SYMPOSIA

Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Abstracts of the Invited Speakers
concept formation, and planning. Those subjects reporting chronic, heavy cannabis use show the most enduring deficits (2). One can
suggest that some of these impairments are not completely reversible upon cessation of cannabis use and moreover may interfere with
the treatment of cannabis addiction. Therefore, targeting cognitive impairment associated with chronic cannabis use may be a promising
novel strategy for the treatment of cannabis addiction (3).
While acute administration of cannabis to patients with schizophrenia exacerbates symptoms and cognitive impairments and may have
enduring effects, cannabis has also been found to have some beneficial effects on cognition, at least in certain subgroups of patients (4).
Cannabis using patients had better attention and executive functions than non-cannabis using patients at baseline and after one year of
treatment in a representative sample of first-episode schizophrenia patients. Cannabis using patients appear to comprise a subgroup of
patients with better premorbid adjustment and premorbid frontal cognitive functions (5).
Thus, while cannabis use is traditionally associated with cognitive impairment, the relationship is more complex in the case of schizophrenia.
Key words: Cannabis, cognitive functions
References:
1. Blume AW, Marlatt GA. The role of executive cognitive functions in changing substance use: what we know and what we need to know. Ann Behav Med 2009;
37:117-25.
2. Crean RD, Tapert SF, Minassian A, Macdonald K, Crane NA, Mason BJ. Effects of chronic, heavy cannabis use on executive functions. J Addict Med 2011; 5:9-15.
3. Sofuoglu M, Sugarman DE, Carroll KM. Cognitive function as an emerging treatment target for marijuana addiction. Exp Clin Psychopharmacol 2010; 18:109-19.
4. Yücel M, Bora E, Lubman DI, Solowij N, Brewer WJ, Cotton SM, Conus P, Takagi MJ, Fornito A, Wood SJ, McGorry PD, Pantelis C. The impact of cannabis use on
cognitive functioning in patients with schizophrenia: a meta-analysis of existing findings and new data in a first-episode sample. Schizophr Bull 2010 (In press)
5. Rodríguez-Sánchez JM, Ayesa-Arriola R, Mata I, Moreno-Calle T, Perez-Iglesias R, González-Blanch C, Periañez JA, Vazquez-Barquero JL, Crespo-Facorro B. Cannabis
use and cognitive functioning in first-episode schizophrenia patients. Schizophr Res 2010;124:142-51.
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S82-3
The differences between marijuana psychosis and other substance induced psychoses
Mükerrem Güven
Akdeniz University Research and Practice Center for Alcohol and Substance Addiction, Antalya,Turkey
E-mail: mguven@akdeniz.edu.tr
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 (flashbacks) 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.
Key words: Addiction, cannabis, psychosis, substance abuse
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