Toxic cannabis psychosis is a valid entity

Department of Psychiatry, University of Witwatersrand, Johannesburg Tvl.
South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde (Impact Factor: 1.63). 11/1990; 78(8):476-81.
Source: PubMed


One hundred black men admitted to hospital with acute psychiatric symptoms were investigated for the presence of urinary cannabis metabolites in order to delineate the psychiatric role played by 'dagga', the potent South African cannabinol, in the study population and to determine the diagnostic value of the entity 'toxic psychosis (dagga)'. Cannabinoids were present in 29% of patients, and 31% were discharged with a diagnosis of toxic psychosis (dagga). Clinical and demographic material was gathered for all patients and no consistent differences were found between dagga-positive and dagga-negative patients or toxic dagga psychotic patients and 'functional' psychotics other than a history of recent dagga use and the dagga screening test result. The latter measure was found to be both more sensitive and more specific than the history of dagga use alone. The findings support the routine use of a simple screening test for dagga in the sample population studied. The study demonstrated the heterogeneous nature of the toxic dagga psychosis syndrome by documenting a variety of different clinical presentations, which included schizophrenia (42%), paranoia (26%), maniform psychosis (16%) and organic psychosis (16%).

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    • "These symptoms are transient and generally disappear when cannabis use ceases (American Psychiatric Association, 2000). Some studies have reported cases of psychosis or psychotic symptoms immediately following the use of cannabis (Chopra & Smith, 1974; Favrat et al., 2005; Solomons, Neppe, & Kuyl, 1990; Wylie, Scott, & Burnett, 1995). However, these studies have been criticised for failing to investigate whether the cases have a family history of psychotic disorder, or whether cannabis use occurred up to symptom onset (Thornicroft, 1990). "
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    ABSTRACT: Over the past five years, the release of cohort studies assessing the link between cannabis and psychosis has increased attention on this relationship. Existing reviews generally conclude that these cohort studies show cannabis has a causal relationship to psychosis, or at least that one cannot be excluded. Few studies have evaluated the relative strengths and limitations of these methodologically heterogeneous cohort studies, and how their relative merits and weaknesses might influence the way the link between cannabis use and psychosis is interpreted. This paper reviews the methodological strengths and limitations of major cohort studies which have looked at the link between cannabis and psychosis, and considers research findings against criteria for causal inference.
    Full-text · Article · Sep 2009 · The International journal on drug policy
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    • "[6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] "
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    ABSTRACT: This paper reviews evidence on two hypotheses about the relationship between cannabis use and psychosis. The first hypothesis is that heavy cannabis use may cause a cannabis psychosis-a psychosis that would not occur in the absence of cannabis use, the symptoms of which are preceded by heavy cannabis use and remit after abstinence. The second hypothesis is that cannabis use may precipitate schizophrenia, or exacerbate its symptoms. Evaluation of these hypotheses requires evidence of an association between cannabis use and psychosis, that is unlikely to be due to chance, in which cannabis use precedes psychosis, and in which we can exclude the hypothesis that the relationship is due to other factors, such as other drug use, or a personal vulnerability to psychosis. There is some clinical support for the first hypothesis. If these disorders exist they seem to be rare, because they require very high doses of THC, the prolonged use of highly potent forms of cannabis, or a pre-existing (but as yet unspecified) vulnerability. There is more support for the second hypothesis, in that a large prospective study has shown a linear relationship between the frequency with which cannabis has been used by age 18 and the risks over the subsequent 15 years of a diagnosis of schizophrenia. It is still unclear whether this means that cannabis use precipitates schizophrenia, whether it is a form of self-medication, or whether the association is due to the use of other drugs, such as amphetamines, which heavy cannabis users are more Likely to use. There is stronger evidence that cannabis use can exacerbate the symptoms of schizophrenia. Mental health services should identify patients with schizophrenia who use alcohol, cannabis and other drugs and advise them to abstain or to greatly reduce their drug use.
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    • "The findings of Chopra & Smith have been supported by case series which suggest that large doses of potent cannabis products can produce a 'toxic' psychotic disorder with 'organic' features of amnesia and confusion. These disorders have been reported in the Caribbean [10], New Zealand [11], Scotland [9], South Africa [8], Sweden [6] and the United Kingdom [12]. These disorders have been attributed to cannabis use for combinations of the following reasons: the onset of the disorders followed the use of large quantities of cannabis; the affected individuals were confused, disorientated and amnesic; some had no personal or family history of psychosis; their symptoms remitted within days to weeks of enforced abstinence from cannabis use; recovery was complete, with the person having no residual psychotic symptoms such as those seen in schizophrenia; and if the disorder recurred, it was only after the individual resumed cannabis use [1]. "
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    ABSTRACT: This paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidence from prospective epidemiological studies. These are that: (1) cannabis use causes a psychotic disorder that would not have occurred in the absence of cannabis use; (2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and (3) that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence of recent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countries have found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis of schizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptoms and they have persisted after adjustment for potentially confounding variables. The absence of any change in the incidence of schizophrenia during the three decades in which cannabis use in Australia has increased makes it unlikely that cannabis use can produce psychoses that would not have occurred in its absence. It seems more likely that cannabis use can precipitate schizophrenia in vulnerable individuals. There is also reasonable evidence for the third hypothesis that cannabis use exacerbates psychosis.
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