View source for Psychosis

{{Short description|Abnormal condition of the mind}}
{{Other uses}}
{{Distinguish|Psychopathy|Sycosis|Psykotic}}
{{More medical citations needed|date=February 2021}}
{{Infobox medical condition
| name = Psychosis
| synonyms = Psychotic break (''colloquial'')
| field = [[Neurology]], [[psychiatry]], [[emergency medicine]], [[clinical psychology]]
| symptoms = [[Delusion]]s, [[hallucination]]s, incoherent speech and behavior<ref name=NIH2018QA/>
| complications = [[Self-harm]], [[suicide]]<ref name=NHS2016/>
| onset = 
| duration = 
| types = 
| causes = [[Mental illness]] ([[schizophrenia]], [[bipolar disorder]]), [[Psychological trauma|trauma]], [[sleep deprivation]], some medical conditions, certain [[medication]]s, drugs (including [[Alcohol (drug)|alcohol]], [[caffeine]] and [[Cannabis (drug)|cannabis]])<ref name=NIH2018QA/>
| risks = 
| diagnosis = 
| differential = 
| prevention = 
| treatment = [[Antipsychotic]]s, [[counselling]], [[social support]]<ref name=NHS2016/>
| medication = 
| prognosis = Depends on cause<ref name=NHS2016/>
| frequency = 3% of people at some point in their lives (U.S.)<ref name=NIH2018QA/>
| deaths = 
}}
<!-- Definition and symptoms -->

In [[psychopathology]], '''psychosis''' is a condition in which one is unable to distinguish, in one's experience of life, between what is and is not [[Reality|real]].<ref name="Continuum">{{cite journal | vauthors = Arciniegas DB | title = Psychosis | journal = Continuum | volume = 21 | issue = 3 Behavioral Neurology and Neuropsychiatry | pages = 715–736 | date = June 2015 | pmid = 26039850 | pmc = 4455840 | doi = 10.1212/01.CON.0000466662.89908.e7 }}</ref> Examples of psychotic symptoms are [[delusion]]s, [[hallucination]]s, and disorganized or [[thought disorder|incoherent thoughts]] or speech.<ref name="Continuum" /> Psychosis is a description of a person's state or symptoms, rather than a particular [[Mental disorder|mental illness]], and it is not related to [[psychopathy]] (a [[personality]] [[Construct (psychology)|construct]]<ref>{{Cite web |last=Blackburn |first=Ronald |date=2005 |title=Psychopathy as a Personality Construct. |url=https://psycnet.apa.org/record/2005-04993-015 |url-status=live |archive-url=https://web.archive.org/web/20230905192012/https://psycnet.apa.org/record/2005-04993-015 |archive-date=5 September 2023 |access-date=12 June 2024 |website=American Psychiatric Association}}</ref><ref>{{Cite journal |last1=Driessen |first1=Josi M. A. |last2=van Baar |first2=Jeroen M. |last3=Sanfey |first3=Alan G. |last4=Glennon |first4=Jeffrey C. |last5=Brazil |first5=Inti A. |date=July 2021 |title=Moral strategies and psychopathic traits |journal=Journal of Abnormal Psychology |volume=130 |issue=5 |pages=550–561 |doi=10.1037/abn0000675 |issn=1939-1846 |pmid=34472890 |hdl-access=free |hdl=2066/236779}}</ref> characterized by impaired [[empathy]] and [[remorse]], along with [[Boldness|bold]], [[disinhibited]], and [[Egocentrism|egocentric]] traits).

<!-- Causes and diagnosis -->
Common causes of [[Chronic condition|chronic]] (i.e. ongoing or repeating) psychosis include [[schizophrenia]] or [[schizoaffective disorder]], [[bipolar disorder]], and [[Wernicke–Korsakoff syndrome|brain damage]] (usually as a result of [[alcoholism]]).<ref>{{cite journal | vauthors = Radua J, Ramella-Cravaro V, Ioannidis JP, Reichenberg A, Phiphopthatsanee N, Amir T, Yenn Thoo H, Oliver D, Davies C, Morgan C, McGuire P, Murray RM, Fusar-Poli P | display-authors = 6 | title = What causes psychosis? An umbrella review of risk and protective factors | journal = World Psychiatry | volume = 17 | issue = 1 | pages = 49–66 | date = February 2018 | pmid = 29352556 | pmc = 5775150 | doi = 10.1002/wps.20490 }}</ref><ref>{{Cite web |title=Korsakoff Psychosis – Special Subjects |url=https://www.msdmanuals.com/en-in/professional/special-subjects/illicit-drugs-and-intoxicants/korsakoff-psychosis |access-date=2024-04-10 |website=MSD Manual Professional Edition |language=en-IN}}</ref> Acute (temporary) psychosis can also be caused by [[Psychological trauma|severe distress]], [[sleep deprivation]], [[sensory deprivation]],<ref name="Oxford Textbook of Psychiatry">{{Cite book |last1=Gelder |first1=Michael G. |url=https://books.google.com/books?id=pN9rAAAAMAAJ |title=Oxford Textbook of Psychiatry |last2=Gath |first2=Dennis |last3=Mayou |first3=Richard |date=1983 |publisher=Oxford University Press |isbn=978-0-19-261294-6 |language=en}}</ref> some [[medication]]s, and [[Drug|drug use]] (including [[Alcohol (drug)|alcohol]], [[Cannabis (drug)|cannabis]], [[hallucinogen]]s, and [[stimulant]]s).<ref name="Griswold">{{cite journal | vauthors = Griswold KS, Del Regno PA, Berger RC | title = Recognition and Differential Diagnosis of Psychosis in Primary Care | journal = American Family Physician | volume = 91 | issue = 12 | pages = 856–863 | date = June 2015 | pmid = 26131945 | url = https://www.aafp.org/afp/2015/0615/p856.html | access-date = 2021-12-06 | archive-date = 2021-02-22 | archive-url = https://web.archive.org/web/20210222162048/https://www.aafp.org/afp/2015/0615/p856.html | url-status = live }}</ref> Acute psychosis is termed primary if it results from a psychiatric condition and secondary if it is caused by another medical condition or drugs.<ref name="Griswold" /> The diagnosis of a mental-health condition requires excluding other potential causes.<ref>{{cite book | vauthors = Cardinal RN, Bullmore ET |title=The Diagnosis of Psychosis |date=2011 |publisher=Cambridge University Press |isbn=978-1-139-49790-9 |page=279 |url=https://books.google.com/books?id=wE3FXgW9gDkC&pg=PA279 |language=en |access-date=2020-06-25 |archive-date=2020-08-06 |archive-url=https://web.archive.org/web/20200806010504/https://books.google.com/books?id=wE3FXgW9gDkC&pg=PA279 |url-status=live }}</ref> Tests can be done to check whether psychosis is caused by [[central nervous system]] diseases, toxins, or other health problems.<ref>{{cite book | vauthors = Foster NL |title=The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry |date=2011 |publisher=American Psychiatric Pub |isbn=978-1-58562-952-7 |page=523 |url=https://books.google.com/books?id=c52vBAAAQBAJ&pg=PA523 |language=en |access-date=2020-06-25 |archive-date=2020-08-19 |archive-url=https://web.archive.org/web/20200819021425/https://books.google.com/books?id=c52vBAAAQBAJ&pg=PA523 |url-status=live }}</ref>

<!-- Treatment and epidemiology -->
Treatment may include [[antipsychotic medication]], [[psychotherapy]], and [[social support]].<ref name="NIH2018QA">{{cite web|title=RAISE Questions and Answers|url=https://www.nimh.nih.gov/health/topics/schizophrenia/raise/raise-questions-and-answers.shtml|archive-url=https://web.archive.org/web/20191008203120/https://www.nimh.nih.gov/health/topics/schizophrenia/raise/raise-questions-and-answers.shtml|archive-date=8 October 2019|access-date=23 January 2018|website=NIMH|language=en}}</ref><ref name="NHS2016" /> Early treatment appears to improve outcomes.<ref name="NIH2018QA" /> Medications appear to have a moderate effect.<ref>{{cite journal | vauthors = Haddad PM, Correll CU | title = The acute efficacy of antipsychotics in schizophrenia: a review of recent meta-analyses | journal = Therapeutic Advances in Psychopharmacology | volume = 8 | issue = 11 | pages = 303–318 | date = November 2018 | pmid = 30344997 | pmc = 6180374 | doi = 10.1177/2045125318781475 }}</ref> Outcomes depend on the underlying cause.<ref name="NHS2016">{{cite web|title=Psychosis|url=https://www.nhs.uk/conditions/psychosis/|website=NHS|access-date=24 January 2018|date=23 December 2016|archive-date=15 October 2018|archive-url=https://web.archive.org/web/20181015043847/https://www.nhs.uk/Conditions/Psychosis/Pages/Prevention-OLD.aspx|url-status=live}}</ref>

Psychosis is not well-understood at the [[neurological]] level, but [[dopamine]] (along with other [[neurotransmitter]]s) is known to play an important role.<ref>{{cite journal | vauthors = Stahl SM | title = Beyond the dopamine hypothesis of schizophrenia to three neural networks of psychosis: dopamine, serotonin, and glutamate | journal = CNS Spectrums | volume = 23 | issue = 3 | pages = 187–191 | date = June 2018 | pmid = 29954475 | doi = 10.1017/S1092852918001013 | s2cid = 49599226 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Grace AA | title = Dysregulation of the dopamine system in the pathophysiology of schizophrenia and depression | journal = Nature Reviews. Neuroscience | volume = 17 | issue = 8 | pages = 524–532 | date = August 2016 | pmid = 27256556 | pmc = 5166560 | doi = 10.1038/nrn.2016.57 }}</ref><ref>{{cite journal | vauthors = Leucht S, Leucht C, Huhn M, Chaimani A, Mavridis D, Helfer B, Samara M, Rabaioli M, Bächer S, Cipriani A, Geddes JR, Salanti G, Davis JM | display-authors = 6 | title = Sixty Years of Placebo-Controlled Antipsychotic Drug Trials in Acute Schizophrenia: Systematic Review, Bayesian Meta-Analysis, and Meta-Regression of Efficacy Predictors | journal = The American Journal of Psychiatry | volume = 174 | issue = 10 | pages = 927–942 | date = October 2017 | pmid = 28541090 | doi = 10.1176/appi.ajp.2017.16121358 | s2cid = 27256686 | doi-access = free }}</ref> In the United States about 3% of people develop psychosis at some point in their lives.<ref name="NIH2018QA" /> Psychosis has been described as early as the 4th century BC by [[Hippocrates]] and possibly as early as 1500 BC in the [[Ebers Papyrus]].<ref>{{cite book| vauthors = Gibbs RS |title=Danforth's Obstetrics and Gynecology|date=2008|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-6937-2 |page=508 |url= https://books.google.com/books?id=v4krPhqFG8sC&pg=PA508 }}</ref><ref>{{cite book| vauthors = Giddens JF |title=Concepts for Nursing Practice – E-Book|date=2015|publisher=Elsevier Health Sciences|isbn=978-0-323-38946-4|page=348|url=https://books.google.com/books?id=lB-KCwAAQBAJ&pg=PA348|access-date=2020-06-25|archive-date=2020-08-19|archive-url=https://web.archive.org/web/20200819141258/https://books.google.com/books?id=lB-KCwAAQBAJ&pg=PA348|url-status=live}}</ref> 
{{TOC limit|3}}

== Signs and symptoms ==

=== Hallucinations ===
A [[hallucination]] is defined as a sensory perception in the absence of external stimuli.<ref name=":9">{{Cite journal |last1=Zmigrod |first1=Leor |last2=Garrison |first2=Jane R. |last3=Carr |first3=Joseph |last4=Simons |first4=Jon S. |date=2016-10-01 |title=The neural mechanisms of hallucinations: A quantitative meta-analysis of neuroimaging studies |url=https://www.sciencedirect.com/science/article/pii/S0149763415302669 |journal=Neuroscience & Biobehavioral Reviews |volume=69 |pages=113–123 |doi=10.1016/j.neubiorev.2016.05.037 |pmid=27473935 |issn=0149-7634 |quote=A hallucination has been formally defined as a "sensory experience which occurs in the absence of corresponding external stimulation of the relevant sensory organ, has a sufficient sense of reality to resemble a veridical perception, over which the subject does not feel they have direct and voluntary control, and which occurs in the awake state" (David, 2004).}}</ref> Hallucinations are different from [[illusion]]s and perceptual distortions, which are the misperception of external stimuli.<ref>{{Cite journal |last1=Barodawala |first1=S. |last2=Mulley |first2=G. P. |date=1997 |title=Visual hallucinations |journal=Journal of the Royal College of Physicians of London |volume=31 |issue=1 |pages=42–48 |doi=10.1016/S0035-8819(25)00268-5 |issn=0035-8819 |pmc=5420857 |pmid=9044197}}</ref><ref>{{Cite journal |last1=Hyatt |first1=Erica |last2=Blom |first2=Jan Dirk |date=2024 |title=Perceptual distortions characteristic of Alice in Wonderland syndrome in contemporary figurative painting |journal=Frontiers in Psychiatry |volume=15 |article-number=1466666 |doi=10.3389/fpsyt.2024.1466666 |doi-access=free |issn=1664-0640 |pmc=11652831 |pmid=39698212 |quote=AIWS is a neurological condition characterized by phenomena known as perceptual distortions. These differ from hallucinations (where something is perceived that is not there) and illusions (where an existing object is perceived as something else) [...]}}</ref> Hallucinations may occur in any of the senses and take on almost any form. They may consist of simple sensations (such as lights, colors, sounds, tastes, or smells) or more detailed experiences (such as seeing and interacting with animals and people, [[Auditory verbal hallucinations|hearing voices]], and having complex tactile sensations). Hallucinations are generally characterized as being vivid and uncontrollable.<ref name=":9" /><ref name="DSM"/> [[Auditory hallucination]]s, particularly experiences of hearing voices, are the most common and often prominent feature of psychosis.

Up to 15% of the general population may experience auditory hallucinations (though not all are due to psychosis).<ref>{{Cite journal |last1=Linszen |first1=Mascha M. J. |last2=de Boer |first2=Janna N. |last3=Schutte |first3=Maya J. L. |last4=Begemann |first4=Marieke J. H. |last5=de Vries |first5=Jacqueline |last6=Koops |first6=Sanne |last7=Blom |first7=Renske E. |last8=Bohlken |first8=Marc M. |last9=Heringa |first9=Sophie M. |last10=Blom |first10=Jan Dirk |last11=Sommer |first11=Iris E. C. |date=2022-04-23 |title=Occurrence and phenomenology of hallucinations in the general population: A large online survey |journal=Schizophrenia (Heidelberg, Germany) |volume=8 |issue=1 |page=41 |doi=10.1038/s41537-022-00229-9 |issn=2754-6993 |pmc=9261095 |pmid=35853871}}</ref> The prevalence of auditory hallucinations in patients with schizophrenia is generally put around 70%.<ref>{{Cite journal |last1=Hugdahl |first1=Kenneth |last2=Løberg |first2=Else-Marie |last3=Specht |first3=Karsten |last4=Steen |first4=Vidar M. |last5=van Wageningen |first5=Heidi |last6=Jørgensen |first6=Hugo A. |date=2007 |title=Auditory hallucinations in schizophrenia: the role of cognitive, brain structural and genetic disturbances in the left temporal lobe |journal=Frontiers in Human Neuroscience |volume=1 |pages=6 |doi=10.3389/neuro.09.006.2007 |doi-access=free |issn=1662-5161 |pmc=2525988 |pmid=18958220 |quote=Auditory hallucinations are among the most common symptoms in schizophrenia, affecting more than 70% of the patients.}}</ref> Reported prevalence in bipolar disorder ranges between 11% and 68%.<ref name="Toh">{{cite journal | vauthors = Toh WL, Thomas N, Rossell SL | title = Auditory verbal hallucinations in bipolar disorder (BD) and major depressive disorder (MDD): A systematic review | journal = Journal of Affective Disorders | volume = 184 | pages = 18–28 | date = September 2015 | pmid = 26066781 | doi = 10.1016/j.jad.2015.05.040 }}</ref> During the early 20th century, auditory hallucinations were second to [[Visual hallucinations in psychosis|visual hallucinations]] in frequency, but they are now the most common manifestation of schizophrenia, although rates vary between cultures and regions. Auditory hallucinations are most commonly intelligible voices. When voices are present, the average number has been estimated at three. Content, like frequency, differs significantly, especially across cultures and demographics. People who experience auditory hallucinations can frequently identify the loudness, location of origin, and may settle on identities for voices. Western cultures are associated with auditory experiences concerning religious content, frequently related to sin. Hallucinations may command a person to do something potentially dangerous when combined with delusions.<ref name="Sadock Psychosis">{{cite book|title=Kaplan and Sadock's Comprehensive Textbook of Psychiatry|vauthors=Lewis S, Escalona R, Keith S|publisher=Wolters Kluwer|year=2017|isbn=978-1-45-110047-1|veditors=Sadock V, Sadock B, Ruiz P|chapter=Phenomenology of Schizophrenia}}</ref>

So-called "minor hallucinations", such as extracampine hallucinations, or false perceptions of people or movement occurring outside of one's visual field, frequently occur in neurocognitive disorders, such as Parkinson's disease.<ref>{{cite journal | vauthors = Lenka A, Pagonabarraga J, Pal PK, Bejr-Kasem H, Kulisvesky J | title = Minor hallucinations in Parkinson disease: A subtle symptom with major clinical implications | journal = Neurology | volume = 93 | issue = 6 | pages = 259–266 | date = August 2019 | pmid = 31289146 | pmc = 6709995 | doi = 10.1212/WNL.0000000000007913 }}</ref>

Visual hallucinations occur in roughly a third of people with schizophrenia, although certain studies show rates higher than 60%, suggesting that the prevelance of visual hallucinatinations may be higher in certain samples than traditionally thought.<ref>{{Cite journal |last1=Silverstein |first1=Steven M. |last2=Lai |first2=Adriann |date=2021 |title=The Phenomenology and Neurobiology of Visual Distortions and Hallucinations in Schizophrenia: An Update |journal=Frontiers in Psychiatry |volume=12 |article-number=684720 |doi=10.3389/fpsyt.2021.684720 |doi-access=free |issn=1664-0640 |pmc=8226016 |pmid=34177665}}</ref> The reported prevalence in bipolar disorder is around 15%.<ref>{{Cite journal |last1=Waters |first1=Flavie |last2=Collerton |first2=Daniel |last3=Ffytche |first3=Dominic H. |last4=Jardri |first4=Renaud |last5=Pins |first5=Delphine |last6=Dudley |first6=Robert |last7=Blom |first7=Jan Dirk |last8=Mosimann |first8=Urs Peter |last9=Eperjesi |first9=Frank |last10=Ford |first10=Stephen |last11=Larøi |first11=Frank |date=July 2014 |title=Visual hallucinations in the psychosis spectrum and comparative information from neurodegenerative disorders and eye disease |journal=Schizophrenia Bulletin |volume=40 Suppl 4 |issue=Suppl 4 |pages=S233–245 |doi=10.1093/schbul/sbu036 |issn=1745-1701 |pmc=4141306 |pmid=24936084 |quote=Psychotic symptoms such as hallucinations and delusions are also a common feature of affective disorders including bipolar disorder. [...] the weighted mean frequency of VH is approximately 15%.}}</ref> Content commonly involves animate objects, although perceptual abnormalities such as changes in lighting, shading, streaks, or lines may be seen. Visual abnormalities may conflict with [[proprioceptive]] information, and visions may include experiences such as the ground tilting. [[Lilliputian hallucinations]] are less common in schizophrenia, and are more common in various types of [[encephalopathy]], such as [[peduncular hallucinosis]].<ref name="Sadock Psychosis"/><ref name="Blom2021">{{cite journal | vauthors = Blom JD | title = Leroy's elusive little people: A systematic review on lilliputian hallucinations | journal = Neurosci Biobehav Rev | volume = 125 | issue = | pages = 627–636 | date = June 2021 | pmid = 33676962 | doi = 10.1016/j.neubiorev.2021.03.002 | url = }}</ref>

