The neuropsychopharmacology of cannabis: A review of human imaging studies

Bloomfield, Michael; Hindocha, Chandni; Green, Sebastian F.; Wall, Matthew B.; Lees, Rachel; Petrilli, Kat; Costello, Harry; Ogunbiyi, M Olabisi; Bossong, Matthijs G.; Freeman, Tom P.

doi:10.1016/j.pharmthera.2018.10.006

Cited by 191 publications

(118 citation statements)

References 322 publications

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“…This remarkable and counterintuitive result can be explained by differences in the underlying mechanism of psychosis associated with frequency of use for CU. Heavy, repeated cannabis use, particularly during adolescence in patients without psychosis, has been associated with adverse effects on the endocannabinoid system, especially in genetically predisposed persons [54]. Chronic and heavy use of cannabis in persons without psychosis affects cognitive domains such as memory and attention, as well as their associated brain areas [55].…”

Section: Discussionmentioning

confidence: 99%

Cannabis use and nonuse in patients with first-episode psychosis: A systematic review and meta-analysis of studies comparing neurocognitive functioning

et al. 2020

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Background. The implications of cannabis use in the onset of early psychosis and the severity of psychotic symptoms have resulted in a proliferation of studies on this issue. However, few have examined the effects of cannabis use on the cognitive symptoms of psychosis (i.e., neurocognitive functioning) in patients with first-episode psychosis (FEP). This systematic review and meta-analysis aim to assess the neurocognitive functioning of cannabis users (CU) and nonusers (NU) with FEP. Methods. Of the 110 studies identified through the systematic review of 6 databases, 7 met the inclusion criteria, resulting in 14 independent samples and 78 effect sizes. The total sample included 304 CU with FEP and 369 NU with FEP. The moderator variables were age at first use, duration of use, percentage of males, and age. Results. Effect sizes were not significantly different from zero in any neurocognitive domain when users and NU were compared. Part of the variability in effect sizes was explained by the inclusion of the following moderator variables: (1) frequency of cannabis use (β = 0.013, F = 7.56, p = 0.017); (2) first-generation antipsychotics (β = 0.019, F = 34.46, p ≤ 0.001); and (3) country where the study was carried out (β = 0.266, t = 2.06, p = 0.043). Conclusions. This meta-analysis indicates that cannabis use is not generally associated with neurocognitive functioning in patients with FEP. However, it highlights the deleterious effect of low doses of cannabis in some patients. It also stresses the importance of the type of antipsychotic prescription and cannabis dose as moderator variables in the neurocognitive functioning of CU with FEP.

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Section: Discussionmentioning

confidence: 99%

Cannabis use and nonuse in patients with first-episode psychosis: A systematic review and meta-analysis of studies comparing neurocognitive functioning

et al. 2020

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“…There is the ever present issue of relying upon retrospective measures to ascertain cannabis use history 56,57 . We did not collect data on the Duration of Untreated Psychosis as should be undertaken in future studies.…”

Section: Discussionmentioning

confidence: 99%

Association of cannabis with glutamatergic levels in patients with early psychosis: Evidence for altered volume striatal glutamate relationships in patients with a history of cannabis use in early psychosis

et al. 2020

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The associative striatum, an established substrate in psychosis, receives widespread glutamatergic projections. We sought to see if glutamatergic indices are altered between early psychosis patients with and without a history of cannabis use and characterise the relationship to grey matter. 92 participants were scanned: Early Psychosis with a history of cannabis use (EPC = 29); Early Psychosis with minimal cannabis use (EPMC = 25); Controls with a history of cannabis use (HCC = 16) and Controls with minimal use (HCMC = 22). Whole brain T1 weighted MR images and localised proton MR spectra were acquired from head of caudate, anterior cingulate and hippocampus. We examined relationships in regions with known high cannabinoid 1 receptor (CB1R) expression (grey matter, cortex, hippocampus, amygdala) and low expression (white matter, ventricles, brainstem) to caudate Glutamine+Glutamate (Glx). Patients were well matched in symptoms, function and medication. There was no significant group difference in Glx in any region. In EPC grey matter volume explained 31.9% of the variance of caudate Glx (p = 0.003) and amygdala volume explained 36.9% (p = 0.001) of caudate Glx. There was no significant relationship in EPMC. The EPC vs EPMC interaction was significant (p = 0.042). There was no such relationship in control regions. These results are the first to demonstrate association of grey matter volume and striatal glutamate in the EPC group. This may suggest a history of cannabis use leads to a conformational change in distal CB1 rich grey matter regions to influence striatal glutamatergic levels or that such connectivity predisposes to heavy cannabis use.

