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Two cases of "cannabis acute psychosis" following the administration of oral cannabis
Bernard Favrat, Annick Ménétrey, Marc Augsburger, Laura E Rothuizen, Monique Appenzeller, Thierry Buclin, Marie Pin, Patrice Mangin, Christian Giroud
BMC Psychiatry , 2005, DOI: 10.1186/1471-244x-5-17
Abstract: We report two cases of healthy subjects who were occasional but regular cannabis users without psychiatric history who developed transient psychotic symptoms (depersonalization, paranoid feelings and derealisation) following oral administration of cannabis. In contrast to most other case reports where circumstances and blood concentrations are unknown, the two cases reported here happened under experimental conditions with all subjects negative for cannabis, opiates, amphetamines, cocaine, benzodiazepines and alcohol, and therefore the ingested dose, the time-events of effects on behavior and performance as well as the cannabinoid blood levels were documented.While the oral route of administration achieves only limited blood concentrations, significant psychotic reactions may occur.As several countries in Europe have taken policies to decrease the penalties for cannabis possession, many people especially young persons have interpreted this move as giving support to consider cannabis as a benign drug [1].However as stated by several reports cannabis is not a harmless substance and requires urgent attention considering public health issues such as car driving for example [2]. The relationship between Cannabis and acute psychosis is another important issue. In Pakistan and also India, Bhang, a beverage made from an infusion of cannabis leaves, and flowering tops combined with milk and nuts is reported to frequently induce psychotic manifestations among consumers [3]. Presenting symptoms include grandiosity, excitement, hostility, uncooperativeness, disorientation, hallucinatory behaviour and unusual thought content [3].Recently five large-scale longitudinal studies and a systematic review have shown that cannabis use in adolescence is associated with a two-to threefold increase in the relative risk of later developing schizophrenia [4]. Furthermore short-term psychotic reactions, particularly in naive users have also been reported. Thomas [5] describes that one in seve
Gone to Pot – A Review of the Association between Cannabis and Psychosis  [PDF]
Rajiv Radhakrishnan,Samuel T. Wilkinson,Deepak Cyril D’Souza
Frontiers in Psychiatry , 2014, DOI: 10.3389/fpsyt.2014.00054
Abstract: Cannabis is the most commonly used illicit drug worldwide, with ~5 million daily users worldwide. Emerging evidence supports a number of associations between cannabis and psychosis/psychotic disorders, including schizophrenia. These associations-based on case-studies, surveys, epidemiological studies, and experimental studies indicate that cannabinoids can produce acute, transient effects; acute, persistent effects; and delayed, persistent effects that recapitulate the psychopathology and psychophysiology seen in schizophrenia. Acute exposure to both cannabis and synthetic cannabinoids (Spice/K2) can produce a full range of transient psychotomimetic symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to symptoms of schizophrenia. In individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Several factors appear to moderate these associations, including family history, genetic factors, history of childhood abuse, and the age at onset of cannabis use. Exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. Individuals with polymorphisms of COMT and AKT1 genes may be at increased risk for psychotic disorders in association with cannabinoids, as are individuals with a family history of psychotic disorders or a history of childhood trauma. The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence. At the present time, the evidence indicates that cannabis may be a component cause in the emergence of psychosis, and this warrants serious consideration from the point of view of public health policy.
Design paper: The CapOpus trial: A randomized, parallel-group, observer-blinded clinical trial of specialized addiction treatment versus treatment as usual for young patients with cannabis abuse and psychosis
Carsten Hjorth?j, Allan Fohlmann, Anne-Mette Larsen, Mette TR Madsen, Lone Vesterager, Christian Gluud, Mikkel C Arendt, Merete Nordentoft
Trials , 2008, DOI: 10.1186/1745-6215-9-42
Abstract: The major objective for the CapOpus trial is to evaluate the additional effect on cannabis abuse of a specialized addiction treatment program adding group treatment and motivational interviewing to treatment as usual.The trial is designed as a randomized, parallel-group, observer-blinded clinical trial. Patients are primarily recruited through early-psychosis detection teams, community mental health centers, and assertive community treatment teams. Patients are randomized to one of two treatment arms, both lasting six months: 1) specialized addiction treatment plus treatment as usual or 2) treatment as usual. The specialized addiction treatment is manualized and consists of both individual and group-based motivational interviewing and cognitive behavioral therapy, and incorporates both the family and the case manager of the patient.The primary outcome measure will be changes in amount of cannabis consumption over time. Other outcome measures will be psychosis symptoms, cognitive functioning, quality of life, social functioning, and cost-benefit analyses.ClinicalTrials.gov NCT00484302.A recent meta-analysis of eleven longitudinal studies concluded that cannabis use is associated with increased risk of lasting psychotic conditions later in life [1]. Assuming causality, as much as 800 annual cases of schizophrenia are preventable in the UK if exposure to cannabis was eliminated [2]. Several studies have shown that use of cannabis increases the risk of developing schizophrenia-like symptoms, especially in young men disposed to developing psychosis [3-10]. Furthermore, use of cannabis among patients with psychosis can maintain and worsen the psychotic symptoms [11-15], and comorbid schizophrenia and substance abuse is associated with lack of compliance to treatment and with more rehospitalizations [15-20]. This indicates both that effective interventions to limit cannabis use in persons with psychosis are needed, and that getting patients to follow such interventions may
Cannabis Use and Mental Health: A Review of Recent Epidemiological Research  [PDF]
T.H. Richardson
International Journal of Pharmacology , 2010,
Abstract: Cannabis is the most commonly used drug in the world. This review examines recent epidemiological research on the relationships between cannabis use and mental health problems. Relationships with depression, anxiety disorders, mania and psychosis are examined, with relevant issues such as the effect of confounding variables, temporal directions and causality being discussed. Factors which influence the relationship such as dose-response effects, age of first cannabis use and risk of mental health problems are also examined. Causality is often difficult to establish, as cannabis is often used by those with mental illness for self-medication. However, there is substantial evidence to suggest that cannabis may induce or exacerbate a number of mental health problems.
