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

Publication ,  Journal Article
Froeliger, B; McConnell, PA; Bell, S; Sweitzer, M; Kozink, RV; Eichberg, C; Hallyburton, M; Kaiser, N; Gray, KM; McClernon, FJ
Published in: JAMA Psychiatry
April 1, 2017

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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Published In

JAMA Psychiatry

DOI

EISSN

2168-6238

Publication Date

April 1, 2017

Volume

74

Issue

4

Start / End Page

379 / 386

Location

United States

Related Subject Headings

  • Thalamus
  • Synaptic Transmission
  • Statistics as Topic
  • Smoking Cessation
  • Smoking
  • Risk Factors
  • Recurrence
  • Prefrontal Cortex
  • Neural Inhibition
  • Nerve Net
 

Citation

APA
Chicago
ICMJE
MLA
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Froeliger, B., McConnell, P. A., Bell, S., Sweitzer, M., Kozink, R. V., Eichberg, C., … McClernon, F. J. (2017). Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability. JAMA Psychiatry, 74(4), 379–386. https://doi.org/10.1001/jamapsychiatry.2017.0017
Froeliger, Brett, Patrick A. McConnell, Spencer Bell, Maggie Sweitzer, Rachel V. Kozink, Christie Eichberg, Matt Hallyburton, Nicole Kaiser, Kevin M. Gray, and F Joseph McClernon. “Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability.JAMA Psychiatry 74, no. 4 (April 1, 2017): 379–86. https://doi.org/10.1001/jamapsychiatry.2017.0017.
Froeliger B, McConnell PA, Bell S, Sweitzer M, Kozink RV, Eichberg C, et al. Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability. JAMA Psychiatry. 2017 Apr 1;74(4):379–86.
Froeliger, Brett, et al. “Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability.JAMA Psychiatry, vol. 74, no. 4, Apr. 2017, pp. 379–86. Pubmed, doi:10.1001/jamapsychiatry.2017.0017.
Froeliger B, McConnell PA, Bell S, Sweitzer M, Kozink RV, Eichberg C, Hallyburton M, Kaiser N, Gray KM, McClernon FJ. Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability. JAMA Psychiatry. 2017 Apr 1;74(4):379–386.

Published In

JAMA Psychiatry

DOI

EISSN

2168-6238

Publication Date

April 1, 2017

Volume

74

Issue

4

Start / End Page

379 / 386

Location

United States

Related Subject Headings

  • Thalamus
  • Synaptic Transmission
  • Statistics as Topic
  • Smoking Cessation
  • Smoking
  • Risk Factors
  • Recurrence
  • Prefrontal Cortex
  • Neural Inhibition
  • Nerve Net