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== 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" /> * 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 | pages = 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}}</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 |pages=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 |page=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}}</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}}</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 or sexual abuse, physical or emotional 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 if he or she is placed in 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 === From a diagnostic standpoint, organic disorders were believed to be caused by physical illness affecting the brain (that is, psychiatric disorders secondary to other conditions) while functional disorders were considered disorders of the functioning of the mind in the absence of physical disorders (that is, primary psychological or psychiatric disorders). 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 | pages = 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 | pages = 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 | pages = 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 |url=https://pubmed.ncbi.nlm.nih.gov/38299647 |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 | pages = 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 three percent 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 }}</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 | s2cid = 53563635 }}</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 | pages = 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 | pages = 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 percent 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 }}</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 individuals with both a family history of psychosis or bipolar disorder and lifetime psychedelic use, while they were lowest among those with lifetime 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 |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>
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