title: Cannabis and psychosis: an update on course and biological plausible mechanisms.
abstract: OBJECTIVE
  Cannabis use is the most commonly abused illicit substance. Its relation with psychosis remains a topic of debate. Epidemiological studies suggest that cannabis is a component cause accounting for approximately 10% of cases. An increasing number of studies have been published on neurobiological effects of cannabis and vulnerability of psychosis.
  
  
  RESULTS
  Acute cannabis administration can induce memory impairments, sometimes persisting months following abstinence. There is no evidence that residual effects on cognition remain after years of abstinence. The scarce literature on neuro-imaging mainly done in nonpsychotic populations, show little evidence that cannabis has effects on brain anatomy. Acute effects of cannabis include increases of cerebral blood flow, whereas long-term effects of cannabis include attenuation of cerebral blood flow. In animals Delta9-tetrahydrocannabinol enhances dopaminergic neurotransmission in brain regions known to be implicated in psychosis. Studies in humans show that genetic vulnerability may add to increased risk of developing psychosis and cognitive impairments following cannabis consumption. Delta9-tetrahydrocannabinol induces psychotic like states and memory impairments in healthy volunteers.
  
  
  CONCLUSIONS
  Simultaneously with increasing understanding of neurobiological cannabis effects, there is a lack of studies in people with psychosis. There are plausible mechanisms that might explain the psychotogenic effects of cannabis.
authors.affiliation: Department of Psychiatry, Academic Medical Centre University of Amsterdam, The Netherlands. d.h.linszen@amc.uva.nl
authors.forename: Don
authors.initials: D
authors.lastname: Linszen
authors.forename: Therese
authors.initials: T
authors.lastname: van Amelsvoort
mesh_terms: D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D015984:Causality; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D003072:Cognition Disorders / Q000139:chemically induced / Q000503:physiopathology; D015897:Comorbidity; D004298:Dopamine / Q000378:metabolism; D013759:Dronabinol / Q000633:toxicity*; D006801:Humans; D002189:Marijuana Abuse / Q000453:epidemiology* / Q000503:physiopathology; D008569:Memory Disorders / Q000139:chemically induced / Q000503:physiopathology; D009483:Neuropsychological Tests; D049268:Positron-Emission Tomography; D011605:Psychoses, Substance-Induced / Q000453:epidemiology* / Q000503:physiopathology; D012307:Risk Factors; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D013759:Dronabinol; D004298:Dopamine