Substance-induced psychosis (commonly known as toxic psychosis or drug-induced psychosis) is a form of psychosis that is attributed to substance intoxication. It is a psychosis that results from the effects of various substances, such as medicinal and nonmedicinal substances, legal and illegal drugs, chemicals, and plants. Various psychoactive substances have been implicated in causing or worsening psychosis in users.[1]
Psychosis manifests as disorientation, visual hallucinations and/or haptic hallucinations.[2] It is a state in which a person's mental capacity to recognize reality, communicate, and relate to others is impaired, thus interfering with the capacity to deal with life's demands.[3] While there are many types of psychosis, the cause of substance-induced psychosis can be pinpointed to intake of specific chemicals. To properly diagnose Substance-Induced Psychotic Disorder, one must conclude that exhibited hallucinations or delusions began during intoxication, withdrawal, or within a month after use of the substance and the symptoms are not related to a non-substance-induced psychotic disorder.[4]
Treatment
Because substance-induced psychosis results from the consumption of a substance or combination of substances, treatment practices heavily rely on detoxification and discontinuation of the substance(s). [1] Detox and addiction treatment centers may often provide rehabilitation programs, including inpatient and outpatient treatment options, support groups, and extended treatment plans. Substance-induced psychosis may persist for hours, days, or weeks, but typically resolves within a month of sobriety. [1] Treating psychosis involves a very thorough evaluation, including medical history, family background, symptoms, and other potential causes.[5] Treatment prioritizes emergent symptoms, evaluates for underlying mental illnesses, and focuses on behavioral and preventative measures against substance use.[1]
Substance use and schizophrenia
Rates of drug use amongst people with schizophrenia are higher than the general population; 50% of those diagnosed with schizophrenia use substances over their life.[6]: 495, 496 There is a model that suggests this arises because those with schizophrenia self-medicate with psychoactive drugs.[6]: 500
Transition to schizophrenia
A 2019 systematic review and meta-analysis found that the 25% (18–38%) of people diagnosed with substance-induced psychosis went on to be diagnosed with schizophrenia, compared with 36% (30–43%) for brief, atypical and not otherwise specified psychoses.[7] The substance present was the primary predictor of transition from drug-induced psychosis to schizophrenia, with highest rates associated with cannabis (34% (25–46%)), hallucinogens (26% (14–43%)) and amphetamines (22% (14–34%)). Lower rates were reported for opioid– (12% (8–18%)), alcohol– (9% (6–15%)) and sedative– (10% (7–15%)) induced psychoses. Transition rates were slightly lower in older cohorts but were not affected by sex, country of the study, hospital or community location, urban or rural setting, diagnostic methods, or duration of follow-up.[7]
Class of substance
Number of studies
Rates of transition to schizophrenia
Estimate
Lower bound
Upper bound
Brief, atypical and NOS
34
36%
30%
43%
Combined
-
25%
18%
38%
Cannabis
6
34%
25%
46%
Hallucinogens
3
26%
14%
43%
Amphetamines
5
22%
14%
34%
Opioid
3
12%
8%
18%
Sedative
3
10%
7%
15%
Alcohol
9
9%
6%
15%
Substances
Psychotic states may occur after using a variety of legal and illegal substances. Substances whose use or withdrawal is implicated in psychosis include the following:
International Classification of Diseases
Psychoactive substance-induced psychotic disorders outlined within the ICD-10 codes F10.5—F19.5:
F10.5 alcohol:[8][9][10] Alcohol is a common cause of psychotic disorders or episodes, which may occur through acute intoxication, chronic alcoholism, withdrawal, exacerbation of existing disorders, or acute idiosyncratic reactions.[8] Research has shown that excessive alcohol use causes an 8-fold increased risk of psychotic disorders in men and a 3 fold increased risk of psychotic disorders in women.[11][12] While the vast majority of cases are acute and resolve fairly quickly upon treatment and/or abstinence, they can occasionally become chronic and persistent.[8] Alcoholic psychosis is sometimes misdiagnosed as another mental illness such as schizophrenia.[13]
F11.5 opioid: Studies show stronger opioids such as fentanyl are more likely to cause psychosis and hallucinations[14]
F12.5 cannabinoid: Some studies indicate that cannabis may trigger full-blown psychosis.[15] Recent studies have found an increase in risk for psychosis in cannabis users.[16]
F17.5 is reserved for tobacco-induced psychosis, but is traditionally not associated with the induction of psychosis.
