Cerebral Blood Flow in the Salience Network of Individuals with Alcohol Use Disorder

Abstract

Aims: Magnetic resonance imaging (MRI) studies have identified structural and functional differences in salience network nodes of individuals with alcohol use disorders (AUDs) after chronic exposure to alcohol. However, no studies have investigated cerebral blood flow (CBF) in nontreatment-seeking (NTS) individuals with AUD.

Methods: In this work, we sought to quantify putative CBF deficits in NTS individuals relative to social drinking (SD) controls and determine if CBF in the salience network is associated with AUD severity. Fifteen NTS (36.5 ± 11.2 years old, 30.0 ± 22.7 drinks/week) and 22 SD (35.6 ± 11.9 years old, 9.1 ± 5.7 drinks/week) underwent pseudocontinuous arterial spin labeling MRI.

Results: Compared with social drinkers, NTS individuals had significantly lower CBF in the right and left dorsal anterior insula, and the left ventral anterior and posterior insula. The Alcohol Use Disorder Identification Test (AUDIT) score showed a significant negative relationship with CBF in the bilateral caudal anterior cingulate cortex. In addition, a significant negative correlation was present between number of standard drinks consumed per week and the left frontal opercular CBF.

Conclusion: These results provide evidence that insular CBF is negatively associated with heavy drinking, and that severity of alcohol use is related to CBF deficits in key nodes of the salience network. Longitudinal data are needed to understand if disruptions of CBF in the insula and the salience network are a predisposition for or a consequence of chronic AUD.

Fig. 1

Insula and salience network masks. (A) Functional subdivisions of the insular cortex used for region of interest analysis overlaid on the Montreal Neurological Institute (MNI152) template with the respective slice coordinates. Green: posterior insula, blue: dorsal AI and yellow: ventral AI. (B) Mask of dorsal anterior insular coactivation used for SVC in the voxel-wise correlation analysis overlaid on the Montreal Neurological Institute (MNI152) template with the respective slice coordinates.

Fig. 2

Voxel-wise illustration of group differences in CBF. (A) Visualization of group differences in CBF in the insular cortex (display height, P < 0.005, uncorrected). The peak effect [−28 26 4] in the dorsal AI is circled. (B) Violin plot of mean CBF values for each participant from the cluster (k = 320) containing the peak effect. NTS AUD; SD controls and CBF values are displayed in units of milliliters per 100-g tissue per minute.

Fig. 3

CBF in salience network regions inversely correlates with degree of alcohol risk behaviors. (A) Linear regression between CBF and AUDIT in the caudal ACC. Peak effect at [−2 10 44] is significant (p_FWE = 0.045, k = 63) after correcting for FWE within the SVC mask (see text for detail). (B) Mean CBF values from the cluster containing the peak effect plotted against AUDIT score. (C) Linear regression between CBF and standard drinks per week in the left frontal operculum (peak voxel at [−38 20 –12], p_FWE = 0.013, k = 76). (D) Mean CBF values from the cluster containing the peak effect plotted against standard drinks per week. Display height, P < 0.001. AUDIT: Alcohol Use Disorder Identification Test; CBF: cerebral blood flow in units of milliliters per 100-g tissue per minute.