Neuropsychological functioning and alcohol dependence

Abstract

Recent studies found widespread compromised fronto-cortico-cerebellar circuits to underlie cognitive deficits. The inclusion of cerebellar structures to support functions traditionally associated with cortical and even prefrontal structures is important. However, most importantly, alcohol-dependent patients use additional and generally higher-order executive functions to compensate for deficient task performance. The compensatory mechanisms might help to explain close to normal functioning in basic cognitive domains enabled by support of executive components. But deficits in executive functions themselves might emerge more directly. New approaches concerning executive functioning, analyzing functional components of executive tasks, found response inhibition and decision-making to be impaired but normal performance in simple working memory tasks. Multiple withdrawals have been shown to lead to a higher degree of executive deficit. The causing mechanism underlying the attentional bias induced by alcohol-related words (stroop effect) is still under debate. Correlation of cognitive deficits with therapy outcome turned out to be weak. However, important interactions of cognitive deficits with personality, therapy-setting and successful coping, together with the finding that cognitive performance of alcohol-dependent patients could be enhanced by motivating instructions, might open new strategies in treatment planning and cognitive rehabilitation.

A Preliminary Prospective Study of an Escalation in ‘Maximum Daily Drinks’, Fronto-Parietal Circuitry and Impulsivity-Related Domains in Young Adult Drinkers

“…This finding is in line with previous research associating binge drinking with increased responseinhibition-related activity in frontal and parietal regions (see (Petit et al, 2013)), and extends support for compensatory models of fronto-parietal hyperactivity in young binge drinkers (ie, increased demand-related activity is needed to overcome tonically deficient control mechanisms) (Scheurich, 2005). Information regarding the chronicity of drinking at MaxDrinks levels prior to baseline was not available in the current study; however, fronto-parietal impairments in young adult drinkers may reflect a combination of predisposing vulnerabilities and neural consequences of heavy drinking (Jacobus and Tapert, 2013).…”

Cognitive control in alcohol use disorder: deficits and clinical relevance

“…Larger ventricles and brain tissue volume loss correlate with the amounts of alcohol consumed (Ding et al, 2004). The notion of compromised fronto-cortico-cerebellar functional networks in AUD appears to be a well-replicated construct, and there is evidence that deficits in a variety of executive functions, and in particular in performance on tasks of cognitive control, are associated with volume loss in the frontal, cerebellar, and subcortical (striatum and thalamus) regions, in particular (Sullivan, 2003; Scheurich, 2005; Chanraud et al, 2007). …”

Neurocognitive Functioning in Alcohol Use Disorder: Cognitive Test Results Do not Tell the Whole Story

“…The present study examined whether at least some of the neurocognitive deficits seen in alcohol-dependent patients stem from poor motivation [4] and other secondary influences. To illustrate, if the individual is not motivated to perform a cognitive task or if he or she is distracted by craving [17] or rumination, tests results may not mirror the full potential of an individual and thus may underestimate true cognitive functioning (secondary malperformance).…”

“…Cognitive deficits in severe alcoholism are usually attributed to brain damage in the frontal and limbic regions [4,5], particularly due to thiamine deficiency/malnutrition and the consequences of liver damage [6][7][8]. Yet, a direct neurotoxic effect of alcohol consumption for neurocognitive deficits in humans is not fully established, and there is an ongoing debate regarding whether mild to moderate alcohol consumption is harmful [9] or even neuroprotective [10,11].…”