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

Suicide is a serious and extensive problem in the clinical management of schizophrenic patients. A retrospective empirical study was conducted on 33 white schizophrenic patients who committed suicide between 1978 and 1989. 'Psychological autopsy' and psychiatric interviews were used for gathering information. A group of 33 schizophrenic patients with a high suicide risk were used as control group. The two groups were correlated as far as possible with regard to age, duration of illness and sex. A statistical analysis was made of the findings. Risk factors revealed by this study, which may be of use in the clinical situation to help prevent suicide in schizophrenic patients, are discussed and include sociodemographic data, depressive and psychotic symptomatology and the misuse of Cannabis. Suggestions are also made regarding future research on schizophrenia and suicide. It is concluded that the clinician should be conservative in his assumptions when identifying schizophrenic patients with a high risk of suicide and should not overestimate his abilities in this field.
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PMID:[Suicide in schizophrenic patients]. 156 61

A review of the evidence shows that there is no convincing support for a separate clinical diagnosis of 'cannabis psychosis'. Cannabis can, however, produce brief acute organic reactions and, in moderate to heavy doses, psychotic episodes in clear consciousness. Ingestion in naive users or increasingly heavy use in habitual users can precipitate a schizophreniform episode. Heavy users may have an increased risk of developing schizophrenia in the subsequent 15 years. Well controlled, longitudinal studies are required to explore these associations further and their possible aetiological significance.
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PMID:Cannabis and psychosis. Is there epidemiological evidence for an association? 220 62

Out of a sample of 220 British psychiatrists, 139 completed a questionnaire regarding a case vignette of psychotic illness. The sex and 'race' of the vignette were varied and the responses compared. The Afro-Caribbean case was regarded as that of an illness of shorter duration, and requiring less neuroleptics than the white case. Respondents judged the Afro-Caribbean case as potentially more violent and thought criminal proceedings were more appropriate. The female vignette was perceived as less violent, less criminal, and less likely to need neuroleptics. Cannabis psychosis and acute reactive psychosis tended to be diagnosed more often and schizophrenia less often in Afro-Caribbean cases, refuting the claim that psychiatrists tend to overdiagnose schizophrenia in this group. Such 'race thinking' (a form of stereotyping which is distinct from ideological racism) could lead to inappropriate management.
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PMID:Are British psychiatrists racist? 1138 82

In this updating review of research on cannabis particular attention has been paid to the increasing number of studies of the disposition of the components of cannabis in man, as well as possible effects on health. Specific binding sites for cannaboids have not been demonstrated. Approximately 80 metabolites of tetrahydrocannabiol (THC) have been discovered, of which 11-OH-THC is the main metabolite, but it contributes little to the overall effect when the drug is smoked or given intravenously. The minimum plasma level of THC associated with the psychotropic effect is 25 ng/ml. Cannabis may produce directly an acute panic reaction, a toxic delirium, and acute paranoid state, or acute mania. Cannabis use may aggrevate schizophrenia, but it is much less certain whether it can lead to sociopathy or even to "amotivational syndrome". Despite widespread use of cannabis in virtually all parts of the world, no catastrophic effects on health have been noted. Cannabis appears to be relatively safe as compared with current social drugs. It is, however, still too early in the history of the present episode of cannabis use to be sanguine about possible bad effects.
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PMID:Cannabis--1988. 285 50

The mental state of 20 psychotic men with high urinary cannabinoid levels on admission to a psychiatric hospital was compared with that of 20 matched cannabis-free controls. All patients underwent toxicological analysis to exclude the presence of alcohol and other exogenous agents. Cannabis levels were measured by a semiquantitative enzyme immunological technique and mental state was assessed by the use of the Present State Examination (PSE), once shortly after admission and again 7 days later. The cannabis group showed significantly more hypomania and agitation and significantly less affective flattening, auditory hallucinations, incoherence of speech, and hysteria than did the controls. Clouding of consciousness was absent in most cannabis patients. After 1 week the cannabis group showed marked improvement (particularly in the psychotic syndromes), whereas the controls remained virtually unchanged. There was no significant difference in amount of medication received between the two groups. Our data suggest that a high intake of cannabis may be related to a rapidly resolving psychosis manifesting with marked hypomanic features, though often presenting as a schizophrenia-like illness.
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PMID:Cannabis-associated psychosis with hypomanic features. 612 63

Patients with the combination of cannabis abuse and psychosis are difficult to treat. The intoxicated state has many similarities to schizophrenia. Like other drugs with abuse potential cannabis affects the brain's reward system. It has not been possible to show major structural changes in the cerebrum, but by electron microscopy structural changes can be shown in animals especially in the hippocampus. The drug is taken in order to escape reality, and a vicious circle tending to maintain the person's abuse pattern which includes reduced energy, judgment and memory may be established. Cannabis may cause toxic psychosis, with a tendency to recurrent psychoses with continued abuse. There is no convincing support for the assumption that cannabis can cause chronic functional psychosis following cessation of abuse. Schizophrenic patients who use cannabis are often trying to reduce the discomfort caused by symptoms in the prodromal phase. By continued abuse positive psychotic symptoms are worsened. Antidepressant drugs may diminish the depressive elements of the disease. Some cannabis users are especially sensitive and develop toxic psychosis. Patients with repeated toxic psychosis may erroneously be diagnosed as schizophrenics. It is therefore important to be aware that a psychotic state may be caused by abuse of cannabis, and adjust treatment to this fact.
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PMID:[Cannabis and psychoses]. 800 23

