Alcohol abuse and dependence. Experimental and clinical evidence Salvatore Campanella University of Brussels, Belgium – Laboratory of Psychological Medicine and Addiction Brescia – 08 Aprile 2017

Alcohol is THE social drug!!!

Consume alcohol is funny! Why?

And even more during adolescence!!!

« When passion faced with rationality » During adolescence, Brain is still maturing; Limbic emotional zones are well-developped; Contrary to more « rationale » frontal zones… « When passion faced with rationality » Period in which youths privilegied sensation seeking, immediate rewarding despite long-term negative consequences

A major problem: the relapse rate There is an urgent need to identify neuro-cognitive mechanisms that may help to identify people at « high risk » to relapse…..

Two main neuro-cognitive mechanisms triggering addictions (1) An Attentional Bias towards drug cues; (2) A lack of Inhibitory resources

Need to focus on the attentional bias Drug cues have a huge motivational salience

Need to focus on the inhibition process

Overall: Alcoholic patients are more attracted by alcohol cues and they also displayed less inhibitory skills; We have no idea about a potential effect of anti-craving medication on these processes; Our main idea: use cognitive ERPs as biomarkers of relapse

Intensity of processing Amplitude = Intensity of processing Latency Speed of processing

Our study based on two cognitive ERP tasks

(1) A Contextual Go-NoGo Task 80% of Go trials: M 20% of NoGo trials: W 3 contexts

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M 25

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M 27

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M 29

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W 33

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(2) An oddball alcohol-related task

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Drinker typology based on AUDIT scores Possible Dependence Heavy Drinkers Light Drinkers

Follow-up at 3 months

The Go Nogo task

BUT THE ERROR RATE IS SIMILAR BETWEEN Relapsers and Non Relapsers!

However, when we look at ERPs… Relapsers vs Controls: p = .026 Non Relap vs Controls: p =1

Patients made more commissions errors than controls; No more errors in alcohol context; The error rate did not predict relapse; However, at the ERP level, the NoGo P3 of Relapsers disclosed higher amplitude than the one of Non Relapsers = Controls : patients who need higher neural resources to perform correct inhibition are more prone to relapse?..! Flaudias et al., 2013

Behavioural Brain Research The oddball task Reduced processing of alcohol cues predicts abstinence in recently detoxified alcoholic patients in a three-month follow up period: an ERP study Behavioural Brain Research Petit et al. 2015

Compared to relapsers, abstainers showed a decreased P3 amplitude for alcohol related compared to non alcohol related pictures (p = .009). Through hierarchical regression, this difference between alcohol and non alcohol related cues was shown to be the best predictor of relapse vulnerability (p = .013). A devaluation of the motivational significance of stimuli related to alcohol, only measurable through electrophysiology, could protect from a relapse within three months following detoxification in alcohol dependent patients.

Conclusions

What is the impact of anti-craving medications on these processes??? Is the NoGo P3 a biological marker of relapse? Clinical impact: increase cognitive control through neuropsychological retraining? Is the P3 a biological marker of abstinence? Clinical impact: decrease motivational salience of alcohol cues through neuropsychological retraining? What is the impact of anti-craving medications on these processes???

Our project: tDCS and cognitive training: still to develop….

… even if we are aware that chronic alcoholism is a multi-factorial disease….

Thank you for your attention!