Neural activation during processing of aversive faces predicts treatment outcome in alcoholism

Abstract

Neuropsychological studies reported decoding deficits of emotional facial expressions in alcohol-dependent patients, and imaging studies revealed reduced prefrontal and limbic activation during emotional face processing. However, it remains unclear whether this reduced neural activation is mediated by alcohol-associated volume reductions and whether it interacts with treatment outcome. We combined analyses of neural activation during an aversive face-cue-comparison task and local gray matter volumes (GM) using Biological Parametric Mapping in 33 detoxified alcohol-dependent patients and 33 matched healthy controls. Alcoholics displayed reduced activation toward aversive faces-neutral shapes in bilateral fusiform gyrus [FG; Brodmann areas (BA) 18/19], right middle frontal gyrus (BA46/47), right inferior parietal gyrus (BA7) and left cerebellum compared with controls, which were explained by GM differences (except for cerebellum). Enhanced functional activation in patients versus controls was found in left rostral anterior cingulate cortex (ACC) and medial frontal gyrus (BA10/11), even after GM reduction control. Increased ACC activation correlated significantly with less (previous) lifetime alcohol intake [Lifetime Drinking History (LDH)], longer abstinence and less subsequent binge drinking in patients. High LDH appear to impair treatment outcome via its neurotoxicity on ACC integrity. Thus, high activation of the rostral ACC elicited by affective faces appears to be a resilience factor predicting better treatment outcome. Although no group differences were found, increased FG activation correlated with patients' higher LDH. Because high LDH correlated with worse task performance for facial stimuli in patients, elevated activation in the fusiform 'face' area may reflect inefficient compensatory activation. Therapeutic interventions (e.g. emotion evaluation training) may enable patients to cope with social stress and to decrease relapses after detoxification.

Cognitive, emotion control, and motor performance of adolescents in the NCANDA study: Contributions from alcohol consumption, age, sex, ethnicity, and family history of addiction.

“…The first is emotion discrimination and identification, which differentiated the drinking group from the no/low drinkers. Impairment in emotion detection and expression of greater negative emotional states has been documented using several different paradigms in adult alcoholics in recovery (Charlet et al, 2014; Clark, Oscar-Berman, Shagrin, & Pencina, 2007; Kornreich et al, 2013; Maurage, Campanella, Philippot, Martin, & de Timary, 2008; O’Daly et al, 2012; Schulte, Müller-Oehring, Rohlfing, Sullivan, & Pfefferbaum, 2011). Misperception of emotion has been speculated to contribute to misinterpretation of intent of another person, potentially serving as a source, for example, of argument or unwanted advances.…”

Predicting the future relapse of alcohol-dependent patients from structural and functional brain images

“…After enrolment in the study, patients' alcohol consumption was recorded biweekly for 3 months using the Form 90 for retrospective assessment of alcohol intake (Miller & Del Boca 1994). Here, relapse was defined as a consumption of more than 60 g alcohol for male patients or more than 40 g alcohol for female patients on one occasion (drinking day) during the assessment period (Grüsser et al 2004;Beck et al 2012;DHS 2014;Charlet et al 2014aCharlet et al ,2014b. According to the follow-up data, 16 patients were labeled as abstainers (5 females) and 30 as relapsers (11 females).…”

The neural correlates of priming emotion and reward systems for conflict processing in alcoholics

“…Automatic allocation of attention to salient stimuli is guided by a person’s individual goals or needs (Vogt et al 2010) and can be driven by alcohol-related stimulus attributes in ALC (Klein et al 2013; Alba-Ferrara et al 2016) promoting the initiation of alcohol consumption (Weafer and Fillmore 2013) or triggering relapse in abstinent alcoholics (Grüsser et al 2004; Cooney et al 1997). Neural dysregulation of the overlapping emotion and addiction systems together with the difficulty to engage executive control mechanisms can put alcohol-dependent individuals at risk for relapse when cortical–limbic–striatal systems are activated by either alcohol cues (e.g., Courtney et al 2015; Cyders et al 2014) or emotional events (e.g., Charlet et al 2014). …”