Vermal atrophy of alcoholics correlate withserum thiamine levels but not with dentateiron concentrations as estimated by MRI (original) (raw)
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Alcohol-related cerebellar degeneration: not all down to toxicity?
Cerebellum & Ataxias, 2016
Background: Alcohol-related cerebellar degeneration is one of the commonest acquired forms of cerebellar ataxia. The exact pathogenic mechanisms by which alcohol leads to cerebellar damage remain unknown. Possible autoreactive immune mediated mechanisms have not been explored previously. In this study, we aim to investigate the potential role of alcohol-induced immune mediated cerebellar degeneration.
High ethanol intake and malnutrition in alcoholic cerebellar shrinkage
QJM, 2000
To determine the influence of chronic ethanol intake lar shrinkage (n=33) were older ( p=0.05) and tended to report greater daily ethanol intake than and nutritional status on cerebellar shrinkage in alcoholism, we studied 12 undernourished patients alcoholics without cerebellar shrinkage (n=15), although not significantly so ( p=0.09). Cerebellar with acute Wernicke's encephalopathy (WE), 12 undernourished and 24 well-nourished asympto-volume correlated negatively with age in controls and asymptomatic alcoholics (rÁ0.52, p∏0.01, matic chronic alcoholics, and 24 age-matched wellnourished controls, using morphometric analysis both), with a significantly greater shrinkage for age in the latter ( p=0.003). Logistic regression anal-of MRI scans with volumetry of the cerebellum. Alcoholics reported a mean daily intake of ethanol ysis showed that malnutrition (OR 6.6 [95%CI 1.7-25.6], p=0.005) and a daily ethanol intake of of 177±8 g over a period of 27±1 years. Most undernourished alcoholics and half of the well-more than 140 g over ten years .5], p=0.003) were independently associated nourished alcoholics, compared to one-tenth of the controls, showed a significant reduction in cerebel-with the development of cerebellar shrinkage. lar volume ( p∏0.01, both). Alcoholics with cerebel-
Acta Neuropathologica, 2006
Alcoholic cerebellar degeneration (ACD) is a pivotal neurological complication in alcoholics. However, although there are a few autopsy reports and some data on its frequency, it is considered very rare in Japan. The aims of this study were (1) to estimate the frequency of the disease in Japanese autopsy cases, and (2) to examine the clinicopathological features of symptomatic and asymptomatic cases of ACD. We reviewed the records of 1,509 Japanese autopsies obtained from three autopsy series in Japan, and selected all 55 cases (3.6%) with alcoholism. On neuropathological reexamination, ACD was confirmed in six male alcoholics [0.4% of all subjects; 10.9% of all alcoholics; mean age at death 59.3±13.4 years (± SD)], including three asymptomatic cases. These frequencies were much lower than some previous Western findings, but more common than that has been expected in Japan. The frequencies of memory impairment and ataxia in ACD cases were significantly higher than those in alcoholics without any alcoholrelated pathologies. In ACD cases, loss of Purkinje cells, narrowing of the width of the molecular layer, and tissue rarefaction in the granular layer were observed in the anterior and superior portions of the vermis of the cerebellum. In adjacent regions, the Purkinje cell and molecular layers were more mildly affected. The distribution of severely affected regions was more restricted in the asymptomatic cases than in the symptomatic cases. This study confirmed the frequency of asymptomatic cerebellar degeneration in alcoholics, suggesting that early intervention in alcoholism in the subclinical phase is important to prevent the development of cerebellar symptoms.
