Fries, GR; Galvez, JF; Valvassori, SS; Soares, JC; Carvalho, AF; Quevedo, J (3 April 2016). "Modeling mania in preclinical settings: A comprehensive review.". Progress in Neuro-Psychopharmacology & Biological Psychiatry 66: 22–34. doi:10.1016/j.pnpbp.2015.11.001. PMID 26545487.
28. ↑ Santos, Catarina O.; Caeiro, Lara; Ferro, José M.; Figueira, M. Luísa (2011). "Mania and Stroke: A Systematic Review". Cerebrovascular Diseases 32 (1): 11–21. doi:10.1159/000327032. PMID 21576938.
29. ↑ Braun, CM; Larocque, C; Daigneault, S; Montour-Proulx, I (January 1999). "Mania, pseudomania, depression, and pseudodepression resulting from focal unilateral cortical lesions.". Neuropsychiatry, Neuropsychology & Behavioral Neurology 12 (1): 35–51. ISSN 0894-878X. PMID 10082332.
30. ↑ Chopra, Amit; Tye, Susannah J.; Lee, Kendall H.; Sampson, Shirlene; Matsumoto, Joseph; Adams, Andrea; Klassen, Bryan; Stead, Matt et al. (January 2012). "Underlying Neurobiology and Clinical Correlates of Mania Status After Subthalamic Nucleus Deep Brain Stimulation in Parkinson's Disease: A Reviews of the Literature". The Journal of Neuropsychiatry and Clinical Neurosciences 24 (1): 102–110. doi:10.1176/appi.neuropsych.10070109. ISSN 0895-0172. PMID 22450620.
31. ↑ Krauthammer, C. (1978). Secondary Mania. Archives of General Psychiatry, 35(11), 1333. doi:10.1001/archpsyc.1978.01770350059005.
32. ↑ "Spring Mania—Deciding If It's Time for Action" (in en-US). 2023-04-05. https://www.bphope.com/blog/spring-mania/.
33. ↑ "Spring Mania: A Different Kind of Spring Fever" (in en-US). https://www.psychologytoday.com/us/blog/a-different-kind-of-therapy/202403/spring-mania-a-different-kind-of-spring-fever.
34. ↑ Eskinazi, Mickael; Nasserdine, Rayan; Cusin, Romane M.; Baniotoupoulos, Pantelis; Saccaro, Luigi F.; De Pieri, Marco; Corino, Tamara; Seragnoli, Federico et al. (May 2026). "Psychedelic-induced hypomania and mania: a systematic review and meta-analysis" (in en). Molecular Psychiatry: 1–15. doi:10.1038/s41380-026-03657-6. ISSN 1476-5578. https://www.nature.com/articles/s41380-026-03657-6.
35. ↑ Clark, L; Sahakian, BJ (2008). "Cognitive neuroscience and brain imaging in bipolar disorder.". Dialogues in Clinical Neuroscience 10 (2): 153–63. doi:10.31887/DCNS.2008.10.2/lclark. PMID 18689286.
36. ↑ 36.0 36.1 Arnsten, AFT; Manji, HK; Haberland, G (March 2008). "Mania: a rational neurobiology". Future Neurology 3 (2): 125–131. doi:10.2217/14796708.3.2.125.
37. ↑ "Regulation of glycogen synthase kinase-3 during bipolar mania treatment". Bipolar Disord 12 (7): 741–52. 2010. doi:10.1111/j.1399-5618.2010.00866.x. PMID 21040291.
38. ↑ Goodman, Brunton L, Chabner B, Knollman B (2011). Goodman Gilman's pharmacological basis of therapeutics (Twelfth ed.). New York: McGraw-Hill Professional. ISBN 978-0-07-162442-8.
39. ↑ Chen, CH; Suckling, J; Lennox, BR; Ooi, C; Bullmore, ET (February 2011). "A quantitative meta-analysis of fMRI studies in bipolar disorder.". Bipolar Disorders 13 (1): 1–15. doi:10.1111/j.1399-5618.2011.00893.x. PMID 21320248.
40. ↑ Strakowski, SM; Adler, CM; Almeida, J; Altshuler, LL; Blumberg, HP; Chang, KD; DelBello, MP; Frangou, S et al. (June 2012). "The functional neuroanatomy of bipolar disorder: a consensus model.". Bipolar Disorders 14 (4): 313–25. doi:10.1111/j.1399-5618.2012.01022.x. PMID 22631617.
