Amphetamine-induced psychosis

Ciraulo DA, Rotrosen J, Leiderman D, et al Nefazodone induced alterations of cocaine craving and use in dysphoric cocaine users. Drug Alcohol Depend 60 S38, 2000 Connell PH Amphetamine Psychosis (Maudsley Monographs No 5). London, Oxford University Press, 1938... 

Van Kammen DP, Docherty JP, Marder SR, et al Lithium attenuates the activation-euphoria but not the psychosis induced by d-amphetamine in schizophrenia. Psychopharmacology 87 111-115, 1985... 

Angrist BM, Gershon S. 1970. The phenomenology of experimentally induced amphetamine psychosis — preliminary observations. Biol Psychiatry 2 95-107. 

Griffith JD, Cavanaugh JH, Held J, et al. Experimental psychosis induced by the administration of d-amphetamine. In Costa E, Garattini S, editors. Amphetamines and Related Compounds. New York Raven Press, 1970 897. 

In addition to acute effects, however, prolonged usage of amphetamines (and other psychostimulants) can produce an "amphetamine psychosis." This syndrome was first clearly documented by Connell (25) and is regarded as very similar to paranoid schizophrenia, characterized by "paranoid psychosis with ideas of reference, delusions of persecution, auditory and visual hallucinations in a setting of clear consciousness" (25). The psychosis clears quickly after the drug is withdrawn. Psychosis has been induced experimentally in normal subjects by continuous amphetamine administration (26). Amphetamine psychosis has... 

Acutely, cocaine can cause anxiety or panic reactions. Used chronically., cocaine can in duce a psychosis that closely resembles that produced by amphetamine. It is generally considered that amphetamine psychosis predominantly mimics the positive symptoms of schizophrenia, but in fact stimulant-induced psychosis can mimic a broad range of symptoms, including negative and bizarre symptoms (44). Paranoid behavior has been produced in experienced cocaine users by continuous (4h) cocaine infusion (45). 

Ephedrine psychosis closely resembles psychosis induced by amphetamines paranoia with delusions of persecution and auditory and visual hallucinations, even though consciousness remains unclouded. Typically, patients with ephedrine psychosis will have ingested more than 1000 mg/d. Recovery is rapid after the drug is withdrawn (Shufman et al., 1994). The ephedrine content per serving of most food supplements is on the order of 10-20 mg, making it extremely unlikely that, in recommended doses, use of any of the products would lead to neurologic symptoms. 

Griffith, J.D. etaL 1970. Psychosis induced by the administration oW-amphetamine to human volunteers In Efron, D.H. 

Stimulants induce both tolerance and sensitization to their behavioral effects. Tolerance develops to the anorectic and euphoric effects of stimulants (Schuster 1981) however, chronic intermittent use of low doses of stimulants delays the development of tolerance. With the doses commonly used in clinical practice, patients treated for narcolepsy or for depressive or apathetic states find that the stimulant properties usually persist without development of tolerance however, the persistence of antidepressant effects remains a matter of controversy. Sensitization has been linked to the development of amphetamine-induced psychosis (Yui et al. 1999). Sensitization to the induction of psychosis is suggested because psychosis is induced by progressively lower doses and shorter periods of consumption of amphetamine following repeated use over time (Sato 1986). Sensitization for amphetamine-induced psychosis may persist despite long periods of abstinence. 

King GR, Ellinwood EH Amphetamines and other stimulants, in Substance Abuse A Comprehensive Textbook, 3rd Edition. Edited by Lowinson JH, Ruiz P, Mill-man RB, et al. Baltimore, MD, Williams Wilkins, 1997, pp 207—233 Klawans HE, Margolin Dl Amphetamine-induced dopaminergic hypersensitivity in guinea pigs implications in psychosis and human movement disorders. Arch Gen Psychiatry 32 725—732, 1975... 

Toxic psychosis Several monoamine stimulants including cocaine are known to produce a temporary or even a lasting psychotic state after heavy use. Reviews of numerous clinical case reports have shown amphetamine to produce a chronic psychotic state, sometimes persisting for months after cessation. There appears to be a sensitization effect in this regard, because after recovery, psychotic states may recur with minimal use of amphetamine or alcohol. When compared to schizophrenic patients, people with amphetamine-induced psychosis demonstrate fewer negative symptoms (Boutros and Bowers 1996). 

In the aftermath of World War II, problems with amphetamine abuse began to arise. An epidemic of amphetamine abuse and related cases of amphetamine-induced psychosis arose first in Japan and later in the United States. Since that time, use of amphetamines and other stimulants has been greatly curtailed and as a class are more tightly regulated than virtually any other psychotropic agents, with the exception of narcotic analgesics. 

Flaum M Schultz SK (1996). When does amphetamine-induced psychosis become schizophrenia. American Journal of Psychiatry, 153, 812-5... 

Inhibition of conditioned (but not unconditioned) avoidance behavior is one of the most predictive tests of antipsychotic action. Another is the inhibition of amphetamine- or apomorphine-induced stereotyped behavior. Other tests that may predict antipsychotic action are reduction of exploratory behavior without undue sedation, induction of a cataleptic state, inhibition of intracranial self-stimulation of reward areas, and prevention of apomorphine-induced vomiting. Most of these tests are difficult to relate to any model of clinical psychosis. 

The hypothetical link between dopamine and schizophrenia was forged by two reciprocally related findings. The first was that potent dopamine agonist stimulants like d-amphetamine and cocaine could cause a psychosis that was schizophrenia-like, in that it had auditory hallucinations and paranoia. The second was that the neuroleptic drugs that were effective in reversing both schizophrenia and stimulant-induced psychosis were dopamine blockers. Moreover, the antipsychotic potency of the neuroleptics was proportional to their binding affinity to the D2 receptor. 

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