The Neuropathology of Alcohol-Related Brain Damage
“Excessive alcohol use can cause structural and functional abnormalities of the brain and this has significant health, social and economic implications for most countries in the world. Even heavy social drinkers who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Changes are more severe and other brain regions are damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke–Korsakoff syndrome). Quantitative studies and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood.”
From the abstract of this paper. Some more stuff from the paper:
“It has long been accepted that excessive alcohol use can cause structural and functional abnormalities of the brain and other organs (Courville, 1955; Victor et al., 1959; Dreyfus and Victor, 1961). In the brain, this has been demonstrated clinically, with imaging techniques and pathologically. Many alcoholics can also develop cirrhosis of the liver that can impact on brain structure and function and others develop nutritional deficiency states (vitamin B1 deficiency) that can cause severe brain damage and dysfunction. These latter two groups of alcoholic cases are often defined as ‘complicated alcoholics’ to differentiate them from those who do not have liver disease or nutritional deficiency states (uncomplicated alcoholics). Nevertheless, ‘uncomplicated alcoholics’ who are cognitively impaired have abnormalities (Pfefferbaum et al., 1997). The risks of ‘moderate’ alcohol consumption are more difficult to assess. Ding and colleagues showed that the more alcohol consumed, the larger the cerebrospinal fluid-filled spaces of the brain became (Ding et al., 2004). This data correspond with a neuropathological study that showed an increase in the cerebrospinal fluid-filled spaces covering the brain (pericerebral space) in men drinking more than eight standard drinks per day and a similar distinctive trend in those drinking five to eight standard drinks per day (Harper et al., 1988). […]
The first quantitative neuropathological study on brain weights in alcoholics (Harper and Blumbergs, 1982) was inspired by the various reports of ‘brain shrinkage’ seen on CT scans in alcoholics (Cala et al., 1978; Ron et al., 1980). Alcoholics have a reduced brain weight compared to controls and the degree of brain atrophy has been shown to correlate with the rate and amount of alcohol consumed over a lifetime (Harding et al., 1996). […]
As noted above, the mechanism for alcoholism-related white matter loss, restoration with alcohol abstinence and disruption of micro structural integrity still remains unclear but probably involves changes in both myelination and axonal integrity. This has been inferred from in vivo human and experimental MR diffusion tensor imaging studies (Pfefferbaum et al., 2006b, 2007) and may explain why tissue volume recovery appears incomplete with abstinence. Thus, alcoholic brain pathology may have two components, one reflecting permanent change and one a transient change. Regarding permanent effects, alcohol-related neuronal loss has been documented in specific regions of the cerebral cortex (superior frontal association cortex), hypothalamus and cerebellum (Harper, 1998). Such loss will result in axonal (Wallerian) degeneration and a permanent reduction in white matter volume. Structural changes in myelin, however, could explain the reversible white matter shrinkage that has been documented with serial MRI studies following periods of abstinence from alcohol (Shear et al., 1994; Pfefferbaum et al., 1995; Gazdzinski et al., 2005). […]
Analysis of the types of neurons lost from the frontal cortex revealed that they were the larger ones with a somal area >90 μm (Harper and Kril, 1989). This population of neurons is also more vulnerable in both Alzheimer’s disease (Terry et al., 1981) and normal aging (Terry and Hansen, 1987). There does not appear to be any link between alcohol-related brain damage and Alzheimer’s disease (Morikawa et al., 1999), although there is some work that suggests a relationship between alcohol and aging (Harper et al., 1998a).”
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