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Stimulant psychosis
Classification and external resources
ICD-10 F15.5
ICD-9 292.1

Stimulant psychosis is a psychotic disorder that occurs in some people who use stimulant drugs. Most commonly, stimulant psychosis occurs in drug abusers who take very large doses but, in rare cases, it can also occur in patients taking therapeutic doses under medical supervision.[1]

The most common causative agents are amphetamines and cocaine, although newer designer drugs such as MDPV, Ethylphenidate and a-PVP can produce severe psychotic episodes that occur more rapidly and are more intense and longer lasting.[citation needed] Other more powerful Norepinephrine-dopamine reuptake inhibitor-type drugs, such as 2-DPMP, can produce multiday stimulant psychotic episodes from an acute overdose.[citation needed]

Signs and symptoms

The symptoms of stimulant psychosis vary slightly between different stimulant drugs, but are shared largely with the symptoms of organic psychosis, including hallucinations, delusions, thought disorder, and, in extreme cases, catatonia.

Physical symptoms of prolonged stimulant abuse or acute overdose tend to accompany these psychotic symptoms in cases of stimulant psychosis (but not organic psychosis). These additional symptoms may include aggression, arrhythmia, dilated pupils, diarrhea, hypertension, hyperthermia, nausea, rapid breathing, restlessness, seizures, sleep deprivation, tremor, and vomiting.[2]

Stimulants known to cause psychosis


Amphetamine and its derivatives are well known to induce psychosis, typically when abused chronically or in high doses.[3] In an Australian study of 309 active methamphetamine users, 18% had experienced a clinical level psychosis in the past year.[4] The generic term "Amphetamines" describes both amphetamine proper, as well as the substituted amphetamines. The amphetamine molecule consists of a phenethylamine core with a methyl group attached to the alpha carbon. The substituted amphetamines consist of the same structure with one or more substitutions; common examples include cathinone, DOM, ephedrine, MDMA, methamphetamine, methcathinone, and methylphenidate, though a large number of such compounds have been synthesized.

The symptoms of amphetamine psychosis include auditory and visual hallucinations, persecutory delusions, and delusions of reference concurrent with both clear consciousness and prominent extreme agitation.[5][6] A Japanese study of recovery from methamphetamine psychosis reported a 64% recovery rate within 10 days rising to an 82% recovery rate at 30 days after methamphetamine cessation.[7] However, it has been suggested that about 5–15% of users fail to make a complete recovery from the psychosis in the long term.[8] Furthermore, the psychosis can be quickly reestablished with further use, even at a small dose.[7] Psychosocial stress has been found to be an independent risk factor for psychosis relapse, even without further amphetamine use in certain cases.[9]

The symptoms of acute amphetamine psychosis are very similar to those of the acute phase of schizophrenia,[3] although in amphetamine psychosis, visual hallucinations are more common and thought disorder is rare.[10] Amphetamine psychosis may be purely related to high drug usage, or high drug usage may trigger an underlying vulnerability to schizophrenia.[3] There is some evidence that vulnerability to amphetamine psychosis and schizophrenia may be genetically related. Relatives of methamphetamine users with a history of amphetamine psychosis are five times more likely to have been diagnosed with schizophrenia than relatives of methamphetamine users without a history of amphetamine psychosis.[11] The disorders are often distinguished by a rapid resolution of symptoms in amphetamine psychosis, while schizophrenia is more likely to follow a chronic course.[12]


Cocaine has a similar potential to induce temporary psychosis,[13] with more than half of cocaine abusers reporting at least some psychotic symptoms at some point.[14] Typical symptoms of sufferers include paranoid delusions that they are being followed and that their drug use is being watched, often with accompanying hallucinations, which support the delusional beliefs.[15] Delusional parasitosis with formication ("cocaine bugs") is also a fairly common reaction.[16]

Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug, meaning psychosis tends to become more severe with repeated, intermittent use.[15][17]


Methylphenidate, better known by its trade name Ritalin, is a central nervous system stimulant with a similar mechanism of action to cocaine,[18][19] and can also lead to psychosis from chronic abuse.[20][21] Although the safety profile of short-term methylphenidate therapy has been well-established, with short-term clinical trials revealing a very low incidence (0.1%) of methylphenidate-induced psychosis at therapeutic dose levels,[22] the specific effects of long-term use of methylphenidate, even at therapeutic doses, remain largely unknown.[23][24] A naturalistic study published in 1999 with an average follow up time of 21 months showed that 6 of 98 children and adolescents who were prescribed methylphenidate in an outpatient clinic developed psychotic symptoms at therapeutic dosages (the exception being a 17 year old on 80 mg daily), with most improving after drug cessation; however, the lack of a control group makes it impossible to attribute these effects to the medication.[25]

Concerns have been raised that long-term therapy might cause drug dependence, paranoia, schizophrenia, and behavioral sensitization in a similar manner to other stimulant drugs.[26] Psychotic symptoms from methylphenidate can include, hearing voices, visual hallucinations, urges to harm oneself, severe anxiety, mania, grandiosity, paranoid delusions, confusion, increased aggression, and irritability. Methylphenidate psychosis is unpredictable in whom it will occur, as family history of mental illness does not predict the incidence of stimulant toxicosis in children with ADHD.

