The neural basis for the acute effects of cannabis on learning and psychosis

TY - CHAP

T1 - The neural basis for the acute effects of cannabis on learning and psychosis

AU - Bhattacharyya, Sagnik

AU - McGuire, Philip

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Accumulating epidemiological evidence (reviewed in Chapter 18 of this book and elsewhere [Moore et al., 2007]) suggests that regular cannabis use can increase the long-term risk of development of psychotic disorders like schizophrenia, and this risk may be particularly high in individuals who start smoking cannabis at a young age. Among the many environmental risk factors for schizophrenia (van Os and Kapur, 2009), the influence of regular frequent cannabis use on the risk of development of psychotic disorders like schizophrenia is particularly important, as it is the most widely used illicit drug in the world (Chawla and Pichon, 2006). Furthermore, the age of first cannabis use is currently decreasing (Hall and Degenhardt, 2007), to the extent that cannabis use is becoming more common than cigarette smoking among young people in some countries (Rey and Tennant, 2002). Evidence has also accumulated regarding the occurrence of a wide range of psychotic symptoms acutely in the context of cannabis use (D’Souza, 2007) and following the experimental administration of its principal psychoactive ingredient, Δ9-tetrahydrocannabinol (THC) (Isbell et al., 1967; Melges et al., 1974). Methodologically improved, placebo-controlled studies have demonstrated that the acute administration of THC can induce psychotic symptoms as measured using standardized rating scales in healthy volunteers (D’Souza et al., 2004; Morrison et al., 2009; Stokes et al., 2009; Bhattacharyya et al., 2009b) and can exacerbate them in patients with schizophrenia (D’Souza et al., 2005). However, while existing anecdotal, experimental and epidemiological studies constitute a very important guiding strand in the evidence supporting the role of cannabis use in the development of psychosis, obvious methodological limitations associated with large-scale epidemiological studies (Moore et al., 2007) that examine a relatively rare outcome, indicate the need for complementary strands of evidence.

AB - Accumulating epidemiological evidence (reviewed in Chapter 18 of this book and elsewhere [Moore et al., 2007]) suggests that regular cannabis use can increase the long-term risk of development of psychotic disorders like schizophrenia, and this risk may be particularly high in individuals who start smoking cannabis at a young age. Among the many environmental risk factors for schizophrenia (van Os and Kapur, 2009), the influence of regular frequent cannabis use on the risk of development of psychotic disorders like schizophrenia is particularly important, as it is the most widely used illicit drug in the world (Chawla and Pichon, 2006). Furthermore, the age of first cannabis use is currently decreasing (Hall and Degenhardt, 2007), to the extent that cannabis use is becoming more common than cigarette smoking among young people in some countries (Rey and Tennant, 2002). Evidence has also accumulated regarding the occurrence of a wide range of psychotic symptoms acutely in the context of cannabis use (D’Souza, 2007) and following the experimental administration of its principal psychoactive ingredient, Δ9-tetrahydrocannabinol (THC) (Isbell et al., 1967; Melges et al., 1974). Methodologically improved, placebo-controlled studies have demonstrated that the acute administration of THC can induce psychotic symptoms as measured using standardized rating scales in healthy volunteers (D’Souza et al., 2004; Morrison et al., 2009; Stokes et al., 2009; Bhattacharyya et al., 2009b) and can exacerbate them in patients with schizophrenia (D’Souza et al., 2005). However, while existing anecdotal, experimental and epidemiological studies constitute a very important guiding strand in the evidence supporting the role of cannabis use in the development of psychosis, obvious methodological limitations associated with large-scale epidemiological studies (Moore et al., 2007) that examine a relatively rare outcome, indicate the need for complementary strands of evidence.

UR - http://www.scopus.com/inward/record.url?scp=84875658579&partnerID=8YFLogxK

U2 - 10.1017/CBO9780511706080.015

DO - 10.1017/CBO9780511706080.015

M3 - Chapter

AN - SCOPUS:84875658579

SN - 9781107000216

SP - 160

EP - 168

BT - Marijuana and Madness

PB - Cambridge University Press

ER -