Cannabis and schizophrenia spectrum disorders: A review of clinical studies  [cached]
Rodrigo Chaturaka,Rajapakse Senaka
Indian Journal of Psychological Medicine , 2009,
Abstract: Cannabis is the most widely used illegitimate substance in the world, and the number of users has increased by 10% over the last decade worldwide. Therefore, it is important to review the evidence on psychoactive properties of cannabis and its possible association with schizophrenia spectrum disorders (SSD). We searched MEDLINE with the key words cannabis and schizophrenia. The search was limited to articles published in English over the last 10 years (1999-2009). Bibliographies of cited literature were also searched. Data sources included reviews published in core clinical journals, cohort studies, interventional studies, case-control studies, cross-sectional analyses and epidemiological data. Results are discussed under 2 topics. Firstly, evidence related to biochemical functioning of cannabinoids and their relationship to endocannabinoid system is discussed briefly. Secondly, the evidence from clinical studies on cannabis, psychosis proneness and SSD are discussed in detail. The discussion is structured to fit in the evidence from results section to 3 plausible hypotheses on cannabis use and SSD. The evidence for and against each hypothesis is discussed. Despite new evidence, the exact relationship between cannabis and SSD is unclear. There is no firm evidence that cannabis causes SSD. The evidence for the argument that schizophrenic patients are attracted to cannabis is also not strong. The most plausible explanation is that cannabis use and psychosis proneness may have synergistic effects in a vulnerable minority.
The effect of cannabis use on memory function: an update
Schoeler T,Bhattacharyya S
Substance Abuse and Rehabilitation , 2013,
Abstract: Tabea Schoeler, Sagnik BhattacharyyaDepartment of Psychosis Studies, King's College London, Institute of Psychiatry, London, UKAbstract: Investigating the effects of cannabis use on memory function appears challenging. While early observational investigations aimed to elucidate the longer-term effects of cannabis use on memory function in humans, findings remained equivocal and pointed to a pattern of interacting factors impacting on the relationship between cannabis use and memory function, rather than a simple direct effect of cannabis. Only recently, a clearer picture of the chronic and acute effects of cannabis use on memory function has emerged once studies have controlled for potential confounding factors and started to investigate the acute effects of delta-9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), the main ingredients in the extract of the cannabis plant in pharmacological challenge experiments. Relatively consistent findings have been reported regarding the acute impairments induced by a single dose of Δ9-THC on verbal and working memory. It is unclear whether they may persist beyond the intoxication state. In the long-term, these impairments seem particularly likely to manifest and may also persist following abstinence if regular and heavy use of cannabis strains high in Δ9-THC is started at an early age. Although still at an early stage, studies that employed advanced neuroimaging techniques have started to model the neural underpinnings of the effects of cannabis use and implicate a network of functional and morphological alterations that may moderate the effects of cannabis on memory function. Future experimental and epidemiological studies that take into consideration individual differences, particularly previous cannabis history and demographic characteristics, but also the precise mixture of the ingredients of the consumed cannabis are necessary to clarify the magnitude and the mechanisms by which cannabis-induced memory impairments occur and to elucidate underlying neurobiological mechanisms.Keywords: cannabis, THC, CBD, memory, neuroimaging, fMRI
Cannabis and Breastfeeding  [PDF]
Aurélia Garry,Virginie Rigourd,Ammar Amirouche,Valérie Fauroux,Sylvie Aubry,Rapha l Serreau
Journal of Toxicology , 2009, DOI: 10.1155/2009/596149
Abstract: Cannabis is a drug derived from hemp plant, Cannabis sativa, used both as a recreational drug or as medicine. It is a widespread illegal substance, generally smoked for its hallucinogenic properties. Little is known about the adverse effects of postnatal cannabis exposure throw breastfeeding because of a lack of studies in lactating women. The active substance of cannabis is the delta 9 TetraHydroCannabinol (THC). Some studies conclude that it could decrease motor development of the child at one year of age. Therefore, cannabis use and abuse of other drugs like alcohol, tobacco, or cocaine must be contraindicated during breastfeeding. Mothers who use cannabis must stop breastfeeding, or ask for medical assistance to stop cannabis use in order to provide her baby with all the benefits of human milk.