41. ↑ Phillips, ML; Swartz, HA (August 2014). "A critical appraisal of neuroimaging studies of bipolar disorder: toward a new conceptualization of underlying neural circuitry and a road map for future research.". The American Journal of Psychiatry 171 (8): 829–43. doi:10.1176/appi.ajp.2014.13081008. PMID 24626773.
42. ↑ Braun, CM; Larocque, C; Daigneault, S; Montour-Proulx, I (January 1999). "Mania, pseudomania, depression, and pseudodepression resulting from focal unilateral cortical lesions.". Neuropsychiatry, Neuropsychology & Behavioral Neurology 12 (1): 35–51. PMID 10082332.
43. ↑ Gawryluk, J; Young, T. "Signal Transduction Pathways in the Pathophysiology of Bipolar Disorder". in Manji, H; Zarate, C. Behavioral Neurobiology of Bipolar Disorder And its Treatment. Springer. pp. 151–152.
44. ↑ MANJI, HUSSEINI K; QUIROZ, JORGE A; PAYNE, JENNIFER L; SINGH, JASKARAN; LOPES, BARBARA P; VIEGAS, JENILEE S; ZARATE, CARLOS A (Oct 2003). "The underlying neurobiology of bipolar disorder". World Psychiatry 2 (3): 136–146. ISSN 1723-8617. PMID 16946919.
45. ↑ Nusslock, Robin; Young, Christina B.; Damme, Katherine S. F. (1 November 2014). "Elevated reward-related neural activation as a unique biological marker of bipolar disorder: assessment and treatment implications". Behaviour Research and Therapy 62: 74–87. doi:10.1016/j.brat.2014.08.011. ISSN 1873-622X. PMID 25241675.
46. ↑ Rolls, ET (September 2016). "A non-reward attractor theory of depression.". Neuroscience and Biobehavioral Reviews 68: 47–58. doi:10.1016/j.neubiorev.2016.05.007. PMID 27181908. http://wrap.warwick.ac.uk/80548/1/WRAP_Rolls_depression16c.pdf. Retrieved 2018-12-19.
47. ↑ "Organic Causes of Mania". September 1988. https://www.mayoclinicproceedings.org/article/S0025-6196(12)62694-9/pdf.
48. ↑ Dailey, Mark W.; Saadabadi, Abdolreza (2023-07-17), "Mania", StatPearls (Treasure Island (FL): StatPearls Publishing), PMID 29630220, http://www.ncbi.nlm.nih.gov/books/NBK493168/, retrieved 2026-03-28
49. ↑ Jauhar, Sameer; Alexandre Wong, Sui Liem (2024). "An Update on the Treatment of Manic and Hypomanic States". Clinical Textbook of Mood Disorders. Cambridge University Press. pp. 206–212. doi:10.1017/9781108973922.021. ISBN 978-1-108-97827-9. https://www.cambridge.org/core/books/abs/clinical-textbook-of-mood-disorders/an-update-on-the-treatment-of-manic-and-hypomanic-states/E698A43E697473E93EF93238F238BE46.
50. ↑ Kane, Nuala B (October 2024). "What it is like to be manic: a response to Director" (in en). Journal of Medical Ethics 50 (10): 716–717. doi:10.1136/jme-2024-110032. ISSN 0306-6800. https://jme.bmj.com/lookup/doi/10.1136/jme-2024-110032.
51. ↑ Director, Samuel (September 2025). "Defending manic competence: a reply to Kane" (in en). Journal of Medical Ethics 51 (9): 653–654. doi:10.1136/jme-2025-110744. ISSN 0306-6800. PMID 39965908. https://jme.bmj.com/lookup/doi/10.1136/jme-2025-110744.
52. ↑ Beckett, Jonathan; Chaplin, Robert (November 2006). "Capacity to consent to treatment in patients with acute mania" (in en). Psychiatric Bulletin 30 (11): 419–422. doi:10.1192/pb.30.11.419. ISSN 0955-6036. https://www.cambridge.org/core/journals/psychiatric-bulletin/article/capacity-to-consent-to-treatment-in-patients-with-acute-mania/0787195B4D6CF3B7022C79A6BFEE535D.
