Alcohol withdrawal and prolonged hospital stay in a patient with neuroimaging abnormalities: a case report.

A hospital stay of 30 days was required in a 47-year-old woman with alcohol withdrawal. Magnetic resonance imaging (MRI) findings revealed a focal brain stem lesion and multiple focal supracortical abnormalities. Could asymptomatic neuroimaging abnormalities predict risk of complicated alcohol withdrawal? Future clinical observations and longitudinal studies may wish to address this potential risk factor.

Psicosis etílica y mortalidad por todas las causas en Bielorrusia / Alcohol psychoses and all-cause mortality in Belarus

Antecedentes: La carga que representan los problemas relacionados con el alcohol en Europa Central y Oriental es la más alta del mundo. El nivel de consumo de alcohol en Bielorrusia se encuentra entre los más altos a nivel mundial, con un índice de consumo estimado de 14 litros de alcohol puro per cápita. Los desórdenes sociales, económicos y políticos experimentados en Bielorrusia durante los años que siguieron a la disolución de la Unión Soviética se han visto acompañados por un incremento sustancial de la mortalidad por todas las causas. Aunque el alcohol, en las antiguas Repúblicas Soviéticas, parece ser un contribuidor importante en la carga sobre dichas enfermedades, se han llevado a cabo pocas investigaciones sistemáticas sobre su impacto en la mortalidad por todas las causas en Bielorrusia. Objetivos: El objetivo del presente estudio es tratar este déficit particular en lo concerniente a la relación con la mortalidad total por alcohol utilizando datos a nivel agregado. Método: Las tendencias en la mortalidad por todas las causas y los índices de incidencia de la psicosis etílica (como sustituto del consumo de alcohol), desde 1970 hasta 2005, fueron examinados utilizando análisis de series temporales ARIMA para evaluar relaciones bivariables entre dos series temporales. Resultados: Los resultados del análisis de estas series temporales apuntan hacia una estrecha relación entre la mortalidad por todas las causas y los índices de psicosis etílica a nivel agregado. Conclusiones: Este estudio refrenda los hallazgos anteriores que sugieren la existencia de vínculos estrechos entre alcohol y mortalidad. Las conclusiones del presente estudio también apoyan la hipótesis de que el alcohol es un factor crucial enla crisis de mortalidad de Bielorrusia. Por lo tanto, el control del alcohol debe ser una prioridad clave en las políticas bielorrusas de salud pública

Background: The burden of alcohol-related problems in central and eastern Europe is the highest in the world. The level of alcohol consumption in Belarus is among the highest in the world, with an annual consumption rate estimated to be 14 litres of pure alcohol per capita. The social, economic and political turmoil that Belarus has experiences in the years following the dissolution of the Soviet Union has been accompanied by a substantial rise in all-cause mortality. Although alcohol seems to be an important contributor to the burden of disease in the former Soviet republics, little systematic research has been undertaken on its impact on all-cause mortality in Belarus. Aims: The aim of the present study was to address this particular deficit concerning the alcohol-total mortality relationship in Belarus by using aggregate-level data. Method: Trends in the all-cause mortality and alcohol psychoses incidence rates (as a proxy for alcohol consumption) from 1970 to 2005 were analyzed employing ARIMA time series analysis in order to asses bivariate relationship between the two time series. Results: The results of time series analysis suggest a close relationship between all-cause mortality and alcohol psychoses rates at the aggregate level. Conclusions: This study replicates the previous findings that suggested close link between alcohol and mortality. The outcome of present study also supports the hypothesis that alcohol is a crucial factor of mortality crisis in Belarus. Therefore, alcohol control must be a key priority for Belorussian public health policy

Tentativa de restabelecimento de saúde em indivíduos que fizeram ou fazem uso de álccol / An attempt on health reestablishment of individuals who where alcohol users and those who are present dependents

O álcool é considerado uma droga psicoativa que, dependendo da dose e freqüência, pode trazer prejuízos a nível social, psicológico e orgânico. Este trabalho teve como objetivo verificar as alterações ocasionadas pelo uso abusivo do álcool, considerando em especial os prejuízos hepáticos, de forma que o acompanhamento laboratorial permita a monitorização de sua saúde, contribuindo para reintegração do indivíduo na sociedade em que vive. Trabalhou-se com 10 pacientes dependentes de álcool e 10 dependente em recuperação,os quais foram na sua maioria funcionários da UFSC e membros do grupo de recuperação desta Instituição. A maioria dos dependentes da ativa apresentaram alterações orgânicas importantes em seu estado de saúde....

Magnetic resonance imaging in alcoholic Korsakoff's syndrome: evidence for an association with alcoholic dementia.