A visceral hallucination, also called a cenesthetic hallucination, is characterized by visceral sensations in the absence of stimuli. Cenesthetic hallucinations may include sensations of burning, or re-arrangement of internal organs.<ref name="Sadock Psychosis"/>

=== Delusions ===
A [[delusion]] is a fixed, false, [[Idiosyncrasy|idiosyncratic]] belief, which does not change even when presented with incontrovertible evidence to the contrary.<ref>{{Cite journal |last1=Kiran |first1=Chandra |last2=Chaudhury |first2=Suprakash |date=January 2009 |title=Understanding delusions |journal=Industrial Psychiatry Journal |volume=18 |issue=1 |pages=3–18 |doi=10.4103/0972-6748.57851 |doi-access=free |issn=0972-6748 |pmc=3016695 |pmid=21234155}}</ref><ref name=":13">{{Cite journal |last1=Collin |first1=Sophie |last2=Rowse |first2=Georgina |last3=Martinez |first3=Anton P. |last4=Bentall |first4=Richard P. |date=2023-08-01 |title=Delusions and the dilemmas of life: A systematic review and meta-analyses of the global literature on the prevalence of delusional themes in clinical groups |url=https://www.sciencedirect.com/science/article/pii/S0272735823000612 |journal=Clinical Psychology Review |volume=104 |article-number=102303 |doi=10.1016/j.cpr.2023.102303 |pmid=37390804 |issn=0272-7358|url-access=subscription }}</ref><ref name=":14" /> Delusions are context- and culture-dependent: a belief that inhibits critical functioning and is widely considered delusional in one population may be common (and even adaptive) in another, or in the same population at a later time.<ref name=":14">{{cite book |last1=Joseph |first1=Shawn M. |last2=Siddiqui |first2=Waquar |title=StatPearls |date=2024 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK539855/ |access-date=19 August 2024 |chapter=Delusional Disorder|pmid=30969677 }}</ref><ref>{{cite journal |last1=Ashinoff |first1=Brandon K. |last2=Singletary |first2=Nicholas M. |last3=Baker |first3=Seth C. |last4=Horga |first4=Guillermo |title=Rethinking delusions: A selective review of delusion research through a computational lens |journal=Schizophrenia Research |date=July 2022 |volume=245 |pages=23–41 |doi=10.1016/j.schres.2021.01.023 |pmid=33676820 |pmc=8413395 }}</ref> Since [[Norm (philosophy)|normative]] views may contradict available evidence, a belief need not contravene cultural standards in order to be considered delusional. However, the [[DSM-5]] considers a belief delusional only if it is not widely accepted within a cultural or subcultural context.<ref>{{Citation |title=Schizophrenia Spectrum and Other Psychotic Disorders |date=2013-08-11 |work=DSM-5® Clinical Cases |publisher=American Psychiatric Publishing |doi=10.1176/appi.books.9781585624836.jb02 |isbn=978-1-58562-463-8}}</ref>

Prevalence in schizophrenia is generally considered at least 90%, and around 50% in bipolar disorder.{{Citation needed|date=September 2025}}

The DSM-5 characterizes certain delusions as "bizarre" if they are clearly implausible, or are incompatible with the surrounding cultural context.<ref name=":13" /> The concept of bizarre delusions has many criticisms, the most prominent being that judging their presence is not highly reliable even among trained individuals.<ref name="Sadock Psychosis"/>

A delusion may involve diverse thematic content. The most common type is a [[persecutory delusion]], in which a person believes that an entity seeks to harm them.<ref name=":13" /><ref name=":14" /> Others include [[delusions of reference]] (the belief that some element of one's experience represents a deliberate and specific act by or message from some other entity), [[delusions of grandeur]] (the belief that one possesses special power or influence beyond one's actual limits), [[thought broadcasting]] (the belief that one's thoughts are audible) and [[thought insertion]] (the belief that one's thoughts are not one's own).<ref name=":14" /> A delusion may also involve [[Delusional misidentification syndrome|misidentification]] of objects, persons, or environs that the afflicted should reasonably be able to recognize; such examples include [[Cotard's syndrome]] (the belief that oneself is partly or wholly [[dead]]) and [[clinical lycanthropy]] (the belief that oneself is or has transformed into an animal).{{Citation needed|date=September 2025}}

The subject matter of delusions seems to reflect the current culture in a particular time and location. For example, in the early 1900s in the United States, [[syphilis]] was a common theme in delusions. During the Second World War, it was Germany. In the [[Cold War]] era, communists became a frequent focus. Now, in recent years, technology is a common subject matter of delusions.<ref name="Cannon Kramer pp. 323–327">{{cite journal | vauthors = Cannon BJ, Kramer LM | title = Delusion content across the 20th century in an American psychiatric hospital | journal = The International Journal of Social Psychiatry | volume = 58 | issue = 3 | pages = 323–327 | date = May 2012 | pmid = 21421637 | doi = 10.1177/0020764010396413 | publisher = SAGE Publications | s2cid = 42421925 }}</ref> Some psychologists, such as those who practice the [[Open Dialogue]] method, believe that the content of psychosis represents an underlying thought process, that may in part, be responsible for psychosis,<ref name="Seikkula, Birgitta Alakare, Jukka A 2001 pp. 247–265">{{cite journal| vauthors = Seikkula J, Alakare B, Aaltonen J |title=Open Dialogue in Psychosis I: An Introduction and Case Illustration |journal=Journal of Constructivist Psychology |volume=14 |issue=4 |year=2001 |pages=247–265 |issn=1072-0537|doi=10.1080/10720530125965|s2cid=216136239 }}</ref> though the accepted medical position is that psychosis is due to a brain disorder.<ref>{{Cite journal |last=Saugstad |first=Letten F. |date=June 2008 |title=What is a psychosis and where is it located? |journal=European Archives of Psychiatry and Clinical Neuroscience |volume=258 Suppl 2 |pages=111–117 |doi=10.1007/s00406-008-2014-1 |issn=0940-1334 |pmid=18516523}}</ref>

Historically, [[Karl Jaspers]] classified psychotic delusions into ''primary'' and ''secondary'' types. Primary delusions are defined as arising suddenly and not being comprehensible in terms of normal mental processes, whereas secondary delusions are typically understood as being influenced by the person's background or current situation (e.g., ethnicity, religious, superstitious, or political beliefs).<ref name=Jaspers>{{cite book | vauthors = Jaspers K |author-link=Karl Jaspers | translator-last1 = Hoenig J, Hamilton M | language = German |title=Allgemeine Psychopathologie | trans-title = General Psychopathology |orig-date=1963 | edition = Reprint |date=1997-11-27 |publisher=Johns Hopkins University Press |location=Baltimore, Maryland |isbn=978-0-8018-5775-1}}</ref>

=== Disorganized speech/thought and disorganized behavior ===
Disorganization is categorized into either disorganized speech (disorganized speech stemming from disorganized thought), and grossly disorganized motor behavior. Disorganized speech or thought, also formally called [[thought disorder]], is disorganization of thinking that is ''inferred'' from speech. Characteristics of disorganized speech include rapidly switching topics which is called [[Derailment (thought disorder)|derailment]] or loose [[Association (psychology)|association]], switching to topics that are unrelated which is called [[Tangential speech|tangential thinking]], incomprehensible speech which is called incoherence and referred to as a [[word salad]]. Disorganized motor behavior includes repetitive, odd, or sometimes purposeless movement. Disorganized motor behavior rarely includes [[catatonia]], and although it was a prominent symptom historically, it is rarely seen today. Whether this may be due to the use of historical treatments or the lack thereof is unknown.<ref name="Sadock Psychosis"/><ref name="DSM"/>

Catatonia describes a profoundly agitated state in which the experience of reality is generally considered impaired. There are two primary manifestations of catatonic behavior. The classic presentation is a person who does not move or interact with the world in any way while awake. This type of catatonia presents with [[waxy flexibility]]. Waxy flexibility is when someone physically moves part of a catatonic person's body and the person stays in the position even if it is bizarre and otherwise nonfunctional (such as moving a person's arm straight up in the air and the arm staying there).<ref>{{Cite web |title=Medical Definition of WAXY FLEXIBILITY |url=https://www.merriam-webster.com/medical/waxy+flexibility |access-date=2025-09-03 |website=www.merriam-webster.com |language=en}}</ref>

The other type of catatonia is more of an outward presentation of the profoundly agitated state described above. It involves excessive and purposeless motor behaviour, as well as an extreme mental preoccupation that prevents an intact experience of reality. An example is someone walking very fast in circles to the exclusion of anything else with a level of mental preoccupation (meaning not focused on anything relevant to the situation) that was not typical of the person prior to the symptom onset. In both types of catatonia, there is generally no reaction to anything that happens outside of them. It is important to distinguish catatonic agitation from severe bipolar mania, although someone could have both.{{citation needed|date=July 2025}}

=== Negative symptoms ===
{{See also|Clouding of consciousness|Depression (mood)}}
Negative symptoms include [[Reduced affect display|reduced emotional expression]], [[avolition|decreased motivation]] ([[avolition]]), and [[alogia|reduced spontaneous speech]] (poverty of speech, [[alogia]]). Individuals with this condition lack interest and spontaneity, and have the [[anhedonia|inability to feel pleasure]] ([[anhedonia]]).<ref>{{cite journal | vauthors = Lyne J, O'Donoghue B, Roche E, Renwick L, Cannon M, Clarke M | title = Negative symptoms of psychosis: A life course approach and implications for prevention and treatment | journal = Early Intervention in Psychiatry | volume = 12 | issue = 4 | pages = 561–571 | date = August 2018 | pmid = 29076240 | doi = 10.1111/eip.12501 | s2cid = 38777906 | hdl = 11343/293781 | url = https://pure.manchester.ac.uk/ws/files/59921199/Negative_Symtpoms_Accepted_Revision.pdf | hdl-access = free }}</ref> Altered Behavioral Inhibition System functioning could possibly cause reduced sustained attention in psychosis and overall contribute to more negative reactions.<ref>{{Cite journal |last1=Osborne |first1=K. Juston |last2=Zhang |first2=Wendy |last3=Gupta |first3=Tina |last4=Farrens |first4=Jaclyn |last5=Geiger |first5=McKena |last6=Kraus |first6=Brian |last7=Krugel |first7=Chloe |last8=Nusslock |first8=Robin |last9=Kappenman |first9=Emily S. |last10=Mittal |first10=Vijay A. |date=November 2023 |title=Clinical high risk for psychosis syndrome is associated with reduced neural responding to unpleasant images. |journal=Journal of Psychopathology and Clinical Science |language=en |volume=132 |issue=8 |pages=1060–1071 |doi=10.1037/abn0000862 |pmid=37796541 |s2cid=263669772 |issn=2769-755X|doi-access=free |pmc=11812458 }}</ref>

=== Psychosis in adolescents ===
Psychosis is relatively rare in adolescents but not uncommon.<ref>{{Cite journal |last1=Kelleher |first1=I. |last2=Connor |first2=D. |last3=Clarke |first3=M. C. |last4=Devlin |first4=N. |last5=Harley |first5=M. |last6=Cannon |first6=M. |date=2012 |title=Prevalence of psychotic symptoms in childhood and adolescence: a systematic review and meta-analysis of population-based studies |url=https://www.cambridge.org/core/journals/psychological-medicine/article/abs/prevalence-of-psychotic-symptoms-in-childhood-and-adolescence-a-systematic-review-and-metaanalysis-of-populationbased-studies/D754B5216E027CE4BB51C1BDF5F0DBD0 |journal=Psychological Medicine |language=en |volume=42 |issue=9 |pages=1857–1863 |doi=10.1017/S0033291711002960 |pmid=22225730 |issn=1469-8978|url-access=subscription }}</ref> Young people who have psychosis may have trouble connecting with the world around them and may experience hallucinations or delusions.<ref name=":3">{{cite journal |vauthors=Datta SS, Daruvala R, Kumar A |date=July 2020 |title=Psychological interventions for psychosis in adolescents |journal=The Cochrane Database of Systematic Reviews |volume=7 |issue=7 |article-number=CD009533 |doi=10.1002/14651858.CD009533.pub2 |pmc=7388907 |pmid=32633858 |collaboration=Cochrane Schizophrenia Group}}</ref> Adolescents with psychosis may also have cognitive deficits that may make it harder for the youth to socialize and work.<ref name=":3" /> Potential impairments include a reduced speed of mental processing, the lack of ability to focus without getting distracted (limited [[attention span]]), and deficits in [[verbal memory]].<ref name=":3" /> If an adolescent is experiencing psychosis, they most likely have comorbidity, meaning that they could have multiple mental illnesses.<ref name=":11">{{cite journal | vauthors = Joyce EM | title = Organic psychosis: The pathobiology and treatment of delusions | journal = CNS Neuroscience & Therapeutics | volume = 24 | issue = 7 | pages = 598–603 | date = July 2018 | pmid = 29766653 | pmc = 6489844 | doi = 10.1111/cns.12973 }}</ref> Because of this, it may be difficult to determine whether it is psychosis or [[autism]], [[Social anxiety disorder|social]] or [[generalized anxiety disorder]], or [[Obsessive–compulsive disorder|obsessive-compulsive disorder]].<ref name=":11" />

== Causes ==
The symptoms of psychosis may be caused by serious [[psychiatric disorders]] such as [[schizophrenia]], a number of medical illnesses, and [[Psychological trauma|trauma]]. Psychosis may also be temporary or transient, and be caused by medications or [[substance use disorder]] ([[substance-induced psychosis]]).

=== Normal states ===
Brief hallucinations are not uncommon in those without any psychiatric disease, including healthy children. Causes or triggers include:<ref name="Cardinal_2011_diagnosis_psychosis" />
* Falling asleep and waking: [[hypnagogic]] and [[hypnopompic]] hallucinations<ref>{{cite journal | vauthors = Waters F, Blom JD, Dang-Vu TT, Cheyne AJ, Alderson-Day B, Woodruff P, Collerton D | title = What Is the Link Between Hallucinations, Dreams, and Hypnagogic–Hypnopompic Experiences? | journal = Schizophrenia Bulletin | volume = 42 | issue = 5 | pages = 1098–1109 | date = September 2016 | pmid = 27358492 | pmc = 4988750 | doi = 10.1093/schbul/sbw076 }}</ref>
* [[Bereavement]], in which hallucinations of a deceased loved one are common<ref name="Cardinal_2011_diagnosis_psychosis" /><ref>{{Cite journal |last1=Elsaesser |first1=Evelyn |last2=Roe |first2=Chris A. |last3=Cooper |first3=Callum E. |last4=Lorimer |first4=David |date=September 2021 |title=The phenomenology and impact of hallucinations concerning the deceased |journal=BJPsych Open |language=en |volume=7 |issue=5 |pages=e148 |doi=10.1192/bjo.2021.960 |issn=2056-4724 |pmc=8388006}}</ref>
* Severe [[sleep deprivation]]<ref>{{cite journal | vauthors = Waters F, Chiu V, Atkinson A, Blom JD | title = Severe Sleep Deprivation Causes Hallucinations and a Gradual Progression Toward Psychosis With Increasing Time Awake | journal = Frontiers in Psychiatry | volume = 9 | article-number = 303 | date = 2018 | pmid = 30042701 | pmc = 6048360 | doi = 10.3389/fpsyt.2018.00303 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Cosgrave J, Wulff K, Gehrman P | title = Sleep, circadian rhythms, and schizophrenia: where we are and where we need to go | language = en-US | journal = Current Opinion in Psychiatry | volume = 31 | issue = 3 | pages = 176–182 | date = May 2018 | pmid = 29537983 | doi = 10.1097/YCO.0000000000000419 | s2cid = 4414751 }}</ref>
* Extreme stress (see below)<ref>{{cite journal | vauthors = Pruessner M, Cullen AE, Aas M, Walker EF | title = The neural diathesis-stress model of schizophrenia revisited: An update on recent findings considering illness stage and neurobiological and methodological complexities | journal = Neuroscience and Biobehavioral Reviews | volume = 73 | pages = 191–218 | date = February 2017 | pmid = 27993603 | doi = 10.1016/j.neubiorev.2016.12.013 | s2cid = 3971965 | url = https://kclpure.kcl.ac.uk/portal/en/publications/the-neural-diathesisstress-model-of-schizophrenia-revisited(e114c9df-04b9-4350-9ef3-acc58a2d336d).html | access-date = 2022-05-05 | archive-date = 2022-06-30 | archive-url = https://web.archive.org/web/20220630153031/https://kclpure.kcl.ac.uk/portal/en/publications/the-neural-diathesisstress-model-of-schizophrenia-revisited(e114c9df-04b9-4350-9ef3-acc58a2d336d).html | url-status = live }}</ref>
* Abnormal brainwaves<ref>{{Cite journal |last1=Grent-'t-Jong |first1=Tineke |last2=Gajwani |first2=Ruchika |last3=Gross |first3=Joachim |last4=Gumley |first4=Andrew I. |last5=Krishnadas |first5=Rajeev |last6=Lawrie |first6=Stephen M. |last7=Schwannauer |first7=Matthias |last8=Schultze-Lutter |first8=Frauke |last9=Uhlhaas |first9=Peter J. |date=2020-08-01 |title=Association of Magnetoencephalographically Measured High-Frequency Oscillations in Visual Cortex With Circuit Dysfunctions in Local and Large-scale Networks During Emerging Psychosis |journal=JAMA Psychiatry |language=en |volume=77 |issue=8 |pages=852–862 |doi=10.1001/jamapsychiatry.2020.0284 |issn=2168-622X |pmc=7097849 |pmid=32211834}}</ref><ref>{{Cite journal |last1=Supekar |first1=Kaustubh |last2=de los Angeles |first2=Carlo |last3=Ryali |first3=Srikanth |last4=Kushan |first4=Leila |last5=Schleifer |first5=Charlie |last6=Repetto |first6=Gabriela |last7=Crossley |first7=Nicolas A. |last8=Simon |first8=Tony |last9=Bearden |first9=Carrie E. |last10=Menon |first10=Vinod |date=October 2024 |title=Robust and replicable functional brain signatures of 22q11.2 deletion syndrome and associated psychosis: a deep neural network-based multi-cohort study |url=https://www.nature.com/articles/s41380-024-02495-8 |journal=Molecular Psychiatry |language=en |volume=29 |issue=10 |pages=2951–2966 |doi=10.1038/s41380-024-02495-8 |pmid=38605171 |issn=1476-5578|url-access=subscription }}</ref>
* Abnormal brain networks<ref>{{Cite journal |last1=Ding |first1=Ningning |last2=Zhang |first2=Entu |last3=Liu |first3=Yangyang |last4=Zhang |first4=Shuaiqi |last5=Lu |first5=Pei |last6=Zhang |first6=Haisan |date=2024-11-30 |title=Network integration and segregation changes in schizophrenia: impact of electroconvulsive therapy |journal=BMC Psychiatry |volume=24 |issue=1 |page=862 |doi=10.1186/s12888-024-06331-9 |doi-access=free |issn=1471-244X |pmc=11607971 |pmid=39616308}}</ref><ref>{{Cite journal |last1=Li |first1=Siyi |last2=Hu |first2=Na |last3=Zhang |first3=Wenjing |last4=Tao |first4=Bo |last5=Dai |first5=Jing |last6=Gong |first6=Yao |last7=Tan |first7=Youguo |last8=Cai |first8=Duanfang |last9=Lui |first9=Su |date=2019-07-12 |title=Dysconnectivity of Multiple Brain Networks in Schizophrenia: A Meta-Analysis of Resting-State Functional Connectivity |journal=Frontiers in Psychiatry |volume=10 |article-number=482 |doi=10.3389/fpsyt.2019.00482 |doi-access=free |issn=1664-0640 |pmc=6639431 |pmid=31354545}}</ref><ref>{{Cite journal |last1=Kinsey |first1=Spencer |last2=Kazimierczak |first2=Katarzyna |last3=Camazón |first3=Pablo Andrés |last4=Chen |first4=Jiayu |last5=Adali |first5=Tülay |last6=Kochunov |first6=Peter |last7=Adhikari |first7=Bhim M. |last8=Ford |first8=Judith |last9=van Erp |first9=Theo G. M. |last10=Dhamala |first10=Mukesh |last11=Calhoun |first11=Vince D. |last12=Iraji |first12=Armin |date=2024-11-21 |title=Networks extracted from nonlinear fMRI connectivity exhibit unique spatial variation and enhanced sensitivity to differences between individuals with schizophrenia and controls |journal=Nature Mental Health |language=en |volume=2 |issue=12 |pages=1464–1475 |doi=10.1038/s44220-024-00341-y |issn=2731-6076 |pmc=11621020 |pmid=39650801}}</ref>
* [[Traumatic brain injury]]<ref>{{Cite journal |last1=Batty |first1=Rachel A. |last2=Rossell |first2=Susan L. |last3=Francis |first3=Andrew J.P. |last4=Ponsford |first4=Jennie |date=May 2013 |title=Psychosis Following Traumatic Brain Injury |url=https://www.cambridge.org/core/product/identifier/S1443964613000107/type/journal_article |journal=Brain Impairment |language=en |volume=14 |issue=1 |pages=21–41 |doi=10.1017/BrImp.2013.10 |issn=1443-9646|url-access=subscription }}</ref><ref>{{Cite journal |last=David |first=A S |date=2005-03-01 |title=Psychosis following head injury: a critical review |journal=Journal of Neurology, Neurosurgery & Psychiatry |language=en |volume=76 |issue=suppl_1 |pages=i53–i60 |doi=10.1136/jnnp.2004.060475 |issn=0022-3050 |pmc=1765686 |pmid=15718223}}</ref><ref>{{Cite journal |last1=Fujii |first1=Daryl |last2=Fujii |first2=Daniel C. |date=July 2012 |title=Psychotic Disorder Due to Traumatic Brain Injury: Analysis of Case Studies in the Literature |url=https://psychiatryonline.org/doi/10.1176/appi.neuropsych.11070176 |journal=The Journal of Neuropsychiatry and Clinical Neurosciences |language=en |volume=24 |issue=3 |pages=278–289 |doi=10.1176/appi.neuropsych.11070176 |pmid=23037642 |issn=0895-0172|url-access=subscription }}</ref>