Neuroscience, 1999
This study examines the effect of chronic alcohol consumption on the human cerebellum using operational criteria for case selection [Caine D. et al. (1997) J. Neurol. Neurosurg. Psychiat. 62, 51-60] and unbiased stereological techniques. We describe, for the first time, structural changes in different functional zones of the cerebellum of chronic alcoholics and correlate these changes with specific clinical symptoms. No consistent changes in the number of neurons or the structural volume for any cerebellar region were observed in the chronic alcoholics without the clinical signs of Wernicke's encephalopathy. In all cerebellar measures, these chronic alcoholics did not differ significantly from the non-alcoholic controls, suggesting that chronic alcohol consumption per se does not necessarily damage human cerebellar tissue. However, several cerebellar changes were noted in the thiamine-deficient alcoholics studied. There was a significant decrease in Purkinje cell density (reduced on average by 43%) and molecular layer volume (reduced by 32%) in the cerebellar vermis in all thiamine-deficient chronic alcoholics. A decrease in cell density and atrophy of the molecular layer, where the dendritic trees of the Purkinje cells are found, without significant cell loss suggests loss of cellular dendritic structure and volume. These thiaminedeficient alcoholics also had a significant decrease (36% loss) in the estimated Purkinje cell number of the flocculi, disrupting vestibulocerebellar pathways.
Effects of Lifelong Ethanol Consumption on Cerebellar Layer Volumes in AA and ANA Rats
Alcoholism: Clinical and Experimental Research, 1997
Aging and chronic alcohol consumption can cause degenerative changes in the cerebellar cortex. In this study, the effects of aging and lifelong alcohol consumption on cerebellar cortical layer volumes (molecular and granular) and also white matter layer volumes were studied in alcohol-preferring (AA) and nonpreferring (ANA) rats of both sexes. The ethanol-consuming animals (EtOH) had 12% (wlv) ethanol as the only available fluid from 4 to 22 months of age, whereas the young (3 month) and old controls (24 months) had only water to drink. The volumes of molecular, granular, and white matter layers of the cerebellar vermis in folia II, IV, VII, and X were measured by using systematic sampling and a point-counting method. The volumes of the granular and white matter layers showed consistent increase between 3 and 24 months of age, whereas the volume of the molecular layer remained unchanged with increasing age. Individual ethanol intake was measured over a 1-week period at the beginning and at the end of chronic ethanol exposure. Significant (ANOVA, p = 0.0oO) sex difference was found in the drinking behavior in both lines, with females consuming more alcohol than males (daily ethanol consumption at 22 months of age 3.2 f 0.3 vs. 7.1 f 0.3 glkg for AA males and females; 3.2 f 0.3 vs. 5.4 f 0.4 glkg for ANA males and females, respectively). The only ethanol-induced effect on the cerebellum was observed in ANA-EtOH females with a 15% reduction in the volumes of the molecular and granular layer in folium II compared with agematched controls and a significant ( p c 0.05, analysis of covariance with ethanol intake as a covariate) line difference in folium II (molecular and granular layers) was observed between ANA-EtOH females and AA-EtOH females. Furthermore, the volume of the molecular layer in folium II was significantly ( p c 0.05, analysis of covariance with ethanol intake and body weights as covariates) reduced for ANA-EtOH females, compared with ANA-EtOH males indicating a sex difference in the cerebellar degeneration due to chronic alcohol consumption. Of the three layers studied, the white matter layer was the most resistant layer to the effects caused by chronic alcohol consumption. In view of the fact that AA and ANA rats of both sexes differ regarding the drinking behavior and ethanol metabolism, they provide an important model for further research on ethanol-induced pathological changes in the central nervous system.
A GOLGI STUDY OF CEREBELLAR ATROPHY IN HUMAN CHRONIC ALCOHOLISM
Neuropathology and Applied Neurobiology, 1984
Instant access to vital information. . I I , , " , ---1 -r-7 --1983 592 pages 668 half-tones + 7 line illus. extensively referenced Embraces topics on the frontiers of this specialty as well as material forming the foundation of neuropathology. Since much of neuropathology is based on the visual evaluation of lesions, abundant illustrations amplify the text. thoroughly indexed hardback €70.00 -Neurobiology Edited by R, N. Rosenberg and W. D. Willis Jr. with 28 contributors 1983 648 pages 43 half-tone + 213 line illus. extensively referenced thoroughly indexed hardback f78.00 Expert coverage of contemporary neurobiology, describing neural mechanisms at cellular level and neural systems at organism level. Volume 3 Volume 5 Neuropathology Ne ur obiolog y Edited b y R. N. Rosenberg and S. S. Schochet 592 pages 668 half-tones + 7 line illus. €70.00 Edited byR. N. Rosenberg and W. D. Willis Jr. 648 pages 43 half-tones + 2131ine illus. €78.00 -. _. ~. -__ ---Five Volumes plus cumulative index volume 3708 pages 3221 illus. 274tables €400.00-asavingof f18.00onthesumcostof individualvolumes.
