Archival ReportEffects of Modafinil on Neural Correlates of Response Inhibition in Alcohol-Dependent Patients
Section snippets
Subjects
Twenty male subjects meeting DSM-IV (30) criteria for alcohol dependence (AD) were recruited from regional addiction treatment centers. In addition, 18 healthy control subjects (HC), matched on sex, education, and age, were included. Exclusion criteria can be found in the Supplemental Methods in Supplement 1. Four AD and two HC subjects were excluded from analyses due to either too many omission errors on go trials or excessive head motion during scanning. The remaining data from 32
Demographics and Clinical Assessments
Demographic, self-report, and substance use characteristics are presented in Table 1. The AD group did not differ from the HC group with regard to age, educational level, or IQ. Alcohol dependence subjects smoked significantly more cigarettes than HC subjects. We did not include smoking as a covariate in subsequent analyses, because smoking behavior was related to alcohol consumption during the past 6 months (r = .47, p = .01) and AUDIT scores (r = .54, p = .001). Therefore, including smoking
Discussion
This study demonstrates that modafinil can improve response inhibition by modulating activation in key regions involved in successful inhibition (SMA and thalamus) but only in alcohol-dependent patients that show poor initial response inhibition. In contrast, response inhibition in better performing subjects deteriorated after receiving modafinil. These observations are in line with findings of modafinil-induced improvements and deteriorations in response inhibition in subjects with low and
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2021, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Small samples consisting of patients with less severe deficits may erroneously result in differences that are statistically non-significant, hence increasing the risk of false negatives (Type-II error). As noted earlier, some CPEAs such as modafinil may be more beneficial in a subgroup of AUD patients with more severe neurocognitive dysfunctions (Joos et al., 2013b; Schmaal et al., 2013b). Screening for neurocognitive dysfunctions prior to baseline assessment would allow for the inclusion of a subgroup of patients with a specific level of neurocognitive impairment, which in turn could increase susceptibility to the effects of the pharmacotherapeutic agent.
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2020, Neuroscience and Biobehavioral ReviewsCitation Excerpt :In a cross-translational IMAGEN study of the ubiquitously expressed GTPase Arf6 and Efa6, mutant flies showed differential sensitivity to alcohol preference, tolerance and sedation; the human ortholog, the PSD3 haplotype associated with AD was localized within the prefrontal cortex associated with response inhibition (Gonzalez et al., 2018). Acute administration of modafanil improved response inhibition and thalamic and supplementary motor area activity in abstinent AD but only in those with underlying baseline inhibitory impairments (Schmaal et al., 2013). AD and binge drinkers also display impaired waiting impulsivity (or the tendency to response prematurely) along with reduced resting state functional connectivity between the subthalamic nucleus, VS and subgenual cingulate cortex (Sanchez-Roige et al., 2014; Morris et al., 2016b).