=== Trauma and stress ===
Traumatic life events have been linked with an elevated risk of developing psychotic symptoms.<ref name=":1">{{cite journal | vauthors = Gibson LE, Alloy LB, Ellman LM | title = Trauma and the psychosis spectrum: A review of symptom specificity and explanatory mechanisms | journal = Clinical Psychology Review | volume = 49 | pages = 92–105 | date = November 2016 | pmid = 27632064 | pmc = 5157832 | doi = 10.1016/j.cpr.2016.08.003 }}</ref> [[Childhood trauma]] has specifically been shown to be a predictor of adolescent and adult psychosis.<ref name=":2">{{cite journal | vauthors = Misiak B, Krefft M, Bielawski T, Moustafa AA, Sąsiadek MM, Frydecka D | title = Toward a unified theory of childhood trauma and psychosis: A comprehensive review of epidemiological, clinical, neuropsychological and biological findings | journal = Neuroscience and Biobehavioral Reviews | volume = 75 | pages = 393–406 | date = April 2017 | pmid = 28216171 | doi = 10.1016/j.neubiorev.2017.02.015 | s2cid = 21614845 }}</ref> Individuals with psychotic symptoms are three times more likely to have experienced childhood trauma (e.g., [[Physical abuse|physical]] or [[Sexual abuse#Children|sexual abuse]], physical or emotional [[Neglect#Child neglect|neglect]]) than those in the general population.<ref name=":2" /> Increased individual vulnerability toward psychosis may interact with traumatic experiences promoting an onset of future psychotic symptoms, particularly during sensitive developmental periods.<ref name=":2" /> Importantly, the relationship between traumatic life events and psychotic symptoms appears to be dose-dependent in which multiple traumatic life events accumulate, compounding symptom expression and severity.<ref name=":1" /><ref name=":2" /> However, acute, stressful events can also trigger brief psychotic episodes.<ref>{{Cite book|url=http://archive.org/details/diagnosticstatis0005unse|title=Diagnostic and statistical manual of mental disorders: DSM-5|date=2013|publisher=Arlington, VA : American Psychiatric Association |isbn=978-0-89042-554-1}}</ref> Trauma prevention and early intervention may be an important target for decreasing the incidence of psychotic disorders and ameliorating its effects.<ref name=":1" /> A healthy person could become psychotic when inside an empty room with no light and sound. After about 15 minutes, psychosis can occur, this is a phenomenon known as [[sensory deprivation]].<ref name="Oxford Textbook of Psychiatry" />

[[Neuroticism]], a personality trait associated with vulnerability to stressors, is an independent predictor of the development of psychosis.<ref name="NeuroticismMA">{{cite journal | vauthors = Jeronimus BF, Kotov R, Riese H, Ormel J | title = Neuroticism's prospective association with mental disorders halves after adjustment for baseline symptoms and psychiatric history, but the adjusted association hardly decays with time: a meta-analysis on 59 longitudinal/prospective studies with 443 313 participants | journal = Psychological Medicine | volume = 46 | issue = 14 | pages = 2883–2906 | date = October 2016 | pmid = 27523506 | doi = 10.1017/S0033291716001653 | url = https://zenodo.org/record/895885 | url-status = live | access-date = 2019-07-03 | s2cid = 23548727 | archive-url = https://web.archive.org/web/20190724213253/https://zenodo.org/record/895885 | archive-date = 2019-07-24 }}</ref>

=== Psychiatric disorders ===
Traditionally psychotic disorders have been believed to have one of two roots: organic (physiological) or functional (mental). Organic disorders being those caused by physical conditions directly affecting the brain with psychosis as a secondary feature, and functional disorders being primary psychological or psychiatric disorders (disorders of the functioning of the mind) in the absence of physiological causes. Subtle physical abnormalities have been found in illnesses traditionally considered functional, such as [[schizophrenia]]. The [[DSM-IV-TR]] avoids the functional/organic distinction, and instead lists traditional psychotic illnesses, psychosis due to general medical conditions, and substance-induced psychosis.

Primary psychiatric causes of psychosis include the following:<ref name="ICD-10">[[World Health Organization]], [https://www.who.int/entity/classifications/icd/en/bluebook.pdf ''The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines (CDDG)''] {{Webarchive|url=https://web.archive.org/web/20041017011412/http://www.who.int/classifications/icd/en/bluebook.pdf |date=2004-10-17 }}, 1992.</ref><ref>{{Cite book|url=http://archive.org/details/diagnosticstatis0005unse|title=Diagnostic and statistical manual of mental disorders: DSM-5|date=2013|publisher=Arlington, VA : American Psychiatric Association| via = Internet Archive|isbn=978-0-89042-554-1}}</ref><ref name="Cardinal_2011_diagnosis_psychosis">{{cite book | vauthors = Cardinal RN, Bullmore, ET | title = The Diagnosis of Psychosis | publisher = Cambridge University Press | date = 2011 | isbn = 978-0-521-16484-9 }}</ref>
* [[schizophrenia]]
* [[mood disorders]] including [[psychotic depression]] and [[bipolar disorder]] in the [[mania|manic]] and [[mixed episode]]s of [[bipolar I disorder]] and depressive episodes of both [[bipolar I]] and [[bipolar II]]
* [[schizoaffective disorder]]
* [[delusional disorder]]
* [[brief psychotic disorder]]
* [[schizophreniform disorder]]
Psychotic symptoms may also be seen in:<ref name="Cardinal_2011_diagnosis_psychosis" />
* [[Personality disorders]] including [[Schizotypal personality disorder]] and [[borderline personality disorder]]
* [[Post-traumatic stress disorder]]
* [[obsessive–compulsive disorder]]
* [[dissociative identity disorder]]
* [[paraphrenia]]

==== Subtypes ====
Subtypes of psychosis include:
* [[Postpartum psychosis]], occurring shortly after [[giving birth]], primarily associated with maternal [[bipolar disorder]]
* [[Monothematic delusion]]s
* [[Myxedematous psychosis]]
* [[Stimulant psychosis]]
* [[Tardive psychosis]]
* [[Shared psychosis]]

==== Cycloid psychosis ====
Cycloid psychosis is typically an acute, self-limiting form of psychosis with psychotic and mood symptoms that progress from normal to full-blown, usually between a few hours to days, and not related to drug intake or [[brain injury]].<ref name=":0">{{cite journal | vauthors = El-Mallakh RS, Furdek C | title = Cycloid Psychosis | journal = The American Journal of Psychiatry | volume = 175 | issue = 6 | pages = 502–505 | date = June 2018 | pmid = 29869551 | doi = 10.1176/appi.ajp.2017.17030282 | doi-access = free }}</ref> While proposed as a distinct entity, clinically separate from schizophrenia and affective disorders, cycloid psychosis is not formally acknowledged by current ICD or DSM criteria.<ref name=":0" /> Its unclear place in psychiatric nosology has likely contributed to the limited scientific investigation and literature on the topic.

==== Postpartum psychosis ====
[[Postpartum psychosis]] is a rare yet serious and debilitating form of psychosis.<ref name=":10">{{cite journal | vauthors = VanderKruik R, Barreix M, Chou D, Allen T, Say L, Cohen LS | title = The global prevalence of postpartum psychosis: a systematic review | journal = BMC Psychiatry | volume = 17 | issue = 1 | article-number = 272 | date = July 2017 | pmid = 28754094 | pmc = 5534064 | doi = 10.1186/s12888-017-1427-7 | doi-access = free }}</ref> Symptoms range from fluctuating moods and insomnia to mood-incongruent delusions related to the individual or the infant.<ref name=":10" /> Women experiencing postpartum psychosis are at increased risk for suicide or infanticide. Many women who experience first-time psychosis from postpartum often have bipolar disorder, meaning they could experience an increase of psychotic episodes even after postpartum.<ref name=":10" />

=== Medical conditions ===
A very large number of medical conditions can cause psychosis, sometimes called ''secondary psychosis''.<ref name="Cardinal_2011_diagnosis_psychosis" /> Examples include:
* disorders causing ''[[delirium]]'' (''toxic psychosis''), in which consciousness is disturbed
* neurodevelopmental disorders and chromosomal abnormalities, including [[velocardiofacial syndrome]]
* neurodegenerative disorders, such as [[Alzheimer's disease]], [[dementia with Lewy bodies]], and [[Parkinson's disease]]<ref>{{cite journal | vauthors = Karameh WK, Murari G, Schweizer TA, Munoz DG, Fischer CE | title = Psychosis in neurodegenerative disorders: recent developments | language = en-US | journal = Current Opinion in Psychiatry | volume = 32 | issue = 2 | pages = 117–122 | date = March 2019 | pmid = 30520740 | doi = 10.1097/YCO.0000000000000476 | s2cid = 54560300 }}</ref>
* focal neurological disease, such as [[stroke]], [[brain tumor]]s,<ref name="Brain_tumor">{{cite journal | vauthors = Lisanby SH, Kohler C, Swanson CL, Gur RE | title = Psychosis Secondary to Brain Tumor | journal = Seminars in Clinical Neuropsychiatry | volume = 3 | issue = 1 | pages = 12–22 | date = January 1998 | pmid = 10085187 }}</ref> [[multiple sclerosis]],<ref name="Continuum" /> and some forms of [[epilepsy]]
* malignancy (typically via masses in the brain, [[paraneoplastic syndrome]]s)<ref name="Continuum" />
* infectious and postinfectious syndromes, including infections causing [[delirium]], [[viral encephalitis]], [[HIV/AIDS]],<ref name="Munjal 681–712">{{cite journal | vauthors = Munjal S, Ferrando SJ, Freyberg Z | title = Neuropsychiatric Aspects of Infectious Diseases: An Update | journal = Critical Care Clinics | volume = 33 | issue = 3 | pages = 681–712 | date = July 2017 | pmid = 28601141 | pmc = 5771230 | doi = 10.1016/j.ccc.2017.03.007 }}</ref> [[malaria]],<ref>{{cite journal | vauthors = Nevin RL, Croft AM | title = Psychiatric effects of malaria and anti-malarial drugs: historical and modern perspectives | journal = Malaria Journal | volume = 15 | article-number = 332 | date = June 2016 | pmid = 27335053 | pmc = 4918116 | doi = 10.1186/s12936-016-1391-6 | doi-access = free }}</ref> [[syphilis]]<ref name="Munjal 681–712" />
* endocrine disease, such as [[hypothyroidism]], [[hyperthyroidism]], [[Cushing's syndrome]], [[hypoparathyroidism]] and [[hyperparathyroidism]];<ref name=":6" /> sex hormones also affect psychotic symptoms and sometimes giving birth can provoke psychosis, termed [[postpartum psychosis]]<ref name=":7">{{cite journal |vauthors=Davies W |date=June 2017 |title=Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches |journal=World Journal of Psychiatry |volume=7 |issue=2 |pages=77–88 |doi=10.5498/wjp.v7.i2.77 |pmc=5491479 |pmid=28713685 |doi-access=free}}</ref>
* inborn errors of metabolism, such as Wilson's disease, porphyria, and homocysteinemia.<ref>{{Cite journal| vauthors = Turkel SB, Wong D, Randolph L |date=2020-09-01|title=Psychiatric Symptoms Associated with Inborn Errors of Metabolism |journal=SN Comprehensive Clinical Medicine|language=en|volume=2|issue=9|pages=1646–1660|doi=10.1007/s42399-020-00403-z|s2cid=221130135|issn=2523-8973}}</ref>
* nutritional deficiency, such as [[vitamin B12 deficiency|vitamin B<sub>12</sub> deficiency]]<ref name="Griswold" />
* other acquired metabolic disorders, including [[electrolyte]] disturbances such as [[hypocalcemia]], [[hypernatremia]], [[hyponatremia]], [[hypokalemia]], [[hypomagnesemia]], [[hypermagnesemia]], [[hypercalcemia]], and [[hypophosphatemia]], but also [[hypoglycemia]], [[Hypoxia (medical)|hypoxia]], and failure of the [[liver]] or [[kidney]]s<ref name=":6">{{cite journal | vauthors = Skikic M, Arriola JA | title = First Episode Psychosis Medical Workup: Evidence-Informed Recommendations and Introduction to a Clinically Guided Approach | language = English | journal = Child and Adolescent Psychiatric Clinics of North America | volume = 29 | issue = 1 | pages = 15–28 | date = January 2020 | pmid = 31708044 | doi = 10.1016/j.chc.2019.08.010 | s2cid = 207965670 }}</ref><ref name="Griswold"/>
* [[autoimmune]] and related disorders, such as [[systemic lupus erythematosus]] (lupus, SLE), [[sarcoidosis]], [[Hashimoto's encephalopathy]], [[anti-NMDA-receptor encephalitis]], and [[non-celiac gluten sensitivity]]<ref name="LosurdoPrincipi2018">{{cite journal | vauthors = Losurdo G, Principi M, Iannone A, Amoruso A, Ierardi E, Di Leo A, Barone M | title = Extra-intestinal manifestations of non-celiac gluten sensitivity: An expanding paradigm | journal = World Journal of Gastroenterology | volume = 24 | issue = 14 | pages = 1521–1530 | date = April 2018 | pmid = 29662290 | pmc = 5897856 | doi = 10.3748/wjg.v24.i14.1521 | type = Review | doi-access = free }}</ref><ref>{{cite journal | vauthors = Najjar S, Steiner J, Najjar A, Bechter K | title = A clinical approach to new-onset psychosis associated with immune dysregulation: the concept of autoimmune psychosis | journal = Journal of Neuroinflammation | volume = 15 | issue = 1 | article-number = 40 | date = February 2018 | pmid = 29433523 | pmc = 5809809 | doi = 10.1186/s12974-018-1067-y | doi-access = free }}</ref>
* poisoning by a range of plants, fungi, metals, organic compounds, and a few animal toxins<ref name="Cardinal_2011_diagnosis_psychosis" />
* sleep disorders, such as in [[narcolepsy]] (in which [[REM sleep]] intrudes into wakefulness)<ref name="Cardinal_2011_diagnosis_psychosis" />
* parasitic diseases, such as [[neurocysticercosis]]

=== Psychoactive drugs ===
{{Main|Substance-induced psychosis}}

Various [[psychoactive substances]] (both legal and illegal) have been implicated in causing, exacerbating, or precipitating psychotic states or disorders in users, with varying levels of evidence.<ref>{{Cite journal |last1=Baldaçara |first1=Leonardo |last2=Ramos |first2=Artur |last3=Castaldelli-Maia |first3=João Maurício |date=2023 |title=Managing drug-induced psychosis |journal=International Review of Psychiatry |volume=35 |issue=5–6 |pages=496–502 |doi=10.1080/09540261.2023.2261544 |issn=1369-1627 |pmid=38299647}}</ref> This may be upon intoxication for a more prolonged period after use, or upon [[drug withdrawal|withdrawal]].<ref name="Cardinal_2011_diagnosis_psychosis" /> Individuals who experience substance-induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels of [[suicidal thinking]] compared to those who have a primary psychotic illness.<ref name="pmid21728034">{{cite journal | vauthors = Grant KM, LeVan TD, Wells SM, Li M, Stoltenberg SF, Gendelman HE, Carlo G, Bevins RA | display-authors = 6 | title = Methamphetamine-associated psychosis | journal = Journal of Neuroimmune Pharmacology | volume = 7 | issue = 1 | pages = 113–139 | date = March 2012 | pmid = 21728034 | pmc = 3280383 | doi = 10.1007/s11481-011-9288-1 | author6-link = Howard E. Gendelman }}</ref> Drugs commonly alleged to induce psychotic symptoms include [[Alcohol (drug)|alcohol]], [[Cannabis (drug)|cannabis]], [[cocaine]], [[amphetamine]]s, [[cathinone]]s, [[psychedelic drug]]s (such as [[LSD]] and [[psilocybin]]), [[κ-opioid receptor]] [[agonist]]s (such as [[enadoline]] and [[salvinorin A]]) and [[NMDA receptor antagonist]]s (such as [[phencyclidine]] and [[ketamine]]).<ref name="Cardinal_2011_diagnosis_psychosis" /><ref>{{cite journal | vauthors = Krebs TS, Johansen PØ | title = Psychedelics and mental health: a population study | journal = PLOS ONE | volume = 8 | issue = 8 | article-number = e63972 | date = August 2013 | pmid = 23976938 | pmc = 3747247 | doi = 10.1371/journal.pone.0063972 | doi-access = free | bibcode = 2013PLoSO...863972K }}</ref> [[Caffeine]] may worsen symptoms in those with schizophrenia and cause psychosis at very high doses in people without the condition.<ref>{{cite journal | vauthors = Alasmari F | title = Caffeine induces neurobehavioral effects through modulating neurotransmitters | journal = Saudi Pharmaceutical Journal | volume = 28 | issue = 4 | pages = 445–451 | date = April 2020 | pmid = 32273803 | pmc = 7132598 | doi = 10.1016/j.jsps.2020.02.005 }}</ref><ref>{{Cite journal | vauthors = Beauchamp G, Amaducci A, Cook M |date=2017-09-01|title=Caffeine Toxicity: A Brief Review and Update |journal=Clinical Pediatric Emergency Medicine|series=Toxicology|language=en|volume=18|issue=3|pages=197–202|doi=10.1016/j.cpem.2017.07.002|issn=1522-8401}}</ref> Cannabis and other illicit recreational drugs are often associated with psychosis in adolescents and cannabis use before 15 years old may increase the risk of psychosis in adulthood.<ref name=":3" />

