Stimulants psychosis induced

In other studies, volunteers previously dependent on amphetamines were dosed to a level at which amfetamine psychosis was produced, in order to examine the mechanism of action and pharmacokinetics of amfetamine and its possible relation to schizophrenia (64,65). Psychosis was induced by moderately high doses of amfetamine and the psychotic symptoms were often a replication of the chronic amfetamine psychosis, raising the question of whether the establishment of chronic stimulant psychosis leaves residual vulnerability to psychosis precipitated by stimulants. The mechanism might be similar to that which operates in the reverse tolerance that has been seen in experimental animals (66). In some cases an underlying psychosis can be precipitated an increase in schizophrenic symptoms (SED-8, 12) was observed in 17 actively ill schizophrenic patients after a single injection of amfetamine. 

According to Carpenter, Conley, and Buchanan (1998), stimulants such as cocaine and amphetamines activate the dopaminergic system in the brain, which explains why the abuse of stimulants can induce a paranoid psychosis that mimics the positive symptoms representative of schizophrenia. In turn, if a person who is diagnosed with schizophrenia is given stimulants of this type, the psychosis may be exacerbated. It follows, therefore, that the typical antipsychotic medications act by blocking the dopamine receptors. 

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... 

Yui, K., Goto, K., Ikemoto, S. et al. Neurobiological basis of relapse prediction in stimulant-induced psychosis and schizophrenia the role of sensitization. Mol. Psychiatry. 4 512, 1999. 

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. 

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. 

We find that the models of stimulant-induced and schizophrenic psychosis share three important elements (1) facilitation of the limbic system, (2) reciprocal disfacilitation of the prefrontal cortex, and (3) orchestration of these reciprocal changes by aminergic neuromodulatory systems. As it is item (3) that is causal in both models, we need to examine similarities and differences in the neuromodulatory mechanisms of the three classes of psychosis under scrutiny here. 

Though psilocybin is known as a natural hallucinogen and has a reputation of being gentler than LSD, it is still known to cause panic attacks, bad trips, and to precipitate mental illness in some people. In 1998, a study at the Psychiatric University Hospital in Zurich, Switzerland, demonstrated that psilocybin produces a psychosis-like syndrome in healthy humans that is similar to early schizophrenia. The study showed that psilocybin-induced psychosis was due to serotonin-2A receptor activation and was not dependent on dopamine stimulation. 

Segal, D. S., and Schuckit, M. A. (1983). Animal models of stimulant-induced psychosis. In Stimulants Neurochemical, Behavioral and Clinical Perspectives (I. Grees, ed.), pp. 131-167. Reven, New York. 

The principle animal model of psychosis has for many years been the hyperactivity and stereotypies induced by stimulant drugs. In animals... 

Ellison G (1994) Stimulant-induced psychosis, the dopamine theory of schizophrenia, and the habenula. Brain Res Rev 79 223-239. 

Adverse effects of catecholaminergic stimulants, such as amfetamine and cocaine, fall into several categories, based on dose, time after dose, chronicity of use, and pattern of use/abuse (for example 4-5 day bingeing episodes). Adverse effects include not only responses during the period of use but also intermediate and longterm residual effects after withdrawal. For example, in some abusers once an amfetamine psychosis has developed with chronic abuse, only one or two moderate doses are required to induce the full-blown psychosis in its original form, even long after withdrawal (1). This is also evidenced by the precipitous slide to severe re-addic-tion in former abusers who are re-introduced to stimulants. 

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