The recent trend towards legalization and commercialization of marijuana in the US has resulted in a significant drop in the perceived risks of cannabis use among all age groups. Thus, legalization has further advances the common misperception that cannabis abuse and dependence are generally safe and devoid of neuropsychiatric sequelae. Yet there are numerous acute, as well as numerous long-term neuropsychiatric consequences of cannabis use. In addition to acute psychosis and agitation, this review will discuss the long-term issues of cognitive decline, permanent psychotic disorders, syndromes of prolonged depersonalization, as well as psychological and physical dependence, and related withdrawal symptoms.Cannabis use, particularly repeated exposure, is an established contributory cause of schizophrenia by way of a classic gene-environment interaction, with the vulnerabilities associated with cannabis-induced schizophrenia involving multiple genes. There is also evidence that in utero cannabinoid exposure will impair brain maturation in developing infants and predispose them to neurodevelopmental disorders during childhood. This summary will inform clinicians of the most prevalent consequences associated with cannabis abuse and dependence, and better equip them to educate patients as to these risks. Further, there are treatments that may help patients achieve abstinence, and even neuroprotective strategies to employ in cases of new-onset cannabisinduced psychosis, as well as for cases of in utero exposure.Keywords: Schizophrenia; Cannabis abuse; Paranoia; Anxiety; Psychosis
Acute Cannabis Induced PsychopathologyFor some individuals, cannabis use does not produce a calming sensation; rather, it will induce anxiety and, in some, panic attacks [1]. Numerous case reports indicate that typical panic attack symptoms often present with intense depersonalization [2]. Though possibly related to an underlying genetic vulnerability, the specifics of this interaction have yet to be discerned, however, individuals who do experience panic and anxiety symptoms during abuse are more likely to abstain from cannabis in the future [3].The mechanism of cannabis-induced paranoia and hallucinations while abusing is believed to involve the relationship between dopamine activity and endocannabinoid transmitters. Stimulation of D2 receptors in the striatum will result in the synthesis and release of endocannabinoids, which act in a retrograde fashion to inhibit GABA and glutamate activity. Researchers have speculated that due to the number of key physiological processes within the striatum dependent on D2 to endocannabinoid signaling, this process is vital for normal functions of the striatum in health [4].They further theorized that the reason antipsychotics are less effective for acute cannabis-induced psychosis is because they exert their effects through D2 blockade, while THC enters the pathway "downstream" from D2 receptors [4]. Further, acute psychosis is often a harbinger of future psychopathology, as those who experience...