| Summary: | Includes bibliographical references. === An association between methamphetamine dependence and neurocognitive impairment has long been established. However, there are a number of research gaps. First, while evidence suggests that the primary cognitive domains affected in methamphetamine dependence are executive functions; previous research fails to employ a comprehensive battery of executive functioning tests. Second, there is little research investigating the specific neuropsychological impairments associated with methamphetamine psychosis in particular. Third, ADHD is highly co-morbid with substance dependence. Symptoms of ADHD were therefore investigated as possible confounders in this study. Fourth, few studies of methamphetamine dependence have explored relationships between neuropsychological data and cortical thickness data; the current study therefore investigated this further. The current study employed a neuropsychological test battery to compare executive functioning across three groups; a methamphetamine dependent group without psychosis (n = 20), a methamphetamine dependent group with psychosis (n =19) and a healthy control group (n = 20); demographically matched. Brain images were acquired using a Siemens Magnetom Allegra 3T system with a high-resolution, T1-weighted, 3D-multiecho MPRAGE sequence with the following scan parameters: TR=2530ms; graded TE=1.53, 3.21, 4.89, 6.57ms; flip angle=7°; FOV=256mm; slice thickness=1mm; 160 slices; and acquisition duration of 10.49 min. Cortical thickness was assessed employing a surface-based cortical reconstruction and automatic labelling tool in the FreeSurfer software package. Four executive domains were identified and evaluated, namely decision making and impulsivity; inhibitory control and setshifting; attention and working memory; and verbal fluency. One-way ANOVAs were conducted in order to assess differences between groups. Analyses indicated significant between group differences on most tasks of executive functioning. Overall the methamphetamine psychosis (MA+) group performed more poorly than the methamphetamine non-psychosis (MA-) group and the controls (NC). Statistically significant between-group differences were observed on inhibitory control and set-shifting (p < .001), attention and working memory (p = .006), and on tasks of generativity (p < .001). Spearman's correlational analyses revealed that in general, executive impairment was associated with cortical thinning of frontal regions in the MA+ group and cortical thickening of frontal regions in the MA- group. This may be reflective of a compensatory response to methamphetamine toxicity in the MA- group. In conclusion, executive functioning was significantly impaired in the MA- group and even more so in the MA+ group. Symptoms of ADHD were not found to be significantly correlated with executive functioning data. Therefore executive dysfunction is more likely the result of MA toxicity than a pre-existing ADHD disorder. An improved understanding of the neuropsychology and neuroanatomy of methamphetamine dependence may ultimately contribute to the clinical management of these individuals.
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