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Query: UMLS:C0036341 (schizophrenia)
60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cannabis sativa L. preparations have been used in medicine for millenia. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the 1930s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds. In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable--instead, we need to work on the development of more selective cannabinoid receptor agonists/antagonists and related compounds, as well as on novel drugs of this family with better selectivity, distribution patterns, and pharmacokinetics, and--in cases where it is impossible to separate the desired clinical action and the psychoactivity--just to monitor these side effects carefully.
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PMID:Cannabinoids in health and disease. 1828 1

Cannabis contains various cannabinoids, two of which have almost opposing actions: Delta9-tetrahydrocannabinol (Delta9-THC) is psychotomimetic, whereas cannabidiol (CBD) has antipsychotic effects. Hair samples were analysed to examine levels of Delta9-THC and CBD in 140 individuals. Three clear groups emerged: ;THC only', ;THC+CBD' and those with no cannabinoid in hair. The THC only group showed higher levels of positive schizophrenia-like symptoms compared with the no cannabinoid and THC+CBD groups, and higher levels of delusions compared with the no cannabinoid group. This provides evidence of the divergent properties of cannabinoids and has important implications for research into the link between cannabis use and psychosis.
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PMID:Effects of cannabidiol on schizophrenia-like symptoms in people who use cannabis. 1837 95

Reduced amplitudes of auditory evoked P300 are a robust finding in schizophrenic patients, indicating deficient attentional resource allocation and active working memory. Delta9-Tetrahydrocannabinol (Delta9-THC), the main active constituent of Cannabis sativa, has been known to acutely impair cognitive abilities in several domains, particularly in memory and attention. Given the psychotic-like effects of Delta9-THC, a cannabinoid hypothesis of schizophrenia has been proposed. This prospective, double-blind, placebo-controlled cross-over study investigated the acute effects of cannabinoids on P300 amplitude in 20 healthy volunteers (age 28.2+/-3.1 years, 10 male) by comparing Delta9-THC and standardized cannabis extract containing Delta9-THC and cannabidiol (CBD). P300 waves were recorded during a choice reaction task. As expected, Delta9-THC revealed a significant reduction of P300 amplitude at midline frontal, central, and parietal electrodes. CBD has been known to abolish many of the psychotropic effects of Delta9-THC, but, unexpectedly, failed to demonstrate a reversal of Delta9-THC-induced P300 reduction. Moreover, there were no correlations between cannabinoid plasma concentrations and P300 parameters. These data suggest that Delta(9)-THC may lead to acute impairment of attentional functioning and working memory. It can be speculated whether the lack of effect of CBD may be due to an insufficient dose used or to an involvement of neurotransmitter systems in P300 generation which are not influenced by CBD.
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PMID:Effects of acute oral Delta9-tetrahydrocannabinol and standardized cannabis extract on the auditory P300 event-related potential in healthy volunteers. 1854 69

Highlighting the association between schizophrenia and Cannabis sativa and the endogenous cannabinoid receptor system, respectively, two opposite aspects are of major relevance. On the one hand, cannabis is the most widely used illegal drug. There is substantial evidence that cannabis has to be classified as an independent risk factor for psychosis that may lead to a worse outcome of the disease. This risk seems to be increased in genetically predisposed people and may depend on the amount of cannabis used. On the other hand, during the last few years, an endogenous cannabinoid receptor system (including two known cannabinoid [CB(1) and CB(2)] receptors and five endogenous ligands) has been discovered. There are several lines of evidence suggesting that, at least in a subgroup of patients, alterations in the endocannabinoid system may contribute to the pathogenesis of schizophrenia (e.g., increased density of CB(1) receptor binding and increased levels of cerebrospinal fluid endocannabinoid anandamide). Accordingly, beside the 'dopamine hypothesis' of schizophrenia, a 'cannabinoid hypothesis' has been suggested. Interestingly, there is a complex interaction between the dopaminergic and the endocannabinoid receptor system. Thus, agents that interact with the cannabinoid receptor system, such as the nonpsychoactive cannabidiol, might be beneficial in the treatment of psychosis.
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PMID:Cannabis and schizophrenia: towards a cannabinoid hypothesis of schizophrenia. 1859 Apr 75

Dual Diagnosis (DD) patients with psychosis and substance use disorders (SUD) represent a large core group among patients with schizophrenia. Cannabis use disorders are most prevalent among DD patients, particularly in adolescent and young adult populations. There are different models to explain the high rates of comorbidity between psychosis and SUD. Currently, evidence is best for the model of cannabis use being a component cause of psychosis in individuals who are highly vulnerable to psychosis. There is also some evidence for the model of common vulnerability factors for psychosis and SUD. DD patients are difficult to treat as they comply poorly, their long-term outcomes are unfavourable and they suffer frequent psychotic relapses and hospitalisations. Successful treatment models integrate traditional psychiatric therapy for psychosis and therapy for addiction in one setting, modifying and adjusting the two components to the special needs of the DD patients. Integrated programmes focus mostly on long-term outpatient treatment and offer pharmacotherapy, motivational enhancement, psychoeducation, cognitive-behavioural therapy and family interventions. Current clinical research demonstrates that integrated treatment programmes can achieve significant improvements with regard to the social adjustment of, as well as decreased substance use by DD patients.
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PMID:[Dual diagnosis psychosis and substance use disorders: theoretical foundations and treatment]. 1865 56

