Editing Mania (section)

==Causes==
Various triggers have been associated with switching from [[Euthymia (medicine)|euthymic]] or depressed states into mania. One common trigger of mania is [[antidepressant]] 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 include [[Glutamate|glutaminergic]] agents and drugs that alter the [[Hypothalamic–pituitary–adrenal axis|HPA axis]]. Lifestyle triggers include irregular sleep-wake schedules and [[sleep deprivation]], as well as extremely emotional or stressful [[Stimulus (psychology)|stimuli]].<ref>{{cite journal|last1=Salvadore|first1=Giacomo|last2=Quiroz|first2=Jorge A.|last3=Machado-Vieira|first3=Rodrigo|last4=Henter|first4=Ioline D.|last5=Manji|first5=Husseini K.|last6=Zarate|first6=Carlos A.|title=The Neurobiology of the Switch Process in Bipolar Disorder: a Review|journal=The Journal of Clinical Psychiatry|date=Nov 2010|volume=71|issue=11|pages=1488–1501|doi=10.4088/JCP.09r05259gre|issn=0160-6689|pmc=3000635|pmid=20492846}}</ref>

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 (gene)|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 [[MAPK3|ERK1]] have also demonstrated mania like behavior in preclinical models.<ref>{{cite journal|last1=Sharma|first1=AN|last2=Fries|first2=GR|last3=Galvez|first3=JF|last4=Valvassori|first4=SS|last5=Soares|first5=JC|last6=Carvalho|first6=AF|last7=Quevedo|first7=J|title=Modeling mania in preclinical settings: A comprehensive review.|journal=Progress in Neuro-Psychopharmacology & Biological Psychiatry|date=3 April 2016|volume=66|pages=22–34|doi=10.1016/j.pnpbp.2015.11.001|pmid=26545487|pmc=4728043}}</ref>

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.<ref>{{cite journal|last1=Santos|first1=Catarina O.|last2=Caeiro|first2=Lara|last3=Ferro|first3=José M.|last4=Figueira|first4=M. Luísa|title=Mania and Stroke: A Systematic Review|journal=Cerebrovascular Diseases|date=2011|volume=32|issue=1|pages=11–21|doi=10.1159/000327032|pmid=21576938|doi-access=free}}</ref><ref>{{cite journal|last1=Braun|first1=CM|last2=Larocque|first2=C|last3=Daigneault|first3=S|last4=Montour-Proulx|first4=I|title=Mania, pseudomania, depression, and pseudodepression resulting from focal unilateral cortical lesions.|journal=Neuropsychiatry, Neuropsychology & Behavioral Neurology|date=January 1999|volume=12|issue=1|pages=35–51|pmid=10082332|issn=0894-878X}}</ref>

[[Deep brain stimulation]] of the [[subthalamic nucleus]] in [[Parkinson's disease]] has been associated with mania, especially with electrodes placed in the ventromedial [[Subthalamic nucleus|STN]]. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.<ref>{{cite journal|last1=Chopra|first1=Amit|last2=Tye|first2=Susannah J.|last3=Lee|first3=Kendall H.|last4=Sampson|first4=Shirlene|last5=Matsumoto|first5=Joseph|last6=Adams|first6=Andrea|last7=Klassen|first7=Bryan|last8=Stead|first8=Matt|last9=Fields|first9=Julie A.|last10=Frye|first10=Mark A.|title=Underlying Neurobiology and Clinical Correlates of Mania Status After Subthalamic Nucleus Deep Brain Stimulation in Parkinson's Disease: A Reviews of the Literature|journal=The Journal of Neuropsychiatry and Clinical Neurosciences|date=January 2012|volume=24|issue=1|pages=102–110|doi=10.1176/appi.neuropsych.10070109|pmid=22450620|issn=0895-0172|pmc=3570815}}</ref>

There are certain psychoactive substances that can induce a state of manic psychosis, including: [[amphetamine]], [[cathinone]], [[cocaine]], [[MDMA]], [[methamphetamine]], [[methylphenidate]], [[oxycodone]], [[phencyclidine]], [[designer drug]]s, etc.<ref>{{Cite journal |last1=Peet |first1=M. |last2=Peters |first2=S. |date=February 1995 |title=Drug-induced mania |url=https://pubmed.ncbi.nlm.nih.gov/7766338/ |journal=Drug Safety |volume=12 |issue=2 |pages=146–153 |doi=10.2165/00002018-199512020-00007 |issn=0114-5916 |pmid=7766338 |s2cid=1226279 |access-date=2022-03-16 |archive-date=2022-03-16 |archive-url=https://web.archive.org/web/20220316195200/https://pubmed.ncbi.nlm.nih.gov/7766338/ |url-status=live }}</ref>

Mania can also be caused by [[Major trauma|physical trauma]] or [[Disease|illness]]. When the causes are physical, it is called [[secondary mania]].<ref name="Krauthammer">Krauthammer, C. (1978). Secondary Mania. ''Archives of General Psychiatry'', 35(11), 1333. doi:10.1001/archpsyc.1978.01770350059005.</ref> In some individuals, manic symptoms are also correlated with the season of spring.<ref>{{Cite web |last= |first= |date=2023-04-05 |title=Spring Mania—Deciding If It's Time for Action |url=https://www.bphope.com/blog/spring-mania/ |access-date=2024-04-27 |website=bphope.com |language=en-US |archive-date=2024-04-27 |archive-url=https://web.archive.org/web/20240427051344/https://www.bphope.com/blog/spring-mania/ |url-status=live }}</ref><ref>{{Cite web |title=Spring Mania: A Different Kind of Spring Fever |url=https://www.psychologytoday.com/us/blog/a-different-kind-of-therapy/202403/spring-mania-a-different-kind-of-spring-fever |access-date=2024-04-27 |website=psychologytoday.com |language=en-US}}</ref>