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Results for “ENCEPHALOMALACIA”

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At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

[Blood clotting disorders in cases of encephalomalacia].

In a group of 22 patients with foci of brain softening certain blood clotting factor were determined at different stages of the disease. The control group consisted of 16 healthy subjects. Shortening of the prothrombin time was observed after 4 weeks in the group of patients as compared with the control group. The fibrinolytic activity was higher in the plasma on the 4th day of the disease and a fall of plasma fibrinolytic activity after 4 weeks to normal values was observed.

Aged↗
PubMed1980

[Etiopathogenesis and prevention of encephalomalacia in chickens].

Studies were carried out on the dissemination of encephalomalation with chickens. The quality of the feeding-mixes, meant for the different categories of fowls, was also studied with regard to the contents of vitamins, fats, aldehyde and peroxide number and antioxidizers. The contents of vitamin E was also determined, as well as its biological activity in a biological material. The prophylactic effect of different vitamin preparations was tested in combination with other means of prophylaxis of broilers against encephalomalation. It was proved that the increase of aldehydes and peroxides in feeding-mixes could lead to the appearance of encephalomalation with chickens. The quantity of santokvin--200 g/t of fodder enabled the good conservation and preservation of the biological activity of vitamin E. The index 'biological activity' is a more appropriate criterium for a supply of chickens with vitamin E, rather than its quantitative contents in biological substrates. On the basis of the experiments made, a disgram is offered about the prophylaxis of encephalomalation with chickens.

Animal Feed↗
PubMedDate not supplied

Cerebral encephalomalacia in commercial turkeys.

A flock of 9 1/2-week-old commercial tom turkeys experienced high mortality after consuming a complete feed containing an unidentified toxic substance. Initially, turkeys were found dead. Clinically, the birds were calm and still but became hyperexcitable with noise. A small percentage of birds exhibited torticollis, opisthotonos, circling, ataxia, and blindness. Findings at necropsy and upon microscopic examination were bilaterally symmetrical areas of necrosis of the cerebral hemispheres in the area of the neostriatum that were well demarcated from the surrounding normal neuropil. A feeding trial with the suspect feed in twelve 4-week-old turkey hens induced clinical disease and gross and microscopic brain changes similar to those observed in the field case. Analyses for the following substances in the suspect feed were either negative or within acceptable limits: salt, selenium, furazolidone, monensin, amprolium, 3-nitro-4-hydroxyphenylarsonic acid, aflatoxin, deoxynivalenol, zearalenone, T-2 toxin, ochratoxin, fumonisin, organophosphates, chlorinated hydrocarbons, and carbamates. The toxic component of the feed remains unidentified.

Animal Feed↗
PubMedDate not supplied

Enterococcus durans infection in young chickens associated with bacteremia and encephalomalacia.

Two unrelated flocks of chicks experienced elevated mortality from 4 to 10 days of age. Clinical signs in affected birds included a full range of neurological disorders. Livers and spleens were grossly enlarged at necropsy. Enterococcus durans was isolated from multiple organs, including brains. Histologically, there were multifocal coagulative necrosis in the liver, areas of malacia in brain stem, and cerebellar white matter. Inoculation of 1-day-old chicks with a suspension of E. durans resulted in bacteremia but did not produce the lesions observed in field cases.

Animals↗
PubMed1979

Neonatal polycystic encephalomalacia: four new cases and review of the literature.

Four patients with pathologically documented polycystic cavitation of the brain had an acute illness characterised by stupor, seizures, CSF erythrocytic and monocytic pleocytosis, increased CSF protein, and diminished CSF glucose. The acute phase was followed by chronic decerebation, disappearance of the CSF abnormalities, and radiological evidence of polycystic cavitation of the brain. In one patient Herpes simplex was isolated from a cutaneous vesicle. The CSF abnormalities in the disorder have received scant attention, and have not previously been correlated with the acute and chronic stages. Clearly some cases are associated with Herpes simplex virus. The clinical profile should now be sufficiently distinctive to permit future identification of the aetiology in more neonates.

Brain↗