53. ↑ "Chapter Six: From provisions to practice: implementing the Convention – Legal capacity and supported decision-making | United Nations Enable". https://www.un.org/development/desa/disabilities/resources/handbook-for-parliamentarians-on-the-convention-on-the-rights-of-persons-with-disabilities/chapter-six-from-provisions-to-practice-implementing-the-convention-5.html.
54. ↑ Pacchiarotti, I.; Anmella, G.; Colomer, L.; Vieta, E. (September 2020). "How to treat mania" (in en). Acta Psychiatrica Scandinavica 142 (3): 173–192. doi:10.1111/acps.13209. ISSN 0001-690X. PMID 33460070. https://onlinelibrary.wiley.com/doi/10.1111/acps.13209. Retrieved 2022-04-20.
55. ↑ "FDA Approves Fanapt for Mixed, Manic Episodes Associated With Bipolar I Disorder" (in en). 2024-04-02. https://www.psychiatrictimes.com/view/fda-approves-fanapt-for-mixed-manic-episodes-associated-with-bipolar-i-disorder.
56. ↑ Tohen, Mauricio; Vieta, Eduard (2009). "Antipsychotic agents in the treatment of bipolar mania". Bipolar Disorders 11 (s2): 45–54. doi:10.1111/j.1399-5618.2009.00710.x. ISSN 1399-5618. PMID 19538685.
57. ↑ Jawad, Ibrahim; Watson, Stuart; Haddad, Peter M; Talbot, Peter S; McAllister-Williams, R Hamish (2018-12-01). "Medication nonadherence in bipolar disorder: a narrative review". Therapeutic Advances in Psychopharmacology 8 (12): 349–363. doi:10.1177/2045125318804364. ISSN 2045-1261. PMID 30524703.
58. ↑ Cappleman, Reed; Smith, Ian; Lobban, Fiona (2015-03-15). "Managing bipolar moods without medication: A qualitative investigation". Journal of Affective Disorders 174: 241–249. doi:10.1016/j.jad.2014.11.055. ISSN 0165-0327. PMID 25527994. https://www.sciencedirect.com/science/article/pii/S0165032714007794.
59. ↑ Novick, Danielle M.; Swartz, Holly A. (2019). "Evidence-Based Psychotherapies for Bipolar Disorder". Focus: Journal of Life Long Learning in Psychiatry 17 (3): 238–248. doi:10.1176/appi.focus.20190004. ISSN 1541-4094. PMID 32047369.
60. ↑ "Long-term lithium therapy for bipolar disorder: systematic review and meta-analysis of randomized controlled trials.". The American Journal of Psychiatry 161 (2): 217–22. February 2004. doi:10.1176/appi.ajp.161.2.217. PMID 14754766.
61. ↑ Nierenberg AA (2010). "A critical appraisal of treatments for bipolar disorder". Primary Care Companion to the Journal of Clinical Psychiatry 12 (Suppl 1): 23–29. doi:10.4088/PCC.9064su1c.04. PMID 20628503.
62. ↑ Behrman, Andy (2002). Electroboy: A Memoir of Mania. Random House Trade Paperbacks. pp. Preface: Flying High. ISBN 978-0-8129-6708-1.
63. ↑ Johnson, Sheri L.; Murray, Greg; Fredrickson, Barbara; Youngstrom, Eric A.; Hinshaw, Stephen; Bass, Julie Malbrancq; Deckersbach, Thilo; Schooler, Jonathan et al. (February 2012). "Creativity and bipolar disorder: Touched by fire or burning with questions?". Clinical Psychology Review 32 (1): 1–12. doi:10.1016/j.cpr.2011.10.001. ISSN 0272-7358. PMID 22088366.
64. ↑ Nolen-Hoeksema, Susan (2014). Abnormal psychology (Sixth ed.). McGraw Hill Education. p. 184. ISBN 978-0-07-803538-8.
65. ↑ 65.0 65.1 "Stephen Fry: My battle with mental illness". The Independent. https://www.independent.co.uk/life-style/health-and-families/health-news/stephen-fry-my-battle-with-mental-illness-416386.html.
66. ↑ "Stephen Fry: my battle with manic depression". The Guardian. https://www.theguardian.com/society/2006/jul/21/mentalhealth.broadcasting.
67. ↑ μανία , Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus Digital Library
68. ↑ μαίνομαι, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus Digital Library

