Alcohol dependence is thought of as a disorder with an overwhelming impulsive and compulsive “drive” towards alcohol consumption (Kamarajan et al. 2005), and an inability to “hit the brakes”, or inhibit alcohol consumption despite negative biological, psychological, legal, and social consequences (American Psychiatric Association 1994). Functional neuroimaging studies suggest that these aspects of alcohol dependence correspond to differences (from non-alcoholic controls) in brain function and organization within both top-down and bottom-up networks that mediate inhibitory control of behavior and appetitive drive toward consummatory behavior (Akine et al. 2007; Gilman et al. 2008; Li et al. 2009; Vollstadt-Klein et al. 2010).

Neural networks in active alcohol dependence

FMRI studies have reported that when actively drinking alcoholics view alcohol cues, crave alcohol, or consume alcohol, they show increased activity in the bottom-up appetitive drive network, particularly in the nucleus accumbens (Ihssen et al. 2011; Myrick et al. 2004;Schacht et al. 2011). The nucleus accumbens (NAcc), an important limbic region that mediates appetitive drive and behavior towards rewards, is presumably involved in the lack of behavioral flexibility necessary to generate new adaptive behavior and the inability to extinguish alcohol-related habits (Chen et al. 2011). Studies have suggested that involvement of brain regions within the bottom-up network differ as a function of the development of dependence. It has been proposed that as alcohol use shifts from habit to compulsion, there is a shift in the involvement of limbic regions, particularly from nucleus accumbens to caudate and putamen (Everitt and Robbins 2005; Vollstadt-Klein et al. 2010).

Functional differences from non-alcoholic controls within the top-down executive control network have been identified in actively drinking alcoholics, particularly those differences associated with poor regulation of behavior and emotion, a core aspect of alcohol dependence (Berking et al. 2011; Fox et al. 2008). Dysfunctional emotion regulation in alcoholics (e.g., extremes in emotional responsiveness to social situations, negative affect, and mood swings) has been associated with prefrontal dysfunction (Lyvers 2000), particularly in the subgenual anterior cingulate cortex (sgACC) (Salloum et al. 2007).

This study (1) looked at whether  there are identifiable differences from normal controls in abstinent alcoholics, which may be related to the length of abstinence and whether the characteristics of top-down and bottom-up networks at different stages of abstinence (short- or long-term abstinence)  may help identify brain mechanisms that support the cessation of drinking and the development of long-term abstinence.

Short-term abstinence

An fMRI study using the monetary incentive delay task (MIDT) in 5–37 day abstinent alcoholics found reduced NAcc activation when processing monetary reward and increased NAcc activation when viewing alcohol related cues in alcoholics compared to controls (Wrase et al. 2007). Results from that study suggest that salience of alcohol cues is present during early stages of abstinence. Another fMRI study in 7–14 day abstinent alcoholics found that reduced NAcc activation during anticipation of reward was associated with higher impulsivity and alcohol craving, suggesting that differences in NAcc activity may impact the maintenance of abstinence (Beck et al. 2009)

Long-term abstinence

There is evidence from the task-evoked fMRI literature supporting the existence of compensatory mechanisms in top-down and bottom-up networks in long-term abstinence. A recent study by Nestor et al. (2011) compared task-evoked brain activity between long-term abstinent smokers, current smokers and non-smoking controls during a task that required a stimulus-response selection. Long-term abstinent smokers showed increased task-evoked activity in executive control regions (e.g. dorsolateral prefrontal cortex, anterior cingulate cortex) and lower activity in reward processing regions (e.g. nucleus accumbens) when compared to current smokers and non-smoking controls.

Nestor et al (2011) suggested that long-term abstinent smokers recruit frontal regions to increase regulation of their responses to achieve performance (Nestor et al. 2011). Their results suggest compensatory mechanisms in long-term abstinence in which individuals ostensibly avoid relapse by enhancing the involvement of executive control regions and attenuating the involvement of reward processing regions when responding to the environment.

A study by Dresler et al (2011) provided evidence suggesting that the engagement of executive control regions during task performance was a function of abstinence length. They found no significant differences in frontal task-evoked brain activity during a verbal fluency task between long-term abstinent alcoholics (abstinent for 264.75 ± 198.24 days) and controls. Since short-term abstinent alcoholics in the same study had significantly lower frontal brain activity when compared to controls (and to long-term abstinent alcoholics), the authors proposed that there is an increase in task-related frontal brain activity with continued abstinence.

This study provided evidence for short-term abstinent alcoholics having a different pattern strength of appetitive drive and inhibitory control networks when compared to non-alcoholic controls – with duration of abstinence so that (a) synchrony of executive control regions progressively increases and (b) synchrony of reward processing regions progressively decreases. In addition, (a) enhanced synchrony between executive control regions was associated with better cognitive flexibility and (b) lack of disengagement of synchrony between reward processing regions was associated with more current antisocial symptoms in short-term abstinence.

For us these findings seem to be hinting at emotional regulation improving and control over distress based impulsivity as these are both the result of the PFC dysfunction mentioned above. Also reward is also connected to emotional regulation.

Main Reference

1. Camchong, J., Stenger, V. A., & Fein, G. (2013). Resting‐State Synchrony in Short‐Term Versus Long‐Term Abstinent Alcoholics. Alcoholism: Clinical and Experimental Research, 37(5), 794-803.