Alcoholism and the Brain: An Overview (original) (raw)
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Neuroimaging in Alcoholism: Ethanol and Brain Damage
Alcoholism: Clinical and Experimental Research, 2001
This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The co-chairs were Karl Mann and Ingrid Agartz. The presentations were (1) Neuropathological changes in alcohol-related brain damage, by Clive Harper; (2) Regional brain volumes including the hippocampus and monoamine metabolites in alcohol dependence, by Ingrid Agartz, Susan Shoaf, Robert R, Rawlings, Reza Momenan, and Daniel W Hommer; (3) Diffusion tensor abnormalities in imaging of white matter alcoholism, by Adolf Pfefferbaum and Edith V. Sullivan; (4) Use of functional MRI to evaluate brain activity during alcohol cue exposure in alcoholics: Relationship to craving, by Raymond F. Anton, David J. Drobes, and Mark S. George; and (5) -Opiate receptor availability in alcoholism: First results from a positron emission tomography study,
Alcohol: Effects on Neurobehavioral Functions and the Brain
Neuropsychology Review, 2007
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.
Impairments of Brain and Behavior The Neurological Effects of Alcohol
1997
Chronic heavy drinking and alcoholism can have serious repercussions for the functioning of the entire nervous system, particularly the brain. These effects include changes in emotions and personality as well as impaired perception, learning, and memory. Neuropathological and imaging techniques have provided evidence of physical brain abnormalities in alcoholics, such as atrophy of nerve cells and brain shrinkage. At the
Brain impairment in well-nourished chronic alcoholics is related to ethanol intake
Annals of Neurology, 1997
To determine the influence of chronic ethanol intake on the central nervous system, we studied 40 asymptomatic, well-nourished, chronic alcoholics (mean age, 42.6 -+ 9.1 years) and 20 age-, sex-, and education-matched control subjects. Studies included neuropsychological testing, visual and short-latency auditory evoked potentials, and morphometric analysis of computed tomography scans. The mean daily ethanol consumption of the alcoholics was 204 gm over an average of 26.4 years. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of the PI00 latency of visual evoked potentials, and a prolongation and reduction in the amplitude of the latency of the V wave of short-latency auditory evoked potentials. These abnormalities were related to the lifetime dose of ethanol consumed. Brain morphometric analysis showed that alcoholics had a significantly greater degree of brain shrinkage with age, compared to control subjects. The cortical atrophy index correlated significantly with the lifetime ethanol consumption. Neuropsychological testing in alcoholics compared to controls revealed a significant impairment of frontal skills that was related to age, degree of scholarship, and the presence of frontal atrophy. In conclusion, well-nourished chronic alcoholics exhibited significant brain impairment, as demonstrated by neuropsychological testing, evoked potentials, and brain morphometric analysis, which was correlated with the lifetime dose of ethanol consumed.
Alcoholism and Brain Damage: Some Psychometric Findings in Addiction Unit Alcoholics
Addiction, 1973
The use of psychometric tests as evidence of brain damage is discussed briejiy, and selected recent literature mentioned Fifty-seven addiction unit alcoholics were examined, using a vocabulary test and a test sensitive to cerebral dysfunction, and compared with a control group of fifty-seven psychkttrk patients with varying degrees of brain damage or dysfunction. It was concluded that very few of the addiction unit alcoholics were suffering from imdoubted brain damage or dysfunction on psychometric evidence, and some implications of this findings are discussed.
Alcohol's effects on brain and behavior
Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism, 2010
Over the past 40 years, rigorous examination of brain function, structure, and attending factors through multidisciplinary research has helped identify the substrates of alcohol-related damage in the brain. One main area of this research has focused on the neuropsychological sequelae of alcoholism, which has resulted in the description of a pattern of sparing and impairment that provided an essential understanding of the functional deficits as well as of spared capabilities that could be useful in recovery. These studies have elucidated the component processes of memory, problem solving, and cognitive control, as well as visuospatial, and motor processes and their interactions with cognitive control processes. Another large area of research has focused on observable brain pathology, using increasingly sophisticated imaging technologies--progressing from pneumoencephalography to computed tomography, magnetic resonance imaging (MRI), diffusion tensor imaging, and functional MRI--that ...