Withdrawal symptoms of methylphenidate can include psychosis and depression[27] and can be minimized by gradually tapering off the medication.[28][29][30] A very small study (19 subjects) of abrupt withdrawal from stimulants used at therapeutic doses for ADHD and chronic tic disorder suggests that withdrawal reactions are not typical. Nonetheless, withdrawal reactions may still occur in susceptible individuals.[31]


There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in normal individuals and worsen pre-existing psychosis in those diagnosed with schizophrenia.[32][33][34]

Caffeine-induced psychosis is infrequently reported in the medical literature and remains controversial due to the lack of supporting information. It is not clear whether it occurs by a similar mechanism to other stimulant psychoses, or whether it is an entirely different process. Like other stimulants, caffeine increases dopamine levels, though only indirectly. A co-factor in caffeine-induced psychosis may be undernourishment, especially a diet lacking in the B-vitamins. High, chronic doses of caffeine, theobromine or theophylline can lead to an exhaustion of the nervous system, which may form the basis for a subsequent psychosis.[35][36]

Prolonged heavy use of caffeine is also known to cause chronic insomnia, the ensuing sleep deprivation may then be source of psychotic-like symptoms.[citation needed]


Treatment consists of supportive care during the acute intoxication phase: maintaining hydration, body temperature, blood pressure, and heart rate at acceptable levels until the drug is sufficiently metabolized to allow vital signs to return to baseline. Typical and atypical antipsychotics have been shown to be helpful in the early stages of treatment.[3] This is followed by abstinence from psychostimulants, supported with counseling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state.

Distinction from excited delirium

Though less common than stimulant psychosis, stimulants such as cocaine and amphetamines as well as the dissociative drug phencyclidine (PCP, angel dust) can also cause a severe and life-threatening condition known as excited delirium. This condition manifests as a combination of delirium, psychomotor agitation, anxiety, delusions, hallucinations, speech disturbances, disorientation, violent and bizarre behavior, insensitivity to pain, elevated body temperature, and superhuman strength.[37] Despite some superficial similarities in presentation, excited delirium is a distinct (and more serious) condition from simple stimulant psychosis.

