When injected, snorted, or inhaled, METH has direct access to the circulatory system and therefore has more immediate effects on the brain ( 26, 27). METH is available in various forms and at different levels of chemical purity. In Australia, there has been a 233% increase in demand for METH related treatment and a 274% increase in METH related hospital admissions since 2010 ( 23, 24), with Queensland specifically witnessing a 20-fold increase in METH related hospital admissions from 2009 to 2015 ( 25). Additionally, admissions to treatment programs for METH use increased 255% from 1997 to 2007 in the USA ( 20, 21), although there is some evidence that the rate of admissions for METH in the USA have remained stable or slightly declined from 2004 to 2014 ( 22). Indeed, worldwide seizures relating to METH have been greater than any other drug category ( 17). Recent reports suggest an increased production of METH around the world and an increasing popularity of METH over the last 5–15 years, which has been linked to increased ease and cost-effective synthesis in clandestine laboratories and augmented importation of METH from Mexico and Asia ( 16, 19). Worldwide statistics on METH use describe it as a global phenomenon, with METH consumption reportedly independent of wealth, geographical location, and culture ( 18). Although all three monoamine systems are involved, the behavioral and reinforcing properties of METH have typically been associated with dopaminergic neurotransmission, particularly in the mesocorticolimbic pathway ( 11, 12).Įpidemiological studies place amphetamine-type stimulants as the most widely used illicit drug in the world after cannabis ( 13, 14), with up to 51 million users globally between 15 and 64 years old ( 15– 17). This causes changes to dopaminergic, serotonergic, and noradrenergic systems via the stimulated release of monoamines, the inhibition and reversal of monoamine reuptake, inactivation of presynaptic vesicular monoamine transporter 2, and by reducing the efficacy of monoamine metabolic enzymes ( 6– 10). This methyl addition reportedly makes METH highly lipophilic, thereby allowing it to increasingly penetrate the blood-brain barrier ( 5). It is a cationic molecule and chiral compound based around a phenylethylamine core ( 4), and distinguishable from its amphetamine analogs by an additional methyl group. Methamphetamine (METH N-methyl-alpha-methylphenethylamine) is a highly potent amphetamine derivative that is frequently abused worldwide and has significant effects on physical, behavioral, cognitive and psychiatric output ( 3). Limitations of the literature and avenues for future research are also discussed.Īmphetamines refer to a class of chemically related compounds that have been used extensively over the last century in both recreational and medicinal settings, with various amphetamine analogs used in the treatment of narcolepsy, attention deficit hyperactivity disorder (ADHD) and obesity ( 1, 2). Preliminary evidence, on the other hand, suggests that chronic METH psychosis may be clinically similar to that of primary psychotic disorders, particularly with respect to positive and cognitive symptomatology, although negative symptoms appear to be more pronounced in schizophrenia. As such, acute METH psychosis may represent a distinct psychotic disorder to schizophrenia and could be clinically distinguished from a primary psychotic disorder based on the aforementioned behavioral and cognitive sequelae. Schizophrenia appears to be associated with pronounced thought disorder, negative symptoms more generally and cognitive deficits mediated by the parietal cortex, such as difficulties with selective visual attention, while visual and tactile hallucinations appear to be more prevalent in acute METH-induced psychosis. We conclude that while there is considerable overlap in the behavioral and cognitive symptoms between METH psychosis and schizophrenia, there appears to be some evidence that suggests there are divergent aspects to each condition, particularly with acute METH psychosis. This review provides a comprehensive critique of research that has directly compared schizophrenia with acute and chronic METH psychosis, with particular focus on psychiatric and neurocognitive symptomatology. Methamphetamine is a potent psychostimulant that can induce psychosis among recreational and chronic users, with some users developing a persistent psychotic syndrome that shows similarities to schizophrenia.
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