CNS Drug Reviews, 2006
Studies of alcohol-induced brain damage have clearly indicated that alcohol is neurotoxic. Alcoholics are at increased risk for brain damage from a variety of causes, including poor nutrition, liver disease, and head trauma. Further, alcoholic dementia is the second leading cause of adult dementia in the United States, accounting for approximately 10% of the cases (Alzheimer's disease is the leading cause, accounting for 40 to 60% of cases). A variety of studies report that 50 to 75% of sober, detoxified, long-term alcohol-dependent individuals suffer from some degree of detectable cognitive impairment with approximately 10% suffering from serious dementia. Although more research is required to precisely delineate the effects of alcohol on various types of brain function, there appears to be a continuum of moderate deficits in the majority of long-term alcoholics, progressing to much more severe deficits of Wernicke's disease and Wernicke's encephalopathy with Korsakoff's amnestic syndrome (12,79). A variety of lifestyle factors, including nutrition, are implicated in the more severe cases. However, all of these on the continuum appear to be related to alcohol consumption and to the amount of alcohol consumed. That is, the more severe cases are associated with more severe and chronic longterm alcoholism (12,79). Alcohol-induced changes in the structure of the adult brain have been studied in both humans and rodents. A variety of postmortem histological analyses, as well as supporting imaging analysis, suggest that chronic alcohol changes brain structure. Computed tomography (CT) and magnetic resonance imaging (MRI) studies of human brain have repeatedly shown enlargement of the cerebral ventricles and sulci in most alcoholics. The enlargement of the ventricles and sulci essentially reflects a shrinking of the brain mass. This is consistent with studies on postmortem brain tissue, where alcoholics have a reduction in total brain weight. Particularly severe alcoholics have reductions in the global cerebral hemisphere and cerebellar brain weights that are significantly reduced compared
2008
Almost all we know about neurobiological brain injury in alcohol use disorders has been derived from convenience samples of treated alcoholics. Recent research has demonstrated more comorbid conditions, poorer psychosocial functioning, and higher dependence levels in treated alcoholics than in their treatment-naive counterparts. Thus, it is not clear whether neuroimaging results from convenience samples of treated alcoholics can be generalized to the entire population with alcohol use disorders. We compared 35 treated alcoholics at 1 week of abstinence (ALC) and 32 treatment-naive heavy drinkers (HD) on regional brain volumes and metabolite concentrations obtained by in vivo magnetic resonance at 1.5 Tesla to evaluate for potential group differences. Then, we evaluated whether comorbid cigarette smoking and common demographic and clinical variables mediated any existing neurobiological group differences. ALC demonstrated smaller lobar gray matter volumes and thalami than HD, exacerbated by chronic smoking. Furthermore, concentrations of N-acetyl-aspartate (an accepted marker of neuronal viability), choline-containing metabolites (involved in membrane turnover), and myo-inositol (a putative marker of glial cells and osmolyte) were lower in multiple brain regions of ALC compared to HD. The lower N-acetyl-aspartate concentrations in white matter of ALC versus HD were explained by average number of drinks per month over the year preceding study. However, the other group differences were not explained by common drinking, demographic, and clinical variables (used as covariates at the same time) or by excluding participants with comorbid mood disorders. Taken together, this suggests that the degree of brain atrophy, as well as neuronal and membrane injury in clinical samples of alcoholics cannot be generalized to the much larger population with alcohol use disorders that does not seek treatment. Ó
Alcohol-Related Brain Damage in Humans Editor
Chronic excessive alcohol intoxications evoke cumulative damage to tissues and organs. We examined prefrontal cortex (Brodmann's area (BA) 9) from 20 human alcoholics and 20 age, gender, and postmortem delay matched control subjects. H & E staining and light microscopy of prefrontal cortex tissue revealed a reduction in the levels of cytoskeleton surrounding the nuclei of cortical and subcortical neurons, and a disruption of subcortical neuron patterning in alcoholic subjects. BA 9 tissue homogenisation and one dimensional polyacrylamide gel electrophoresis (PAGE) proteomics of cytosolic proteins identified dramatic reductions in the protein levels of spectrin b II, and aand b-tubulins in alcoholics, and these were validated and quantitated by Western blotting. We detected a significant increase in a-tubulin acetylation in alcoholics, a non-significant increase in isoaspartate protein damage, but a significant increase in protein isoaspartyl methyltransferase protein levels, the enzyme that triggers isoaspartate damage repair in vivo. There was also a significant reduction in proteasome activity in alcoholics. One dimensional PAGE of membrane-enriched fractions detected a reduction in b-spectrin protein levels, and a significant increase in transmembranous a3 (catalytic) subunit of the Na + ,K + -ATPase in alcoholic subjects. However, control subjects retained stable oligomeric forms of a-subunit that were diminished in alcoholics. In alcoholics, significant loss of cytosolic aand b-tubulins were also seen in caudate nucleus, hippocampus and cerebellum, but to different levels, indicative of brain regional susceptibility to alcohol-related damage. Collectively, these protein changes provide a molecular basis for some of the neuronal and behavioural abnormalities attributed to alcoholics.