Implications of Chronic Methamphetamine Use: A Literature Review

Abstract

Methamphetamine (MA) abuse is increasing to epidemic proportions, both nationally and globally. Chronic MA use has been linked to significant impairments in different arenas of neuropsychological function. To better understand this issue, a computerized literature search (PubMed, 1964-2004) was used to collect research studies examining the neurobiological and neuropsychiatric consequences of chronic MA use. Availability of MA has markedly increased in the United States due to recent technological improvements in both mass production and clandestine synthesis, leading to significant public health, legal, and environmental problems. MA intoxication has been associated with significant psychiatric and medical comorbidity. Research in animal models and human subjects reveals complicated mechanisms of neurotoxicity by which chronic MA use affects catecholamine neurotransmission. This pathology may underlie the characteristic cognitive deficits that plague chronic MA users, who experience impairments in memory and learning, psychomotor speed, and information processing. These impairments have the potential to compromise, in turn, the ability of MA abusers to engage in, and benefit from, psychosocially based chemical-dependency treatment. Development of pharmacological interventions to improve these cognitive impairments in this population may significantly improve the degree to which they may be able to participate in treatment. Atypical antipsychotics may have some promise in this regard.

Effect of (+)-methamphetamine on path integration learning, novel object recognition, and neurotoxicity in rats

“…The significance of the path integration deficits in rats in relation to human MA users is not yet known because no human study has assessed this specific function, but it is noteworthy that MA affects cortical regions in humans (Meredith et al, 2005;Barr et al, 2006;Baicy and London, 2007) and path integration is a cortically-mediated function. Moreover, human virtual path integration tasks have recently been developed and used in fMRI experiments to map the locations of path integration in humans (Wolbers et al, 2007).…”

“…Chronic MA use can result in cognitive deficits, even after periods of abstinence (Meredith et al, 2005;Barr et al, 2006;Baicy and London, 2007). Autopsy and imaging studies on chronic users reveal reductions in brain dopamine and of dopamine transporter density (Wilson et al, 1996;Meredith et al, 2005;Barr et al, 2006;Baicy and London, 2007) and reductions in brain serotonin (Wilson et al, 1996) and of serotonin transporter density (Sekine et al, 2006).…”

“…Acutely, methamphetamine (MA) heightens attention and decreases fatigue, appetite, and anxiety along with stimulating the sympathetic nervous system and cortisol release (Meredith et al, 2005) (Fehm et al, 1984). Chronic MA use can result in cognitive deficits, even after periods of abstinence (Meredith et al, 2005;Barr et al, 2006;Baicy and London, 2007).…”

Extended methamphetamine self-administration enhances reinstatement of drug seeking and impairs novel object recognition in rats

“…Aside from public health concerns (e.g., increased rates of sexually transmitted diseases), methamphetamine addiction poses greater concern than other drugs of abuse, given its capacity to produce deleterious psychiatric symptoms and cognitive impairments. Methamphetamine abuse contributes to depression, aggression, anxiety, attention deficits, and a variety of cognitive deficits (Meredith et al 2005). Clinical data indicate that long-term methamphetamine users exhibit deficits in specific tests of cognitive function, such as poor recall for both words and pictures (Simon et al 2000;Woods et al 2005), impairments of decision making (Paulus et al 2002), vigilance task performance (London et al 2005), and verbal encoding and retrieval (Woods et al 2005).…”

Long-Term Methamphetamine Administration in the Vervet Monkey Models Aspects of a Human Exposure: Brain Neurotoxicity and Behavioral Profiles

“…Although behavioral consequences associated with long-term METH exposure have been extensively documented in METH abusers (Cretzmeyer et al, 2003;Ling et al, 2006;Meredith et al, 2005), the corresponding magnitude and duration of brain alterations remain unclear due, in part, to the paucity of relevant human data. The framework for postulating METH-associated brain changes in humans has been derived mainly from results of experimental METH studies, predominantly in rodents (Seiden, 1985(Seiden, , 1996Bowyer and Holson, 1995;Davidson et al, 2001;Cadet et al, 2003) and relatively fewer in nonhuman primates (Fischman and Schuster, 1977;Melega et al, 1997;Madden et al, 2005).…”