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“…L'exposition prénatale au cannabis a aussi des effets persistants jusqu'à l'âge adulte sur la mémoire de travail et les fonctions exécutives [15,23] et elle augmenterait la vulnérabilité aux addictions [24]. De plus, des études d'imagerie par résonance magnétique fonctionnelle (IRMf) ont montré que l'exposition prénatale est associée à une altération du fonctionnement de plusieurs zones du cerveau chez le jeune adulte lors de tests impliquant la mémoire de travail visuospatiale et l'inhibition [15,25]. Ces travaux confirment les risques associés à l'exposition au cours du développement précoce au cannabis.…”

Section: Exposition Au Cours Du Développement Précoceunclassified

Cannabis et neurodéveloppement

Krebs¹,

Demars²,

Frajerman³

et al. 2020

Bulletin de l'Académie Nationale de Médecine

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Le développement cérébral est un phénomène complexe, qui s'étend de la vie foetale à l'adolescence, pendant laquelle la maturation cérébrale suit une série d'événements ordonnés incluant des périodes critiques de plasticité. Le cerveau est particulièrement sensible à l'environnement pendant ces remaniements. Le système endocannabinoïde participe directement et indirectement à ces processus de plasticité et de maturation. Le delta-9tetrahydrocanabinol, principal composant psychoactif du cannabis, diffuse dans le placenta, le lait maternel et le cerveau. Il interagit avec le système endocannabinoïde, notamment par l'activation des récepteurs aux cannabinoïdes 1 CB1R, ce qui peut entraîner des altérations du neurodéveloppement et du fonctionnement des circuits neuronaux. Par conséquent, l'exposition au cannabis in utero, en période périnatale ainsi qu'à l'adolescence est susceptible d'entraîner des perturbations de la maturation cérébrale dont les conséquences, sur le plan cognitif, psychotique et addictif, persistent bien au-delà de la période d'exposition. Plusieurs facteurs modulent le risque de telles complications mais les études réalisées sur des modèles animaux ainsi que chez l'homme ont montré qu'une exposition durant les phases critiques, en particulier durant la phase de développement périnatal et à l'adolescence, constitue en soi un facteur de risque. Les données actuelles incitent à diffuser une information objective aux jeunes, pour prévenir et limiter les consommations précoces. © 2020 Publié par Elsevier Masson SAS au nom de l'Académie nationale de médecine. ଝ Étant donné le contexte sanitaire épidémique lié au Covid-19 du mois de mars 2020, la présentation orale de cette communication en séance à l'Académie a été reportée.Summary. -Brain development is a complex phenomenon, stretching from fetal life to adolescence, during which brain maturation proceeds through a series of ordered events including critical periods of plasticity. The brain is particularly sensitive to the environment during these changes. The endocannabinoid system participates directly and indirectly in these plasticity and maturation processes. The main psychoactive component of cannabis, the delta-9-tetrahydrocanabinol, can cross the placental barrier, is present in breastmilk and diffuses in the brain. It interacts with the endocannabinoid signaling, especially through the activation of cannabinoid receptors 1 CB1R, which can lead to abnormal neurodevelopmental processes and neuronal circuits functions. Therefore, exposure to cannabis in utero, in perinatal phase, as well as during the adolescence disrupts the brain maturation and can cause disturbances on the cognitive, psychotic and addictive levels that persist far beyond the period of exposure. Several factors modulate the risk of such complications, but studies performed in animal models as well as in human cohorts have shown that exposure during both the critical perinatal and adolescence phases is a risk factor per se. Current knowledge encourages the dissemination of obje...

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The neuropsychopharmacology of cannabis: A review of human imaging studies

Cited by 191 publications

References 322 publications

Cannabis use and nonuse in patients with first-episode psychosis: A systematic review and meta-analysis of studies comparing neurocognitive functioning

Cannabis use and nonuse in patients with first-episode psychosis: A systematic review and meta-analysis of studies comparing neurocognitive functioning

Association of cannabis with glutamatergic levels in patients with early psychosis: Evidence for altered volume striatal glutamate relationships in patients with a history of cannabis use in early psychosis

Cannabis et neurodéveloppement

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