## Further reading

* Expert Opin Pharmacother. 2001 December;2(12):1963–73.
* Schizoaffective Disorder . 2007 September Mayo Clinic. Retrieved October 1, 2007.
* Schizoaffective Disorder . 2004 May. All Psych Online: Virtual Psychology Classroom. Retrieved October 2, 2007.
* Psychotic Disorders. 2004 May. All Psych Online: Virtual Psychology Classroom. Retrieved October 2, 2007.
* Sajatovic, Martha; DiBiovanni, Sue Kim; Bastani, Bijan; Hattab, Helen; Ramirez, Luis F. (1996). "Risperidone therapy in treatment refractory acute bipolar and schizoaffective mania". Psychopharmacology Bulletin 32 (1): 55–61. PMID 8927675.

## External links

* Depression and Bipolar Support Alliance

Classification|

* ICD-11: 6A60.0, 6A60.1, 6E62.1, 6A25.3
* ICD-10: F30.1, F30.2, F30.8, F30.9, F31.1, F31.2
* ICD-10-CM: F06.30
* ICD-9-CM: 296.0, 296.4, 296.6
* MeSH: D001714

|

* v
* t
* e

Mood disorder (F30–F39, 296)

History|

* Emil Kraepelin
* Karl Leonhard
* John Cade
* Mogens Schou
* Frederick K. Goodwin
* Kay Redfield Jamison

Symptoms|

* Hallucination
* Delusion
* Emotional dysregulation
* Anhedonia
* Dysphoria
* Suicidal ideation
* Mood swing
* Sleep disorder
* Hypersomnia
* Insomnia
* Psychosis
* Racing thoughts
* Reduced affect display
* Depression (differential diagnoses)

Spectrum|

* Bipolar disorder
* Bipolar I
* Bipolar II
* Cyclothymia
* Bipolar NOS
* Depression
* Major depressive disorder
* Dysthymia
* Seasonal affective disorder
* Atypical depression
* Melancholic depression
* Schizoaffective disorder
* Mania
* Mixed affective state
* Hypomania
* Major depressive episode
* Rapid cycling

Treatment|

| Anticonvulsants|

* Carbamazepine
* Lamotrigine
* Oxcarbazepine
* Valproate
* Sodium valproate
* Valproate semisodium

|

Sympathomimetics,
SSRIs & similar|

* Dextroamphetamine
* Methylphenidate
* Bupropion
* Sertraline
* Fluoxetine
* Escitalopram

Other mood stabilizers|

* Antipsychotics
* Lithium
* Lithium carbonate
* Lithium citrate
* Lithium sulfate
* Lithium toxicity
* Atypical antipsychotics

Non-pharmaceutical|

* Clinical psychology
* Electroconvulsive therapy
* Involuntary commitment
* Light therapy
* Psychotherapy
* Transcranial magnetic stimulation
* Cognitive behavioral therapy
* Dialectical behavior therapy

* v
* t
* e

Mental and behavioral disorders (F00–F99 & 290–319)

Adult personality and behavior

| Gender dysphoria|

* Ego-dystonic sexual orientation
* Paraphilia
* Fetishism
* Voyeurism
* Sexual maturation disorder
* Sexual relationship disorder

|

Other|

* Factitious disorder
* Munchausen syndrome
* Impulse control disorder
* Dermatillomania
* Kleptomania
* Pyromania
* Trichotillomania
* Personality disorder

