Cannabis is one of the most widely used drugs throughout the world. The psychoactive constituent of cannabis, delta 9-tetrahydrocannabinol (delta 9-THC), produces a myriad of pharmacological effects in animals and humans. For many decades, the mechanism of action of cannabinoids, compounds which are structurally similar to delta 9-THC, was unknown. Tremendous progress has been made recently in characterizing cannabinoid receptors both centrally and peripherally and in studying the role of second messenger systems at the cellular level. Furthermore, an endogenous ligand, anandamide, for the cannabinoid receptor has been identified. Anandamide is a fatty-acid derived compound that possesses pharmacological properties similar to delta 9-THC. The production of complex behavioral events by cannabinoids is probably mediated by specific cannabinoid receptors and interactions with other neurochemical systems. Cannabis also has great therapeutic potential and has been used for centuries for medicinal purposes. However, cannabinoid-derived drugs on the market today lack specificity and produce many unpleasant side effects, thus limiting therapeutic usefulness. The advent of highly potent analogs and a specific antagonist may make possible the development of compounds that lack undesirable side effects. The advancements in the field of cannabinoid pharmacology should facilitate our understanding of the physiological role of endogenous cannabinoids.

Cannabis: pharmacology and toxicology in animals and humans.

Data on the history of cannabis use and a spot urine test for cannabinoids were obtained for 137 schizophrenics in treatment. Subjects who were using cannabis during the 6-month observation period presented with a significantly higher degree of delusional and hallucinatory activity than those who did not. Moreover, the group using cannabis made a higher average number of visits to the hospital during the same period. The status of cannabis use appeared to contribute to such variance more than did other relevant factors (age, stage of the illness, amount of medication prescribed, occasional use of other psychoactive substances).

Cannabis affects the severity of schizophrenic symptoms: results of a clinical survey.

Objective: The existence of cannabis-induced psychosis (CP) remains controversial, partly because of methodological problems. We hypothesize that acute schizophrenia (AS) and CP can have distinct demographic, premorbid and clinical features. Method: We compared 26 patients with CP to 35 with AS, after their cannabis-consumption status was confirmed by repeated urine screens. Patients with CP were assessed after at least 1 week but not more than 1 month of abstinence. Symptoms were evaluated with the Present State Examination (PSE). Results: In group CP, male gender, expansive mood and ideation, derealization/depersonalization, visual hallucinations, and disturbances of sensorium were more frequent than in group AS. Premorbid schizoid personality traits were more frequently associated to AS and antisocial personality traits to CP. Conclusion: The continuous heavy use of cannabis can induce a psychotic disorder distinct from AS. These two clinical entities share some features but they diAer in others.

Cannabis-induced psychosis: a cross-sectional comparison with acute schizophrenia.

The aim of this study was to find out whether there are any similarities between cannabis psychosis on the one hand and schizophrenia and mania on the other, and to delineate any consistency in the pattern of clinical symptoms of cannabis psychosis. Relevant data were collected from patient's case-notes depicting biographical information and the frequencies of mental symptoms. Age and duration in hospital agreed between the 3 groups. Although several significant differences were recorded in the distribution of mental symptoms, it was not possible to demonstrate a consistent pattern of symptoms typical of cannabis psychosis.

A retrospective study of symptom patterns of cannabis-induced psychosis.

Twelve male patients with chronic drug consumption including cannabis (ICD=304.3) and morphine (ICD=304.7), who required inpatient treatment for drug-induced paranoid hallucinatory states (ICD=292.1) were investigated using computed tomography for macroscopic structural changes in the brain. The findings were compared with those in a control group of schizophrenic patients who did not consume drugs. The brain scans were measured and not show any significant morphological differences between the two groups.

A cerebral computed tomography study of patients with drug-induced psychoses.

From 237 patients examined for drug-induced psychoses, 50 cannabis psychoses were examined according to the criterion "main cause of addiction" and 107 were examined according to the criterion "consumption during the last three months before hospitalization". The cannabis psychoses were compared to the other drug-induced psychoses as well as to a control group consisting of 219 schizophrenic patients. General agreement was found with the other drug-induced psychoses as well as with the group of schizophrenic patients. The variation from the symptomatology of the schizophrenics is generally common to both the cannabis psychoses and the other drug-induced psychoses. Judging by the results of our investigations, it must be concluded that there is no disease "cannabis psychosis" in its own right, just as the disease "drug-induced psychosis" also does not exist in its own right. While there is a certain slight drug-specific psychopathological undertone, it does not entitle us to speak of a syndromatic or indeed a nosological entity. The psychopathological cross section does not permit a differentiation in the individual psychoses groups mentioned, although this has often been attempted in the literature. That there are no relevant psychopathological differences between cannabis psychoses and endogenous schizophrenia could, for one, be based on the fact that we are observing the final stage of one and the same underlying pathological process. In this case both syndromes would in practice be endogenous psychoses, with the cause not being known in one case. The psychopathologic similarity of these two psychoses forms could, however, also be based on the assumption that cannabis psychoses are triggered schizophrenias, so that we could in both cases be dealing with one and the same disease. We see the solution to the problem of diagnosing symptomatic psychoses, and in particular cannabis psychoses, in making a diagnosis that takes the etiology into consideration in addition to the syndrome diagnosis.

Zur Psychopathologie und Differentialdiagnose sogenannter Cannabispsychosen

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Zur Psychopathologie und Differentialdiagnose sogenannter Cannabispsychosen