Sarah Aronson Fischell1, Thomas J Ross2, Zhi-De Deng3, Betty Jo Salmeron2, Elliot A Stein4. 1. Neuroimaging Research Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, Maryland; School of Medicine, University of Maryland, Baltimore, Maryland. 2. Neuroimaging Research Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, Maryland. 3. Noninvasive Neuromodulation Unit, Experimental Therapeutics and Pathophysiology Branch, National Institute of Mental Health, Intramural Research Program, National Institutes of Health, Bethesda, Maryland. 4. Neuroimaging Research Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, Maryland. Electronic address: estein@nih.gov.
Abstract
BACKGROUND: The nicotine withdrawal syndrome remains a major impediment to smoking cessation. Cognitive and affective disturbances are associated with altered connectivity within and between the executive control network, default mode network (DMN), and salience network. We hypothesized that functional activity in cognitive control networks, and downstream amygdala circuits, would be modified by application of transcranial direct current stimulation (tDCS) to the left (L) dorsolateral prefrontal cortex (dlPFC, executive control network) and right (R) ventromedial prefrontal cortex (vmPFC, DMN). METHODS: A total of 15 smokers (7 women) and 28 matched nonsmokers (14 women) participated in a randomized, sham-controlled, double-blind, exploratory crossover study of 3 tDCS conditions: anodal-(L)dlPFC/cathodal-(R)vmPFC, reversed polarity, and sham. Cognitive tasks probed withdrawal-related constructs (error monitoring, working memory, amygdalar reactivity), while simultaneous functional magnetic resonance imaging measured brain activity. We assessed tDCS impact on trait (nonsmokers vs. sated smokers) and state (sated vs. abstinent) smoking aspects. RESULTS: Single-session, anodal-(L)dlPFC/cathodal-(R)vmPFC tDCS enhanced deactivation of DMN nodes during the working memory task and strengthened anterior cingulate cortex activity during the error-monitoring task. Smokers were more responsive to tDCS-induced DMN deactivation when sated (vs. withdrawn) and displayed greater cingulate activity during error monitoring than nonsmokers. Nicotine withdrawal reduced task engagement and attention and reduced suppression of DMN nodes. CONCLUSIONS: Cognitive circuit dysregulation associated with nicotine withdrawal may be modifiable by anodal tDCS applied to L-dlPFC and cathodal tDCS applied to R-vmPFC. tDCS may have stronger effects as a complement to existing therapies, such as nicotine replacement, owing to possible enhanced plasticity in the sated state. Published by Elsevier Inc.
RCT Entities:
BACKGROUND: The nicotinewithdrawal syndrome remains a major impediment to smoking cessation. Cognitive and affective disturbances are associated with altered connectivity within and between the executive control network, default mode network (DMN), and salience network. We hypothesized that functional activity in cognitive control networks, and downstream amygdala circuits, would be modified by application of transcranial direct current stimulation (tDCS) to the left (L) dorsolateral prefrontal cortex (dlPFC, executive control network) and right (R) ventromedial prefrontal cortex (vmPFC, DMN). METHODS: A total of 15 smokers (7 women) and 28 matched nonsmokers (14 women) participated in a randomized, sham-controlled, double-blind, exploratory crossover study of 3 tDCS conditions: anodal-(L)dlPFC/cathodal-(R)vmPFC, reversed polarity, and sham. Cognitive tasks probed withdrawal-related constructs (error monitoring, working memory, amygdalar reactivity), while simultaneous functional magnetic resonance imaging measured brain activity. We assessed tDCS impact on trait (nonsmokers vs. sated smokers) and state (sated vs. abstinent) smoking aspects. RESULTS: Single-session, anodal-(L)dlPFC/cathodal-(R)vmPFC tDCS enhanced deactivation of DMN nodes during the working memory task and strengthened anterior cingulate cortex activity during the error-monitoring task. Smokers were more responsive to tDCS-induced DMN deactivation when sated (vs. withdrawn) and displayed greater cingulate activity during error monitoring than nonsmokers. Nicotine withdrawal reduced task engagement and attention and reduced suppression of DMN nodes. CONCLUSIONS: Cognitive circuit dysregulation associated with nicotine withdrawal may be modifiable by anodal tDCS applied to L-dlPFC and cathodal tDCS applied to R-vmPFC. tDCS may have stronger effects as a complement to existing therapies, such as nicotine replacement, owing to possible enhanced plasticity in the sated state. Published by Elsevier Inc.
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