==== Alcohol ====
{{Further|Long-term effects of alcohol consumption#Mental health effects}}
Approximately 3% of people with [[alcoholism]] experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a [[kindling (sedative-hypnotic withdrawal)|kindling mechanism]]. The mechanism of alcohol-related psychosis is due to the [[long-term effects of alcohol consumption]] resulting in distortions to neuronal membranes, [[gene expression]], as well as [[thiamine]] deficiency. It is possible that hazardous alcohol use via a kindling mechanism can cause the development of a chronic substance-induced psychotic disorder, i.e. schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments.<ref>{{cite journal | vauthors = Castillo-Carniglia A, Keyes KM, Hasin DS, Cerdá M | title = Psychiatric comorbidities in alcohol use disorder | journal = The Lancet. Psychiatry | volume = 6 | issue = 12 | pages = 1068–1080 | date = December 2019 | pmid = 31630984 | pmc = 7006178 | doi = 10.1016/S2215-0366(19)30222-6 }}</ref> [[Delirium tremens]], a symptom of chronic alcoholism that can appear in the acute withdrawal phase, shares many symptoms with alcohol-related psychosis suggesting a common mechanism.<ref>{{cite journal | vauthors = Jordaan GP, Emsley R | title = Alcohol-induced psychotic disorder: a review | journal = Metabolic Brain Disease | volume = 29 | issue = 2 | pages = 231–243 | date = June 2014 | pmid = 24307180 | doi = 10.1007/s11011-013-9457-4 | url = http://link.springer.com/10.1007/s11011-013-9457-4 | access-date = 2021-01-20 | url-status = live | s2cid = 17239167 | archive-url = https://web.archive.org/web/20211018155817/https://link.springer.com/article/10.1007%2Fs11011-013-9457-4 | archive-date = 2021-10-18 | url-access = subscription }}</ref>

==== Cannabis ====
{{Further|Causes of schizophrenia#Cannabis|Long-term effects of cannabis#Chronic psychosis and schizophrenia spectrum disorders}}
According to current studies, cannabis use is associated with increased risk of psychotic disorders, and the more often cannabis is used the more likely a person is to develop a psychotic illness.<ref name=":8">{{cite journal | vauthors = Hasan A, von Keller R, Friemel CM, Hall W, Schneider M, Koethe D, Leweke FM, Strube W, Hoch E | display-authors = 6 | title = Cannabis use and psychosis: a review of reviews | journal = European Archives of Psychiatry and Clinical Neuroscience | volume = 270 | issue = 4 | pages = 403–412 | date = June 2020 | pmid = 31563981 | doi = 10.1007/s00406-019-01068-z | s2cid = 203567900 }}</ref> Furthermore, people with a history of cannabis use develop psychotic symptoms earlier than those who have never used cannabis.<ref name=":8" /> Some debate exists regarding the causal relationship between cannabis use and psychosis with some studies suggesting that cannabis use hastens the onset of psychosis primarily in those with pre-existing vulnerability.<ref name=":8" /><ref>{{cite journal | vauthors = Ortiz-Medina MB, Perea M, Torales J, Ventriglio A, Vitrani G, Aguilar L, Roncero C | title = Cannabis consumption and psychosis or schizophrenia development | journal = The International Journal of Social Psychiatry | volume = 64 | issue = 7 | pages = 690–704 | date = November 2018 | pmid = 30442059 | doi = 10.1177/0020764018801690 | hdl = 10366/163120 | s2cid = 53563635 | hdl-access = free }}</ref><ref>{{cite journal | vauthors = Hamilton I, Monaghan M | title = Cannabis and Psychosis: Are We any Closer to Understanding the Relationship? | journal = Current Psychiatry Reports | volume = 21 | issue = 7 | article-number = 48 | date = June 2019 | pmid = 31161275 | pmc = 6546656 | doi = 10.1007/s11920-019-1044-x }}</ref> Indeed, cannabis use plays an important role in the development of psychosis in vulnerable individuals, and cannabis use in adolescence should be discouraged.<ref>{{cite journal | vauthors = van der Steur SJ, Batalla A, Bossong MG | title = Factors Moderating the Association Between Cannabis Use and Psychosis Risk: A Systematic Review | journal = Brain Sciences | volume = 10 | issue = 2 | page = 97 | date = February 2020 | pmid = 32059350 | pmc = 7071602 | doi = 10.3390/brainsci10020097 | doi-access = free }}</ref> Some studies indicate that the effects of two active compounds in cannabis, [[tetrahydrocannabinol]] (THC) and [[cannabidiol]] (CBD), have opposite effects with respect to psychosis. While THC can induce psychotic symptoms in healthy individuals, limited evidence suggests that CBD may have antipsychotic effects.<ref>{{cite journal | vauthors = Chesney E, Oliver D, McGuire P | title = Cannabidiol (CBD) as a novel treatment in the early phases of psychosis | journal = Psychopharmacology | date = July 2021 | volume = 239 | issue = 5 | pages = 1179–1190 | pmid = 34255100 | doi = 10.1007/s00213-021-05905-9 | pmc = 9110455 | s2cid = 235807339 }}</ref>

==== Methamphetamine ====
{{Main|Stimulant psychosis}}

[[Methamphetamine]] induces a psychosis in 26%–46% of heavy users. Some of these people develop a long-lasting psychosis that can persist for longer than six months. Those who have had a short-lived psychosis from methamphetamine can have a relapse of the methamphetamine psychosis years later after a stressful event such as severe insomnia or a period of hazardous alcohol use despite not relapsing back to methamphetamine.<ref>{{cite journal | vauthors = Shin EJ, Dang DK, Tran TV, Tran HQ, Jeong JH, Nah SY, Jang CG, Yamada K, Nabeshima T, Kim HC | display-authors = 6 | title = Current understanding of methamphetamine-associated dopaminergic neurodegeneration and psychotoxic behaviors | journal = Archives of Pharmacal Research | volume = 40 | issue = 4 | pages = 403–428 | date = April 2017 | pmid = 28243833 | doi = 10.1007/s12272-017-0897-y | s2cid = 22791168 }}</ref> Individuals who have a long history of methamphetamine use and who have experienced psychosis in the past from methamphetamine use are highly likely to re-experience methamphetamine psychosis if drug use is recommenced. {{citation needed|date=March 2025}} Methamphetamine-induced psychosis is likely gated by genetic vulnerability, which can produce long-term changes in brain neurochemistry following repetitive use.<ref>{{cite journal | vauthors = Greening DW, Notaras M, Chen M, Xu R, Smith JD, Cheng L, Simpson RJ, Hill AF, van den Buuse M | display-authors = 6 | title = Chronic methamphetamine interacts with BDNF Val66Met to remodel psychosis pathways in the mesocorticolimbic proteome | journal = Molecular Psychiatry | volume = 26 | issue = 8 | pages = 4431–4447 | date = August 2021 | pmid = 31822818 | doi = 10.1038/s41380-019-0617-8 | url = https://www.nature.com/articles/s41380-019-0617-8 | access-date = 2020-01-05 | url-status = live | s2cid = 209169489 | archive-url = https://web.archive.org/web/20200806232220/https://www.nature.com/articles/s41380-019-0617-8 | archive-date = 2020-08-06 | url-access = subscription }}</ref> Methamphetamine users with more ADHD-related behaviours in childhood experience methamphetamine-related psychosis more frequently.<ref>{{Cite journal |last1=Salo |first1=Ruth |last2=Fassbender |first2=Catherine |last3=Iosif |first3=Ana-Maria |last4=Ursu |first4=Stefan |last5=Leamon |first5=Martin H |last6=Carter |first6=Cameron |date=2013-12-15 |title=Predictors of methamphetamine psychosis: History of ADHD-relevant childhood behaviors and drug exposure |journal=Psychiatry Research |volume=210 |issue=2 |pages=529–535 |doi=10.1016/j.psychres.2013.06.030 |pmid=23896355 |pmc=3818411 |issn=0165-1781}}</ref>

==== Psychedelics ====
A 2024 meta-analysis found an incidence of psychedelic-induced psychosis at 0.002% in population studies, 0.2% in uncontrolled clinical trials, and 0.6% in randomised controlled trials.<ref>{{Cite journal |last1=Sabé |first1=Michel |last2=Sulstarova |first2=Adi |last3=Glangetas |first3=Alban |last4=De Pieri |first4=Marco |last5=Mallet |first5=Luc |last6=Curtis |first6=Logos |last7=Richard-Lepouriel |first7=Héléne |last8=Penzenstadler |first8=Louise |last9=Seragnoli |first9=Federico |last10=Thorens |first10=Gabriel |last11=Zullino |first11=Daniele |last12=Preller |first12=Katrin |last13=Böge |first13=Kerem |last14=Leucht |first14=Stefan |last15=Correll |first15=Christoph U. |date=November 2024 |title=Reconsidering evidence for psychedelic-induced psychosis: an overview of reviews, a systematic review, and meta-analysis of human studies |journal=Molecular Psychiatry |language=en |volume=30 |issue=3 |pages=1223–1255 |doi=10.1038/s41380-024-02800-5 |pmid=39592825 |issn=1476-5578|pmc=11835720 }}</ref> This meta-analysis found that in uncontrolled clinical trials involving only patients with schizophrenia, 3.8% developed prolonged psychotic reactions. A 2024 study found that [[psychedelic]] use was not generally associated with a change in the number of psychotic symptoms.<ref>{{Cite journal |last1=Honk |first1=Ludwig |last2=Stenfors |first2=Cecilia U. D. |last3=Goldberg |first3=Simon B. |last4=Hendricks |first4=Peter S. |last5=Osika |first5=Walter |last6=Dourron |first6=Haley Maria |last7=Lebedev |first7=Alexander |last8=Petrovic |first8=Predrag |last9=Simonsson |first9=Otto |date=2024-04-15 |title=Longitudinal associations between psychedelic use and psychotic symptoms in the United States and the United Kingdom |journal=Journal of Affective Disorders |volume=351 |pages=194–201 |doi=10.1016/j.jad.2024.01.197 |pmid=38280572 |pmc=10922895 |issn=0165-0327}}</ref> This study found that psychedelic use interacted with a family history of bipolar disorder, such that in those with a family history of bipolar disorder, psychedelic use was associated with an increase in the number of psychotic symptoms, while in those with a personal history of psychosis but no family history of psychotic disorders, psychedelic use was associated with a decrease in the number of psychotic symptoms. A 2023 study found an interaction between lifetime psychedelic use and family history of psychosis or bipolar disorder on psychotic symptoms over the past two weeks. Psychotic symptoms were highest among those with both a family history of psychosis or bipolar disorder and life-time psychedelic use, while they were lowest among those with life-time psychedelic use but no family history of these disorders.<ref>{{Cite journal |last1=Simonsson |first1=Otto |last2=Goldberg |first2=Simon B. |last3=Chambers |first3=Richard |last4=Osika |first4=Walter |last5=Simonsson |first5=Charlotta |last6=Hendricks |first6=Peter S. |date=2023-10-24 |title=Psychedelic use and psychiatric risks |journal=Psychopharmacology |volume=242 |issue=7 |pages=1577–1583 |language=en |doi=10.1007/s00213-023-06478-5 |issn=1432-2072 |pmc=11039563 |pmid=37874345}}</ref>

=== Medication ===
Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms.<ref name="Cardinal_2011_diagnosis_psychosis" /> Drugs that can induce psychosis experimentally or in a significant proportion of people include:
* stimulants, such as [[amphetamine]] and other [[sympathomimetics]],
* [[dopamine]] agonists,
* [[ketamine]],
* [[corticosteroid]]s (often with mood changes in addition),
* and some anticonvulsants such as [[vigabatrin]].<ref>{{Cite journal| vauthors = Guadalupe MT, Páramo IA |date=2020-03-23|title=Corticosteroid-induced psychosis: Case report and review of the literature |journal=European Psychiatry|language=en|volume=41|issue=S1|pages=s840|doi=10.1016/j.eurpsy.2017.01.1659|s2cid=232174454|issn=0924-9338}}</ref><ref>{{Cite journal| vauthors = Gray LA |date=2020-03-01|title=Anticonvulsant toxicity |journal=Medicine|language=en|volume=48|issue=3|pages=192–193|doi=10.1016/j.mpmed.2019.12.011|s2cid=243053658|issn=1357-3039}}</ref><ref>{{cite journal | vauthors = Ward K, Citrome L | title = Lisdexamfetamine: chemistry, pharmacodynamics, pharmacokinetics, and clinical efficacy, safety, and tolerability in the treatment of binge eating disorder | journal = Expert Opinion on Drug Metabolism & Toxicology | volume = 14 | issue = 2 | pages = 229–238 | date = February 2018 | pmid = 29258368 | doi = 10.1080/17425255.2018.1420163 | s2cid = 3494618 }}</ref>

== Pathophysiology ==
=== Neuroimaging ===
The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called [[pneumoencephalography]]<ref>{{cite journal | vauthors = Moore MT, Nathan D, Elliott AR, Laubach C |title=Encephalographic studies in mental disease |journal=American Journal of Psychiatry|volume=92|issue=1|pages=43–67|doi= 10.1176/ajp.92.1.43|year=1935 }}</ref> (a painful and now obsolete procedure where [[cerebrospinal fluid]] is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on an [[X-ray]] picture).

Both [[Antipsychotic#First episode psychosis|first episode psychosis]], and high risk status is associated with reductions in grey matter volume (GMV). First episode psychotic and high risk populations are associated with similar but distinct abnormalities in GMV. Reductions in the right [[middle temporal gyrus]], right [[superior temporal gyrus]] (STG), right [[parahippocampus]], right [[hippocampus]], right [[middle frontal gyrus]], and left [[anterior cingulate cortex]] (ACC) are observed in high risk populations. Reductions in first episode psychosis span a region from the right STG to the right insula, left insula, and cerebellum, and are more severe in the right ACC, right STG, insula and cerebellum.<ref>{{cite journal | vauthors = Fusar-Poli P, Radua J, McGuire P, Borgwardt S | title = Neuroanatomical maps of psychosis onset: voxel-wise meta-analysis of antipsychotic-naive VBM studies | journal = Schizophrenia Bulletin | volume = 38 | issue = 6 | pages = 1297–1307 | date = November 2012 | pmid = 22080494 | pmc = 3494061 | doi = 10.1093/schbul/sbr134 }}</ref><ref>{{cite journal | vauthors = Palaniyappan L, Balain V, Liddle PF | title = The neuroanatomy of psychotic diathesis: a meta-analytic review | journal = Journal of Psychiatric Research | volume = 46 | issue = 10 | pages = 1249–1256 | date = October 2012 | pmid = 22790253 | doi = 10.1016/j.jpsychires.2012.06.007 }}</ref>

Another meta analysis reported bilateral reductions in insula, operculum, STG, medial frontal cortex, and ACC, but also reported increased GMV in the right [[lingual gyrus]] and left [[precentral gyrus]].<ref name="Radua">{{cite journal | vauthors = Radua J, Borgwardt S, Crescini A, Mataix-Cols D, Meyer-Lindenberg A, McGuire PK, Fusar-Poli P | title = Multimodal meta-analysis of structural and functional brain changes in first episode psychosis and the effects of antipsychotic medication | journal = Neuroscience and Biobehavioral Reviews | volume = 36 | issue = 10 | pages = 2325–2333 | date = November 2012 | pmid = 22910680 | doi = 10.1016/j.neubiorev.2012.07.012 | quote = Patients with an FEP showed large and robust bilateral decreases of GMV in a peri-Sylvian cluster that included the insula, operculum and the superior temporal gyrus, and in the medial frontal and anterior cingulate cortices (MeF/ACC) (Fig. 2A and Supplementary Table S2). Patients had relatively greater GMV than controls in the right lingual gyrus and left precentral gyrus. | doi-access = free }}</ref>  The [[Kraepelinian dichotomy]] is made questionable{{Clarify | date = November 2019 | reason = Non sequitur.  Also, even the provided link doesn't clarify why GMV abnormalities would make the Kraepelinian dichotomy, which also separates schizophrenia from bipolar disorder, questionable. }} by grey matter abnormalities in bipolar and schizophrenia; schizophrenia is distinguishable from bipolar in that regions of grey matter reduction are generally larger in magnitude, although adjusting for gender differences reduces the difference to the left [[dorsomedial prefrontal cortex]], and right [[dorsolateral prefrontal cortex]].<ref>{{cite journal | vauthors = Bora E, Fornito A, Yücel M, Pantelis C | title = The effects of gender on grey matter abnormalities in major psychoses: a comparative voxelwise meta-analysis of schizophrenia and bipolar disorder | journal = Psychological Medicine | volume = 42 | issue = 2 | pages = 295–307 | date = February 2012 | pmid = 21835091 | doi = 10.1017/S0033291711001450 | s2cid = 206252132 }}</ref>

During attentional tasks, first episode psychosis is associated with hypoactivation in the right middle frontal gyrus, a region generally described as encompassing the dorsolateral prefrontal cortex (dlPFC).Altered Behavioral Inhibition System functioning could possibly cause reduced sustained attention in psychosis and overall contribute to more negative reactions.<ref>{{Cite journal |last1=Osborne |first1=K. Juston |last2=Zhang |first2=Wendy |last3=Gupta |first3=Tina |last4=Farrens |first4=Jaclyn |last5=Geiger |first5=McKena |last6=Kraus |first6=Brian |last7=Krugel |first7=Chloe |last8=Nusslock |first8=Robin |last9=Kappenman |first9=Emily S. |last10=Mittal |first10=Vijay A. |date=November 2023 |title=Clinical high risk for psychosis syndrome is associated with reduced neural responding to unpleasant images. |journal=Journal of Psychopathology and Clinical Science |language=en |volume=132 |issue=8 |pages=1060–1071 |doi=10.1037/abn0000862 |pmid=37796541 |issn=2769-755X|doi-access=free |pmc=11812458 }}</ref> In congruence with studies on grey matter volume, hypoactivity in the right insula, and right inferior parietal lobe is also reported.<ref>{{cite journal | vauthors = Del Casale A, Kotzalidis GD, Rapinesi C, Sorice S, Girardi N, Ferracuti S, Girardi P | title = Functional Magnetic Resonance Imaging Correlates of First-Episode Psychoses during Attentional and Memory Task Performance | journal = Neuropsychobiology | volume = 74 | issue = 1 | pages = 22–31 | date = 2016 | pmid = 27698323 | doi = 10.1159/000448620 | s2cid = 5806628 }}</ref> During cognitive tasks, hypoactivities in the right insula, dACC, and the left precuneus, as well as reduced deactivations in the right [[basal ganglia]], right [[thalamus]], right [[Inferior frontal gyrus|inferior frontal]] and left precentral gyri are observed. These results are highly consistent and replicable possibly except the abnormalities of the right inferior frontal gyrus.<ref>{{harvnb|Radua|Borgwardt|Crescini|Mataix-Cols|2012|loc=3.3. Changes in regional brain response to cognitive tasks.}} "In the anterior part of the right insula and in the dorsal ACC there was hypoactivation relative to controls, whereas in the right basal ganglia/thalamus extending to the posterior part of the insula and in the medial frontal cortex, there was a relative reduction in deactivation... Patients also showed reductions in deactivation in the right inferior frontal and left precentral gyri, as well as hypoactivation in left precuneus. ... The analyses of robustness showed that all these results were highly replicable, with the possible exception of the abnormalities in right inferior frontal gyrus..."</ref> Decreased grey matter volume in conjunction with bilateral hypoactivity is observed in anterior insula, dorsal medial frontal cortex, and dorsal ACC. Decreased grey matter volume and bilateral hyperactivity is reported in posterior insula, ventral medial frontal cortex, and ventral ACC.<ref>{{Harvnb|Radua|Borgwardt|Crescini|Mataix-Cols|2012|loc=3.4. Multimodal analysis of grey matter volume and brain response.}} "Specifically, the anterior parts of the insulae and the dorsal part of the MeF/ACC showed hypoactivation, whereas the posterior parts of the insulae and the ventral part of the MeF/ACC showed reductions in deactivation (Fig. 3 and Table 1)."</ref>

