In amixed affective state, the individual, though meeting the general criteria for ahypomanic (discussed below) or manic episode, experiences three or more concurrentdepressive 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 forsuicide.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 onsuicidal impulses.
Hypomania, which means "less than mania",[7] is a lowered state of mania that does not always impair function or decrease quality of life.[8] Althoughcreativity 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.[9] 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.[10] Though the elevated mood and energy level typical of hypomania could be seen positively, mania itself generally has many undesirable consequences, includingsuicidal tendencies. Hypomania can also have these effects, if the prominent mood isirritable as opposed toeuphoric. 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,[11] exaggerated in hypomania, such a person can display excessiveoptimism,grandiosity, and poor decision-making, often with little regard to the consequences.[11]
Evidence indicates avitamin B12 deficiency can also cause symptoms characteristic of mania and psychosis.[12]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.[13][14]Postpartum psychosis can also cause manic episodes (unipolar mania).
Amanic episode is defined in theAmerican Psychiatric Association'sdiagnostic 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),"[15] 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 haspsychosis.[16]
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:
Excessive involvement in activities with a high likelihood of painful consequences. (e.g., extravagant shopping, improbable commercial schemes,hypersexuality).[16]
Though the activities one participates in while in a manic state are notalways negative, those with the potential to have negative outcomes are more common.
If the person is concurrently depressed, they are said to be having amixed episode.[16]
TheWorld Health Organization'sInternational Classification of Diseases (ICD) definesa manic episode as one where mood is higher than the person's situation warrants and may vary from relaxed high spirits to barely controllable exuberance, 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. Behavior that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.[6]
Some people also have physical symptoms, such assweating, pacing, andweight 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.[17]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.[18]
One of the signature symptoms of mania (and to a lesser extent,hypomania) is what many have described asracing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli.[19] 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 duringeuthymia. 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 eithergrandeur orpersecution, 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.[20][21]
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.[22] Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprivedpsychosis 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 asgregariousness andeuphoria. In stages II and III mania, however, the patient may be extraordinarily irritable,psychotic or evendelirious. These latter two stages are referred to as acute and delirious (or Bell's), respectively.
Various triggers have been associated with switching fromeuthymic or depressed states into mania. One common trigger of mania isantidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69 percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medications possibly includeglutaminergic agents and drugs that alter theHPA axis. Lifestyle triggers include irregular sleep-wake schedules andsleep deprivation, as well as extremely emotional or stressfulstimuli.[23]
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 andDBP 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 asGSK-3, andERK1 have also demonstrated mania like behavior in preclinical models.[24]
Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.[25][26]
Mania can also be caused byphysical trauma orillness. When the causes are physical, it is calledsecondary mania.[29] In some individuals, manic symptoms are also correlated with the season of spring.[30][31]
The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the rightprefrontal cortex, a common finding in neuroimaging studies.[32][33] Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities inGSK-3,[34]dopamine,Protein kinase C, andInositol monophosphatase.[35]
Meta analysis of neuroimaging studies demonstrate increasedthalamic activity, and bilaterally reduced inferiorfrontal gyrus activation.[36] Activity in theamygdala and other subcortical structures such as theventral 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.[37] A bias towardspositively valenced stimuli, and increased responsiveness inreward circuitry may predispose towards mania.[38] Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.[39]
Post-mortem examinations of bipolar disorder demonstrate increased expression ofProtein Kinase C (PKC).[40] While limited, some studies demonstrate manipulation of PKC in animals produces behavioral changes mirroring mania, and treatment with PKC inhibitortamoxifen (also ananti-estrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.[33]
Manic episodes may be triggered bydopamine receptor agonists, and this combined with tentative reports of increasedVMAT2 activity, measured viaPET scans ofradioligand binding, suggestsa role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite5-HIAA have been found in manic patients too, which may be explained by a failure ofserotonergic regulation anddopaminergic hyperactivity.[41]
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 frontalEEG activity with mania. As left frontal EEG activity is generally thought to be a reflection ofbehavioral 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 elevatedorbitofrontal 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.[42] Punishmenthyposensitivity, 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.[43]
In theICD-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 ofschizoaffective disorder (F25.0),bipolar disorder, current episode manic without psychotic symptoms (F31.1), bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).[44]
When the manic behaviours have gone, long-term treatment then focuses onprophylactic treatment to try to stabilize the patient's mood, typically through a combination ofpharmacotherapy andpsychotherapy.[22] The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important 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, includingpsychotherapy, self-help coping strategies, and healthy lifestyle choices.[49][50]
In some cases, long-actingbenzodiazepines, particularlyclonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms,lorazepam, combined withhaloperidol, is used to promptly alleviate symptoms of agitation,aggression, andpsychosis.
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. Someatypical antidepressants, however, such asmirtazapine andtrazodone, have been occasionally used after other options have failed.[52]
InElectroboy: 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."[53] 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 people in the creative industries have bipolar disorder more often than those in other occupations.[54]Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.[55]
English actorStephen Fry, who hasbipolar disorder,[56] 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 theSavoy andRitz and drink cocktails."[57] While he has experiencedsuicidal thoughts, he says the manic side of his condition has had positive contributions on his life.[56]
Thenosology of the various stages of a manic episode has changed over the decades. The word derives from theAncient Greek μανία (manía), "madness, frenzy"[58] and the verb μαίνομαι (maínomai), "to be mad, to rage, to be furious."[59]
^Soares, Jair; Walss-Bass, Consuelo; Brambilla, Paolo (2018).Bipolar Disorder Vulnerability: Perspectives from Pediatric and High-Risk Populations. London: Academic Press. p. 218.ISBN9780128123478.
^abDoran, Christopher M. (2007).The Hypomania Handbook: The Challenge of Elevated Mood. Philadelphia. PA: Lippincott Williams & Wilkins. p. 75.ISBN9780781775205.
^AJ Giannini.Biological Foundations of Clinical Psychiatry, NY Medical Examination Publishing Company, 1986.
^Lakshmi N. Ytham, Vivek Kusumakar, Stanley P. Kutchar. (2002).Bipolar Disorder: A Clinician's Guide to Biological Treatments, page 3.
^Fletcher K, Parker G, Paterson A, Synnott H (2013). "High-risk behaviour in hypomanic states".J Affect Disord.150 (1):50–6.doi:10.1016/j.jad.2013.02.018.PMID23489397.
^Pawlak J, Dmitrzak-Węglarz M, Skibińska M, Szczepankiewicz A, Leszczyńska-Rodziewicz A, Rajewska-Rager A, Maciukiewicz M, Czerski P, Hauser J (2013). "Suicide attempts and psychological risk factors in patients with bipolar and unipolar affective disorder".Gen Hosp Psychiatry.35 (3):309–13.doi:10.1016/j.genhosppsych.2012.11.010.PMID23352318.
^abDailey, Mark W.; Saadabadi, Abdolreza (2023),"Mania",StatPearls, Treasure Island (FL): StatPearls Publishing,PMID29630220,archived from the original on 2024-01-11, retrieved2023-12-29
^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.PMID10082332.
^Gawryluk, J; Young, T. "Signal Transduction Pathways in the Pathophysiology of Bipolar Disorder". In Manji, H; Zarate, C (eds.).Behavioral Neurobiology of Bipolar Disorder And its Treatment. Springer. pp. 151–152.
^Melinda Smith; Lawrence Robinson; Jeanne Segal; Damon Ramsey (1 March 2012)."The Bipolar Medication Guide". HelpGuide.org. Archived fromthe original on 10 March 2012. Retrieved23 March 2012.
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.PMID8927675.