This study explored explanatory models used by individuals with schizophrenia in relation to continuing cannabis abuse. Cannabis is known to exacerbate positive symptoms, compound the effects of negative symptoms, and lead to relapse, having a negative effect upon quality of life. If this is so, why would people choose to continue the drug use? Most previous studies exploring this phenomenon have used quantitative methodology where the questions asked have been preset by the researchers and the subjective experience of the patient has been minimized. Qualitative methodology was utilized in this study in order to give voice to the patients' perspectives, and contribute to the knowledge of the frameworks of meanings employed by patients. The majority of participants in this study did not perceive that they had a mental illness and they held strong beliefs regarding the usefulness of cannabis. They gave explanations for their continuing cannabis use that expanded the understanding from previous studies. These included that they sought the drug effects of cannabis use for clarity of voices, control of symptoms, to feel normal, perceived improvement in cognitive function, reduced psychological pain and increased energy. These beliefs may influence a person's adherence with treatment and their future cannabis use. This research has implications for clinical practice as clinicians may lack insight into the importance of the phenomenological beliefs of a person with schizophrenia. This lack of insight by the clinician into the phenomenological beliefs may impact on the development of a therapeutic relationship.
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PMID:The effects of cannabis abuse on the symptoms of schizophrenia: patient perspectives. 1866 5

Cannabis use is considered a contributory cause of schizophrenia and psychotic illness. However, only a small proportion of cannabis users develop psychosis. This can partly be explained by the amount and duration of the consumption of cannabis and by its strength but also by the age at which individuals are first exposed to cannabis. Genetic factors, in particular, are likely to play a role in the short- and the long-term effects cannabis may have on psychosis outcome. This review will therefore consider the interplay between genes and exposure to cannabis in the development of psychotic symptoms and schizophrenia. Studies using genetic, epidemiological, experimental, and observational techniques will be discussed to investigate gene-environment correlation gene-environment interaction, and higher order interactions within the cannabis-psychosis association. Evidence suggests that mechanisms of gene-environment interaction are likely to underlie the association between cannabis and psychosis. In this respect, multiple variations within multiple genes--rather than single genetic polymorphisms--together with other environmental factors (eg, stress) may interact with cannabis to increase the risk of psychosis. Further research on these higher order interactions is needed to better understand the biological pathway by which cannabis use, in some individuals, may cause psychosis in the short- and long term.
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PMID:Gene-environment interplay between cannabis and psychosis. 1872 41

Cannabis is the most consumed illicit drug. For a number of years it was thought to be not very toxic, although this idea has no scientific backup. The object of much controversy, it is a public health problem for the most vulnerable populations, adolescents, subjects with evolutive psychopathologies and certain highly cognitive situations: driving a car, the professional environment and students. Cannabis breeds, in international classifications of mental disorders, intoxication charts, abuse and dependence, although this last could have been challenged. The complications are basically anxious and psychotic. It is the object of a number of debates associated with schizophrenic disorders, where it seems to be a risk factor where there is a large consumption before the age of fourteen. Like all psychoactive substances, it is an aggravating factor in all evolutive psychopathologies.
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PMID:[Induced psychiatric and somatic disorders to cannabis]. 1884 72

Cannabis use has often been associated with various forms of psychosis. Today it is well established that everyone produces marijuana-like compounds known as endocannabinoids. The endocannabinoid system is a homeostatic regulator of all body systems including the nervous system. As a result, imbalances in the endocannabinoid system have been considered as possible causes of various forms of mental illness and abnormal behavior. In this paper, a novel hypothesis is presented that suggests that an as yet undefined subset of schizophrenia is caused by an excess of endocannabinoids that are produced to protect the brain in response to infections by agents such as Toxoplasma gondii.
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PMID:Parasitic brain infection, endocannabinoids, and schizophrenia. 1899 70

Cannabis use has increased greatly over the last three decades. The various types of cannabis differ in their concentration of the main psychoactive component, Delta-9-tetrahydrocannabinol (THC), and the other major ingredient, cannabidiol (CBD). Plant engineering has maximized levels of THC, thus increasing the potency of street cannabis. It is well known that cannabis intoxication can cause brief psychotic symptoms like paranoia, whilst recent evidence demonstrates that heavy use of cannabis increases the risk of chronic psychoses like schizophrenia; genetic vulnerability seems to predispose some people to a higher risk. This paper starts to consider the neurochemical mechanisms whereby cannabis use increases the risk of psychosis.
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PMID:What is the mechanism whereby cannabis use increases risk of psychosis? 1907 18


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