Citation

Mayer AR, Hanlon FM, Claus ED, Dodd AB, Miller B, Mickey J, Quinn DK, Hagerty SL, Seaman B, Hutchison KE. Biol. Psychiatry Cogn. Neurosci. Neuroimaging 2018; 3(3): 294-302.

Affiliation

Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, Colorado.

Copyright

(Copyright © 2018, Society of Biological Psychiatry, Publisher Elsevier Publishing)

DOI

10.1016/j.bpsc.2017.09.012

PMID

29486871

Abstract

BACKGROUND: Chronic alcohol use disorders (AUDs) and traumatic brain injury (TBI) are highly comorbid and share commonly affected neuronal substrates (i.e., prefrontal cortex, limbic system, and cerebellum). However, no studies have examined how combined physical trauma and heavy drinking affect neurocircuitry relative to heavy drinking alone.

METHODS: The current study investigated whether comorbid AUDs and mild or moderate TBI (AUDs+TBI) would negatively affect maladaptive drinking behaviors (n = 90 AUDs+TBI; n = 62 AUDs) as well as brain structure (i.e., increased atrophy; n = 62 AUDs+TBI; n = 44 AUDs) and function (i.e., activation during gustatory cue reactivity; n = 55 AUDs+TBI; n = 37 AUDs) relative to AUDs alone.

RESULTS: Participants reported a much higher incidence of trauma (59.2%) compared with the general population. There were no differences in demographic and clinical measures between groups, suggesting that they were well matched. Although maladaptive drinking behaviors tended to be worse for the AUDs+TBI group, effect sizes were small and not statistically significant. Increased alcohol-cue reactivity was observed in bilateral anterior insula and orbitofrontal cortex, anterior cingulate cortex, medial prefrontal cortex, posterior cingulate cortex, dorsal striatum, thalamus, brainstem, and cerebellum across both groups relative to a carefully matched appetitive control. However, there were no significant differences in structural integrity or functional activation between AUDs+TBI and AUDs participants, even when controlling for AUD severity.

CONCLUSIONS: Current results indicate that a combined history of mild or moderate TBI was not sufficient to alter drinking behaviors and/or underlying neurocircuitry at detectable levels relative to heavy drinking alone. Future studies should examine the potential long-term effects of combined alcohol and trauma on brain functioning.

Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Language: en

Keywords

Alcohol use disorders; Alcohol-cue reactivity; Limbic; Prefrontal; Structure; Traumatic brain injury