Attentional Control and Brain Metabolite Levels in Methamphetamine Abusers

Salo, Ruth; Nordahl, Thomas E.; Natsuaki, Yutaka; Leamon, Martin H.; Galloway, Gantt P.; Waters, Christy; Moore, Carl A.; Buonocore, Michael H.

doi:10.1016/j.biopsych.2006.07.031

Cited by 118 publications

(121 citation statements)

References 59 publications

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“…Because tCr has been used successfully as an internal metabolite reference in several proton MRS studies in abstinent methamphetamine users (Nordahl et al, 2005(Nordahl et al, , 2002Salo et al, 2007) as well as other human studies (see review, Xu et al, 2008), and does not become enriched during the time scale of the present studies, we have used this as an internal reference to quantify HCO 3 À and its subsequent enrichment from [1-…”

Section: ) Productionmentioning

confidence: 99%

Glial Dysfunction in Abstinent Methamphetamine Abusers

Sailasuta

Abulseoud

Harris

et al. 2009

J Cereb Blood Flow Metab

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Persistent neurochemical abnormalities in frontal brain structures are believed to result from methamphetamine use. We developed a localized 13 C magnetic resonance spectroscopy (MRS) assay on a conventional MR scanner, to quantify selectively glial metabolic flux rate in frontal brain of normal subjects and a cohort of recovering abstinent methamphetamine abusers. Steady-state bicarbonate concentrations were similar, between 11 and 15 mmol/L in mixed gray-white matter of frontal brain of normal volunteers and recovering methamphetamine-abusing subjects (P > 0.1). However, glial 13 C-bicarbonate production rate from [1-13 C]acetate, equating with glial tricarboxylic acid (TCA) cycle rate, was significantly reduced in frontal brain of abstinent methamphetamineaddicted women (methamphetamine 0.04 lmol/g per min (N = 5) versus controls 0.11 lmol/g per min (N = 5), P = 0.001). This is equivalent to 36% of the normal glial TCA cycle rate. Severe reduction in glial TCA cycle rate that normally comprises 10% of total cerebral metabolic rate may impact operation of the neuronal glial glutamate cycle and result in accumulation of frontal brain glutamate, as observed in these recovering methamphetamine abusers. Although these are the first studies to define directly an abnormality in glial metabolism in human methamphetamine abuse, sequential studies using analogous 13 C MRS methods may determine 'cause and effect' between glial failure and neuronal injury.

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Section: ) Productionmentioning

confidence: 99%

Glial Dysfunction in Abstinent Methamphetamine Abusers

Sailasuta

Abulseoud

Harris

et al. 2009

J Cereb Blood Flow Metab

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“…Results: At the first assessment, the methamphetamine-dependent subjects showed significantly worse performance than the comparison group on a test of processing speed; they also performed 0.31 SDs worse than the control group on a global battery composite score (p < .05). After a month of abstinence, methamphetamine-dependent subjects demonstrated slightly more cognitive improvement than healthy control subjects on the entire cognitive battery, but this difference did not approach statistical significance (p = .33 (Gonzalez et al, 2004(Gonzalez et al, , 2007Hoffman et al, 2006;Kalechstein et al, 2003;Monterosso et al, 2005;Paulus et al, 2003;Salo et al, 2002Salo et al, , 2005Salo et al, , 2007Simon et al, 2000 Simon et al, , 2002Woods et al, 2005). In a meta-analysis of studies comparing individuals with MA abuse or dependence to healthy control subjects (Scott et al, 2007) Despite evidence provided by meta-analytic data, which is collapsed across studies, individual MA-dependent subjects vary in the severity of cognitive deficits they exhibit (Dean and London, 2010), and not all studies of MA-abusing subjects have demonstrated weaknesses.…”

mentioning

confidence: 96%

“…M ETHAMPHETAMINE (MA) USE HAS been associated with various cognitive deficits (Gonzalez et al, 2004(Gonzalez et al, , 2007Hoffman et al, 2006;Kalechstein et al, 2003;Monterosso et al, 2005;Paulus et al, 2003;Salo et al, 2002Salo et al, , 2005Salo et al, , 2007Simon et al, 2000Simon et al, , 2002Woods et al, 2005). In a meta-analysis of studies comparing individuals with MA abuse or dependence to healthy control subjects (Scott et al, 2007), the largest MA-associated deficits were noted in the domains of learning (d = -0.66), executive functions (d = -0.63), memory (d = -0.59), and processing speed (d = -0.52), with milder deficits in visuoconstruction (d = -0.37) and language (d = -0.34).…”

mentioning

confidence: 99%

Methamphetamine Dependence and Neuropsychological Functioning: Evaluating Change During Early Abstinence

