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Psychosis may be observed in intoxication from cannabis, alcohol, opiates, inhalants, stimulants, amphetamines, hallucinogens, phencyclidine, anxiolytics, sedatives and hypnotics. The condition of psychosis may also occur due to abstinence from alcohol, anxiolytics, sedatives, and hypnotics (1). Although mostly alcohol-dependent psychotic disorders are reported, the cannabis-psychosis relationship arouses more interest among researchers. Hypomania and agitation are more frequently noted in cannabis users compared with users receiving other substances. The symptoms of cannabis-psychosis usually disappear with a decrease in cannabis use, but the true nature of perception (şashbacks) hallucinations may be re-lived. As distinct from psychosis depending on other substances, evidence regarding the relationship between cannabis usage and the first attack of schizophrenia is increasing (2). There are long-term clinical follow-up studies to distinguish the acute toxic psychosis revealed in cannabis users from psychoses similar to schizophrenia, and also some studies conducted on the assumption that "cannabis psychosis" is distinct from other psychoses caused by other substances. Auditory hallucinations and emotional blunting are reported less commonly in cannabis psychosis compared to non-substance dependent psychoses. In a study investigating cannabis-induced psychoses, no significant relationship was determined between usage and the onset age of receiving cannabis; however, it has been put forth that a relation exists between cannabis use, the length of addiction and the quality and amount of cannabis received (3). Capsi et al. have reported that the risk for cannabis-induced psychosis is high in people carrying the valine-158 allele of the catechol-O-methyltransferase (COMT) gene (2005). Abuse substances affect different neurotransmitters in the central nervous system (4). Positive psychotic symptoms such as paranoid delusions and hallucinations are observed in half of cocaine addicts. As the period of cocaine use increases, negative symptoms and paranoid psychosis can be recorded. Stimulants such as cocaine and amphetamine can reveal psychosis by increasing dopaminergic activity in the central nervous system (CNS). Cannabinoid-1 (CB-1) receptors are responsible for the effects of cannabis in the CNS. In the lateral putamen, pallidum and substantia nigra, CB-1 receptors are determined to be present in a high degree. Many neurotransmitter systems taking part in the etiology of schizophrenia, especially glutamatergic and dopaminergic systems, are affected by activation of the CB-1 receptor (5). Effects of substances on neurotransmission should be better investigated to understand how substance-induced psychotic disorder develops. References:
1. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA.
2. Van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 2002;15:319-327.
3. Makkos Z, Fejes L, Inczedy-Farkas G, Kassai-Farkas A, Faludi G, Lazary J. Clinical characteristics of cannabis-induced schizophrenia spectrum disorder. Neuropsychopharmacol Hung. 2011 Sep;13(3):127-38.
4. Caspi A, Moffitt TE, Cannon M, McClay J, Murray R, Harrington H, Taylor A, Arseneault L, Williams B, Braithwaite A, Poulton R, Craig IW. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O methyltransferase gene: longitudinal evidence of a gene X environment interaction. Biol Psychiatry 2005; 15;57(10):1117-7.
5. Müller-Vahl KR, Emrich HM. Cannabis and schizophrenia: towards a cannabinoid hypothesis of schizophrenia. Expert Rev Neurother. 2008 Jul;8(7):1037-48. Review.