Cases Of Chronic Alcoholism Research Articles

Cognitive functioning in Wernicke's encephalopathy following chronic alcoholism

Background: Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome caused by a deficiency of thiamine (Vitamin B1) in chronic alcoholics. In chronic alcoholics, there is always deficiency of thiamine because of an inadequate supply of thiamine and neurotoxic effect of alcohol. The thiamine deficiency in the neuronal cells of the brain usually results in cognitive dysfunctions in chronic alcoholics. Objectives: To assess the memory functioning, intelligence, spatial ability, and visuomotor coordination in patients with WE following chronic alcoholism. Materials and Methods: This study was conducted in the Deaddiction Centre of Mental Health Institute (COE), S.C.B. Medical College and in another Deaddiction Centre of Cuttack. A total number of 34 cases, among 70 cases of chronic alcoholics, had symptoms of WE (global confusion, unsteady gait, and ophthalmologic signs) during admission and were finally selected for the study. The study was conducted from July 2014 to 2016. PGI-battery of brain dysfunction was administered to assess cognitive functioning of these patients, after 1-2 months of the admission in the Deaddiction Centre. Results: Findings suggested dysfunctions in attention-concentration, recent memory, mental balance, immediate recall, delayed recall, visual retention, recognition, abstract reasoning, planning, visual acuity, depth perception, and visuomotor coordination domains of neurocognitive functioning. Conclusion: It is highly essential to take into account the cognitive dimensions of chronic alcoholics before preparing their treatment plan in the long-term management while the patients are in the rehabilitation phase or in the domiciliary treatment and palliate their difficulties in activities of daily living.

Wernicke’s Encephalopathy and Korsakoff’s Syndrome Revisited

Carl Wernicke, a German neurologist, published the formal description of the encephalopathy for whom it is named 131 years ago. The clinical symptoms included lethargy, ophthalmoplegia, ataxia, andmental compromise.Within the same decade but unaware of Wernicke’s description, Sergei Korsakoff, a Russian psychiatrist, presented his doctoral dissertation, “Alcoholic Paralysis,” on the circumscribed amnesia occurring in certain cases of chronic alcoholism. More than half a century lapsed before the common etiology of thiamine deficiencywas discovered as the cause of the signs, symptoms, and link between these conditions (for historical reviews, see Charness, et al. 1989; Victor, et al. 1989). We now acknowledge the temporal linkage of Wernicke’s Encephalopathy (WE) and Korsakoff’s Syndrome (KS), depicted in Fig. 1 (cover image): 1) the acute phase of the encephalopathy, which results in bilateral lesions of periventricular nuclei, thalami, and structures of Papez’s circuit, notably the mammillary bodies; and 2) the chronic phase of the syndrome, which resolves into relatively permanent bilateral lesions and enduring global amnesia. In recognition of this linkage, the resulting condition is often referred to as the Wernicke-Korsakoff Syndrome (WKS). The profound amnesia provided a compelling link to neuropsychology and set the stage for dissecting memory’s component processes and identifying its dissociable neural substrates. Why is Study of WE and KS Still important?

The pathomorphology of chronic alcohol-associated myocardial changes

Forensic cases of sudden cardiac death were reviewed from the point of view of a history of alcohol consumption. A group of known cases of chronic alcoholism and another group of cases known to have been normal social drinkers without evidence of chronic alcoholism were selected. Cases with evidence of hypertension, ischemic or coronary heart disease, as well as cases with positive toxicological findings, were excluded. Applying the same criteria, cases of sudden death from other causes without a known history of alcohol consumption were selected to form a control group. With particular reference to histological myocardial changes, which are often documented in association with alcohol consumption, no noteworthy differences were found between the two major groups despite the significantly much lower frequency in the control group.

Alcohol and the integrity of the pancreas.

Alcohol may affect the integrity of the pancreatic parenchyma, as seen in alcoholic pancreatitis, some cases of chronic alcoholism without clinical pancreatitis, and experimental studies. The composition of pancreatic juice may reflect some of these changes. One type of parenchymal alteration is the loss of differentiative features of acinar cells, so that they take on the characteristics of ductular cells. Concomitant fibrosis completes the formation of the tubular complexes found in association with alcoholic chronic pancreatitis. Sustained alcohol intake may produce the accumulation of lipid droplets in parenchymal cells, some of which may be shown to be within the rough endoplasmic reticulum of acinar cells. Epithelial cells may undergo mucous metaplasia. The epithelial-basal lamina barrier frequently is breached in the area of intraluminal aggregates, with or without obvious inflammation in the immediate area. Loss of barrier function may lead to interaction among components of the external compartment (lumen) and the internal compartment (stroma). Increased levels of blood proteins and glycosaminoglycans in the juice, enzyme activation, fibrin formation, and complement activation are potential consequences of barrier loss. Increased lactoferrin levels could result in part from the activity and degranulation of polymorphonuclear leukocytes.

Isotopic cisternography and computerized tomography in chronic alcoholism with neurologic syndromes.

20 cases of chronic alcoholism with neurologic syndromes were studied by means of both isotopic cisternography and brain CT scan. In 11 cases (55%) there was total reversal of CSF circulation and in a further 4 cases there was a mixed cisternographic pattern. Brain CT scan showed either cortical or subcortical atrophy or both. The magnitude of these findings seems peculiar to chronic alcoholism. Reduction of atrophy in serial CT scan is possible.

Histopathological Changes of Chronic Alcoholism

The brains of six cases of chronic alcoholics without arteriosclerosis and the other diseases were examined histopathologically. The results obtained were as follows: there were chronic nerve cell sclerosis and deletion with slightly increased glial cells in the cortex of the cerebrum, hypothalamus, mamillary body, amygdal body, dentate endplate of Ammon's horn and cerebellum. Increased vascularity was observed in the cortex of the cerebrum, while no increased vascularity was found in the mamillary bodies. In many areas, widening of Virchow-Robin spaces were observed. The above-described findings were common changes in the brains in our six cases and they might have been induced by alcoholic effect on the brain tissue for a long time. Chronic nerve cell sclerosis in many areas, especially the diencephalon and limbic system, might have a deep relation to the character change of chronic alcoholics.

Serum creatine phosphokinase activity in newly admitted chronic alcoholics.

Serum CPK activity was measured for a total of 33 cases of chronic alcoholics who were admitted to the mental hospital from April, 1975 to January, 1976. The result was examined in relation to the manifestation of the psychotic symptoms in the patients: (1) Twenty six (78.8%) out of 33 cases showed increased serum CPK activity within 48 hours of admission. (2) In most cases that showed abnormal CPK activity, CPK value was the highest at the moment of admission, and then began to fall rapidly, and after one or two weeks settled to the normal CPK level. (3) There was a positive correlation between abnormal CPK activity and the manifestation of the psychotic symptoms in the month before and after entering hospital. In this cases of those having more than 101 IU in serum CPK value, the rate of presenting the psychotic symptoms in a month before or after admission was 90.5% and 71.4%, respectively. The author has given here a report on the above-mentioned results and made some considerations as to pathogenesis of abnormal CPK activity in chronic alcoholism.

Two Cases of Chronic Alcoholism

Two Cases of Chronic Alcoholism