The code F15.5 also includes caffeine-induced psychosis, despite not being specifically listed in the DSM-IV. However, there is evidence that caffeine, in extreme acute doses or when taken in excess for long periods of time, may induce psychosis.[34][35]
JWH-018 and some other synthetic cannabinoids, or mixtures containing them (e.g. "Spice", "Kronic", "MNG" or "Mr. Nice Guy", "Relaxinol", etc.).[66] Various "JWH-..." compounds in "Spice" or "Incense" have also been found and have been found to cause psychosis in some people.[67][68][69]
^Pitts, Ferris N; Allen, Robert E; Aniline, Orm; Burgoyne, Rodney W (August 1982). "The Dilemma of the Toxic Psychosis: Differential Diagnosis and the PCP Psychosis". Psychiatric Annals. 12 (8): 762–8. doi:10.3928/0048-5713-19820801-07. OCLC5584879101.
^"toxic psychosis". TheFreeDictionary.com. Archived from the original on 2019-04-25. Retrieved 2020-01-21.
^Tien, Allen Y.; Anthony, James C. (August 1990). "Epidemiological Analysis of Alcohol and Drug Use as Risk Factors for Psychotic Experiences". The Journal of Nervous and Mental Disease. 178 (8): 473–480. doi:10.1097/00005053-199017880-00001. PMID2380692.
^Cargiulo, Thomas (1 March 2007). "Understanding the health impact of alcohol dependence". American Journal of Health-System Pharmacy. 64 (5 Supplement 3): S5–S11. doi:10.2146/ajhp060647. PMID17322182.
^Schuckit, Marc A. (November 1983). "Alcoholism and Other Psychiatric Disorders". Psychiatric Services. 34 (11): 1022–1027. doi:10.1176/ps.34.11.1022. PMID6642446.
^Sarrecchia C, Sordillo P, Conte G, Rocchi G (1998). "[Barbiturate withdrawal syndrome: a case associated with the abuse of a headache medication]". Annali Italiani di Medicina Interna (in Italian). 13 (4): 237–9. PMID10349206.
^White MC, Silverman JJ, Harbison JW (February 1982). "Psychosis associated with clonazepam therapy for blepharospasm". The Journal of Nervous and Mental Disease. 170 (2): 117–9. doi:10.1097/00005053-198202000-00010. PMID7057171.
^Hallberg RJ, Lessler K, Kane FJ (August 1964). "Korsakoff-Like Psychosis Associated With Benzodiazepine Overdosage". The American Journal of Psychiatry. 121 (2): 188–9. doi:10.1176/ajp.121.2.188. PMID14194223.
^Brady, K. T.; R. B. Lydiard; R. Malcolm; J. C. Ballenger (December 1991). "Cocaine-induced psychosis". Journal of Clinical Psychiatry. 52 (12): 509–512. PMID1752853.
^Jung IK, Lee HJ, Cho BH (December 2004). "Persistent psychotic disorder in an adolescent with a past history of butane gas dependence". European Psychiatry. 19 (8): 519–20. doi:10.1016/j.eurpsy.2004.09.010. PMID15589716. S2CID46068168.
^Hernandez-Avila, Carlos A.; Hector A. Ortega-Soto; Antonio Jasso; Cecilia A. Hasfura-Buenaga; Henry R. Kranzler (1998). "Treatment of Inhalant-Induced Psychotic Disorder With Carbamazepine Versus Haloperidol". Psychiatric Services. 49 (6): 812–815. doi:10.1176/ps.49.6.812. PMID9634163.
