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Magnetic resonance imaging of the living brain: evidence for brain degeneration among alcoholics and recovery with abstinence.

Rosenbloom MJ, Pfefferbaum A - Alcohol Res Health (2008)

Bottom Line: In addition, functional imaging studies provide evidence that the brain compensates for cognitive deficits.The myriad concomitants of alcoholism, the antecedents, and the consumption patterns each may influence the observed brain changes associated with alcoholism, which tend to be more deleterious with increasing age.The multifaceted nature of alcoholism presents unique challenges and opportunities to understand the mechanisms underlying alcoholism-induced neuropathology and its recovery.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California, and the Neuroscience Program, SRI International, Menlo Park, California.

ABSTRACT
Magnetic resonance imaging (MRI) provides a safe, noninvasive method to examine the brain's macrostructure, microstructure, and some aspects of how the living brain functions. MRI is capable of detecting abnormalities that can occur with alcoholism as well as changes that can occur with sobriety and relapse. The brain pathology associated with chronic excessive alcohol consumption is well documented with imaging of the living body (i.e., in vivo imaging). Consistent findings include shrinkage of the frontal cortex,1 underlying white matter, and cerebellum and expansion of the ventricles. Some of these changes are reversible with abstinence, but some appear to be enduring. Research showing correlations between brain structure and quantitative neuropsychological testing demonstrates the functional consequences of the pathology. In addition, functional imaging studies provide evidence that the brain compensates for cognitive deficits. The myriad concomitants of alcoholism, the antecedents, and the consumption patterns each may influence the observed brain changes associated with alcoholism, which tend to be more deleterious with increasing age. The multifaceted nature of alcoholism presents unique challenges and opportunities to understand the mechanisms underlying alcoholism-induced neuropathology and its recovery. Longitudinal MRI studies of animal models of alcoholism, however, can address questions about the development and course of alcohol dependence and the scope and limits of in vivo degeneration and recovery of brain structure and concomitant function that may not be readily addressed in clinical studies.

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Axial MR fluid attenuated inversion recovery (FLAIR) (a subtype of MRI) image of a 35-year-old man with an acute nutritional deficiency-induced Wernicke’s encephalopathy (WE). Prominent are the hyperintense signals in the mammillary bodies (A) and thalamus (B) indicating tissue pathology. Sagittal slice of a structural image of an individual rat that has been treated with pyrithiamine to model the acute thiamine deficiency of WE (C) and a difference image—created by subtracting the mean image acquired from all rats before treatment from the mean image acquired after treatment—that highlights changes induced by pyrithiamine in pyrithiamine-treated rats (D) (taken from Pfefferbaum et al. 2007). Note the hyperintense areas in the thalamus and mammillary nuclei in the rat images that are comparable to similar areas of hyperintensity in the man with acute WE.
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f6-arh-31-4-362: Axial MR fluid attenuated inversion recovery (FLAIR) (a subtype of MRI) image of a 35-year-old man with an acute nutritional deficiency-induced Wernicke’s encephalopathy (WE). Prominent are the hyperintense signals in the mammillary bodies (A) and thalamus (B) indicating tissue pathology. Sagittal slice of a structural image of an individual rat that has been treated with pyrithiamine to model the acute thiamine deficiency of WE (C) and a difference image—created by subtracting the mean image acquired from all rats before treatment from the mean image acquired after treatment—that highlights changes induced by pyrithiamine in pyrithiamine-treated rats (D) (taken from Pfefferbaum et al. 2007). Note the hyperintense areas in the thalamus and mammillary nuclei in the rat images that are comparable to similar areas of hyperintensity in the man with acute WE.

Mentions: A 1-year study of genetically selected alcohol-preferring rats, which voluntarily drank large amounts of alcohol, found sustained ventricular enlargement and stunting of corpus callosum growth, possibly modeling the human condition (Pfefferbaum et al. 2006a). Following several bouts of voluntary drinking, some rats underwent thiamine depletion followed by repletion. Rats with a history of alcohol exposure plus thiamine deficiency were especially prone to developing brain lesions identified with alcoholic Wernicke’s encephalopathy (Victor et al. 1989) (see figure 6). Some of the lesions resolved following dietary improvement (Pfefferbaum et al. 2007), suggesting that, at least in rats bred to prefer alcohol, nutritional deficiency must be combined with alcohol to produce severe neurodegeneration. In a study with wild-type rats, alcohol was administered by inhalation. Animals were maintained on a good diet and did not suffer withdrawal seizures; however, they developed significant ventricular enlargement (Pfefferbaum et al. 2008), suggesting that among animals who are not selected for alcohol preference, alcohol alone can be neurotoxic. (Additional information regarding translational studies using animal models can be found in the article by Zahr and Sullivan in “Neuroscience: Part I”) (Zahr and Sullivan 2008).