Childhood and learning

| Emotional and behavioral|

* ADHD
* Conduct disorder
* ODD
* Emotional and behavioral disorders
* Separation anxiety disorder
* Movement disorders
* Stereotypic
* Social functioning
* DAD
* RAD
* Selective mutism
* Speech
* Stuttering
* Cluttering
* Tic disorder
* Tourette syndrome

|

Intellectual disability|

* X-linked intellectual disability
* Lujan–Fryns syndrome

Psychological development
(developmental disabilities)|

* Pervasive
* Specific

Mood (affective)

* Bipolar
* Bipolar I
* Bipolar II
* Bipolar NOS
* Cyclothymia
* Depression
* Atypical depression
* Dysthymia
* Major depressive disorder
* Melancholic depression
* Seasonal affective disorder
* Mania

Neurological and symptomatic

| Autism spectrum|

* Autism
* Asperger syndrome
* High-functioning autism
* PDD-NOS
* Savant syndrome

|

Dementia|

* AIDS dementia complex
* Alzheimer's disease
* Creutzfeldt–Jakob disease
* Frontotemporal dementia
* Huntington's disease
* Mild cognitive impairment
* Parkinson's disease
* Pick's disease
* Sundowning
* Vascular dementia
* Wandering

Other|

* Delirium
* Organic brain syndrome
* Post-concussion syndrome

Neurotic, stress-related and somatoform

| Adjustment|

* Adjustment disorder with depressed mood

|

Anxiety|

| Phobia|

* Agoraphobia
* Social anxiety
* Social phobia
* Anthropophobia
* Specific social phobia
* Specific phobia
* Claustrophobia

|

Other|

* Generalized anxiety disorder
* OCD
* Panic attack
* Panic disorder
* Stress
* Acute stress reaction
* PTSD

Dissociative|

* Depersonalization disorder
* Dissociative identity disorder
* Fugue state
* Psychogenic amnesia

Somatic symptom|

* Body dysmorphic disorder
* Conversion disorder
* Ganser syndrome
* Globus pharyngis
* Da Costa's syndrome
* Hypochondriasis
* Mass psychogenic illness
* Neurasthenia
* Nosophobia
* Psychalgia
* Somatization disorder

Physiological and physical behavior

| Eating|

* Anorexia nervosa
* Bulimia nervosa
* Rumination syndrome
* Other specified feeding or eating disorder

|

Nonorganic
sleep|

* Hypersomnia
* Insomnia
* Parasomnia
* Night terror
* Nightmare
* REM sleep behavior disorder

Postnatal|

* Postpartum depression
* Postpartum psychosis

Sexual dysfunction|

| Arousal|

* Erectile dysfunction
* Female sexual arousal disorder

|

Desire|

* Hypersexuality
* Hypoactive sexual desire disorder

Orgasm|

* Anorgasmia
* Delayed ejaculation
* Premature ejaculation
* Sexual anhedonia

Pain|

* Nonorganic dyspareunia
* Nonorganic vaginismus

Psychoactive substances, substance abuse and substance-related

* Drug overdose
* Intoxication
* Physical dependence
* Rebound effect
* Stimulant psychosis
* Substance dependence
* Withdrawal

Schizophrenia, schizotypal and delusional

| Delusional|

* Delusional disorder
* Folie à deux

|

Psychosis and
schizophrenia-like|

* Brief reactive psychosis
* Schizoaffective disorder
* Schizophreniform disorder

Schizophrenia|

* Childhood schizophrenia
* Disorganized (hebephrenic) schizophrenia
* Paranoid schizophrenia
* Pseudoneurotic schizophrenia
* Simple-type schizophrenia

Symptoms and uncategorized

* Catatonia
* False pregnancy
* Intermittent explosive disorder
* Klüver–Bucy syndrome
* Psychogenic non-epileptic seizures
* Psychomotor agitation
* Stereotypy

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