Browsing by Subject "Chronic alcoholism"

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    Effect of chronic alcoholism on the human hippocampus
    (Murcia : F. Hernández, 1990) Bengochea, O.; Gonzalo, L. M.
    The effect of chronic alcoholism on the human hippocampus was studied in 21 patients, divided in 4 groups: Group A under 45 years, group B 46-59 years, group C 60-69, and Group D over 70 years; and compared with age-matched control patients who died without neurological complications. The gyrus d~ntatus and the ammonic fields CA1 through CA4 were analyzed by counting the number of neurons and the size of the nuclear area. Both parameters were evaluated statistically. The most important findings were a high neuronal loss in alcoholics in the first age group. In addition, the hippocampal neurons failed to display a vicarious reaction, since the nuclei did not show any increase in size despite the intense neuronal loss. Our results point out an early neuronal loss in the hippocampus of alcoholic patients higher than agematched controls, as well as a lack of reaction to the neuronal insult .
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    Effects of chronic alcoholism on the amygdaloid complex. A study in human and rats
    (Murcia : F. Hernández, 2011-01-24) Alvarez, I.; Gonzalo, L. M.; Llor, J.
    The effect of chronic alcoholism on the amygdaloid complex was st~idied in 16 humans and 10 rats. Eighteen patients whose death was due to extraneural causes were selected as controls with 3 rats. Thc alcoholic cases, in addition to the data collected in their clinical history. showed, niicroscopically confirmed. liver cirrhosis or steatosis. The alcoholics and controls were divided into 4 groups: 35-44 years old (4 cases). 45- 54 (5 cases). 55-63 (5 cases) over 65 (2 alcoholics and 4 controls). The alcoholic ingestion in the rats (Wistar, 10 weeks old) was 3 ml at a concentration of 30% in water solution administered by esophagic intubation, for 38 (5 rats) or 58 weeks (5 rats). To judge the state of the amygdaloid nuclei, a neuronal count and caryometry were carried out. The numerical data obtained in this study were analyzed statistically. The results in humans have paralleled those obtained in rats and the behaviour of the different nuclei of the amygdala was uniform and can be summarized as follows: 1) ethanol provoked a prominent and early loss of neurons, and 2) the remainder of non-affected neurons did not react in order to compensate for this neuronal loss.