Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke's encephalopathy (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.
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.
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.
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-
Ethanol consumption has been linked with social and medical problems, coupled with damage of multiple organs including the cerebellum. The present study is aimed at investigating the histological and biochemical changes in the cerebellum of Wistar rats associated with ethanol exposure. The experimental animals were grouped into five groups designated as Group 1 which served as the control group and was given distilled water, Groups 2,3,4 and 5were given 40%, 25%, 12% and 5% v/v of ethanol respectively. Each of the experimental animals was administered 10mls/kg body weight of the stock solution for 42days after which the animals were sacrificed humanely. The cerebellum was removed, fixed in Bouins fluid for histological study while brain homogenates were prepared and used for the biochemical studies. Data was analyzed using one-way ANOVA and Tukey HSD Post-Hoc comparison test was used to determine where the difference lies. Oxidative stress studies showed significant increase and decrease in some oxidative stress markers when compared to the control group (p<0.05). The sialic acid studies showed a dose dependent decrease in the mean sialic acid concentration of the cerebellum across the groups when compared to the control (p<0.05). The histological studies showed the following changes; necrotic Purkinje cells with reduced linear distribution of Purkinje cells, in section of the cerebellar tissue of rats in Groups 2 and 3 with sections from Groups 4 and 5 remaining relatively normal when compared to the slide from the control group. Exposure to ethanol from the present studies showed a dose dependent effect on the cerebellum, as manifested in the histological and biochemical studies.
Journal of Neurology, 2005
Chronic alcohol consumption is frequently accompanied by cerebellar degeneration. The exact aetiology of alcoholic cerebellar degeneration is still a matter of debate. The aim of the present study was to investigate whether patients with chronic alcohol consumption exhibit a decrease in dentate nuclei intensity as measured by MRI, and if so, whether this decrease correlates with cerebellar atrophy as revealed by MR imaging or with clinical signs of cerebellar ataxia. A decrease in dentate nuclei intensity would indirectly indicate that iron accumulation, and therefore, oxidative stress may play a role in alcoholic cerebellar degeneration. MRI of 45 alcoholics and 44 ageand sex–matched healthy control subjects was performed using a 3D–T1–weighted fast low angle shot (FLASH) echo sequence. Signal intensities of the dentate nuclei and cerebellar white matter were bilaterally measured. Planimetric measurements of cerebellar size were performed using a 3D–T1–weighted magnetization prepared rapid acquisition gradient echo (MPRAGE) sequence. Results demonstrated that dentate nuclei intensity was not significantly decreased in patients with chronic alcohol consumption (mean ± SD signal intensity 65.36 ± 13.0) if compared with control subjects (mean ± SD signal intensity 68.95 ± 9.4) (p = 0.15). Dentate nuclei intensity did not correlate with cerebellar size neither in control subjects nor in alcoholics. In contrast, vitamin B1 level correlated with cerebellar size in alcoholics even if the vitamin B1 concentration was within normal values (r = 0.344, p = 0.028). These results support the view that thiamine deficiency rather than direct neurotoxic effects of alcohol is the main causative factor for the development of alcoholic cerebellar degeneration.
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
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.