=== Hallucinations ===
Studies during acute experiences of hallucinations demonstrate increased activity in primary or secondary sensory cortices. As auditory hallucinations are most common in psychosis, most robust evidence exists for increased activity in the left [[middle temporal gyrus]], left [[superior temporal gyrus]], and left [[inferior frontal gyrus]] (i.e. [[Broca's area]]). Activity in the [[ventral striatum]], [[hippocampus]],<ref>{{cite journal |last1=Pines |first1=Andrew R. |last2=Frandsen |first2=Summer B. |last3=Drew |first3=William |last4=Meyer |first4=Garance M. |last5=Howard |first5=Calvin |last6=Palm |first6=Stephan T. |last7=Schaper |first7=Frederic L. W. V. J. |last8=Lin |first8=Christopher |last9=Butenko |first9=Konstantin |last10=Ferguson |first10=Michael A. |last11=Friedrich |first11=Maximilian U. |last12=Grafman |first12=Jordan H. |last13=Kappel |first13=Ari D. |last14=Neudorfer |first14=Clemens |last15=Rost |first15=Natalia S. |last16=Sanderson |first16=Lauren L. |last17=Taylor |first17=Joseph J. |last18=Wu |first18=Ona |last19=Kletenik |first19=Isaiah |last20=Vogel |first20=Jacob W. |last21=Cohen |first21=Alexander L. |last22=Horn |first22=Andreas |last23=Fox |first23=Michael D. |last24=Silbersweig |first24=David |last25=Siddiqi |first25=Shan H. |title=Mapping Lesions That Cause Psychosis to a Human Brain Circuit and Proposed Stimulation Target |journal=JAMA Psychiatry |doi=10.1001/jamapsychiatry.2024.4534 |date=12 February 2025|volume=82 |issue=4 |pages=368–378 |pmid=39937525 |pmc=11822627 |pmc-embargo-date=February 12, 2026 }}</ref> and ACC are related to the lucidity of hallucinations, and indicate that activation or involvement of emotional circuitry are key to the impact of abnormal activity in sensory cortices. Together, these findings indicate abnormal processing of internally generated sensory experiences, coupled with abnormal emotional processing, results in hallucinations. One proposed model involves a failure of feedforward networks from sensory cortices to the inferior frontal cortex, which normally cancel out sensory cortex activity during internally generated speech. The resulting disruption in expected and perceived speech is thought to produce lucid hallucinatory experiences.<ref>{{cite book| vauthors = Brown G, Thompson W | veditors = Swerdlow N |title=Behavioral Neurobiology of Schizophrenia and its Treatment|publisher=Springer|pages=185–189|chapter=Functional Brain Imaging in Schizophrenia: Selected Results and Methods}}</ref>

=== Delusions ===
The two-factor model of delusions posits that dysfunction in both belief formation systems and belief evaluation systems are necessary for delusions. Dysfunction in evaluations systems localized to the right lateral prefrontal cortex, regardless of delusion content, is supported by neuroimaging studies and is congruent with its role in conflict monitoring in healthy persons. Abnormal activation and reduced volume is seen in people with delusions, as well as in disorders associated with delusions such as [[frontotemporal dementia]], psychosis and [[Lewy body dementia]]. Furthermore, lesions to this region are associated with "jumping to conclusions", damage to this region is associated with post-stroke delusions, and hypometabolism this region associated with caudate strokes presenting with delusions.

The [[Aberrant salience|aberrant salience model]] suggests that delusions are a result of people assigning excessive importance to irrelevant stimuli. In support of this hypothesis, regions normally associated with the [[salience network]] demonstrate reduced grey matter in people with delusions, and the neurotransmitter [[dopamine]], which is widely implicated in salience processing, is also widely implicated in psychotic disorders.

Specific regions have been associated with specific types of delusions. The volume of the hippocampus and parahippocampus is related to paranoid delusions in [[Alzheimer's disease]], and has been reported to be abnormal post mortem in one person with delusions. [[Capgras delusion]]s have been associated with occipito-temporal damage, and may be related to failure to elicit normal emotions or memories in response to faces.<ref>{{cite book | vauthors = Naasan G | chapter=The Anatomy of Delusions | veditors = Lehner T, Miller B, State M | title=Genomics, Circuits, and Pathways in Clinical Neuropsychiatry|publisher=Elsevier Science|pages=366–369}}</ref>

=== Negative symptoms ===
{{Technical|section|date=November 2019}}<!-- Probably need further explanations on: 1) implicit/explicit contingencies 2) reward prediction + positive/negative reward prediction errors. -->
Psychosis is associated with the [[ventral striatum]] (VS), which is the part of the brain that is involved with the desire to naturally satisfy the body's needs.<ref name=":02">{{cite journal | vauthors = Jensen J, McIntosh AR, Crawley AP, Mikulis DJ, Remington G, Kapur S | title = Direct activation of the ventral striatum in anticipation of aversive stimuli | journal = Neuron | volume = 40 | issue = 6 | pages = 1251–1257 | date = December 2003 | pmid = 14687557 | doi = 10.1016/S0896-6273(03)00724-4 | s2cid = 14691522 | doi-access = free }}</ref> When high reports of [[Symptom#Negative symptoms|negative symptoms]] were recorded, there were significant irregularities in the left VS. Anhedonia, defined as the inability to feel joy or pleasure,<ref>{{cite web |title=Anhedonia |url=https://my.clevelandclinic.org/health/symptoms/25155-anhedonia |website=Cleveland Clinic |access-date=19 September 2025}}</ref> is a commonly reported symptom in psychosis; experiences with the condition are present in most people with schizophrenia.<ref name=":12">{{Cite journal| vauthors = Germans MK, Kring AM |date=April 2000|title=Hedonic deficit in anhedonia: support for the role of approach motivation|url=https://linkinghub.elsevier.com/retrieve/pii/S0191886999001294|journal=Personality and Individual Differences|language=en|volume=28|issue=4|pages=659–672|doi=10.1016/S0191-8869(99)00129-4|access-date=2021-10-16|archive-date=2018-07-01|archive-url=https://web.archive.org/web/20180701042319/https://linkinghub.elsevier.com/retrieve/pii/S0191886999001294|url-status=live|url-access=subscription}}</ref> Previous research has indicated that a deficiency in the [[neural representation]] in regards to goals and the motivation to achieve them, has demonstrated that when a reward is not present, a strong reaction is noted in the ventral striatum; reinforcement learning is intact when contingencies about stimulus-reward are implicit, but not when they require explicit neural processing; reward prediction errors are what the actual reward is versus what the reward was predicted to be.<ref name=":22">{{cite journal | vauthors = Schultz W | title = Reward prediction error | journal = Current Biology | volume = 27 | issue = 10 | pages = R369–R371 | date = May 2017 | pmid = 28535383 | doi = 10.1016/j.cub.2017.02.064 | s2cid = 29170534 | doi-access = free | bibcode = 2017CBio...27.R369S }}</ref> In most cases positive prediction errors are considered an abnormal occurrence. A positive prediction error response occurs when there is an increased activation in a brain region, typically the [[striatum]], in response to unexpected rewards. A negative prediction error response occurs when there is a decreased activation in a region when predicted rewards do not occur. [[Anterior Cingulate Cortex (ACC)]] response, taken as an indicator of effort allocation, does not increase with reward or reward probability increase, and is associated with negative symptoms; deficits in [[Dorsolateral prefrontal cortex|Dorsolateral Prefrontal Cortex (dlPFC)]] activity and failure to improve performance on cognitive tasks when offered monetary incentives are present; and dopamine mediated functions are abnormal.

=== Neurobiology ===
{{Further|Dopamine hypothesis of schizophrenia}}
{{Technical|section|date=November 2019}}<!-- Probably need further explanations on: NMDA mediated top down predictions and bottom up AMPA mediated predictions errors. -->
Psychosis has been traditionally linked to the overactivity of the [[neurotransmitter]] [[dopamine]], in particular to its effect in the [[mesolimbic pathway]], spanning from the [[ventral tegmental area]] to the ventral [[striatum]]. Additionally, recent evidence suggests a crucial involvement of the pathway spanning from the [[substantia nigra]] to the dorsal [[striatum]].<ref>{{cite journal |last1= Grimaldi |first1=D-A |last2= Patane' |first2=A |last3= Cattarinussi |first3=G |last4= Sambataro |first4=F |title= Functional connectivity of the striatum in psychosis: Meta-analysis of functional magnetic resonance imaging studies and replication on an independent sample |journal=Neuroscience & Biobehavioral Reviews |date=2 May 2025 |volume=174 |article-number=106179 |doi=10.1016/j.neubiorev.2025.106179 |pmid= 40288705 |url=https://kclpure.kcl.ac.uk/portal/en/publications/0ef853cb-265b-4b9d-91fa-b47e44695851 }}</ref> The two major sources of evidence given to support this theory are that [[dopamine receptor D2]] blocking drugs (i.e., [[antipsychotic]]s) tend to reduce the intensity of psychotic symptoms, and that drugs that accentuate dopamine release, or inhibit its reuptake (such as [[amphetamine]]s and [[cocaine]]) can trigger psychosis in some people (see [[stimulant psychosis]]).<ref name="Kapur">{{cite journal | vauthors = Kapur S, Mizrahi R, Li M | title = From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis | journal = Schizophrenia Research | volume = 79 | issue = 1 | pages = 59–68 | date = November 2005 | pmid = 16005191 | doi = 10.1016/j.schres.2005.01.003 | s2cid = 2654713 }}</ref> However, there is substantial evidence that dopaminergic overactivity does not fully explain psychosis, and that neurodegerative pathophysiology plays a significant role. This is evidenced by the fact that psychosis commonly occurs in neurodegenerative diseases of the dopaminergic nervous system, such as Parkinson's disease, which involved reduced, rather than increased, dopaminergic activity.<ref>{{Cite journal |last1=Fénelon |first1=Gilles |last2=Alves |first2=Guido |date=2010-02-15 |title=Epidemiology of psychosis in Parkinson's disease |url=https://www.sciencedirect.com/science/article/abs/pii/S0022510X09007679 |journal=Journal of the Neurological Sciences |series=Mental Dysfunction in Parkinson's Disease |volume=289 |issue=1 |pages=12–17 |doi=10.1016/j.jns.2009.08.014 |pmid=19740486 |issn=0022-510X|url-access=subscription }}</ref>

The [[endocannabinoid system]] is also implicated in psychosis. This is evidenced by the propensity of [[Cannabinoid receptor 1|CB<sub>1</sub> receptor]] agonists such as [[THC]] to induce psychotic symptoms,<ref>{{Citation |last=D'Souza |first=Deepak Cyril |title=Cannabinoids and Psychosis |date=2007-01-01 |journal=International Review of Neurobiology |volume=78 |pages=289–326 |url=https://www.sciencedirect.com/science/article/abs/pii/S0074774206780102 |access-date=2024-11-06 |series=Integrating the Neurobiology of Schizophrenia |publisher=Academic Press|doi=10.1016/S0074-7742(06)78010-2 |pmid=17349865 |isbn=978-0-12-373737-3 |url-access=subscription }}</ref> and the efficacy of [[Cannabinoid receptor 1|CB<sub>1</sub> receptor]] antagonists such as [[Cannabidiol|CBD]] in ameliorating psychosis.<ref>{{Cite journal |last1=Chesney |first1=Edward |last2=Oliver |first2=Dominic |last3=McGuire |first3=Philip |date=2022-05-01 |title=Cannabidiol (CBD) as a novel treatment in the early phases of psychosis |journal=Psychopharmacology |language=en |volume=239 |issue=5 |pages=1179–1190 |doi=10.1007/s00213-021-05905-9 |issn=1432-2072 |pmc=9110455 |pmid=34255100}}</ref>

NMDA receptor dysfunction has been proposed as a mechanism in psychosis.<ref>{{cite journal | vauthors = Egerton A, Fusar-Poli P, Stone JM | title = Glutamate and psychosis risk | journal = Current Pharmaceutical Design | volume = 18 | issue = 4 | pages = 466–478 | date = 2012 | pmid = 22239577 | doi = 10.2174/138161212799316244 }}</ref>  This theory is reinforced by the fact that [[dissociative]] [[NMDA receptor antagonist]]s such as [[ketamine]], [[Phencyclidine|PCP]] and [[dextromethorphan]] (at large overdoses) induce a psychotic state. The symptoms of dissociative [[Substance intoxication|intoxication]] are also considered to mirror the symptoms of schizophrenia, including [[Schizophrenia#Negative symptoms|negative symptoms]].<ref>{{cite journal | vauthors = Bergeron R, Coyle JT | title = NAAG, NMDA receptor and psychosis | journal = Current Medicinal Chemistry | volume = 19 | issue = 9 | pages = 1360–1364 | date = 2012 | pmid = 22304714 | pmc = 3424071 | doi = 10.2174/092986712799462685 }}</ref>  NMDA receptor antagonism, in addition to producing symptoms reminiscent of psychosis, mimics the neurophysiological aspects, such as reduction in the amplitude of [[P50 (neuroscience)|P50]], [[P300 (neuroscience)|P300]], and [[Mismatch negativity|MMN]] [[evoked potential]]s.<ref>{{cite journal | vauthors = Adams RA, Stephan KE, Brown HR, Frith CD, Friston KJ | title = The computational anatomy of psychosis | journal = Frontiers in Psychiatry | volume = 4 | page = 47 | date = 2013 | pmid = 23750138 | pmc = 3667557 | doi = 10.3389/fpsyt.2013.00047 | doi-access = free }}</ref> Hierarchical Bayesian neurocomputational models of sensory feedback, in agreement with neuroimaging literature, link NMDA receptor hypofunction to delusional or hallucinatory symptoms via proposing a failure of NMDA mediated top down predictions to adequately cancel out enhanced bottom up AMPA mediated predictions errors.<ref>{{cite journal | vauthors = Corlett PR, Frith CD, Fletcher PC | title = From drugs to deprivation: a Bayesian framework for understanding models of psychosis | journal = Psychopharmacology | volume = 206 | issue = 4 | pages = 515–530 | date = November 2009 | pmid = 19475401 | pmc = 2755113 | doi = 10.1007/s00213-009-1561-0 }}</ref> Excessive prediction errors in response to stimuli that would normally not produce such a response is thought to root from conferring excessive salience to otherwise mundane events.<ref>{{cite journal | vauthors = Corlett PR, Honey GD, Krystal JH, Fletcher PC | title = Glutamatergic model psychoses: prediction error, learning, and inference | journal = Neuropsychopharmacology | volume = 36 | issue = 1 | pages = 294–315 | date = January 2011 | pmid = 20861831 | pmc = 3055519 | doi = 10.1038/npp.2010.163 }}</ref> Dysfunction higher up in the hierarchy, where representation is more abstract, could result in delusions.<ref>{{cite journal | vauthors = Corlett PR, Taylor JR, Wang XJ, Fletcher PC, Krystal JH | title = Toward a neurobiology of delusions | journal = Progress in Neurobiology | volume = 92 | issue = 3 | pages = 345–369 | date = November 2010 | pmid = 20558235 | pmc = 3676875 | doi = 10.1016/j.pneurobio.2010.06.007 }}</ref> The common finding of reduced [[GAD67]] expression in psychotic disorders may explain enhanced AMPA mediated signaling, caused by reduced GABAergic inhibition.<ref>{{cite journal | vauthors = Kalkman HO, Loetscher E | title = GAD(67): the link between the GABA-deficit hypothesis and the dopaminergic- and glutamatergic theories of psychosis | journal = Journal of Neural Transmission | volume = 110 | issue = 7 | pages = 803–812 | date = July 2003 | pmid = 12811640 | doi = 10.1007/s00702-003-0826-8 | s2cid = 31685339 }}</ref><ref>{{cite journal | vauthors = Akbarian S, Huang HS | title = Molecular and cellular mechanisms of altered GAD1/GAD67 expression in schizophrenia and related disorders | journal = Brain Research Reviews | volume = 52 | issue = 2 | pages = 293–304 | date = September 2006 | pmid = 16759710 | doi = 10.1016/j.brainresrev.2006.04.001 | s2cid = 25771139 }}</ref>

The connection between dopamine and psychosis is generally believed to be complex. While dopamine receptor D2 suppresses [[adenylate cyclase]] activity, the [[Dopamine receptor D1|D1]] receptor increases it. If D2-blocking drugs are administered, the blocked dopamine spills over to the D1 receptors. The increased adenylate cyclase activity affects [[genetic expression]] in the nerve cell, which takes time. Hence antipsychotic drugs take a week or two to reduce the symptoms of psychosis. Moreover, newer and equally effective antipsychotic drugs actually block slightly less dopamine in the brain than older drugs whilst also blocking 5-HT2A receptors, suggesting the 'dopamine hypothesis' may be oversimplified.<ref>{{cite journal | vauthors = Jones HM, Pilowsky LS | title = Dopamine and antipsychotic drug action revisited | journal = The British Journal of Psychiatry | volume = 181 | issue = 4 | pages = 271–275 | date = October 2002 | pmid = 12356650 | doi = 10.1192/bjp.181.4.271 | doi-access = free }}</ref> Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis<ref>{{cite journal | vauthors = Soyka M, Zetzsche T, Dresel S, Tatsch K | title = FDG-PET and IBZM-SPECT suggest reduced thalamic activity but no dopaminergic dysfunction in chronic alcohol hallucinosis | journal = The Journal of Neuropsychiatry and Clinical Neurosciences | volume = 12 | issue = 2 | pages = 287–288 | date = May 2000 | pmid = 11001615 | doi = 10.1176/appi.neuropsych.12.2.287 }}</ref> and Zoldan et al. reported moderately successful use of [[ondansetron]], a 5-HT<sub>3</sub> receptor antagonist, in the treatment of [[levodopa]] psychosis in [[Parkinson's disease]] patients.<ref name="Zoldan_et_al_1995">{{cite journal | vauthors = Zoldan J, Friedberg G, Livneh M, Melamed E | title = Psychosis in advanced Parkinson's disease: treatment with ondansetron, a 5-HT3 receptor antagonist | journal = Neurology | volume = 45 | issue = 7 | pages = 1305–1308 | date = July 1995 | pmid = 7617188 | doi = 10.1212/WNL.45.7.1305 | s2cid = 45540572 }}</ref>

A review found an association between a first-episode of psychosis and prediabetes.<ref>{{cite journal | vauthors = Perry BI, McIntosh G, Weich S, Singh S, Rees K | title = The association between first-episode psychosis and abnormal glycaemic control: systematic review and meta-analysis | journal = The Lancet. Psychiatry | volume = 3 | issue = 11 | pages = 1049–1058 | date = November 2016 | pmid = 27720402 | doi = 10.1016/S2215-0366(16)30262-0 | url = http://wrap.warwick.ac.uk/84089/1/WRAP-association-episode-abnormal-review-Perry-2016.pdf | access-date = 2019-07-03 | url-status = live | archive-url = https://web.archive.org/web/20201001200220/http://wrap.warwick.ac.uk/84089/1/WRAP-association-episode-abnormal-review-Perry-2016.pdf | archive-date = 2020-10-01 }}</ref>

Prolonged or high dose use of [[psychostimulants]] can alter normal functioning, making it similar to the manic phase of bipolar disorder.<ref>{{cite journal | vauthors = Curran C, Byrappa N, McBride A | title = Stimulant psychosis: systematic review | journal = The British Journal of Psychiatry | volume = 185 | issue = 3 | pages = 196–204 | date = September 2004 | pmid = 15339823 | doi = 10.1192/bjp.185.3.196 | doi-access = free }}</ref> NMDA antagonists replicate some of the so-called "negative" symptoms like [[thought disorder]] in subanesthetic doses (doses insufficient to induce [[anesthesia]]), and [[catatonia]] in high doses. Psychostimulants, especially in one already prone to psychotic thinking, can cause some "positive" symptoms, such as delusional beliefs, particularly those persecutory in nature.

