There has only been little research on the neurocognitive and neurophysiological effects of cannabis. There have been introductory neuroimaging studies in mainly non-psychotic populations, which show that cannabis does not affect gross brain anatomy. On the other hand however, it has been proved that cannabis does acutely increase cerebral blood flow (temporarily; in the right hemisphere) on the long run, exposure will cause an overall reduction in cerebral blood flow.
There have been studies with animals where they used an active cannabinol called delta-9-THC to demonstrate enhanced dopaminergic neurotransmission in brain regions which are usually associated and known to be implicated in psychosis.
In humans the delta-9-THC causes psychotic-like states and memory impairments. The effect of a CNS cannabinoid system, on humans is still tested by neuroimaging studies.
The endogenous cannabinoid system is sensitive to contact with exogenous cannabinoids such as the delta-9-THC, which is known to impair memory in humans.
In a further study is was examined what impact chronic cannabis use has on memory-related functions by examination of the subsequent memory effect (SME) of the event-related potential (ERP). The study concluded that comparing the group to the control group that chronic users of cannabis have an altered memory related brain activation in the form of dysfunctional SME production which may also go hand in hand with reduced neural efficiency.
Several investigators studied the acute effects of cannabis specifically on attentional processing. Hart et al. (2001) studied the effects of placebo, light (1.8%), and heavy (3.9%) THC cigarettes in chronic, daily cannabis users and found no significant differences in the accuracy of response to attentional tasks. However, performance on a tracking task, which requires sustained attention, was found to improve significantly after the high dose of THC, relative to the other conditions.
In one study of 37 adults with a history of light cannabis use, acute intoxication with a high dose of THC resulted in significant impairment on a measure of impulsivity (McDonald et al., 2003). Another study (Ramaekers et al., 2006) found similar impairment on a task of inhibition in intoxicated, chronic cannabis users. The results measured where in a timespan from 0-6 hours after consumption.
In another study from 2010, researchers investigated "semantic-priming".
Under the influence of cannabis, users showed increases in both automatic semantic priming and schizotypal symptoms compared with controls. When abstinent, cannabis users exhibited hyper-priming at long SOAs.
References and further reading:
- Linszen D, van Amelsvoort T. Cannabis and psychosis: An update on course and biological plausible mechanisms. Curr Opin Psychiatry. 2007;20:116–20
- de la Serna E, Mayoral M, Baeza I, Arango C, Andres P, Bombin I, et al. Cognitive functioning in children and adolescents in their first episode of psychosis: Differences between previous cannabis users and nonusers. J Nerv Ment Dis. 2010;198:159–62.
- Bossong MG, Niesink RJ. Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophrenia. Prog Neurobiol. 2010;92:370–85.
- Battisti RA, Roodenrys S, Johnstone SJ, Respondek C, Hermens DF, Solowij N. Chronic use of cannabis and poor neural efficiency in verbal memory ability. Psychopharmacology (Berl) 2010;209:319–30.
- Hart CL, van Gorp W, Haney M, Foltin RW, Fischman MW
Neuropsychopharmacology. 2001 Nov; 25(5):757-65.
- McDonald J, Schleifer L, Richards JB, de Wit H
Neuropsychopharmacology. 2003 Jul; 28(7):1356-65.
- Ramaekers JG, Kauert G, van Ruitenbeek P, Theunissen EL, Schneider E, Moeller MR
Neuropsychopharmacology. 2006 Oct; 31(10):2296-303.