Medical Marijuana and Other Cannabinoids _____________________________________________________
Observational studies suggest that THC may have psychoto- genic effects while CBD may have antipsychotic effects. However, whether these effects on brain function are con- sistent with their opposing behavioral effects is unclear. One systematic review sought to identify the key brain substrates where these opposing effects can be observed [153]. Evidence suggests that the opposing effects may be present in the stria- tum, parahippocampus, anterior cingulate/medial prefrontal cortex, and amygdala, with opposite effects less consistently identified in other regions. Broadly, THC seems to increase brain activation and blood flow, while CBD seems to decrease brain activation and blood flow [153]. While cognitive function in long-term medical cannabis users has not been evaluated, a review of the published research on short- and long-term cognitive function in recreational users suggests that cognitive impairment is unlikely to persist beyond the acute intoxication state, even with high-THC cannabis, in late-onset users, short-term users, and occasional users [150]. Amotivational Syndrome Amotivational syndrome is not a medical diagnosis but a term used to describe adolescents and young adults who lose inter- est in and drop out from school, work, socializing, and other goal-directed activities. Cannabis has been cited as the cause when its heavy use accompanies these symptoms, but evidence of causality is lacking [8; 126]. Schizophrenia and Psychoses An acute psychotic reaction to cannabis has been described and is more likely to occur in young adults who are under stress and have a pre-existing vulnerability to psychoses or schizophrenia. An association has been found between cannabis use history and schizophrenia, but the causal direction of this link has not been established, with many studies suggesting causality showing instead a non-specific association between the most severe levels of cannabis use and a wide range of adverse psy- chosocial outcomes [126; 154]. Furthermore, cannabis use in the general population soared between 1949 and 1995, while the population rates of schizophrenia remained stable [155]. However, a subgroup of patients who are genetically vulnerable to cannabis-induced acute psychoses, and possibly cannabis- initiated schizophrenia, carry a functional polymorphism in the catechol- O -methyltransferase gene and a polymorphism in the brain-derived neurotrophic factor gene. Considering the potentially substantial risks, cannabis should be avoided in adolescents and adults with current, past, or family history of any psychotic disorder [59; 156]. Toxicity and Overdose There are no cases in the literature of death due to toxicity fol- lowing the maximum oral THC dose in dogs (up to 3,000 mg/ kg THC) and monkeys (up to 9,000 mg/kg THC). In animals and humans, it is virtually impossible to induce fatal toxicity, and no human fatalities resulting from cannabis ingestion have been documented to date [37].
The side effect profile of medical cannabis is comparable to those produced by other medications tolerated by patients and approved for clinical use by the FDA [126; 157]. The rare acute complications resulting in emergency department presenta- tion, such as panic attacks, psychosis, or convulsions, can be managed with conservative measures such as reassurance in a quiet environment and IV administration of benzodiazepines if needed [14; 158]. The greatest risk for toxicity and potential overdose is among children who may consume cannabis edibles, beverages, or candies inadvertently [159; 160]. A concern with toxic reac- tions is self-harm. In 2014, a young man (19 years of age) from Colorado died after consuming an edible marijuana product (a cookie). The decedent initially ate only a single serving (one- sixth of the cookie), as directed by the salesclerk. Each serving contained approximately 10 mg of THC. Approximately 30 to 60 minutes later, after not feeling any effects, the decedent consumed the remainder of the cookie. For the next two hours, the young man exhibited erratic speech and hostile behaviors. About 3.5 hours following initial ingestion, he jumped off a fourth floor balcony and died from trauma [161]. In adults, most toxic reactions are mild, but in children, overdose can result in significant respiratory depression [160]. Signs can include somnolence, hallucinations, dyspnea, CNS depression, and even coma. Healthcare professionals should assess for availability of cannabis in the household if these signs present with no known explanation. If necessary, airway management and ventilation may be administered. As “Gateway Drug” The sensationalized 1980s theory of marijuana as the gateway to hard drug use lacks empirical support. While heavy adoles- cent use is associated with risk of other drug abuse, there is no good evidence of causality or directionality, and the large majority of cannabis users do not progress to “hard” drug use [19; 162]. Alcohol and nicotine use are more significant primers for hard drug use in many individuals [162]. Further research is necessary to clarify these points. Cannabis Withdrawal Syndrome Until recently, considerable doubt surrounded the possibility of a cannabis withdrawal syndrome; however, cannabis with- drawal syndrome has now been unequivocally demonstrated in heavy chronic recreational users [163]. With abrupt cessation, withdrawal symptoms emerge within one to two days, reach peak intensity after two to six days, and generally resolve within one to two weeks. Common symptoms include irritability or anger, nervousness, tension, restlessness, reduced appetite, insomnia and sleep difficulties, dysphoria, and craving. Less frequent symptoms are chills, stomach pain, shakiness, and sweating [164]. Cannabis withdrawal can resemble a low-grade opioid withdrawal but usually lacks the severe aches and pains, piloerection, diarrhea, sweating, stuffy nose, and muscle spasms common to opioid withdrawal [28; 126].
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