Contributions of Studies on Alcohol Use Disorders to Understanding Cerebellar Function
Neuropsychology Review, 2010
Neuropathological, neuropsychological, and neuroimaging studies of human alcoholism provide evidence for degradation of frontal, pontine, thalamic, and cerebellar brain sites and disturbed associated functions. Current studies using neuroimaging combined with examination of executive functions, traditionally considered the sole purview of the frontal lobes, have identified a role for the cerebellum serving as a compensatory processing adjunct to enable normal performance
Cerebellar Vermis Proteome of Chronic Alcoholic Individuals
Alcoholism: Clinical and Experimental Research, 2007
Background: Cerebellar changes are commonly associated with alcoholism and chronic alcohol consumption can produce profound impairments in motor functioning and various aspects of cognition. Although the mechanisms underlying alcohol-induced changes in the cerebellar vermis are poorly understood, observations in the alcoholic vermis are thought to be consequential to common alcohol-related factors, particularly thiamine deficiency.
Alcohol and Alcoholism, 2007
Objectives: Brain atrophy is a common finding in alcoholics. Several mechanisms may be involved, including ethanol itself, malnutrition, liver failure, and, possibly, ethanol-induced hormone and cytokine changes. The aim of this study was to analyse the relation of brain atrophy-assessed by computerized tomography (CT) scan-and the aforementioned alterations. Methods: Serum insulin-like growth factor 1 (IGF-1), interleukin (IL)-6, IL-8, IL-10, TNF alpha, PTH, estradiol, free testosterone, and corticosterone were measured in 36 alcoholics, ten of them cirrhotics, who also underwent brain CT, which recorded the presence of cortical atrophy or cerebellar atrophy, Evan's, Huckmann's, cella media, bicaudate, cortical atrophy, bifrontal, and ventricular indices, and diameter of the third ventricle; subjective nutritional assessment, midarm anthropometry, and evaluation of liver function. Results: Patients showed marked alterations of all the CT indices compared with 12 controls, but poor relations between these indices and the other parameters analysed (IGF-1, handgrip strength and years of addiction with bifrontal index (P < 0.025 in all cases); PTH and Evan's index (r = 0.36, P = 0.032); mean corpuscular volume with cella index and cortical atrophy (P < 0.05). Cerebellar atrophy was associated with a greater daily ethanol consumption (t = 2.19, P = 0.034). Conclusion: Brain atrophy is frequently observed in alcoholics, but relationships with liver function, cytokines, nutritional status, and hormone levels are poor.
Brain atrophy in chronic alcoholic patients: a quantitative pathological study
Journal of Neurology, Neurosurgery & Psychiatry, 1985
There are essentially no objective neuropathological data on brain atrophy in chronic alcoholic patients despite numerous neuroradiological studies which show a high incidence of shrinkage or atrophy. Therefore measurements were made of the intracranial volume (ICV) and brain volume (BV) in a necropsy study of 25 chronic alcoholic patients and 44 controls. The pericerebral space (PICS) was calculated according to the formula PICS = ICV BV x The PICS will increase in patients with brain atrophy since the ICV remains constant throughout life. The mean PICS value was 8-3% in controls, 11-3% in the alcoholic group, 14-7% in alcoholics with superimposed Wernicke's encephalopathy (thiamine deficiency) and 16-2% in those alcoholics with associated liver disease. Thus there was a statistically significant loss of brain tissue in chronic alcoholic patients which appeared to be more severe in those with associated nutritional vitamin deficiencies or alcoholic liver disease.