^Cerimele JM, Stern AP, Jutras-Aswad D (March 2010). "Psychosis following excessive ingestion of energy drinks in a patient with schizophrenia". The American Journal of Psychiatry. 167 (3): 353. doi:10.1176/appi.ajp.2009.09101456. PMID20194494.
^Christie MJ, Wong K, Ting RH, Tam PY, Sikaneta TG (May 2005). "Generalized seizure and toxic epidermal necrolysis following levofloxacin exposure". Ann Pharmacother. 39 (5): 953–5. doi:10.1345/aph.1E587. PMID15827068. S2CID8470095.
^Marsepoil T, Petithory J, Faucher JM, Ho P, Viriot E, Benaiche F (1993). "[Encephalopathy and memory disorders during treatments with mefloquine]". Rev Méd Interne (in French). 14 (8): 788–91. doi:10.1016/S0248-8663(05)81426-2. PMID8191092.
^Price, L. H.; Lebel, J (1 February 2000). "Dextromethorphan-Induced Psychosis". American Journal of Psychiatry. 157 (2): 304. doi:10.1176/appi.ajp.157.2.304. PMID10671422.
^Sexton, J. D.; Pronchik, D. J. (1997). "Diphenhydramine-induced psychosis with therapeutic doses". The American Journal of Emergency Medicine. 15 (5): 548–549. doi:10.1016/S0735-6757(97)90212-6. PMID9270406.
^Lang, K.; Sigusch, H.; Müller, S. (1995). "Anticholinergisches Syndrom mit halluzinatorischer Psychose nach Diphenhydramin-Intoxikation" [An anticholinergic syndrome with hallucinatory psychosis after diphenhydramine poisoning]. Deutsche Medizinische Wochenschrift (in German). 120 (49): 1695–1698. doi:10.1055/s-2008-1055530. PMID7497894.
^Schreiber, W.; Pauls, A. M.; Krieg, J. C. (1988). "Toxische Psychose als Akutmanifestation der Diphenhydraminvergiftung" [Toxic psychosis as an acute manifestation of diphenhydramine poisoning]. Deutsche Medizinische Wochenschrift (in German). 113 (5): 180–183. doi:10.1055/s-2008-1067616. PMID3338401.
^Bergman, K. R.; Pearson, C.; Waltz, G. W.; Evans R. III (1980). "Atropine-induced psychosis. An unusual complication of therapy with inhaled atropine sulfate". Chest. 78 (6): 891–893. doi:10.1378/chest.78.6.891. PMID7449475.
^Varghese, S.; Vettath, N.; Iyer, K.; Puliyel, J. M.; Puliyel, M. M. (1990). "Ocular atropine induced psychosis--is there a direct access route to the brain?". Journal of the Association of Physicians of India. 38 (6): 444–445. PMID2384469.
^Ellison Gaylord (1995). "The N-methyl-d-aspartate antagonists phencyclidine, ketamine and dizocilpine as both behavioral and anatomical models of the dementias". Brain Research Reviews. 20 (2): 250–267. doi:10.1016/0165-0173(94)00014-G. PMID7795658. S2CID24071513.
^Carey, R. J.; Pinheiro-Carrera, M.; Dai, H.; Tomaz, C.; Huston, J. P. (1995). "l-DOPA and psychosis: Evidence for l-DOPA-induced increases in prefrontal cortex dopamine and in serum corticosterone". Biological Psychiatry. 38 (10): 669–676. doi:10.1016/0006-3223(94)00378-5. PMID8555378. S2CID26029044.
^Müller H, et al. (2010). "The synthetic cannabinoid Spice as a trigger for an acute exacerbation of cannabis induced recurrent psychotic episodes". Schizophr. Res. 118 (1–3): 309–10. doi:10.1016/j.schres.2009.12.001. PMID20056392. S2CID205066297.
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