Cannabis, abuse

Bovasso GB Cannabis abuse as a risk factor for depressive symptoms. Am J Psychiatry... 

Alcohol Abuse, Alcohol Dependence Amphetamine Abuse, Amphetamine Dependence Cannabis Abuse, Cannabis Dependence Cocaine Abuse, Cocaine Dependence Hallucinogen Abuse, Hallucinogen Dependence Inhalant Abuse, Inhalant Dependence Nicotine Dependence Opiate Abuse, Opiate Dependence Phencyclidine Abuse, Phencyclidine Dependence... 

Cannabinoid hyperemesis. Nineteen patients were identified with chronic cannabis abuse and a cyclical vomiting illness. Pol-low-up was provided with serial urine drug... 

Jockers-Scherubl, M. C., H. Danker-Hopfe, R. Mahlberg, et al. Brain-derived neurotrophic factor serum concentrations are increased in drug-naive schizophrenic patients with chronic cannabis abuse and multiple substance abuse. Neurosci Lett 2004 371(1) 79-83. 

Allen, J. H., G. M. de Moore, R. Heddle, and J. C. Twartz. Cannabinoid hyperemesis cyclical hyperemesis in association with chronic cannabis abuse. Gut 2004 53(11) 1566-1570. Carroll, C.B., P. G. Bain, L. Teare, et al. Cannabis for dyskinesia in Parkinson disease a randomized double-blind crossover study. Neurology 2004 63(7) 1245-1250. 

H. Danker-Hopfe, U. E. Lang, R. Mahlberg, and R. Hellweg. Chronic cannabis abuse raises nerve growth fac- CS315 tor serum concentrations in drug-naive schizophrenic patients. ] Psycho-Pharmacol 2003 17(4) 439-445. 

Balle, J., M. J. Olofsson, and J. Hilden. Cannabis and pregnancy. Ugeskr Laeger 1999 161(36) 5024-5028. Von Mandach, U., M. M. Rabner, J. Wisser, and A. Huch. LSD and cannabis abuse in early pregnancy with good perinatal outcome. Case report and review of the literature. Gynakol Geburtshilfliche Rundsch 1999 39(3) 125-129. 

To date, little postmortem work has been done in human cannabis abusers. Preclinical studies indicate that chronic treatment with 5 -THC markedly reduces CBj receptor binding in all brain areas containing this receptor (cerebellum, hippocampus, cortex, globus pal-lidus, striatum), and enhances the cAMP pathway (Rubino et ah, 2000). Other preclinical work has shown that the cannabinoid receptor reserve is larger than that for most other G protein-coupled receptor systems (Gifford et ah, 1999). This means that at occupancies as low as 0.13%, 50% of maximal inhibition of Ach release is achieved. 

As in the case of chronic opiate abuse, few brain morphometric studies of human cannabis abusers have been conducted. However, recent preclinical work has demonstrated that 5 -THC concentrations as low as 0.5 to 1 lM, which are compatible with plasma 5 -THC levels achieved by humans ingesting marijuana, are toxic to hippocampal neurons (Chan et ah, 1998). This hippocampal toxicity may underlie the cognitive deficits observed in chronic marijuana users, which have been shown to persist after abstinence (Pope and Yurgel un-Todd, 1996). 

Chronic cannabis users frequently exhibit the amotivational syndrome", characterized by apathy, impaired judgement, memory defects and loss of interest in normal social pursuits. Whether chronic cannabis abuse leads to more permanent changes in brain function is uncertain, but it is known that chronic administration to animals results in permanent damage to the hippocampus. Regular use of cannabis by adolescents frequently predisposes them to other types of drug abuse later. This may reflect the social pressures placed upon them rather than the pharmacological consequences of abusing cannabis. 

Through random urine testing of draftees to the Italian army, 133 marijuana users were identified, tested, and interviewed (98). Among these marijuana users, 83% of those with cannabis dependence, 46% with cannabis abuse, and 29% of occasional users had at least one DSM-IIIR psychiatric diagnosis. With greater cannabis use, the risk of associated psychiatric disabilities tended to increase progressively. 

The causal relation between cannabis abuse and schizophrenia is controversial. Cannabis abuse, and particularly heavy abuse, can exacerbate symptoms of schizophrenia and can be considered as a risk factor eliciting relapse in schizophrenia (110). Chronic cannabis use can precipitate schizophrenia in vulnerable individuals (111). 

Neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor (BDNF), are implicated in neuronal development, growth, plasticity, and maintenance of function. Neurodevelopment is impaired in schizophrenia and vulnerable schizophrenic brains may be more sensitive to toxic influences. Thus, cannabis may be more neurotoxic to schizophrenic brains than to nonschizophrenic brains when used chronically. In 157 drug-naive first-episode schizophrenic patients there were significantly raised BDNF serum concentrations by up to 34% in patients with chronic cannabis abuse or multiple substance abuse before the onset of the disease (114). Thus, raised BDNF serum concentrations are not related to schizophrenia and /or substance abuse itself but may reflect cannabis-related idiosyncratic damage to the schizophrenic brain. Disease onset was 5.2 years earlier in the cannabis-consuming group. 

Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent-onset schizophrenic disorders. Arch Gen Psychiatry 1994 51(4) 273-9. 

Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis cyclical hyperemesis in association with chronic cannabis abuse. Gut 2004 53 1566-70. 

Carney MW, Bacelle L, Robinson B. Psychosis after cannabis abuse. BMJ (Clin Res Ed) 1984 288(6423) 1047. 

Only the detection in hair of metabolites would provide convincing evidence of cannabis abuse. The presence in hair of THC-COOH, which is not detected in cannabis smoke, can be considered as a potential marker of chronic cannabis exposure and evidence that THC excretion occurs in hair after active use. 

While performing a memory task, cannabis abusers showed less neuronal activation than control subjects in the middle temporal gyrus but areas of higher and lower activation within the parahippocampal gyrus, together with differences in hippocampal activation (Block et al., 2002). 

Suitable immunological reagents for the detection of cannabis abuse from urine tests are available from several companies. In normal circumstances, the sensitivity of a test corresponds to a cut-off value of 50 ng/ml based on 11-nor-A9-THC-9-carboxylic acid. The cut-off values of some cannabinoids are listed in Table 8-29. Only U-nor-A9-THC-9-carboxylic acid is relevant to the determination of consumption from urine tests. 

D. Bourquin and R. Brenneisen, Confirmation of cannabis abuse by the determination of 11-nor-delta 9-tetrahydrocannabinol-9-carboxylic acid in urine with high-performance liquid chromatography and electrochemical detection, J. Chromatogr., 1987, 414, 187—191. 

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