=== Culture ===
Cross-cultural studies into schizophrenia have found that individual experiences of psychosis and 'hearing voices' vary across cultures.<ref name=":5">{{cite journal | vauthors = Luhrmann TM, Padmavati R, Tharoor H, Osei A | title = Hearing Voices in Different Cultures: A Social Kindling Hypothesis | journal = Topics in Cognitive Science | volume = 7 | issue = 4 | pages = 646–663 | date = October 2015 | pmid = 26349837 | doi = 10.1111/tops.12158 | doi-access = free }}</ref><ref>{{Cite book|title=Our Most Troubling Madness|date=2016-09-27|publisher=University of California Press|doi=10.1525/california/9780520291089.001.0001|isbn=978-0-520-29108-9| veditors = Luhrmann TM, Marrow J }}</ref> In countries such as the [[United States]] where there exists a predominantly biomedical understanding of the body, the mind and in turn, mental health, subjects were found to report their hallucinations as having 'violent content' and self-describing as 'crazy'.<ref name=":5" /> This experience is at odds with the experiences of subjects in [[Accra, Ghana]], who describe the voices they hear as having 'spiritual meaning' and are often reported as positive in nature; or subjects in [[Chennai, India]], who describe their hallucinations as kin, family members or close friends, and offering guidance.<ref name=":5" />

These differences are attributed to 'social kindling' or how one's social context shapes the way they interpret and experience sensations such as hallucinations. This concept aligns with preexisting cognitive theory such as reality modelling and is supported by recent research that demonstrates that individuals with psychosis can be taught to attend to their hallucinations differently, which in turn alters the hallucinations themselves.<ref>{{cite journal | vauthors = Jenner JA, van de Willige G, Wiersma D | title = Effectiveness of cognitive therapy with coping training for persistent auditory hallucinations: a retrospective study of attenders of a psychiatric out-patient department | journal = Acta Psychiatrica Scandinavica | volume = 98 | issue = 5 | pages = 384–389 | date = November 1998 | pmid = 9845177 | doi = 10.1111/j.1600-0447.1998.tb10103.x | url = https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0447.1998.tb10103.x | access-date = 2021-08-26 | url-status = live | s2cid = 39279836 | archive-url = https://web.archive.org/web/20210826024511/https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0447.1998.tb10103.x | archive-date = 2021-08-26 | url-access = subscription }}</ref> Such research creates pathways for social or community-based treatment, such as reality monitoring, for individuals with schizophrenia and other psychotic disorders, providing alternatives to, or supplementing traditional pharmacologic management.

Cross-cultural studies explore the way in which psychosis varies in different cultures, countries and religions. The cultural differences are based on the individual or shared illness narratives surrounding cultural meanings of illness experience.<ref name="Jenkins J 2018">Jenkins J (2018) 'Anthropology and Psychiatry: A contemporary convergence for global mental health', in Bhugra D and Bhui K (eds) Textbook of Cultural Psychiatry, 2nd edn, Cambridge University Press, London.</ref> In countries such as [[India]], [[Cambodia]] and [[Muslim]] majority countries, they each share alternative epistemologies. These are known as knowledge systems that focus on the connections between mind, body, culture, nature and society.<ref>Scheper-Hughes N and Lock M (1987) 'The mindful body: a prolegomenon to future work in medical anthropology', Medical Anthropology Quarterly, 1(1):6–41</ref> Cultural perceptions of mental disorders such as psychosis or schizophrenia are believed to be caused by [[jinn]] (spirits) in Muslim majority countries.<ref name="doi.org">{{Cite journal |last1=Valaitė |first1=Dovilė |last2=Berniūnas |first2=Renatas |date=2024 |title=Majnūn or Mental Disorders: Between Cultural Traditions and Western Psychology in Jordan |url=https://link.springer.com/article/10.1007/s11013-022-09787-0 |journal=Culture, Medicine, and Psychiatry |language=en |volume=48 |issue=1 |pages=136–157 |doi=10.1007/s11013-022-09787-0|pmid=35948861 |url-access=subscription }}</ref> Furthermore, those in [[Arab]]-Muslim societies perceive those who act differently than the social norm as "crazy" or as abnormal behaviour.<ref name="doi.org" /> This differs from the experiences of individuals in India and how they attain their perspectives on mental health issues through a variety of spiritual and healing traditions.<ref>{{Cite journal |last1=Raghavan |first1=Raghu |last2=Brown |first2=Brian |last3=Horne |first3=Francesca |last4=Kamal |first4=Sreedevi Ram |last5=Parameswaran |first5=Uma |last6=Raghu |first6=Ardra |last7=Wilson |first7=Amanda |last8=Venkateswaran |first8=Chitra |last9=Svirydzenka |first9=Nadia |last10=Lakhanpaul |first10=Monica |last11=Dasan |first11=Chandra |date=2023 |title=Multiple Mental Health Literacies in a Traditional Temple Site in Kerala: The Intersection Between Beliefs, Spiritual and Healing Regimes |url=https://link.springer.com/article/10.1007/s11013-022-09800-6 |journal=Culture, Medicine, and Psychiatry |language=en |volume=47 |issue=3 |pages=743–765 |doi=10.1007/s11013-022-09800-6|pmid=35771306 |hdl=2086/21950 |hdl-access=free }}</ref> In Cambodia, hallucinations are linked with spirit visitation, a term they call "cultural kindling".<ref>{{Cite journal |last1=Hinton |first1=Devon E. |last2=Reis |first2=Ria |last3=de Jong |first3=Joop |date=2020 |title=Ghost Encounters Among Traumatized Cambodian Refugees: Severity, Relationship to PTSD, and Phenomenology |url=https://link.springer.com/article/10.1007/s11013-019-09661-6 |journal=Culture, Medicine, and Psychiatry |language=en |volume=44 |issue=3 |pages=333–359 |doi=10.1007/s11013-019-09661-6|pmid=31701326 |url-access=subscription }}</ref> These examples of differences are attributed to culture and the way it shapes conceptions of mental disorders.<ref name="doi.org" /> These cultural differences can be useful in bridging the gap of cultural understanding and psychiatric signs and symptoms.<ref name="Jenkins J 2018" />

== Diagnosis ==
To make a diagnosis of a mental illness in someone with psychosis [[diagnosis of exclusion|other potential causes must be excluded]].<ref name="Ol2012">{{cite web| vauthors = Freudenreich O |title=Differential Diagnosis of Psychotic Symptoms: Medical "Mimics"|url=http://www.psychiatrictimes.com/forensic-psychiatry/differential-diagnosis-psychotic-symptoms-medical-%E2%80%9Cmimics%E2%80%9D|website=Psychiatric Times|publisher=UBM Medica|date=3 December 2012|access-date=16 March 2017|archive-date=4 June 2013|archive-url=https://web.archive.org/web/20130604094749/http://www.psychiatrictimes.com/forensic-psychiatry/differential-diagnosis-psychotic-symptoms-medical-%E2%80%9Cmimics%E2%80%9D|url-status=live}}</ref> An initial assessment includes a comprehensive history and physical examination by a health care provider. Tests may be done to exclude substance use, medication, toxins, surgical complications, or other medical illnesses. A person with psychosis is referred to as psychotic.

[[Delirium]] should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses.<ref name="Med_News">{{cite news| vauthors = Nordqvist C |title=What Is Schizoaffective Disorder? What Causes Schizoaffective Disorder?|url=http://www.medicalnewstoday.com/articles/190678.php|access-date=March 16, 2017|newspaper=Medical News Today|date=August 8, 2016|archive-date=June 5, 2010|archive-url=https://web.archive.org/web/20100605080349/http://www.medicalnewstoday.com/articles/190678.php|url-status=live}}</ref> Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:
* [[thyroid-stimulating hormone]] to exclude [[hypothyroidism|hypo-]] or [[hyperthyroidism]],
* [[Vitamin B12|vitamin B<sub>12</sub>]] serum and urinary [[Methylmalonic acid|MMA]] to role out [[pernicious anemia]] or [[Vitamin B12 deficiency|vitamin B<sub>12</sub> deficiency]],
* [[Blood tests#Blood chemistry tests|basic electrolytes]] and [[serum calcium]] to rule out a metabolic disturbance,
* [[full blood count]] including [[erythrocyte sedimentation rate|ESR]] to rule out a systemic infection or chronic disease, and
* [[serology]] to exclude [[syphilis]] or [[HIV]] infection.

Other investigations include:
* [[EEG]] to exclude [[epilepsy]], and an
* [[MRI]] or [[CT scan]] of the head to exclude brain lesions.

Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be [[diagnosis of exclusion|ruled out]], particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be [[diagnosis of exclusion|excluded]] to a high level of certainty, using toxicology screening.

Because some [[dietary supplement]]s may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements.<ref>{{cite journal | title = Final rule declaring dietary supplements containing ephedrine alkaloids adulterated because they present an unreasonable risk. Final rule | journal = Federal Register | volume = 69 | issue = 28 | pages = 6787–6854 | date = February 2004 | pmid = 14968803 | url = http://www.federalregister.gov/a/04-2912/p-276 | access-date = 2014-09-29 | url-status = live | archive-url = https://web.archive.org/web/20210829020131/https://www.federalregister.gov/documents/2004/02/11/04-2912/final-rule-declaring-dietary-supplements-containing-ephedrine-alkaloids-adulterated-because-they | archive-date = 2021-08-29 | author-link1 = Food and Drug Administration | last1 = Food Drug Administration | first1 = HHS }} ({{Federal Register|69|6814}} and {{Federal Register|69|6818}})</ref>

Common mistakes made when diagnosing people who are psychotic include:<ref name="Ol2012" />
* Not properly excluding [[delirium]],
* Not appreciating medical abnormalities (e.g., vital signs),
* Not obtaining a medical history and family history,
* Indiscriminate screening without an organizing framework,
* Missing a toxic psychosis by not screening for substances ''and'' medications,
* Not asking their families or others about dietary supplements,
* Premature diagnostic closure, and
* Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.

Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric [[differential diagnosis]] using a person's family history, incorporating information from the person with psychosis, and information from family, friends or romantic partners.

Types of psychosis in psychiatric disorders may be established by formal rating scales. The [[Brief Psychiatric Rating Scale]] (BPRS)<ref>{{cite journal | vauthors = Overall JE, Gorham DR | title = The Brief Psychiatric Rating Scale. | journal = Psychol. Rep. | date = 1962 | volume = 10 | issue = 3 | pages = 799–812 | doi = 10.2466/pr0.1962.10.3.799 | s2cid = 143531021 }}</ref> assesses the level of 18 symptom constructs of psychosis such as [[hostility]], [[Suspicion (emotion)|suspicion]], [[hallucination]], and [[grandiosity]]. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also answer questions on the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale ([[PANSS]]).<ref>{{cite journal | vauthors = Kay SR, Fiszbein A, Opler LA | title = The positive and negative syndrome scale (PANSS) for schizophrenia | journal = Schizophrenia Bulletin | volume = 13 | issue = 2 | pages = 261–276 | year = 1987 | pmid = 3616518 | doi = 10.1093/schbul/13.2.261 | doi-access = free }}</ref>

The [[DSM-5]] characterizes disorders as psychotic or on the schizophrenia spectrum if they involve hallucinations, delusions, disorganized thinking, grossly disorganized motor behavior, or negative symptoms.<ref name="DSM">{{cite book | author = American Psychiatric Association |title=Diagnostic and statistical manual of mental disorders: DSM-5.|date=2013|publisher=American Psychiatric Association|location=Washington, D.C.|isbn=978-0-89042-554-1|page=[https://archive.org/details/diagnosticstatis0005unse/page/125 125]|edition=5th|url=https://archive.org/details/diagnosticstatis0005unse/page/125}}</ref> The DSM-5 does not include psychosis as a definition in the glossary, although it defines "psychotic features", as well as "psychoticism" with respect to personality disorder. The [[ICD-10]] has no specific definition of psychosis.<ref name="Gaebel">{{cite journal | vauthors = Gaebel W, Zielasek J | title = Focus on psychosis | journal = Dialogues in Clinical Neuroscience | volume = 17 | issue = 1 | pages = 9–18 | date = March 2015 | pmid = 25987859 | pmc = 4421906 | doi = 10.31887/DCNS.2015.17.1/wgaebel }}</ref>

The PSQ (Psychosis Screening Questionnaire) is the most common tool in detecting psychotic symptoms and it includes five root questions that assess the presence of PLE (mania, thought insertion, paranoia, strange experiences and perceptual disturbances)<ref>{{Cite journal |last1=Thungana |first1=Yanga A. |last2=Zingela |first2=Zukiswa |last3=Wyk |first3=Stefan J. Van |last4=Kim |first4=Hannah H. |last5=Ametaj |first5=Amantia |last6=Stevenson |first6=Anne |last7=Stroud |first7=Rocky E. |last8=Stein |first8=Dan J. |last9=Gelaye |first9=Bizu |date=2023 |title=Psychosis screening questionnaire: Exploring its factor structure among South African adults |url=https://sajp.org.za/index.php/sajp/article/view/2051 |journal=South African Journal of Psychiatry |language=en |volume=29 |page=7 |doi=10.4102/sajpsychiatry.v29i0.2051 |pmc=10696556 |pmid=38059200}}</ref> The different tools used to assess symptom severity include the Revised Behavior and Symptom Identification Scale (BASIS-R), a 24-item self-report instrument with six scales: psychosis, depression/functioning, interpersonal problems, alcohol/drug use, self-harm, and emotional lability. The Symptom Checklist-90-Revised (SCL-90-R), a 90-item self assessment tool that measures psychoticism and paranoid ideation in addition to seven other symptom scales. Finally, the Brief Symptom Inventory (BSI), a 53-item self-administered scale developed from the SCL-90-R. The BSI has good psychometric properties and is an acceptable brief alternative to the SCL-90-R.<ref>U.S. Department of Veterans Affairs. (2024, February 15). ''VA.gov | Veterans affairs''. MIRECC / CoE Home. <nowiki>https://www.mirecc.va.gov/visn22/Assessment_Tools_for_Measuring_Outcomes_in_Psychosis.asp#top</nowiki></ref> These seem to be the most accurate tools at the moment,{{when|date=November 2025}} but a research in 2007 that focused on quantifying self-reports of auditory verbal hallucinations (AVH) in persons with psychosis, suggest that The Hamilton Program for Schizophrenia Voices Questionnaire (HPSVQ) is also potentially a reliable and useful measure for specifically quantifying AVHs in relation to psychosis.<ref>Van Lieshout, R. J., & Goldberg, J. O. (2007). Quantifying self-reports of auditory verbal hallucinations in persons with psychosis. ''Canadian Journal of Behavioural Science/Revue Canadienne Des Sciences Du Comportement, 39''(1), 73–77. <nowiki>https://doi.org/10.1037/cjbs2007006</nowiki></ref>

[[Factor analysis]] of symptoms generally regarded as psychosis frequently yields a five factor solution, albeit five factors that are distinct from the five domains defined by the DSM-5 to encompass [[psychotic]] or schizophrenia spectrum disorders. The five factors are frequently labeled as hallucinations, delusions, disorganization, excitement, and emotional distress.<ref name="Gaebel" /> The DSM-5 emphasizes a [[psychotic spectrum]], wherein the low end is characterized by schizoid personality disorder, and the high end is characterized by schizophrenia.<ref name="Continuum" />

Gouzoulis-Mayfrank et al. said that the pleasant or emotionally positive experiences that are common in psychosis, particularly in the early stages, are more easily overlooked in clinical practice than the negative experiences.<ref name="ReferenceA">Friesen P. Psychosis and psychedelics: Historical entanglements and contemporary contrasts.&nbsp;Transcultural Psychiatry. 2022;59(5):592-609. https://doi.org/10.1177/13634615221129116</ref> Nev Jones and Mona Shattel wrote that there is less curiosity towards the complications, or towards the richness of the good things as well as the bad things.<ref name="ReferenceA"/>

== Prevention ==
The evidence for the effectiveness of early interventions to [[Mental disorder#Prevention|prevent]] psychosis appeared inconclusive.<ref>{{cite journal | vauthors = Marshall M, Rathbone J | title = Early intervention for psychosis | journal = The Cochrane Database of Systematic Reviews | issue = 6 | article-number = CD004718 | date = June 2011 | pmid = 21678345 | pmc = 4163966 | doi = 10.1002/14651858.CD004718.pub3 }}</ref> But psychosis caused by drugs can be prevented.<ref>{{Cite web|url=https://www.nhs.uk/Conditions/Psychosis/Pages/Prevention-OLD.aspx|title=Psychosis – Prevention – NHS Choices|last=NHS|website=www.nhs.uk|language=en|access-date=2018-10-15|date=2017-10-23|archive-date=2018-10-15|archive-url=https://web.archive.org/web/20181015043847/https://www.nhs.uk/Conditions/Psychosis/Pages/Prevention-OLD.aspx|url-status=live}}</ref> Whilst early intervention in those with a psychotic episode might improve short-term outcomes, little benefit was seen from these measures after five years.<ref name="Lancet09">{{cite journal | vauthors = van Os J, Kapur S | title = Schizophrenia | journal = Lancet | volume = 374 | issue = 9690 | pages = 635–645 | date = August 2009 | pmid = 19700006 | doi = 10.1016/S0140-6736(09)60995-8 | s2cid = 208792724 }}</ref> However, there is evidence that [[cognitive behavioral therapy]] (C.B.T.) may reduce the risk of  becoming psychotic in those at high risk,<ref>{{cite journal | vauthors = Stafford MR, Jackson H, Mayo-Wilson E, Morrison AP, Kendall T | title = Early interventions to prevent psychosis: systematic review and meta-analysis | journal = BMJ | volume = 346 | pages = f185 | date = January 2013 | pmid = 23335473 | pmc = 3548617 | doi = 10.1136/bmj.f185 }}</ref> and in 2014 the U.K. [[National Institute for Health and Care Excellence|National Institute for Health and Care Excellence (N.I.C.E.)]] recommended preventive C.B.T. for people at risk of psychosis.<ref>{{cite web |url=http://www.nice.org.uk/newsroom/news/OfferTalkingTherapiesPeopleRiskPsychosisSchizophrenia.jsp |title=Offer talking therapies to people at risk of psychosis and schizophrenia |publisher=Nice.org.uk |date=2014-02-12 |access-date=2014-04-15 |archive-date=2014-03-05 |archive-url=https://web.archive.org/web/20140305175232/http://www.nice.org.uk/newsroom/news/OfferTalkingTherapiesPeopleRiskPsychosisSchizophrenia.jsp |url-status=live }}</ref><ref>{{cite web |url=http://www.nice.org.uk/guidance/index.jsp?action=byID&o=14382 |title=Psychosis and schizophrenia in adults |publisher=Nice.org.uk |date=2014-03-31 |access-date=2014-04-15 |archive-date=2014-03-05 |archive-url=https://web.archive.org/web/20140305175149/http://www.nice.org.uk/guidance/index.jsp?action=byID&o=14382 |url-status=live }}</ref>

== Treatment ==
The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first-line treatment for many psychotic disorders is antipsychotic medication,
<ref name="fn_72">{{cite web |url=https://www.nice.org.uk/guidance/cg178 |title=Schizophrenia: Full national clinical guideline on core interventions in primary and secondary care |date= 12 February 2014 |author=National Collaborating Centre for Mental Health |access-date= 21 September 2022 |archive-date= 1 September 2022 |archive-url= https://web.archive.org/web/20220901012650/https://www.nice.org.uk/guidance/cg178 |url-status=live }}</ref> which can reduce the positive symptoms of psychosis in about 7 to 14 days. For youth or adolescents, treatment options include medications, psychological interventions, and social interventions.<ref name=":3" />

