Neurocognitive Effects of Methamphetamine: A Critical Review and Meta-analysis

Joint Doctoral Program in Clinical Psychology, San Diego State University and University of California, San Diego, CA 92120, USA.
Neuropsychology Review (Impact Factor: 4.59). 10/2007; 17(3):275-97. DOI: 10.1007/s11065-007-9031-0
Source: PubMed


This review provides a critical analysis of the central nervous system effects of acute and chronic methamphetamine (MA) use, which is linked to numerous adverse psychosocial, neuropsychiatric, and medical problems. A meta-analysis of the neuropsychological effects of MA abuse/dependence revealed broadly medium effect sizes, showing deficits in episodic memory, executive functions, information processing speed, motor skills, language, and visuoconstructional abilities. The neuropsychological deficits associated with MA abuse/dependence are interpreted with regard to their possible neural mechanisms, most notably MA-associated frontostriatal neurotoxicity. In addition, potential explanatory factors are considered, including demographics (e.g., gender), MA use characteristics (e.g., duration of abstinence), and the influence of common psychiatric (e.g., other substance-related disorders) and neuromedical (e.g., HIV infection) comorbidities. Finally, these findings are discussed with respect to their potential contribution to the clinical management of persons with MA abuse/dependence.

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    • "Neurocognitive deficits occur not only in individuals currently using METH (Simon et al., 2000) but can also persist long after METH is discontinued (4 days to 7 months) (Kalechstein et al., 2003, 2009; Gonzalez et al., 2004; Hoffman et al., 2006; Cherner et al., 2010; Casaletto et al., 2014). Among the different types of neurocognitive deficits caused by METH abuse, METH-associated neurocognitive deficits are greater for episodic memory, executive functions, information processing speed, and motor skills and lesser for attention, working memory , and verbal fluency (Scott et al., 2007). Notably, relapse is associated with episodic memory deficits but not other types of cognitive dysfunction among METH abusers (Simon et al., 2004). "
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    ABSTRACT: Previous studies have demonstrated that methamphetamine (METH) abuse leads to memory deficits and these are associated with relapse. Furthermore, extensive evidence indicates that nicotine (NIC) prevents and/or improves memory deficits in different models of cognitive dysfunction and these nicotinic effects might be mediated by hippocampal or cortical nicotinic acetylcholine receptors (nAChRs). The present study investigated whether NIC attenuates METH-induced novel object recognition (NOR) deficits in rats and explored potential underlying mechanisms. Adolescent or adult male Sprague-Dawley rats received either NIC water (10-75 μg/ml) or tap water for several weeks. METH (4 x 7.5 mg/kg/injection) or saline was administered either before or after chronic NIC exposure. Novel object recognition was evaluated 6 d after METH or saline. Serotonin transporter function and density, and α4β2 nAChR density were assessed on the following day. Chronic NIC intake via drinking water beginning during either adolescence or adulthood attenuated the NOR deficits caused by a high-dose METH administration. Similarly, NIC attenuated METH-induced deficits in NOR when administered after METH treatment. However, NIC did not attenuate the serotonergic deficits caused by METH in adults. Conversely, NIC attenuated METH-induced deficits in α4β2 nAChR density in the hippocampal CA1 region. Furthermore, NIC increased α4β2 nAChR density in the hippocampal CA3, dentate gyrus and perirhinal cortex (PRh) in both saline- and METH-treated rats. Overall, these findings suggest that NIC-induced increases in α4β2 nAChRs in the hippocampus and PRh might be one mechanism by which NOR deficits are attenuated by NIC in METH-treated rats. © The Author 2015. Published by Oxford University Press on behalf of CINP.
    The International Journal of Neuropsychopharmacology 07/2015; DOI:10.1093/ijnp/pyv073 · 4.01 Impact Factor
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    • "From a pathological standpoint, chronic methamphetamine abuse has devastating effects on the neural system and predisposes people to movement disorders, stroke, seizures, aggressiveness, memory deficits, and psychosis (Hsieh et al., 2014; Panenka et al., 2013; Yamamoto et al., 2010). These changes can remain for years after discontinued use and may reflect risk factors for relapse (Grant et al., 2012; Scott et al., 2007). "
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    DESCRIPTION: Quantitative mass spectrometry based proteomics on the PFC identified one potential hit; the synaptic signaling protein phosphatidylethanolamine-binding protein 1 (PEBP1). While methamphetamine intake was associated with reduced PEBP1 protein levels, treatment with ibudilast reversed this effect. Furthermore, decreased PEBP1 expression was correlated with subsequent activation of Raf-1, MEK, and ERK signaling components of the mitogen-activated protein kinase cascade (MAPK). Future work will need to confirm the causal link between chronic methamphetamine intake, the alterations in PEBP1 by this intake, and the reversal of these alterations by ibudilast.
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    • "Despite the indirect link between acute exercise and substance abuse, the role of acute exercise in MA craving has not yet been examined. Cognitive deficits have been linked to MA; in particular, MA-users perform worse on multiple cognitive performance measures, such as inhibition [14] [15], executive function [16], memory [16], and real-life functional ability [17]. Among these cognitive impairments, inhibition is one of the particularly relevant executive functions [18]. "
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    ABSTRACT: This study aimed to determine the effect of acute exercise in the potential context of non-pharmacological intervention for methamphetamine (MA)-related craving; we additionally determine its effect on the inhibitory control induced by standard and MA-related tasks according to behavioral and neuroelectric measurements among MA-dependent individuals. The present study employed a within-subjects, counterbalanced design. A total of 24 participants who met the DSM-IV criteria for MA dependence were recruited. The craving level, reaction time, and response accuracy, as well as the event-related potential (ERP) components N2 and P3, were measured following exercise and the control treatment in a counterbalanced order. The exercise session consisted of an acute stationary cycle exercise at a moderate intensity, whereas the control treatment consisted of an active reading session. The self-reported MA craving was significantly attenuated during, immediately following, and 50min after the exercise session compared with the pre-exercise ratings, whereas the craving scores at these time points following exercise were lower than those for the reading control session. Acute exercise also facilitated inhibitory performance in both the standard and MA-related Go/Nogo tasks. A larger N2 amplitude, but not a larger P3 amplitude, was observed during both tasks in the exercise session and the Nogo condition compared with the reading control session and the Go condition. This is the first empirical study to demonstrate these beneficial effects of acute aerobic exercise at a moderate intensity on MA-related craving and inhibitory control in MA-dependent individuals. These results suggest a potential role for acute aerobic exercise in treating this specific type of substance abuse. Copyright © 2015. Published by Elsevier Inc.
    Physiology & Behavior 04/2015; 147. DOI:10.1016/j.physbeh.2015.04.008 · 2.98 Impact Factor
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