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Original Investigation
April 2017

Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability

Author Affiliations
  • 1Department of Neuroscience, Medical University of South Carolina, Charleston
  • 2Department of Psychiatry, Medical University of South Carolina, Charleston
  • 3Hollings Cancer Center, Medical University of South Carolina, Charleston
  • 4Center for Biomedical Imaging, Medical University of South Carolina, Charleston
  • 5Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina
  • 6Brain Imaging and Analysis Center, Duke University Medical Center, Durham, North Carolina
JAMA Psychiatry. 2017;74(4):379-386. doi:10.1001/jamapsychiatry.2017.0017
Key Points

Question  What is the association between corticothalamic-mediated inhibitory control and smoking relapse vulnerability?

Findings  In 2 functional magnetic resonance imaging studies, a smoking cessation study (n = 81) and a laboratory-based smoking assessment (n = 26), corticothalamic circuitry function during inhibitory control was associated with smoking relapse vulnerability.

Meaning  Findings that baseline differences in corticothalamic circuitry function mediate inhibitory control and smoking relapse vulnerability warrant further examination of interventions for augmenting corticothalamic neurotransmission during the course of tobacco use disorder treatment.

Abstract

Importance  Tobacco use disorder is associated with dysregulated neurocognitive function in the right inferior frontal gyrus (IFG)—one node in a corticothalamic inhibitory control (IC) network.

Objective  To examine associations between IC neural circuitry structure and function and lapse/relapse vulnerability in 2 independent studies of adult smokers.

Design, Setting, and Participants  In study 1, treatment-seeking smokers (n = 81) completed an IC task during functional magnetic resonance imaging (fMRI) before making a quit attempt and then were followed up for 10 weeks after their quit date. In study 2, a separate group of smokers (n = 26) performed the same IC task during fMRI, followed by completing a laboratory-based smoking relapse analog task. Study 1 was performed at Duke University Medical Center between 2008 and 2012; study 2 was conducted at the Medical University of South Carolina between 2013 and 2016.

Main Outcomes and Measures  Associations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse.

Results  Of the 81 study participants in study 1 (cessation study), 45 were women (56%), with mean (SD) age, 38.4 (10.2) years. In study 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P threshold = 0.03), greater IC task-related blood oxygenation level–dependent (BOLD) response in the right IFG (F1,78 = 14.87) and thalamus (F1,78 = 14.97) (P < .05), and weaker corticothalamic task-based functional connectivity (tbFC) (F1,77 = 5.87; P = .02). Of the 26 participants in study 2 (laboratory study), 15 were women (58%), with mean (SD) age, 34.9 (10.3). Similar to study 1, in study 2, greater IC-BOLD response in the right IFG (t23 = −2.49; β = −0.47; P = .02), and weaker corticothalamic tbFC (t22 = 5.62; β = 0.79; P < .001) were associated with smoking sooner during the smoking relapse-analog task. In both studies, corticothalamic tbFC mediated the association between IC performance and smoking outcomes.

Conclusions and Relevance  In these 2 studies, baseline differences in corticothalamic circuitry function were associated with mediated IC and smoking relapse vulnerability. These findings warrant further examination of interventions for augmenting corticothalamic neurotransmission and enhancing IC during the course of tobacco use disorder treatment.

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