=== Medication ===
The choice of which [[antipsychotic]] to use is based on benefits, risks, and costs.<ref name="Lancet09" /> It is debatable whether, as a class, [[typical antipsychotic|typical]] or [[atypical antipsychotic]]s are better.<ref>{{cite journal | vauthors = Kane JM, Correll CU | title = Pharmacologic treatment of schizophrenia | journal = Dialogues in Clinical Neuroscience | volume = 12 | issue = 3 | pages = 345–357 | year = 2010 | pmid = 20954430 | pmc = 3085113 | doi = 10.31887/DCNS.2010.12.3/jkane }}</ref><ref>{{cite journal | vauthors = Hartling L, Abou-Setta AM, Dursun S, Mousavi SS, Pasichnyk D, Newton AS | title = Antipsychotics in adults with schizophrenia: comparative effectiveness of first-generation versus second-generation medications: a systematic review and meta-analysis | journal = Annals of Internal Medicine | volume = 157 | issue = 7 | pages = 498–511 | date = October 2012 | pmid = 22893011 | doi = 10.7326/0003-4819-157-7-201210020-00525 | doi-access = free }}</ref> Tentative evidence supports that [[amisulpride]], [[olanzapine]], [[risperidone]] and [[clozapine]] may be more effective for positive symptoms but result in more side effects.<ref name="barry 2012" /> Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages.<ref name="AFP07">{{cite journal | vauthors = Schultz SH, North SW, Shields CG | title = Schizophrenia: a review | journal = American Family Physician | volume = 75 | issue = 12 | pages = 1821–1829 | date = June 2007 | pmid = 17619525 }}</ref> There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people.<ref name="AFP10">{{cite journal | vauthors = Smith T, Weston C, Lieberman J | title = Schizophrenia (maintenance treatment) | journal = American Family Physician | volume = 82 | issue = 4 | pages = 338–339 | date = August 2010 | pmid = 20704164 }}</ref> Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia),<ref>{{cite journal | vauthors = Taylor DM, Duncan-McConnell D | title = Refractory schizophrenia and atypical antipsychotics | journal = Journal of Psychopharmacology | volume = 14 | issue = 4 | pages = 409–418 | year = 2000 | pmid = 11198061 | doi = 10.1177/026988110001400411 | s2cid = 27270415 }}</ref> but it has the potentially serious side effect of [[agranulocytosis]] (lowered [[white blood cell]] count) in less than 4% of people.<ref name="Lancet09" /><ref name="BMJ07">{{cite journal | vauthors = Picchioni MM, Murray RM | title = Schizophrenia | journal = BMJ | volume = 335 | issue = 7610 | pages = 91–95 | date = July 2007 | pmid = 17626963 | pmc = 1914490 | doi = 10.1136/bmj.39227.616447.BE }}</ref><ref>{{cite journal | vauthors = Essali A, Al-Haj Haasan N, Li C, Rathbone J | title = Clozapine versus typical neuroleptic medication for schizophrenia | journal = The Cochrane Database of Systematic Reviews | issue = 1 | article-number = CD000059 | date = January 2009 | volume = 2009 | pmid = 19160174 | pmc = 7065592 | doi = 10.1002/14651858.CD000059.pub2 }}</ref>

Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of [[extrapyramidal side effects]] while some atypicals are associated with considerable weight gain, diabetes and risk of [[metabolic syndrome]]; this is most pronounced with olanzapine, while risperidone and [[quetiapine]] are also associated with weight gain.<ref name="barry 2012">{{cite journal | vauthors = Barry SJ, Gaughan TM, Hunter R | title = Schizophrenia | journal = BMJ Clinical Evidence | volume = 2012 | date = June 2012 | pmid = 23870705 | pmc = 3385413 | url = http://www.clinicalevidence.bmj.com/x/systematic-review/1007/archive/06/2012.html | archive-url = https://archive.today/20140911114812/http://www.clinicalevidence.bmj.com/x/systematic-review/1007/archive/06/2012.html | archive-date = 2014-09-11 }}</ref> Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.<ref name="barry 2012" />

=== Psychotherapy ===
Psychological treatments such as [[acceptance and commitment therapy]] (A.C.T.) are possibly useful in the treatment of psychosis, helping people to focus more on what they can do in terms of valued life directions despite challenging symptomology.<ref>{{cite journal | vauthors = Ost LG | title = The efficacy of Acceptance and Commitment Therapy: an updated systematic review and meta-analysis | journal = Behaviour Research and Therapy | volume = 61 | pages = 105–121 | date = October 2014 | pmid = 25193001 | doi = 10.1016/j.brat.2014.07.018 }}</ref> [[Metacognitive training]] (MCT) is associated with reduced [[delusion]]s, [[hallucination]]s and [[negative symptoms]] as well as improved [[self-esteem]] and functioning in individuals with schizophrenia spectrum disorders.<ref>{{cite journal | vauthors = Penney D, Sauvé G, Mendelson D, Thibaudeau É, Moritz S, Lepage M | title = Immediate and Sustained Outcomes and Moderators Associated With Metacognitive Training for Psychosis: A Systematic Review and Meta-analysis | journal = JAMA Psychiatry | date = March 2022 | volume = 79 | issue = 5 | pages = 417–429 | pmid = 35320347 | pmc = 8943641 | doi = 10.1001/jamapsychiatry.2022.0277 }}</ref>

There are many psychosocial interventions that seek to treat the symptoms of psychosis:  [[need adapted treatment]], [[Open Dialogue]], psychoanalysis/psychodynamic psychotherapy, [[major role therapy]], [[Soteria (psychiatric treatment)|soteria]], psychosocial outpatient and inpatient treatment, [[milieu therapy]], and  cognitive behavioral therapy ([[Cognitive behavioral therapy|C.B.T.]]). In relation to the success of C.B.T. for psychosis, a randomized controlled trial for a web-based C.B.T.P. (Cognitive Behavioral Therapy for Psychosis) skills program named Coping With Voices (C.W.V.) suggest that the program has promise for increasing access to C.B.T.P. It also associated benefits in the management of distressing psychotic symptoms and improved social functioning. When C.B.T. and the other psychosocial interventions<ref>Gottlieb, J. D., Gidugu, V., Maru, M., Tepper, M. C., Davis, M. J., Greenwold, J., Barron, R. A., Chiko, B. P., & Mueser, K. T. (2017). Randomized controlled trial of an internet cognitive behavioral skills-based program for auditory hallucinations in persons with psychosis. ''Psychiatric Rehabilitation Journal, 40''(3), 283–292. <nowiki>https://doi.org/10.1037/prj0000258</nowiki></ref> these are used without antipsychotic medications, they may be somewhat effective for some people, especially for C.B.T., need-adapted treatment, and soteria.<ref name="Schizophrenia Research 2019 p.">{{cite journal | vauthors = Cooper RE, Laxhman N, Crellin N, Moncrieff J, Priebe S | title = Psychosocial interventions for people with schizophrenia or psychosis on minimal or no antipsychotic medication: A systematic review | journal = Schizophrenia Research | volume = 225 | pages = 15–30 | date = November 2020 | pmid = 31126806 | doi = 10.1016/j.schres.2019.05.020 | url = https://www.sciencedirect.com/science/article/abs/pii/S0920996419301823 | access-date = 2020-05-28 | url-status = live | s2cid = 159040608 | archive-url = https://web.archive.org/web/20200625185822/https://www.sciencedirect.com/science/article/abs/pii/S0920996419301823 | archive-date = 2020-06-25 }}</ref>

=== Early intervention ===
{{Main|Early intervention in psychosis}}

[[Early intervention in psychosis]] is based on the observation that identifying and treating someone in the early stages of a psychosis can improve his or her longer-term outcome.<ref>{{cite journal | vauthors = Birchwood M, Todd P, Jackson C | title = Early intervention in psychosis. The critical period hypothesis | journal = The British Journal of Psychiatry. Supplement | volume = 172 | issue = 33 | pages = 53–59 | year = 1998 | pmid = 9764127 | doi = 10.1192/S0007125000297663 | s2cid = 32411917 }}</ref> This approach advocates the use of an intensive multi-disciplinary approach during what is known as the [[critical period]], where intervention is the most effective, and prevents the long-term morbidity associated with chronic psychotic illness.

=== Systematic reform ===
Addressing systematic reform is essential to creating effective prevention as well as supporting treatments and recovery for those with psychosis.

Waghorn et al.<ref name=":4">{{Cite journal| vauthors = Waghorn G, Still M, Chant D, Whiteford H |date=2004|title=Specialised Supported Education for Australians with Psychotic Disorders |journal=Australian Journal of Social Issues|language=en|volume=39|issue=4|pages=443–458|doi=10.1002/j.1839-4655.2004.tb01193.x |doi-access=free}}</ref> suggest that education interventions can be a building block to support those with psychosis to successfully participate in society. In their study they analyse the relationship between successful education attainment and psychosis. Findings suggest proportionately more school-aged persons with psychosis discontinued their education compared to those without psychosis.<ref name=":4" />

Waghorn et al.<ref name=":4" /> finds that specialised supported education for those with psychotic disorders can help lead to successful education attainment. Additionally, future employment outcomes are relative to such education attainment. Established approaches to supported education in the U.S. include three basic models, self-contained classrooms, onsite support model and the mobile support model. Each model includes the participation of mental health service staff or educational facility staff in the student's education arrangements.<ref name=":4" />

Potential benefits of specialised supported education found from this study include coordination with other service providers (e.g. income support, housing, etc.) to prevent disrupting education, providing specialised career counselling, development of coping skills in the academic environment.<ref name=":4" /> These examples provide beneficial ways for people with psychosis to finish studies successfully as well as counter future experiences of psychosis.<ref name=":4" />

== History ==

=== Etymology ===
The word ''psychosis'' was introduced to the psychiatric literature in 1841 by [[Karl Friedrich Canstatt]] in his work ''Handbuch der Medizinischen Klinik''. He used it as a shorthand for 'psychic neurosis'. At that time neurosis meant any disease of the [[nervous system]], and Canstatt was thus referring to what was considered a psychological manifestation of brain disease.<ref name="Burgy">{{cite journal |vauthors=Bürgy M |date=November 2008 |title=The concept of psychosis: historical and phenomenological aspects |journal=Schizophrenia Bulletin |volume=34 |issue=6 |pages=1200–1210 |doi=10.1093/schbul/sbm136 |pmc=2632489 |pmid=18174608}}</ref> [[Ernst von Feuchtersleben]] is also widely credited as introducing the term in 1845,<ref>{{cite journal |vauthors=Beer MD |date=June 1995 |title=Psychosis: from mental disorder to disease concept |journal=History of Psychiatry |volume=6 |issue=22 Pt 2 |pages=177–200 |doi=10.1177/0957154X9500602204 |pmid=11639691 |s2cid=36424931}}</ref> as an alternative to [[insanity]] and [[mania]].

The term stems from [[Modern Latin]] ''psychosis'', "a giving soul or life to, animating, quickening" and that from [[Ancient Greek]] ψυχή ({{Lang|grc|psyche}}), "soul" and the suffix -ωσις (-''{{Lang|grc|osis}}''), in this case  "abnormal condition".<ref>{{cite web |title=Psychosis, Henry George Liddell, Robert Scott, ''A Greek-English Lexicon'', at Perseus |url=https://www.perseus.tufts.edu/cgi-bin/ptext?doc=Perseus%3Atext%3A1999.04.0057%3Aentry%3D%23115982 |url-status=live |archive-url=https://web.archive.org/web/20211018155816/http://www.perseus.tufts.edu/hopper/text?doc=Perseus%3Atext%3A1999.04.0057%3Aentry%3D%23115982&redirect=true |archive-date=2021-10-18 |access-date=2011-06-11 |publisher=Perseus.tufts.edu}}</ref><ref>{{cite web |year=2001 |title=Online Etymology Dictionary |url=http://www.etymonline.com/index.php?search=psychosis&searchmode=none |url-status=live |archive-url=https://web.archive.org/web/20071011142745/http://etymonline.com/index.php?search=psychosis&searchmode=none |archive-date=2007-10-11 |access-date=2006-08-19 |publisher=Douglas Harper}}</ref>

In its adjective form "psychotic", references to psychosis can be found in both clinical and non-clinical discussions. However, in a ''non''-clinical context, "psychotic" is a nonspecific colloquialism used to mean "insane".

=== Classification ===
The word was also used to distinguish a condition considered a disorder of the mind, as opposed to ''[[neurosis]]'', which was considered a disorder of the nervous system.<ref>{{cite journal |vauthors=Berrios GE |date=July 1987 |title=Historical aspects of psychoses: 19th century issues |journal=British Medical Bulletin |volume=43 |issue=3 |pages=484–498 |doi=10.1093/oxfordjournals.bmb.a072197 |pmid=3322481}}</ref> The psychoses thus became the modern equivalent of the old notion of [[Insanity|madness]], and hence there was much debate on whether there was only one [[Unitary psychosis|(unitary)]] or many forms of the new disease.<ref>{{cite journal |vauthors=Berrios GE, Beer D |date=March 1994 |title=The notion of a unitary psychosis: a conceptual history |journal=History of Psychiatry |volume=5 |issue=17 Pt 1 |pages=13–36 |doi=10.1177/0957154X9400501702 |pmid=11639278 |s2cid=21417530}}</ref> One type of broad usage would later be narrowed down by [[Julius Ludwig August Koch|Koch]] in 1891 to the 'psychopathic inferiorities'—later renamed abnormal personalities by [[Kurt Schneider|Schneider]].<ref name="Burgy" />

The division of the major psychoses into manic depressive illness (now called [[bipolar disorder]]) and dementia praecox (now called [[schizophrenia]]) was made by [[Emil Kraepelin]], who attempted to create a synthesis of the various mental disorders identified by 19th-century [[Psychiatry|psychiatrists]], by grouping diseases together based on classification of common symptoms. Kraepelin used the term 'manic depressive insanity' to describe the whole spectrum of [[mood disorder]]s, in a far wider sense than it is usually used today.

In Kraepelin's classification this would include 'unipolar' [[clinical depression]], as well as bipolar disorder and other mood disorders such as [[cyclothymia]]. These are characterised by problems with mood control and the psychotic episodes appear associated with disturbances in mood, and patients often have periods of normal functioning between psychotic episodes even without medication. [[Schizophrenia]] is characterized by psychotic episodes that appear unrelated to disturbances in mood, and most non-medicated patients show signs of disturbance between psychotic episodes.

=== Treatment ===
Written record of supernatural causes and resultant treatments can be traced back to the [[New Testament]]. [[Mark 5]]:8–13 describes a man displaying what would today be described as psychotic symptoms. [[Christ]] cured this "[[demon]]ic madness" by casting out the demons and hurling them into a herd of swine. Exorcism is still utilized in some religious circles as a treatment for psychosis presumed to be demonic possession.<ref>{{cite journal |vauthors=Vlachos IO, Beratis S, Hartocollis P |year=1997 |title=Magico-religious beliefs and psychosis |journal=Psychopathology |volume=30 |issue=2 |pages=93–99 |doi=10.1159/000285035 |pmid=9168565}}</ref> A research study of out-patients in psychiatric clinics found that 30% of religious patients attributed the cause of their psychotic symptoms to evil spirits. Many of these patients underwent exorcistic healing rituals that, though largely regarded as positive experiences by the patients, had no effect on symptomology. Results did however show a significant worsening of psychotic symptoms associated with exclusion of medical treatment for coercive forms of exorcism.<ref>{{cite journal |vauthors=Pfeifer S |date=September 1994 |title=Belief in demons and exorcism in psychiatric patients in Switzerland |journal=The British Journal of Medical Psychology |volume=67 |issue=3 |pages=247–258 |doi=10.1111/j.2044-8341.1994.tb01794.x |pmid=7803317}}</ref>
[[File:Hippocrates.jpg|thumb|Bust of Hippocrates]]
The medical teachings of the fourth-century philosopher and physician [[Hippocrates of Cos]] proposed a natural, rather than supernatural, cause of human illness. In Hippocrates' work, the [[Hippocratic corpus]], a holistic explanation for health and disease was developed to include madness and other "diseases of the mind". Hippocrates writes:

{{Blockquote|text=Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughter, and jests, as well as our sorrows, pains, griefs and tears. Through it, in particular, we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant.... It is the same thing which makes us mad or delirious, inspires us with dread and fear, whether by night or by day, brings sleeplessness, inopportune mistakes, aimless anxieties, absentmindedness, and acts that are contrary to habit.<ref>[[Hippocratic corpus]]</ref>}}

Hippocrates espoused a theory of [[humoralism]] wherein disease is resultant of a shifting balance in bodily fluids including [[blood]], [[phlegm]], [[black bile]], and [[yellow bile]].<ref>{{cite book |vauthors=Bennet S |title=History of Psychiatry and Medical Psychology |chapter=Mind and Madness in Classical Antiquity |year=2008 |pages=175–197 |doi=10.1007/978-0-387-34708-0_3 |isbn=978-0-387-34707-3}}</ref> According to humoralism, each fluid or "[[humour]]" has temperamental or behavioral correlates. In the case of psychosis, symptoms are thought to be caused by an excess of both blood and yellow bile. Thus, the proposed surgical intervention for psychotic or manic behavior was [[bloodletting]].<ref>{{cite book |vauthors=Spring B, Weinstein L, Lemon M, Haskell A |title=Clinical Psychology |chapter=Schizophrenia from Hippocrates to Kraepelin |year=1991 |pages=259–277 |doi=10.1007/978-1-4757-9715-2_10 |isbn=978-1-4757-9717-6}}</ref>

18th-century physician, educator, and widely considered "founder of American psychiatry", [[Benjamin Rush]], also prescribed bloodletting as a first-line treatment for psychosis. Although not a proponent of humoralism, Rush believed that active purging and bloodletting were efficacious corrections for disruptions in the circulatory system, a complication he believed was the primary cause of "insanity".<ref>{{cite book |title=Medical Inquiries and Observations upon Diseases of the Mind |vauthors=Rush B |year=1830 |isbn=978-0-559-92167-4 |location=Philadelphia |pages=98–190}}</ref> Although Rush's treatment modalities are now considered antiquated and brutish, his contributions to psychiatry, namely the biological underpinnings of psychiatric phenomenon including psychosis, have been invaluable to the field. In honor of such contributions, Benjamin Rush's image is in the official seal of the [[American Psychiatric Association]].

