Clinical and pathological features of alcohol-related brain damage.
paper
Cited
Public
- Authors
- Zahr, Natalie M; Kaufman, Kimberley L; Harper, Clive G
- Year
- 2011
- Journal
- Nature reviews. Neurology
- PMID
- 21487421
- DOI
- 10.1038/nrneurol.2011.42
- PMCID
- PMC8121189
One of the sequelae of chronic alcohol abuse is malnutrition. Importantly, a deficiency in thiamine (vitamin B(1)) can result in the acute, potentially reversible neurological disorder Wernicke encephalopathy (WE). When WE is recognized, thiamine treatment can elicit a rapid clinical recovery. If WE is left untreated, however, patients can develop Korsakoff syndrome (KS), a severe neurological disorder characterized by anterograde amnesia. Alcohol-related brain damage (ARBD) describes the effects of chronic alcohol consumption on human brain structure and function in the absence of more discrete and well-characterized neurological concomitants of alcoholism such as WE and KS. Through knowledge of both the well-described changes in brain structure and function that are evident in alcohol-related disorders such as WE and KS and the clinical outcomes associated with these changes, researchers have begun to gain a better understanding of ARBD. This Review examines ARBD from the perspective of WE and KS, exploring the clinical presentations, postmortem brain pathology, in vivo MRI findings and potential molecular mechanisms associated with these conditions. An awareness of the consequences of chronic alcohol consumption on human behavior and brain structure can enable clinicians to improve detection and treatment of ARBD.
Brain regions targeted by alcohol-related disease. Figure courtesy of A. Pfefferbaum, SRI International, CA, USA and E. V. Sullivan, Stanford University, CA, USA.
LLM interpretation
This figure consists of six sagittal brain MRI diagrams illustrating the brain regions targeted by different alcohol-related diseases: malnutrition, liver disease, inflammation, Marchiafava-Bignami disease, and central pontine myelinolysis. Color-coded overlays highlight specific affected areas, such as the frontal lobes, cerebellum, and thalamus, with specific labels for the mammillary bodies in the malnutrition and liver disease panels. A legend at the bottom maps the colors to their corresponding anatomical structures, including the pons, hippocampus, caudate, putamen, amygdala, and hypothalamus.
Interactions between alcohol consumption and thiamine deficiency.
LLM interpretation
This is a flow diagram illustrating the mechanisms by which alcohol consumption leads to thiamine deficiency. The chart shows that alcohol consumption triggers a decrease in dietary thiamine, gastrointestinal absorption, and brain phosphorylation, which collectively result in reduced thiamine pyrophosphate ('active thiamine') in the brain. This deficiency is further linked to decreased liver storage and ultimately leads to reduced energy (ATP) and impaired biosynthesis of amino acids and proteins.
Functions and associated brain regions targeted by alcohol abuse and alcoholism. Figure courtesy of A. Pfefferbaum, SRI International, CA, USA and E. V. Sullivan, Stanford University, CA, USA.
LLM interpretation
This figure consists of six sagittal brain MRI slices, each highlighting specific brain regions associated with different cognitive and motor functions targeted by alcohol abuse. Color-coded overlays identify regions such as the frontal lobes (orange), cerebellum (teal), and hippocampus (blue), with a legend mapping these colors to specific anatomical structures. The panels are categorized by function: executive functioning, memory (including the mammillary bodies), visuospatial abilities, upper and lower limb motor control, and ocular motor control.
Graded brain-volume deficits in alcoholism and its sequelae. T1-weighted MRI scans from a | a 63-year-old healthy control male, b | a 59-year-old man with alcoholism, and c | a 63-year-old man with WKS. Graded enlargement of the ventricles (indicating shrinkage of the surrounding tissue) can be observed from the healthy control to the individual with WKS. Sagittal (left column), axial (middle column) and coronal (right column) brain images are shown. Abbreviation: WKS, Wernicke–Korsakoff syndrome. Figure courtesy of A. Pfefferbaum, SRI International, CA, USA.
LLM interpretation
This figure consists of T1-weighted MRI scans presented in sagittal, axial, and coronal views for three subjects: a healthy control (a), a man with alcoholism (b), and a man with Wernicke–Korsakoff syndrome (WKS) (c). The images demonstrate a graded increase in ventricular enlargement from the healthy control to the individual with WKS. This pattern indicates a progressive loss of surrounding brain tissue volume across the three conditions.
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| The effects of acamprosate on prefrontal cortical function are mimicked by CaCl2 and they are influenced by the history of alcohol exposure. | Melugin PR et al. | — | 2022 | → |
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| Optimized preparation of gastric acid-response sulfhydryl functionalized chitosan/alginate/tilapia peptide hydrogel and its protective effects on alcohol-induced liver and brain injury. | Lu S et al. | — | 2021 | → |
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| Ethanol Exposure Induces Microglia Activation and Neuroinflammation through TLR4 Activation and SENP6 Modulation in the Adolescent Rat Hippocampus. | Li Q et al. | — | 2019 | → |
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