There is clear evidence of illicit drug abuse in psychiatric hospitals (Deahl, 1991), and illicit drug use has been associated with relapse in people with serious mental health problems. Cannabis abuse in the general population is common and has both desirable and undesirable effects on users. However, when cannabis is used by people with serious mental health problems, a more pronounced effect may be seen. There is little evidence to suggest that cannabis 'causes' schizophrenia, but its abuse may prove to be a trigger in vulnerable individuals. Studies have demonstrated that cannabis abuse can exacerbate the symptoms of schizophrenia and may reduce the effectiveness of antipsychotic drugs. Mental health nurses need to develop interventions in order to manage illicit drug abuse effectively in both the hospital and community settings.
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PMID:Effects of cannabis abuse on people with serious mental health problems. 870 51

In the context of a prospective, controlled treatment study, contrasting family interventions with individual treatment, the role of expressed emotion (EE) as a predictor of relapse was examined in patients with recent-onset schizophrenia and related disorders (n = 97). EE was compared with 13 predictor variables. The variables, taken from EE and family intervention studies, related to demography, premorbid functioning, present and past illness history, and comorbid substance abuse. Psychotic relapse was operationalized with a conservatively measured relapse criterion, composed of monthly ratings based on the Brief Psychiatric Rating Scale and on clinical judgment during the 12 months of outpatient treatment. Of the 14 predictor variables entered in stepwise survival analyses, 6 variables had probable predictive power on the conservative relapse criterion. These variables were entered in a Cox regression model. EE turned out to be the major predictor of relapse in the overall sample (hazard ratio [HR] 4.90; confidence interval [CI] 1.05-22.92). This finding remained when only patients with a first psychotic episode (p = 0.02) and patients in the individual treatment condition (p = 0.001) were examined. Cannabis abuse was the major predictor of relapse in patients with high-EE families (HR 4.27; CI 1.12-16.29).
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PMID:Patient attributes and expressed emotion as risk factors for psychotic relapse. 905 Jan 18

Clinical and basic research studies have linked cannabinoid consumption to the onset of psychosis, specially schizophrenia. In the present study we have evaluated the effects of the natural psychoactive constituent of Cannabis (-)-delta9-tetrahydrocannabinol on the acute actions of the psychostimulant, D-amphetamine, on behaviour displayed by male rats on a hole-board, a proposed animal model of amphetamine-induced psychosis. Cannabinoid-amphetamine interactions were studied (1) 30 min after acute injection of (-)-delta9-tetrahydrocannabinol (0.1 or 6.4 mg/kg, i.p.); (2) 30 min after the last injection of 14-daily treatment with (-)-delta9-tetrahydrocannabinol (0.1 or 6.4 mg/kg) and 3) 24 h after the last injection of 14-daily treatment with (-)-delta9-tetrahydrocannabinol (6.4 mg/kg). Acute cannabinoid exposure antagonized the amphetamine-induced dose-dependent increase in locomotion, exploration and the decrease in inactivity. Chronic treatment with (-)-delta9-tetrahydrocannabinol resulted in tolerance to this antagonistic effect on locomotion and inactivity but not on exploration, and potentiated amphetamine-induced stereotypies. Lastly, 24 h of withdrawal after 14 days of cannabinoid treatment resulted in sensitization to the effects of D-amphetamine on locomotion, exploration and stereotypies. Since (-)-delta9-tetrahydrocannabinol is a cannabinoid CB1 receptor agonist, densely present in limbic and basal ganglia circuits, and since amphetamine enhances monoaminergic inputs (i.e., dopamine, serotonin) in these brain areas, the present data support the hypothesis of a role for the cannabinoid CB1 receptor as a regulatory mechanism of monoaminergic neuron-mediated psychomotor activation. These findings may be relevant for the understanding of both cannabinoid-monoamines interactions and Cannabis-associated psychosis.
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PMID:Chronic (-)-delta9-tetrahydrocannabinol treatment induces sensitization to the psychomotor effects of amphetamine in rats. 998 95

Cannabis can induce schizophrenic-like symptoms in healthy individuals. A principal active ingredient of cannabis, delta-9-tetrahydrocannabinol, acts in the brain on a specific receptor, termed the cannabinoid receptor 1 (CNR1). The human gene for CNR1 is mapped to chromosome 6q14-15, and linkage studies have produced evidence for a schizophrenia-susceptibility locus in this region. To explore a possible role for CNR1 in the pathogenesis of schizophrenic disorders, we used an association study to genotype the CNR1 polymorphism for 127 schizophrenic patients and 146 control subjects. The results demonstrate no association between CNR1 genotypes and schizophrenic disorders (P = 0.409), with these negative findings suggesting that, for Chinese populations, the (AAT)n triplet repeat in the promoter region of the CNR1 gene is not directly involved in the pathogenesis of schizophrenic disorders.
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PMID:Association study of a cannabinoid receptor gene (CNR1) polymorphism and schizophrenia. 1120 52


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