Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENCEPHALOMALACIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

Correlation between confirmed sites of neurological lesions and abnormalities of far-field auditory brainstem responses.

Far-field auditory brainstem responses were recorded in ten patients in whom the distribution of pathology was defined at autopsy or at operation. The response normally consists of seven components in the initial 10 msec following click signals. Interruption of audiotory pathway at the junction of VII nerve with brainstem results in loss of response components after Wave I. Interruption of auditory pathway at the midbrain results in loss of response components after Wave III. We conclude that Wave I reflects activity of VIII nerve, Waves II and III reflect activity of cochlear nucleus, trapezoid body, and superior olive and Waves IV and V reflect activity of lateral lemniscus and inferior colliculus. The generators of Waves VI and VII were not defined.

Acoustic Stimulation↗

Histopathological changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

The distribution, severity and frequency of brain lesions produced in mice by the administration of Clostridium perfringens Type D epsilon toxin were examined by light microscopy. The granular layer of the cerebellum was the area most frequently affected in mice given single doses of toxin. Sequential changes in brain morphology were examined from 1 h to 7 days after injection of toxin. Lesions progressed from an initial vasogenic oedema to malacic foci which commonly were focal and bilaterally symmetrical, with a predilection for white matter. The topographical distribution of these malacic areas is discussed.

Animals↗

Ultrastructural changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

Mice were given lethal and sublethal doses of Clostridium perfringens Type D epsilon toxin and the early morphological changes in perfusion-fixed intoxicated brains were examined from 30 min to 6 h post-inoculation. The initial ultrastructural finding was swelling of astrocytes, especially the perivascular extensions of these cells. Astrocytes in the cerebellum appeared to be particularly sensitive to this toxin. These changes were quickly followed by evidence of severe endothelial damage, with the endothelial cytoplasm becoming attenuated, vacuolated and very electron-dense. A pathogenetic sequence of events leading to malacia, derived from ultrastructural observations, is proposed.

Animals↗

The cortical form of subacute necrotizing encephalopathy of the Leigh type. A light- and electron-microscopic study.

The present paper is a clinico-pathological study of a 14-year-old boy with a chronic, progressive occipital syndrome for which he was operated upon. Postoperatively, metabolic acidosis developed. Pathological anatomy revealed spongy necrosis of the thalamus and corpora quadrigemina with the typical histological features of Leigh's necrotizing encephalopathy. Similar necrotic lesions had developed in the occipital cortex. At this level apart from the typical foci, cavitating necrosis was found as well as involvement of the smaller vessels of the pial circulation. Electron microscopy revealed vascular and glial changes suggestive of primary mesenchymoglial dystrophy. The histiocytes presented intracytoplasmic multiplication of lysosomes and their transformation into lipofuscin pigment. The changes demonstrate a juvenile cortical form of Leigh's subacute necrotizing encephalopathy.

Adolescent↗

Role of thiamine status in sulphur induced polioencephalomalacia in sheep.

The effects of excess dietary sulphur were studied in sheep supplemented and unsupplemented with thiamine. The diets contained either 0.19 per cent sulphur (LS) or 0.63 per cent sulphur (HS) in combinations with 14 mg kg-1 thiamine (LB1) or 243 mg kg-1 thiamine (HB1). A total of 56 two-month-old lambs were used. Groups consisting of nine, nine, 22 and 16 lambs were fed LS-LB1, LS-HB1, HS-LB1 and HS-HB1 diets, respectively for 14 weeks. Out of 22 lambs fed the HS-LB1 diet, seven lambs developed neurological signs between the third and eighth week of the trial. Two of these lambs died, three that were in extremis were euthanased, and two recovered completely. All clinically affected animals had extensive malacic lesions in the cerebral cortex, midbrain and brainstem. None of the lambs from the LS groups or HS-HB1 group developed clinical signs. Several clinically normal lambs from the HS-LB1 group had necrotic lesions in their brains at gross and microscopic examination. Supplementation with dietary thiamine prevented development of clinical signs, but did not totally prevent development of microscopic brain lesions. Brain thiamine concentration, transketolase activity and thiamine pyrophosphate (TPP) effect were not different (P greater than 0.05) among groups. There was a strong effect (P less than 0.0001) of dietary thiamine supplementation on blood thiamine concentration and TPP effect. Blood thiamine concentration was higher whereas TPP effect was lower in the thiamine supplemented sheep. Blood and tissue thiamine concentrations in sheep exposed to high dietary sulphur did not indicate either systemic or local thiamine deficiency per se. Increased TPP effect in sheep fed the HS-LB1 diet indicated mild to moderate metabolic thiamine deficiency. Thiamine inadequacy may be an effect of an increased requirement for thiamine in animals exposed to excess dietary sulphur.

Animals↗

Toxicity to beef cattle of sulfur in saline well water: a case study.

A disorder diagnosed as polioencephalomalacia occurred in yearling Hereford heifers, but not in mature cows, within 2 months of exposure to saline well water. The physiological effects of the disorder matched most of the symptoms for bovine polioencephalomalacia. The water contained 3875 mg l-1 total dissolved salts, sulfate and sodium being the dominant ions. Calculated daily sulfur and sodium intakes were near the upper limit of their range for recommended maximum tolerance level. Sulfur toxicity was implicated as the causative agent for the disorder. Differences in effect of waters with similar sulfur contents were attributed to the total dietary sulfur intake by the cattle rather than to the saline water alone. Established guidelines for saline drinking water were deemed not applicable when fodder from saline land is supplied to or grazed by cattle.

Animal Feed↗

Low attenuation lesions in the midline posterior fossa: differential diagnosis.

A wide variety of cystic appearing or low attenuation lesions in the midline posterior fossa can so closely resemble one another as to render specific histologic diagnosis from CT scans alone fraught with error. Absorption coefficients often overlap and are too nonspecific to infer consistently accurate histologic diagnosis. It is virtually impossible to separate cystic from noncystic, benign from malignant, and neoplastic from non-neoplastic lesions by absorption coefficients alone.

Brain↗

Hepatotoxicity and renal toxicity in rats of corn samples associated with field cases of equine leukoencephalomalacia.

Currently there is no convenient bioassay to determine the potential toxicity of corn naturally contaminated with Fusarium moniliforme. A short-term bioassay would be useful for future investigations aimed at isolating as yet unidentified toxins produced by this fungus. Two groups of five male Sprague-Dawley rats were each fed one of two F. moniliforme contaminated corn samples, designated CS-1 and CS-2, that were associated with separate field cases of equine leukoencephalomalacia (ELEM). A control group, also consisting of five male rats, was fed uncontaminated seed corn. All animals survived to the end of the study and there were no apparent differences in appearance or behaviour among groups. Weight loss and irregular food consumption occurred in all groups and probably resulted from nutritional deficiencies inherent in the corn diets. Hepatocellular degeneration, necrosis and hyperplasia as well as biliary hyperplasia were found in the test groups only and were attributed to F. moniliforme. Serum transaminase and alkaline phosphatase activities in animals fed CS-1 and CS-2 for 4 wk were significantly increased compared with the controls, while serum bilirubin concentration was increased only in the CS-1 group. Tubular nephrosis was also present in the renal cortex of all animals fed CS-1 and CS-2. These effects may have been related to fumonisins B1 and B2, recently discovered metabolites of F. moniliforme, that were found in both CS-1 and CS-2. Short-term studies of this type may be useful in screening naturally-contaminated grains and other materials for hepatotoxic metabolites produced by F. moniliforme.

Animals↗