A magnetic resonance imaging study of 19 alcoholic Korsakoff patients, 17 non-amnesic alcoholics and 23 non-alcoholic controls was undertaken. Several measures of ventricular size and interhemispheric area were significantly greater in the Korsakoff patients. Interhemispheric fissure size was greater in the non-amnesic alcoholics than the non-alcoholic controls. Cortical grey matter T1 values were essentially the same for the three groups, whereas the deep grey and the white matter T1 values for the Korsakoff patients were significantly greater than the non-alcoholic controls. These results indicate widespread cerebral atrophy in alcoholic Korsakoff patients, which is largely subcortical and does not develop independently of the diencephalic pathology. Alcoholic dementia may be a more severe form of alcoholic Korsakoff syndrome, aetiologically related to the nutritionally-induced diencephalic pathology, rather than the neurotoxic effects of alcohol on the cortex.

[The neurobiology of alcoholism. Neuropathology and CT/NMR findings]. / Zur Neurobiologie der Alkoholabhängigkeit. Neuropathologie und CT/NMR-Befunde.

The authors deal with the heuristic value of the "neurobiological model of alcohol dependence". It allows the study of the influence of a defined noxe on different brain structures. Additionally, it enables the quantification of regeneration and restitution processes in abstinence. Because of this, the alcoholism model goes beyond dementia, the model which has dominated brain research so far. Neuropathological studies in humans and animals found a reduction in the volume of white matter and a partial degeneration, or even loss of specific neurons. According to animal data, this could to a certain extent be genetically determined. Alcohol exerts a distinct influence on different neurotransmitter systems. This research will deepen our understanding of the neurotoxic and psychotropic properties of alcohol, and of the development of dependence. Little is known about the role of astrocytes in the reaction of the brain to alcohol. Here again, the neurobiological model of alcohol dependence could be of value in learning more about their interactions with neurons. Using Magnetic Resonance Imaging and CAT-scans, the decrease in volume of white and grey matter was demonstrated in vivo. The degree and the time course of brain damage seems to be influenced less by drinking history than by age and gender. There is evidence that female alcoholics develop brain damage more readily than men. When abstinent, an increase in the volume of white and grey matter can be observed. This is not due to the rehydration of brain tissue alone. Future research will need to deal with the question of whether the central nervous system is capable of partial regeneration. For the study of neuroplasticity, the neurobiological model of alcohol dependence seems to be particularly well suited.

Alcoholic dementia.

At least four distinct cerebral diseases--Wernicke-Korsakoff, Marchiafava-Bignami, pellagrous encephalopathy, and acquired hepatocerebral degeneration--have a close association with chronic alcoholism. Each is characterized by a distinctive pathologic change and a reasonably well-established pathogenesis; in each the role of alcohol in the causation is secondary. The question posed in this review is whether there is, in addition to the established types of dementia associated with alcoholism, a persistent dementia attributable to the direct toxic effects of alcohol on the brain--i.e., a primary alcoholic dementia. The clinical, psychologic, radiologic, and pathologic evidence bearing on this question is critically reviewed. None of the evidence permits the clear delineation of such an entity. The most serious flaw in the argument for a primary alcoholic dementia is that it lacks a distinctive, well-defined pathology, and it must remain ambiguous until such time as its morphologic basis is established.

[Clinical and lesion-related bases of alcoholic brain damage]. / Fundamentos lesionales y clínicos del daño cerebral alcohólico.

Alcohol-induced brain damage is known since long, with classical descriptions of lesions. There is no constant correlation between them and any of the clinical presentations of chronic intoxication. New neuroimaging techniques, neuropsychology and basic investigation have supplied with new data. The so-called alcoholic dementia and its possible reversibility are major issues of this problem. This paper reviews radiological, pathological, vascular and neuropsychological studies related to this point.

Anatomo-pathological studies on alcoholic dementia: a review and up to date research.

Neuropathological studies of cerebral disorders in alcoholics which started by means of macroscopic observation have issued many important articles until now. However, we can not yet stretch out the essential core of alcoholic dementia. Plenty of animal experiments also suggest some possibility fo neurotoxicity by ethanol but do not offer a definitive resolution. Moreover, there is the strict criticism concerning neuropathological evidence on alcoholic dementia. Nevertheless, we know that there are some alcoholics who have no evidence of Wernicke-Korsakoff syndrome, but manifest persistent cerebral impairment after long-term heavy drinking. Under such circumstances it might be necessary to consider and study cerebral disorders in alcoholics, particularly relating to subcortical lesions. Pathomorphological investigations in our laboratory have put forward some significant findings.