Simon¹,

Dean²,

Cordova³

et al. 2010

J. Stud. Alcohol Drugs

102

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ABSTRACT. Objective: The purpose of this work was to assess neuropsychological functioning of individuals in early abstinence from methamphetamine dependence and to test for cognitive change over the first month of abstinence. Method: Methamphetamine-dependent subjects in very early abstinence from methamphetamine (4-9 days; n = 27) were compared with healthy comparison subjects (n = 28) on a test battery that evaluated five cognitive domains (attention/processing speed, learning/memory, working memory, timed executive functioning, and untimed executive functioning). A subsample of the methamphetaminedependent subjects (n =18), who maintained abstinence for 1 month, as well as a subsample of the comparison subjects (n = 21), were retested. Results: At the first assessment, the methamphetamine-dependent subjects showed significantly worse performance than the comparison group on a test of processing speed; they also performed 0.31 SDs worse than the control group on a global battery composite score (p < .05). After a month of abstinence, methamphetamine-dependent subjects demonstrated slightly more cognitive improvement than healthy control subjects on the entire cognitive battery, but this difference did not approach statistical significance (p = .33 (Gonzalez et al., 2004(Gonzalez et al., , 2007Hoffman et al., 2006;Kalechstein et al., 2003;Monterosso et al., 2005;Paulus et al., 2003;Salo et al., 2002Salo et al., , 2005Salo et al., , 2007Simon et al., 2000 Simon et al., , 2002Woods et al., 2005). In a meta-analysis of studies comparing individuals with MA abuse or dependence to healthy control subjects (Scott et al., 2007) Despite evidence provided by meta-analytic data, which is collapsed across studies, individual MA-dependent subjects vary in the severity of cognitive deficits they exhibit (Dean and London, 2010), and not all studies of MA-abusing subjects have demonstrated weaknesses. In one study, MA-dependent subjects (n = 44), who were abstinent for a week, did not significantly differ from matched comparison subjects (n = 28) on a battery of motor functioning, verbal memory, attention/processing speed, working memory, reaction time, and executive functioning (Chang et al

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“…Of these eight studies (see Table 1), five found that the MA-dependent participants performed worse than the control participants on a subset of the cognitive tests administered (Hoffman et al, 2006;Kim et al, 2006;Rippeth et al, 2004;Salo et al, 2007Salo et al, , 2009. The other three studies did not find significant differences between the groups on multiple cognitive tests (Chang et al, 2005;King et al, 2010;Simon et al, 2010), although two of these studies used Bonferroni correction for statistical significance, and this method may be overly conservative when dependent variables are interrcorrelated (Miller, 1981), as is the case with performance on most cognitive tests (Warner et al, 1987).…”

Section: Individuals Who Abuse Ma Will Have Worse Cognitive Performanmentioning

confidence: 99%

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

Dean

Groman

Morales

et al. 2012

Neuropsychopharmacol

203

127

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Methamphetamine (MA) is one of the most commonly abused illicit substances worldwide. Among other problems, abuse of the drug has been associated with reduced cognitive function across several domains. However, much of the literature has not attempted to differentiate cognitive difficulties caused by MA abuse from preexisting cognitive difficulties that are likely caused by other factors. Here, we address this question, evaluating evidence for a priori hypotheses pertaining to six lines of research: (a) animal studies; (b) crosssectional human studies; (c) a twin study; (d) studies of changes in cognition with abstinence from MA; (e) studies of changes in brain structure and function with abstinence from MA; and (f) studies of the relationship between the severity of MA abuse and the extent of cognitive deficits observed. Overall the findings were mixed, with some support for a causal relationship between MA abuse and cognitive decline, and other findings suggesting that there is no relationship. The preponderance of the data, however, does support the possibility that MA abuse causes cognitive decline, of unknown duration, in at least some users of the drug. When averaged across individuals, this decline is likely to be mild in early-to-middle adulthood. However, moderator variables are likely to contribute to the presence and/or severity of cognitive decline exhibited by a given individual.

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Attentional Control and Brain Metabolite Levels in Methamphetamine Abusers

Cited by 118 publications

References 59 publications

Glial Dysfunction in Abstinent Methamphetamine Abusers

Glial Dysfunction in Abstinent Methamphetamine Abusers

Methamphetamine Dependence and Neuropsychological Functioning: Evaluating Change During Early Abstinence

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

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