See also


  1. Curran, Catherine et al., Stimulant psychosis: systematic review, The British Journal of Psychiatry (2004) 185: 196–204
  2. Amphetamine –
  3. 3.0 3.1 3.2 3.3 Shoptaw SJ, Kao U, Ling W. Treatment for amphetamine psychosis (Review). Cochrane Database of Systematic Reviews 2009 Issue 1.
  4. McKetin R, McLaren J, Lubman DI, Hides L. The prevalence of psychotic symptoms among methamphetamine users. Addiction 2006;101(10):1473–8.
  5. Dore G, Sweeting M. Drug-induced psychosis associated with crystalline methamphetamine. Australasian Psychiatry 2006;14(1):86–9.
  6. Srisurapanont M, Ali R, Marsden J, Sunga A, Wada K,Monteiro M. Psychotic symptoms in methamphetamine psychotic in-patients. International Journal of Neuropsychopharmacology 2003;6(4):347–52.
  7. 7.0 7.1 Sato M, Numachi Y, Hamamura T. Relapse of paranoid psychotic state in methamphetamine model of schizophrenia. Schizophrenia Bulletin 1992;18(1):115–22.
  8. Hofmann FG. A handbook on drug and alcohol abuse: the biomedical aspects. 2nd Edition. New York: Oxford University Press, 1983.
  9. Yui K, Ikemoto S, Goto K. Factors for susceptibility to episode recurrence in spontaneous recurrence of methamphetamine psychosis. Annals of the New York Academy of Sciences 2002;965:292–304.
  10. Alan F. Schatzberg, Charles B. Nemeroff (2009). The American Psychiatric Publishing Textbook of Psychopharmacology, 847–48, The American Psychiatric Publishing.
  11. Chen CK, Lin SK, Pak CS, Ball D, Loh EW, Murray RM. Morbid risk for psychiatric disorder among the relatives of methamphetamine users with and without psychosis. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics 2005;136(1):87–91.
  12. McIver C, McGregor C, Baigent M, Spain D, Newcombe D, Ali R. Guidelines for the medical management of patients with methamphetamine-induced psychosis. Drug and Alcohol Services: South Australia 2006.
  13. Brady KT, Lydiard RB, Malcolm R, Ballenger JC. Cocaine-induced psychosis. J Clin Psychiatry. 1991;52:509–512.
  14. Thirthalli, Jagadisha, Vivek Benegal Department of Psychiatry, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore, India. MD. Psychosis Among Substance Users. National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore. URL accessed on 8 August 2011.
  15. 15.0 15.1 Psychosis Among Substance Users: Cocaine, Medscape
  16. Elliott, A., Mahmood, T. and Smalligan, R. D. (2012), Cocaine Bugs: A Case Report of Cocaine-Induced Delusions of Parasitosis. The American Journal on Addictions, 21: 180–181.
  17. Drug-induced psychosis: Emergency diagnosis and management, Psychosomatics. DiSCLAFANI et al. 22 (10): 845. 1981 Accessed 5-20-2010
  18. Auriel E, Hausdorff JM, Giladi N (October 2008). Methylphenidate for the Treatment of Parkinson Disease and Other Neurological Disorders. Clin Neuropharmacol 32 (2): 75–81.
  19. Abramowicz MJ, Van Haecke P, Demedts M, Delcroix M (September 2003). Primary pulmonary hypertension after amfepramone (diethylpropion) with BMPR2 mutation. Eur. Respir. J. 22 (3): 560–2.
  20. Morton WA, Stockton GG. Methylphenidate abuse and psychiatric side effects. Prim Care Companion J Clin Psychiatry 2000;2:159–64.
  21. Spensley J, Rockwell D (April 1972). Psychosis during Methylphenidate Abuse. New England Journal of Medicine 286: 880–1.
  22. (2007). Ritalin & Ritalin-SR Prescribing Information. (PDF) Novartis.
  23. Ashton H, Gallagher P, Moore B (September 2006). The adult psychiatrist's dilemma: psychostimulant use in attention deficit/hyperactivity disorder. J. Psychopharmacol. (Oxford) 20 (5): 602–10.
  24. Kimko HC, Cross JT, Abernethy DR (December 1999). Pharmacokinetics and clinical effectiveness of methylphenidate. Clin Pharmacokinet 37 (6): 457–70.
  25. Cherland E, Fitzpatrick R (October 1999). Psychotic side effects of psychostimulants: a 5-year review. Can J Psychiatry 44 (8): 811–3.
  26. Dafny N, Yang PB. (15). The role of age, genotype, sex, and route of acute and chronic administration of methylphenidate: A review of its locomotor effects.. Brain research bulletin. 68 (6): 393–405.
  27. Rosenfeld AA (February 1979). Depression and psychotic regression following prolonged methylphenidate use and withdrawal: case report. Am J Psychiatry 136 (2): 226–8.
  28. Cohen D, Leo J, Stanton T, et al (2002). A boy who stops taking stimulants for "ADHD": commentaries on a Pediatrics case study. Ethical Hum Sci Serv 4 (3): 189–209.
  29. Schwartz RH, Rushton HG (May 2004). Stuttering priapism associated with withdrawal from sustained-release methylphenidate. J. Pediatr. 144 (5): 675–6.
  30. Garland EJ (1998). Pharmacotherapy of adolescent attention deficit hyperactivity disorder: challenges, choices and caveats. J. Psychopharmacol. (Oxford) 12 (4): 385–95.
  31. Nolan EE, Gadow KD, Sprafkin J (April 1999). Stimulant medication withdrawal during long-term therapy in children with comorbid attention-deficit hyperactivity disorder and chronic multiple tic disorder. Pediatrics 103 (4 Pt 1): 730–7.
  32. Hedges, D. W., F. L. Woon, S. P. Hoopes (September 2009). Caffeine-induced psychosis.. CNS Spectrums 14 (3): 127–9.
  33. Cerimele, J. M., A. P. Stern, D. Jutras-Aswad (September 2010). Psychosis following excessive ingestion of energy drinks in a patient with schizophrenia.. American Journal of Psychiatry 167 (3): 353.
  34. PMID 15732884 (PMID 15732884)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  35. Solinas, Marcello, Sergi Ferre,Zhi-Bing You, Marzena Karcz-Kubicha,Patrizia Popoli, and Steven R. Goldberg (August 2002). Caffeine Induces Dopamine and Glutamate Release in the Shell of the Nucleus Accumbens. The Journal of Neuroscience 14 (3): 127–9.
  36. How Caffeine Works
  37. "White Paper Report on Excited Delirium Syndrome", ACEP Excited Delirium Task Force, American College of Emergency Physicians, September 10, 2009

Further reading

  • Connell, P.H. (1961) Amphetamine Psychosis. Oxford University Press.

External links


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