Early 20th-century treatments for severe and persisting psychosis were characterized by an emphasis on shocking the nervous system. Such therapies include [[insulin shock therapy]], [[cardiazol]] shock therapy, and [[electroconvulsive therapy]].<ref>{{cite book |title=A History of Psychiatry: From the Era of the Asylum to the Age of Prozac |vauthors=Shorter E |publisher=John Wiley & Sons |year=1998 |isbn=978-0-471-24531-5 |location=Hoboken, New Jersey}}</ref> Despite considerable risk, shock therapy was considered highly efficacious in the treatment of psychosis including [[schizophrenia]]. The acceptance of high-risk treatments led to more invasive medical interventions including [[psychosurgery]].<ref>{{cite journal |vauthors=Stone JL |date=March 2001 |title=Dr. Gottlieb Burckhardt—the pioneer of psychosurgery |journal=Journal of the History of the Neurosciences |volume=10 |issue=1 |pages=79–92 |doi=10.1076/jhin.10.1.79.5634 |pmid=11446267 |s2cid=29727830}}</ref>
[[File:Gottlieb Burckhardt (1836-1907).jpg|thumb|Gottlieb Burckhardt (1836–1907)]]
In 1888, Swiss psychiatrist [[Gottlieb Burckhardt]] performed the first medically sanctioned psychosurgery in which the [[cerebral cortex]] was excised. Although some patients showed improvement of symptoms and became more subdued, one patient died and several developed [[aphasia]] or seizure disorders. Burckhardt would go on to publish his clinical outcomes in a scholarly paper. This procedure was met with criticism from the medical community and his academic and surgical endeavors were largely ignored.<ref>{{cite journal |vauthors=Gross D, Schäfer G |date=February 2011 |title=Egas Moniz (1874–1955) and the "invention" of modern psychosurgery: a historical and ethical reanalysis under special consideration of Portuguese original sources |journal=Neurosurgical Focus |volume=30 |issue=2 |pages=E8 |doi=10.3171/2010.10.FOCUS10214 |pmid=21284454 |s2cid=25332947 |doi-access=free}}</ref> In the late 1930s, [[Egas Moniz]] conceived the [[leucotomy]] (AKA [[prefrontal lobotomy]]) in which the fibers connecting the [[frontal lobe]]s to the rest of the brain were severed. Moniz's primary inspiration stemmed from a demonstration by neuroscientists John Fulton and Carlyle's 1935 experiment in which two chimpanzees were given leucotomies and pre- and post-surgical behavior was compared. Prior to the leucotomy, the chimps engaged in typical behavior including throwing feces and fighting. After the procedure, both chimps were pacified and less violent. During the Q&A, Moniz asked if such a procedure could be extended to human subjects, a question that Fulton admitted was quite startling.<ref name="Pressman1998">{{cite book |title=Last Resort: Psychosurgery and the Limits of Medicine |vauthors=Pressman JD |publisher=Cambridge University Press |year=1998 |isbn=978-0-521-35371-7 |series=Cambridge Studies in the History of Medicine |location=Cambridge, UK |pages=18–40 |oclc=36729044}}</ref> Moniz would go on to extend the controversial practice to humans with various psychotic disorders, an endeavor for which he received a [[Nobel Prize]] in 1949.<ref>{{cite journal |vauthors=Berrios GE |date=March 1997 |title=The origins of psychosurgery: Shaw, Burckhardt and Moniz |journal=History of Psychiatry |volume=8 |issue=29 pt 1 |pages=61–81 |doi=10.1177/0957154X9700802905 |pmid=11619209 |s2cid=22225524}}</ref> Between the late 1930s and early 1970s, the leucotomy was a widely accepted practice, often performed in non-[[Sterilization (microbiology)|sterile]] environments such as small [[outpatient]] clinics and patient homes.<ref name="Pressman1998" /> Psychosurgery remained standard practice until the discovery of antipsychotic pharmacology in the 1950s.<ref>{{cite journal |vauthors=Mashour GA, Walker EE, Martuza RL |date=June 2005 |title=Psychosurgery: past, present, and future |journal=Brain Research. Brain Research Reviews |volume=48 |issue=3 |pages=409–419 |doi=10.1016/j.brainresrev.2004.09.002 |pmid=15914249 |s2cid=10303872}}</ref>

The first clinical trial of [[antipsychotic]]s (also commonly known as neuroleptics) for the treatment of psychosis took place in 1952. [[Chlorpromazine]] (brand name: Thorazine) passed clinical trials and became the first antipsychotic medication approved for the treatment of both acute and chronic psychosis. Although the mechanism of action was not discovered until 1963, the administration of chlorpromazine marked the advent of the [[dopamine antagonist]], or first generation antipsychotic.<ref>{{cite journal |vauthors=Stip E |date=May 2002 |title=Happy birthday neuroleptics! 50 years later: la folie du doute |journal=European Psychiatry |volume=17 |issue=3 |pages=115–119 |doi=10.1016/S0924-9338(02)00639-9 |pmid=12052571 |s2cid=29883863|doi-access=free }}</ref> While clinical trials showed a high response rate for both acute psychosis and disorders with psychotic features, the [[side effect]]s were particularly harsh, which included high rates of often irreversible Parkinsonian symptoms such as [[tardive dyskinesia]]. With the advent of [[atypical antipsychotic]]s (also known as second generation antipsychotics) came a dopamine antagonist with a comparable response rate but a far different, though still extensive, side-effect profile that included a lower risk of Parkinsonian symptoms but a higher risk of cardiovascular disease.<ref>{{cite journal |vauthors=Crossley NA, Constante M, McGuire P, Power P |date=June 2010 |title=Efficacy of atypical v. typical antipsychotics in the treatment of early psychosis: meta-analysis |journal=The British Journal of Psychiatry |volume=196 |issue=6 |pages=434–439 |doi=10.1192/bjp.bp.109.066217 |pmc=2878818 |pmid=20513851}}</ref>  Atypical antipsychotics remain the first-line treatment for psychosis associated with various psychiatric and [[neurological disorder]]s including schizophrenia, [[bipolar disorder]], [[major depressive disorder]], [[anxiety disorder]]s, [[dementia]], and some [[autism spectrum]] disorders.<ref>{{cite journal |display-authors=6 |vauthors=Maher AR, Maglione M, Bagley S, Suttorp M, Hu JH, Ewing B, Wang Z, Timmer M, Sultzer D, Shekelle PG |date=September 2011 |title=Efficacy and comparative effectiveness of atypical antipsychotic medications for off-label uses in adults: a systematic review and meta-analysis |journal=JAMA |volume=306 |issue=12 |pages=1359–1369 |doi=10.1001/jama.2011.1360 |pmid=21954480 |doi-access=free}}</ref>

Dopamine is now one of the primary neurotransmitters implicated in psychotic symptomology. Blocking dopamine receptors (namely, the dopamine D2 receptors) and decreasing dopaminergic activity continues to be an effective but highly unrefined effect of antipsychotics, which are commonly used to treat psychosis. Recent pharmacological research suggests that the decrease in dopaminergic activity does not eradicate psychotic [[delusion]]s or [[hallucination]]s, but rather attenuates the reward mechanisms involved in the development of delusional thinking; that is, connecting or finding meaningful relationships between unrelated stimuli or ideas.<ref name="Kapur" /> The author of this research paper acknowledges the importance of future investigation:

{{Blockquote|text=The model presented here is based on incomplete knowledge related to dopamine, schizophrenia, and antipsychotics—and as such will need to evolve as more is known about these.|sign=Shitij Kapur|source=From dopamine to salience to psychosis—linking biology, pharmacology and phenomenology of psychosis}}

[[Freud]]'s former student Wilhelm Reich explored independent insights into the physical effects of neurotic and traumatic upbringing, and published his holistic psychoanalytic treatment with a schizophrenic. With his incorporation of breathwork and insight with the patient, a young woman, she achieved sufficient self-management skills to end the therapy.<ref>{{cite book |title=Character Analysis |vauthors=Reich W |date=1980 |publisher=Macmillan |isbn=978-1-4668-4687-6 |veditors=Higgins M, Raphael CM |page=437 |translator=Carfango VR |chapter=The Schizophrenic Split |access-date=2022-04-29 |chapter-url=https://books.google.com/books?id=ez7nNDjECOQC&pg=PA437 |archive-url=https://web.archive.org/web/20220429013530/https://books.google.com/books?id=ez7nNDjECOQC&pg=PA437 |archive-date=2022-04-29 |url-status=live |name-list-style=vanc}}</ref>

[[Lacan]] extended Freud's ideas to create a psychoanalytic model of psychosis based upon the concept of "[[foreclosure (psychoanalysis)|foreclosure]]", the rejection of the symbolic concept of the father.

Psychiatrist [[David Healy (psychiatrist)|David Healy]] has criticised pharmaceutical companies for promoting simplified biological theories of mental illness that seem to imply the primacy of pharmaceutical treatments while ignoring social and developmental factors that are known important influences in the etiology of psychosis.<ref>{{cite book |title=The Creation of Psychopharmacology |vauthors=Healy D |publisher=Harvard University Press |year=2002 |isbn=978-0-674-00619-5 |location=Cambridge |author-link=David Healy (psychiatrist)}}</ref>

== Society and culture ==

Symptoms of psychosis can also include visions or quasi-visual experiences, felt presences, alterations of time, alterations of space, or alterations of spatiotemporal qualities of objects and things.<ref name="ReferenceA"/> While there are many overwhelmingly negative experiences of psychosis, some experiences of psychosis can be overwhelmingly positive and can be experienced as uplifting or as healing or as difficult but meaningful.<ref name="ReferenceA"/> Jones and Shattell said that mutual dialogue in clinical practice would in theory allow the meaning and complexity of psychotic experiences to emerge.<ref name="ReferenceA"/>

=== Disability ===
The classification of psychosis as a [[Social model of disability|social disability]] is a common occurrence.

Psychosis is considered to be among the top ten causes of social disability among adults in developed countries.<ref>{{cite journal |vauthors=Green MF, Horan WP, Lee J, McCleery A, Reddy LF, Wynn JK |date=February 2018 |title=Social Disconnection in Schizophrenia and the General Community |journal=Schizophrenia Bulletin |volume=44 |issue=2 |pages=242–249 |doi=10.1093/schbul/sbx082 |pmc=5814840 |pmid=28637195}}</ref> The traditional, negative narrative around disability has been shown to adversely influence employment and education for people experiencing psychosis.<ref>{{cite journal |vauthors=Blajeski S |date=September 2020 |title=Family support, forming careers, and breaking the disability mindset: implications for addressing structural barriers to employment pathways in coordinated specialty care for first-episode psychosis. |journal=Social Work in Mental Health. |volume=18 |issue=5 |pages=461–81 |doi=10.1080/15332985.2020.1785603 |s2cid=221380722}}</ref>

Social disability by way of social disconnection is a significant public health concern and is associated with a broad range of negative outcomes, including premature mortality. Social disconnection refers to the ongoing absence of family or social relationships with marginal participation in social activities.

Research on psychosis found that reduced participation in social networks, not only negatively effects the individual on a physical and mental level, it has been shown that failure to be included in social networks influences the individual's ability to participate in the wider community through employment and education opportunities.<ref name="Myers_2019">{{cite journal |vauthors=Myers N |date=2019 |title=Beyond the "Crazy House": Mental/Moral Breakdowns and Moral Agency in First-Episode Psychosis. |journal=Ethos |volume=47 |issue=1 |pages=13–34 |doi=10.1111/etho.12225 |s2cid=151061439}}</ref><ref name="Myers_2012">{{cite journal |vauthors=Myers NA |date=May 2012 |title=Toward an Applied Neuroanthropology of Psychosis: the Interplay of Culture, Brains, and Experience. |journal=Annals of Anthropological Practice |volume=36 |issue=1 |pages=113–130 |doi=10.1111/j.2153-9588.2012.01095.x}}</ref><ref name="pmid21699009">{{cite journal |vauthors=Brown JA |date=June 2011 |title=Talking about life after early psychosis: the impact on occupational performance |journal=Canadian Journal of Occupational Therapy |volume=78 |issue=3 |pages=156–163 |doi=10.2182/cjot.2011.78.3.3 |pmid=21699009 |s2cid=34151007}}</ref>

Equal opportunity to participate in meaningful relationships with friends, family and romantic partners, as well as engaging in social constructs such as employment, can provide significant physical and mental value to people's lives.<ref name="Myers_2019" /> And how breaking the disability mind-set around people experiencing psychosis is imperative for their overall, long-term health and well-being as well as the contributions they are able to make to their immediate social connections and the wider community.<ref name="Myers_2012" />

== Research ==
{{See also|List of investigational antipsychotics}}

Further research in the form of randomized controlled trials is needed to determine the effectiveness of treatment approaches for helping ''adolescents'' with psychosis.<ref name=":3" /> Through 10 randomized clinical trials, studies showed that Early Intervention Services (EIS) for patients with early-phase schizophrenia spectrum disorders have generated promising outcomes.<ref name=":05">{{cite journal | vauthors = Correll CU, Galling B, Pawar A, Krivko A, Bonetto C, Ruggeri M, Craig TJ, Nordentoft M, Srihari VH, Guloksuz S, Hui CL, Chen EY, Valencia M, Juarez F, Robinson DG, Schooler NR, Brunette MF, Mueser KT, Rosenheck RA, Marcy P, Addington J, Estroff SE, Robinson J, Penn D, Severe JB, Kane JM | display-authors = 6 | title = Comparison of Early Intervention Services vs Treatment as Usual for Early-Phase Psychosis: A Systematic Review, Meta-analysis, and Meta-regression | journal = JAMA Psychiatry | volume = 75 | issue = 6 | pages = 555–565 | date = June 2018 | pmid = 29800949 | pmc = 6137532 | doi = 10.1001/jamapsychiatry.2018.0623 }}</ref> EIS are specifically intended to fulfill the needs of patients with early-phase psychosis.<ref name=":05"/> In addition, one meta-analysis that consisted of four randomized clinical trials has examined and discovered the efficacy of EIS to Therapy as Usual (TAU) for early-phase psychosis, revealing that EIS techniques are superior to TAU.<ref name=":05"/>

A study suggests that combining cognitive behavioral therapy (C.B.T.) with SlowMo, an application that helps notice their "unhelpful quick-thinking", might be more effective for treating paranoia in people with psychosis than C.B.T. alone.<ref>{{Cite journal |date=2022-05-19 |title=Mobile app combined with face-to-face therapy helped people with psychosis |url=https://evidence.nihr.ac.uk/alert/slowmo-app-reduced-paranoia-in-people-with-psychosis/ |journal=NIHR Evidence |type=Plain English summary |publisher=National Institute for Health and Care Research |doi=10.3310/nihrevidence_50569|s2cid=249945572 |url-access=subscription }}</ref><ref>{{Cite journal |last1=Garety |first1=Philippa |last2=Ward |first2=Thomas |last3=Emsley |first3=Richard |last4=Greenwood |first4=Kathryn |last5=Freeman |first5=Daniel |last6=Fowler |first6=David |last7=Kuipers |first7=Elizabeth |last8=Bebbington |first8=Paul |last9=Dunn |first9=Graham |last10=Hardy |first10=Amy |date=August 2021 |title=Digitally supported CBT to reduce paranoia and improve reasoning for people with schizophrenia-spectrum psychosis: the SlowMo RCT |url=https://www.journalslibrary.nihr.ac.uk/eme/eme08110 |journal=Efficacy and Mechanism Evaluation |language=en |volume=8 |issue=11 |pages=1–90 |doi=10.3310/eme08110 |pmid=34398537 |s2cid=238644547 |issn=2050-4365|doi-access=free }}</ref>

== References ==
{{reflist}}

== Bibliography ==
* {{cite book | veditors = Badcock JC, Paulik G |year=2019 |title=A Clinical Introduction to Psychosis: Foundations for Clinical Psychologists and Neuropsychologists |edition=1st |location=[[Cambridge, Massachusetts]] |publisher=[[Academic Press]], imprint of [[Elsevier]] |doi=10.1016/C2017-0-01829-3 |isbn=978-0-12-815012-2|s2cid=243510002 }}
* {{cite book | veditors = Lewandowski KE, Moustafa A |year=2019 |title=Social Cognition in Psychosis |edition=1st |location=[[Cambridge, Massachusetts]] |publisher=[[Academic Press]], imprint of [[Elsevier]] |doi=10.1016/C2017-0-03061-6 |isbn=978-0-12-815315-4|s2cid=239126550 }}
* {{cite book | vauthors = Semple D, Smyth R |year=2019 |chapter=Schizophrenia and related psychoses | veditors = Semple D, Smyth R |title=Oxford Handbook of Psychiatry |pages=179–240 |edition=4th |location=[[Oxford]] |publisher=[[Oxford University Press]] |doi=10.1093/med/9780198795551.003.0005 |isbn=978-0-19-879555-1}}
* {{cite book | veditors = Tamminga CA, van Os J, Reininghaus U, Ivleva E |year=2020 |title=Psychotic Disorders: Comprehensive Conceptualization and Treatments |edition=1st |location=[[Oxford]] |publisher=[[Oxford University Press]] |doi=10.1093/med/9780190653279.001.0001 |isbn=978-0-19-065327-9}}
* {{cite book | veditors = Thompson AD, Broome MR |year=2020 |title=Risk Factors for Psychosis: Paradigms, Mechanisms, and Prevention |edition=1st |location=[[Cambridge, Massachusetts]] |publisher=[[Academic Press]], imprint of [[Elsevier]] |doi=10.1016/B978-0-12-813201-2.00001-6 |isbn=978-0-12-813201-2|s2cid=213499429 }}

== Further reading ==
{{Refbegin}}
* {{cite news |url=https://medicine.umich.edu/dept/psychiatry/michigan-psychiatry-resources-covid-19/specific-mental-health-conditions/psychosis-spectrum-disorders-managing-stress-during-covid-19-pandemic |title=Psychosis Spectrum Disorders & Managing Stress during the COVID-19 Pandemic |author=Program for Risk Evaluation and Prevention (PREP) Early Psychosis Clinic |date=2021 |newspaper=Psychiatry |publisher=[[Michigan Medicine]] ([[University of Michigan]]) |access-date=28 February 2021 |archive-date=3 February 2021 |archive-url=https://web.archive.org/web/20210203193215/https://medicine.umich.edu/dept/psychiatry/michigan-psychiatry-resources-covid-19/specific-mental-health-conditions/psychosis-spectrum-disorders-managing-stress-during-covid-19-pandemic |url-status=live }}
* {{cite book | vauthors = Sims A | year = 2002 | title = Symptoms in the mind: An introduction to descriptive psychopathology | edition = 3rd | location = Edinburgh | publisher = Elsevier Science Ltd. | isbn = 978-0-7020-2627-0 }}
* {{cite book | vauthors = Murray ED, Buttner N, Price BH  | chapter = Depression and Psychosis in Neurological Practice | title = Neurology in Clinical Practice | edition = 6th | veditors = Bradley WG, Daroff RB, Fenichel GM, Jankovic J | publisher =  Butterworth Heinemann | date = April 2012 | isbn = 978-1-4377-0434-1 }}
* {{cite book | vauthors = Williams P | year = 2012 | title = Rethinking Madness: Towards a Paradigm Shift In Our Understanding and Treatment of Psychosis | publisher = Sky's Edge Publishing | isbn = 978-0-9849867-0-5 }}
{{Refend}}

; Personal accounts :
{{Refbegin}}
* {{cite book |author-link=Philip K. Dick |vauthors=Dick PK |date=1981 |title=VALIS |location=London |publisher=Gollancz |isbn=978-0-679-73446-8 |title-link=VALIS}} [Semi-autobiographical]
* {{cite book |author-link=Kay Redfield Jamison |vauthors=Jamison KR |date=1995 |title=An Unquiet Mind: A Memoir of Moods and Madness |location=London |publisher=Picador |isbn=978-0-679-76330-7 |url=https://archive.org/details/unquietmindmemoi00jami}}
* {{cite book |author-link=Daniel Paul Schreber |vauthors=Schreber DP |year=2000 |title=Memoirs of My Nervous Illness |location=New York |publisher=New York Review of Books. |isbn=978-0-940322-20-2}}
* {{cite book |vauthors=Hinshaw SP |year=2002 |title=The Years of Silence are Past: My Father's Life with Bipolar Disorder |url=https://archive.org/details/yearsofsilencear00step |url-access=registration |location=Cambridge |publisher=Cambridge University Press |isbn=978-0-521-81780-6}}
* {{cite book |vauthors=McLean R |date=2003 |title=Recovered Not Cured: A Journey Through Schizophrenia |publisher=Allen & Unwin |location=Australia |isbn=978-1-86508-974-4 |url=https://archive.org/details/recoverednotcure00mcle_0}}
* {{cite book |author-link=Elyn Saks |vauthors=Saks ER |date=2007 |title=The Center Cannot Hold – My Journey Through Madness |location=New York |publisher=Hyperion |isbn=978-1-4013-0138-5 |url=https://archive.org/details/centercannothold00saks_0}}
{{Refend}}

== External links ==
{{sister project links||d=Q170082|c=Category:Psychosis|n=no|b=no|v=no|voy=no|m=no|mw=no|s=no|wikt=no|species=no}}
* [https://web.archive.org/web/20151105074035/http://www.nimh.nih.gov/health/topics/schizophrenia/raise/what-is-psychosis.shtml National Institute of Mental Health]

{{Medical resources
|  DiseasesDB     =
|  ICD11          = {{ICD11|6A25.0}}, {{ICD11|6A25.1}}, {{ICD11|6A2Z}}
|  ICD10          = {{ICD10|F|20}}-{{ICD10|F|29}}
|  ICD9           = {{ICD9|290}}-{{ICD9|299}}
|  ICDO           =
|  OMIM           = 603342
|  MedlinePlus    = 001553
|  eMedicineSubj  =
|  eMedicineTopic =
| oMIM_mult       = {{OMIM2|608923}} {{OMIM2|603175}} {{OMIM2|192430}}
| meshName        = Psychotic+Disorders
| meshNumber      = F03.700.675
}}
{{Psychiatry}}
{{Bipolar disorder}}
{{Mental and behavioral disorders|selected = schizophrenia}}
{{Authority control}}

[[Category:Psychosis| ]]
[[Category:1840s neologisms]]
[[Category:Wikipedia medicine articles ready to translate]]