Alcoholism results from an interplay between genetic and environmental factors, and is linked to brain defects and associated cognitive, emotional, and behavioral impairments. A confluence of findings from neuroimaging, physiological, neuropathological, and neuropsychological studies of alcoholics indicate that the frontal lobes, limbic system, and cerebellum are particularly vulnerable to damage and dysfunction. An integrative approach employing a variety of neuroscientific technologies is essential for recognizing the interconnectivity of the different functional systems affected by alcoholism. In that way, relevant experimental techniques can be applied to assist in determining the degree to which abstinence and treatment contribute to the reversal of atrophy and dysfunction.

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Alcohol: Effects on Neurobehavioral Functions and the Brain

Decisions about using addictive substances are influenced by distractions by addiction-related stimuli, of which the user might be unaware. The addiction-Stroop task is a paradigm used to assess this distraction. The empirical evidence for the addiction-Stroop effect is critically reviewed, and meta-analyses of alcohol-related and smoking-related studies are presented. Studies finding the strongest effects were those in which participants had strong current concerns about an addictive substance or such concerns were highlighted through experimental manipulations, especially those depriving participants of the substance. Theories to account for addiction-related attentional bias are discussed, of which the motivational theory of current concerns appears to provide the most complete account of the phenomenon. Recommendations are made for maximizing the precision of the addiction-Stroop test in future research.

The addiction-stroop test: Theoretical considerations and procedural recommendations.

The chronic, excessive consumption of alcohol results in significant modification of selective neural systems of the brain structure, physiology, and function. Quantitative MR structural imaging, diffusion tensor imaging (DTI), and functional MRI (fMRI), together with neuropsychological challenges, have enabled rigorous in vivo characterization of the results of alcoholism on the brain in the human condition. Neuroimaging has also enabled longitudinal study for the examination of alcoholism’s dynamic course through periods of drinking and sobriety. Controlled studies have revealed compelling evidence for alcohol-related brain structural and functional modification—some longstanding, some transient, and some compensatory. Patterns of circuitry disruption identified through structural and functional MRI studies suggest a central role for degradation of frontocerebellar neuronal nodes and connecting circuitry affecting widespread brain regions and contributing to alcoholism’s salient, enduring, and debilitating cognitive and motor deficits—executive dysfunction, visuospatial impairment, and ataxia.

Neurocircuitry in alcoholism: a substrate of disruption and repair

Decision-making deficits reflected by risky decisions in gambling tasks have been associated with frontal lobe dysfunctions in various neurologic and psychiatric populations. The question remains whether decision-making impairments are related to executive functions. The authors developed a new gambling task, the Game of Dice Task, with explicit and stable rules for reinforcement and punishment, to investigate relations between executive functions and risk-taking behavior in an explicit decision-making situation. A sample of 35 alcoholic Korsakoff patients and 35 healthy controls was examined with the Game of Dice Task and a neuropsychological test battery. Results show that Korsakoff patients are strongly impaired in this explicit decision-making task and that these disturbances are correlated with specific executive functions.

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Decision-making deficits of Korsakoff patients in a new gambling task with explicit rules: Associations with executive functions

Background: 
In adults, prefrontal, thalamic, and cerebellar brain injury is associated with excessive ethanol intake. As these brain structures are actively maturing during adolescence, we hypothesized that subjects with adolescent-onset alcohol use disorders, compared with control subjects, would have smaller brain volumes in these areas. Thus, we compared prefrontal-thalamic-cerebellar measures of adolescents and young adults with adolescent-onset alcohol use disorders (AUD, defined as DSM-IV alcohol dependence or abuse) with those of sociodemographically similar control subjects.

Methods: 
Magnetic resonance imaging was used to measure prefrontal cortex, thalamic, and cerebellar volumes in 14 subjects (eight males, six females) with an AUD (mean age, 17.0 ± 2.1 years) and 28 control subjects (16 males, 12 females; 16.9 ± 2.3 years). All AUD subjects were recruited from substance abuse treatment programs and had comorbid mental disorders.

Results: 
Subjects with alcohol use disorders had smaller prefrontal cortex and prefrontal cortex white matter volumes compared with control subjects. Right, left, and total thalamic, pons/brainstem, right and left cerebellar hemispheric, total cerebellar, and cerebellar vermis volumes did not differ between groups. There was a significant sex-by-group effect, indicating that males with an adolescent-onset AUD compared with control males had smaller cerebellar volumes, whereas the two female groups did not differ in cerebellar volumes. Prefrontal cortex volume variables significantly correlated with measures of alcohol consumption.

Conclusions: 
These findings suggest that a smaller prefrontal cortex is associated with early-onset drinking in individuals with comorbid mental disorders. Further studies are warranted to examine if a smaller prefrontal cortex represents a vulnerability to, or a consequence of, early-onset drinking.

Prefrontal Cortex, Thalamus, and Cerebellar Volumes in Adolescents and Young Adults with Adolescent-Onset Alcohol Use Disorders and Comorbid Mental Disorders

Alcohol can induce a wide spectrum of effects on the central nervous system. These effects can be recognized at the neurophysiological, morphological and neuropsychological levels. Several studies of the effect of alcohol on the frontal lobes were identified for review from MedLine, PsychLIT databases and by manual searching. In this review article, the different changes are examined in detail. Computed tomography studies have reported changes of frontal lobe in alcoholism, while magnetic resonance imaging studies supported these findings. Neurophysiological studies with positron emission tomography and single photon emission computed tomography have reported a decreased frontal lobe glucose utilization and reduced cerebral blood flow. There is also evidence from neuropsychological studies that there are specific deficits in alcoholism that suggest frontal lobe dysfunction. Considered together, these studies lend a strong credence to the concept of frontal lobe pathology in alcoholism. However, frontal lobe is not an isolated part of the brain and should be considered with its heavy connections to different cortical and subcortical areas of the brain.

Ashraf Kahn

Papers

Frontal lobe changes in alcoholism: a review of the literature.