Magnetic resonance imaging of the living brain: evidence for brain degeneration among alcoholics and recovery with abstinence.

Rosenbloom MJ, Pfefferbaum A - Alcohol Res Health (2008)

Axial MR fluid attenuated inversion recovery (FLAIR) (a subtype of MRI) image of a 35-year-old man with an acute nutritional deficiency-induced Wernicke’s encephalopathy (WE). Prominent are the hyperintense signals in the mammillary bodies (A) and thalamus (B) indicating tissue pathology. Sagittal slice of a structural image of an individual rat that has been treated with pyrithiamine to model the acute thiamine deficiency of WE (C) and a difference image—created by subtracting the mean image acquired from all rats before treatment from the mean image acquired after treatment—that highlights changes induced by pyrithiamine in pyrithiamine-treated rats (D) (taken from Pfefferbaum et al. 2007). Note the hyperintense areas in the thalamus and mammillary nuclei in the rat images that are comparable to similar areas of hyperintensity in the man with acute WE.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3860463&req=5

f6-arh-31-4-362: Axial MR fluid attenuated inversion recovery (FLAIR) (a subtype of MRI) image of a 35-year-old man with an acute nutritional deficiency-induced Wernicke’s encephalopathy (WE). Prominent are the hyperintense signals in the mammillary bodies (A) and thalamus (B) indicating tissue pathology. Sagittal slice of a structural image of an individual rat that has been treated with pyrithiamine to model the acute thiamine deficiency of WE (C) and a difference image—created by subtracting the mean image acquired from all rats before treatment from the mean image acquired after treatment—that highlights changes induced by pyrithiamine in pyrithiamine-treated rats (D) (taken from Pfefferbaum et al. 2007). Note the hyperintense areas in the thalamus and mammillary nuclei in the rat images that are comparable to similar areas of hyperintensity in the man with acute WE.
Mentions: A 1-year study of genetically selected alcohol-preferring rats, which voluntarily drank large amounts of alcohol, found sustained ventricular enlargement and stunting of corpus callosum growth, possibly modeling the human condition (Pfefferbaum et al. 2006a). Following several bouts of voluntary drinking, some rats underwent thiamine depletion followed by repletion. Rats with a history of alcohol exposure plus thiamine deficiency were especially prone to developing brain lesions identified with alcoholic Wernicke’s encephalopathy (Victor et al. 1989) (see figure 6). Some of the lesions resolved following dietary improvement (Pfefferbaum et al. 2007), suggesting that, at least in rats bred to prefer alcohol, nutritional deficiency must be combined with alcohol to produce severe neurodegeneration. In a study with wild-type rats, alcohol was administered by inhalation. Animals were maintained on a good diet and did not suffer withdrawal seizures; however, they developed significant ventricular enlargement (Pfefferbaum et al. 2008), suggesting that among animals who are not selected for alcohol preference, alcohol alone can be neurotoxic. (Additional information regarding translational studies using animal models can be found in the article by Zahr and Sullivan in “Neuroscience: Part I”) (Zahr and Sullivan 2008).

Bottom Line: In addition, functional imaging studies provide evidence that the brain compensates for cognitive deficits.The myriad concomitants of alcoholism, the antecedents, and the consumption patterns each may influence the observed brain changes associated with alcoholism, which tend to be more deleterious with increasing age.The multifaceted nature of alcoholism presents unique challenges and opportunities to understand the mechanisms underlying alcoholism-induced neuropathology and its recovery.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California, and the Neuroscience Program, SRI International, Menlo Park, California.

ABSTRACT
Magnetic resonance imaging (MRI) provides a safe, noninvasive method to examine the brain's macrostructure, microstructure, and some aspects of how the living brain functions. MRI is capable of detecting abnormalities that can occur with alcoholism as well as changes that can occur with sobriety and relapse. The brain pathology associated with chronic excessive alcohol consumption is well documented with imaging of the living body (i.e., in vivo imaging). Consistent findings include shrinkage of the frontal cortex,1 underlying white matter, and cerebellum and expansion of the ventricles. Some of these changes are reversible with abstinence, but some appear to be enduring. Research showing correlations between brain structure and quantitative neuropsychological testing demonstrates the functional consequences of the pathology. In addition, functional imaging studies provide evidence that the brain compensates for cognitive deficits. The myriad concomitants of alcoholism, the antecedents, and the consumption patterns each may influence the observed brain changes associated with alcoholism, which tend to be more deleterious with increasing age. The multifaceted nature of alcoholism presents unique challenges and opportunities to understand the mechanisms underlying alcoholism-induced neuropathology and its recovery. Longitudinal MRI studies of animal models of alcoholism, however, can address questions about the development and course of alcohol dependence and the scope and limits of in vivo degeneration and recovery of brain structure and concomitant function that may not be readily addressed in clinical studies.

Show MeSH
Related in: MedlinePlus