What does a mouse tell us about neuregulin 1—cannabis interactions?  [PDF]
Tim Karl,Jonathon C. Arnold
Frontiers in Cellular Neuroscience , 2013, DOI: 10.3389/fncel.2013.00018
Abstract: The link between cannabis and psychosis has been debated although there is substantial epidemiological evidence showing that cannabis increases the risk of psychosis. It has been hypothesized that schizophrenia patients carrying particular risk genes might be more sensitive to the psychosis-inducing effects of cannabis than other patients and healthy test subjects. Here we review the effects of cannabinoids on a mutant mouse model for the schizophrenia candidate gene neuregulin 1 (Nrg1). The studies suggest a complex interaction between cannabis and Nrg1: the neuro-behavioral effects of cannabinoids were different in Nrg1 mutant and control mice and depended on exposure time, sex, and age of test animals. This research provides the first evidence of complex cannabis-Nrg1 interactions suggesting Nrg1 as a prime target for future clinical investigations. Furthermore, it highlights that animal model research can broaden our understanding of the complex multi-factorial etiology of schizophrenia. Finally, the findings are important to preventive psychiatry: if the genes that confer genetic vulnerability to cannabis-induced psychosis were identified patients at-high risk could be forewarned of the potential dangers of cannabis abuse.
Alcohol and relatively pure cannabis use, but not schizotypy, are associated with cognitive attenuations  [PDF]
Daniela A. Herzig,David Nutt,Christine Mohr
Frontiers in Psychiatry , 2014, DOI: 10.3389/fpsyt.2014.00133
Abstract: Elevated schizotypy relates to similar cognitive attenuations as seen in psychosis and cannabis/polydrug use. Also, in schizotypal populations cannabis and polydrug (including licit drug) use are enhanced. These cognitive attenuations may therefore either be a behavioural marker of psychotic (-like) symptoms or the consequence of an enhanced drug use in schizotypal populations. To elucidate this, we investigated the link between cognitive attenuation and cannabis use in largely pure cannabis users (35 CU) and non-using controls (48 nCU), accounting for the potential additional influence of both schizotypy and licit drug use (alcohol, nicotine). Cognitive attenuations commonly seen in psychosis were associated with cannabis and alcohol use, but not schizotypy. Future studies should therefore consider i) non-excessive licit substance use (e.g. alcohol) in studies investigating the effect of cannabis use on cognition and ii) both enhanced illicit and licit substance use in studies investigating cognition in schizotypal populations.
The effect of cannabis use on memory function: an update
Schoeler T, Bhattacharyya S
Substance Abuse and Rehabilitation , 2013, DOI: http://dx.doi.org/10.2147/SAR.S25869
Abstract: t of cannabis use on memory function: an update Review (918) Total Article Views Authors: Schoeler T, Bhattacharyya S Published Date January 2013 Volume 2013:4 Pages 11 - 27 DOI: http://dx.doi.org/10.2147/SAR.S25869 Received: 05 November 2012 Accepted: 17 December 2012 Published: 23 January 2013 Tabea Schoeler, Sagnik Bhattacharyya Department of Psychosis Studies, King's College London, Institute of Psychiatry, London, UK Abstract: Investigating the effects of cannabis use on memory function appears challenging. While early observational investigations aimed to elucidate the longer-term effects of cannabis use on memory function in humans, findings remained equivocal and pointed to a pattern of interacting factors impacting on the relationship between cannabis use and memory function, rather than a simple direct effect of cannabis. Only recently, a clearer picture of the chronic and acute effects of cannabis use on memory function has emerged once studies have controlled for potential confounding factors and started to investigate the acute effects of delta-9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), the main ingredients in the extract of the cannabis plant in pharmacological challenge experiments. Relatively consistent findings have been reported regarding the acute impairments induced by a single dose of Δ9-THC on verbal and working memory. It is unclear whether they may persist beyond the intoxication state. In the long-term, these impairments seem particularly likely to manifest and may also persist following abstinence if regular and heavy use of cannabis strains high in Δ9-THC is started at an early age. Although still at an early stage, studies that employed advanced neuroimaging techniques have started to model the neural underpinnings of the effects of cannabis use and implicate a network of functional and morphological alterations that may moderate the effects of cannabis on memory function. Future experimental and epidemiological studies that take into consideration individual differences, particularly previous cannabis history and demographic characteristics, but also the precise mixture of the ingredients of the consumed cannabis are necessary to clarify the magnitude and the mechanisms by which cannabis-induced memory impairments occur and to elucidate underlying neurobiological mechanisms.
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