[Microcirculation in patients with alcoholic delirium (data of conjunctival biomicroscopy)]. / Mikrotsirkuliatsiia u bol'nykh alkogol'nym deliriem po dannym kon''iunktival'noi biomikroskopii.

Using conjunctival microscopy the authors examined 66 males with alcoholic delirium, 25 normal subjects and 20 patients with chronic alcoholism. Examination was carried out in the acute stage of psychosis and 12-16 days after its cessation. Patients with chronic alcoholism and alcoholic delirium had marked microcirculatory disturbances. Microcirculatory disturbances tended to get more serious with prolongation of psychosis and were also more prominent in patients with alcoholic delirium versus patients with chronic alcoholism. The therapy led only to a reduction in the conjunctival index reflecting perivascular changes.

Alcohol withdrawal causes a loss of cerebellar Purkinje cells in mice.

Mice received a liquid diet containing alcohol for 4 months, after which half of them were sacrificed and the others given a 4-month recovery period before being sacrificed. They were compared with similar mice receiving the diet with alcohol replaced isocalorically by sucrose. No damage was detected in the cerebellum during alcohol consumption, but the number of Purkinje cells was significantly reduced in the recovery period. The experiment was repeated twice with mice consuming a normal diet but exposed to alcohol vapor. The first group was exposed to alcohol vapor 24 hr/day for 3 weeks and then given alternating 1-week periods of recovery and exposure 24 hr/day until a total of 6 weeks of exposure to alcohol vapor and 4 one-week recovery periods had been experienced. They were compared with similar mice exposed to alcohol vapor 24 hr/day for 6 weeks without a recovery period. The second group was exposed to alcohol vapor 9 hr/day for 3 weeks, when part of the group was given a 3-week recovery period. In both experiments, damage was not detected in the cerebellum during alcohol exposure, but in mice withdrawn from alcohol, the number of Purkinje cells was reduced and qualitative evidence of neuronal degeneration was found with a silver stain. In a further group of mice, exposure to alcohol vapor was tapered off gradually, and no evidence of neuronal loss was found. Indications in the literature that withdrawal from alcohol can cause brain damage are briefly reviewed.

Morphological alterations in rat CA1 hippocampal pyramidal cell dendrites resulting from chronic ethanol consumption and withdrawal.

Hippocampal CA1 pyramidal cell dendrites were studied in rats after 5 months of consumption of an ethanol liquid diet and 5 months of ethanol diet followed by 2 months of withdrawal. Morphometric data were compared with those obtained from matched littermate, yoke -fed control animals. Dendritic branching in Golgi-Cox-stained tissues was assessed by standard and modified Sholl analysis techniques and basilar dendrites were analysed three-dimensionally by computer. Five months of chronic ethanol consumption caused a significant decrease in the number of second-order basilar dendrites, 60-90 micron from the apical border of the cell layer. No significant changes in the neuronal density of CA1 or CA3 cells were found; however, the thickness of the strata oriens and radiatum of the CA1 field was significantly decreased in the ethanol-fed group. After 5 months of chronic ethanol consumption and 2 months of withdrawal, the thickness of the strata returned to control sizes and the frequency of proximal basilar branching recovered. Evidence of lengthening and new branching of distal basilar dendrites occurred in the third-, fourth-, and fifth-order segments when control animals 6 and 8 months of age were compared. During the 2-month period of withdrawal, the number and length of third-, fourth-, and fifth-order segments of basilar dendrites increased when compared to the nonwithdrawn ethanol group while the number and length of second- and third-order segments decreased. This is comparable to the changes seen during normal aging and suggests that withdrawal may interact with aging to produce enhanced dendritic growth in "compensation" for the developmental retardation induced by chronic ethanol intake.

A comparison of cerebral atrophy in CT scan findings among alcoholic groups.

Seventy-five alcoholic patients and 94 control subjects were examined by CT scans and measured by 11 measurement items on CT. The alcoholics were classified and compared. Enlargement of ventricles was recognized in the alcoholics. The degree of enlargement of ventricles was extremely striking in alcoholic dementia. The increasing tendencies toward cerebral atrophy in a given age stratum were almost parallel in the controls and the alcoholics, with a difference in the degree of atrophy. It was suggested that the enlargement of the ventricular system in the alcoholics might be induced in the initial stage of alcohol dependence, and that physiological atrophy due to aging might progress thereafter. The results of multivariate canonical analysis of these CT items suggested that the CT indicators effective for evaluating alcoholic cerebral atrophy were the transverse diameter of the third ventricle, Ventricle index and Evans' index.