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Results for “Encephalomalacia”

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At least 19 recordsLinked to original sources

PubMed1977

Preventive effect of selenium, methionine and antioxidants against encephalomalacia of chicks induced by dilauryl succinate.

The protective effect of supplemental selenium, methionine, ascorbic acid, menaquinone and five antioxidants against encephalomalacia of chicks fed a diet containing dilauryl succinate was examined. Diauryl succinate induces vitamin E deficiency signs such as fragility of the erythrocytes and encephalomalacia. Supplementation of selenium and methionine with or without simultaneous supplementation of a low level of dl-alpha-tocopheryl acetate had little effect on preventing encephalomalacia. The preventive effect of ascorbic acid, methylene blue, ethoyquine, 2,6-ditertiary-butyl-p-cresol and butylated hydroxyanisole was roughly in proportion to their dietary level, and a high level of any of them could almost completely protect the chicks from encephalomalacia, while diphenyl-p-phenylenediamine was not as effective and the effect was not proportional to the dose. Menaquinone had little effect. No difference was observed in the plasma tocopherol levels and peroxide levels in the adipose tissueof the chick fed eith er dilauryl succinate or cornstarch. The effect of dilauryl succinate appears to be independent of peroxides generated in the chick.

Adipose Tissue↗

PubMed1979

Phagocytic astrocytes and neurons in old encephalomalacia.

Cytoplasmic accumulation of hemosiderin was observed within astrocytes and neurons as well as in other phagocytes associated with old encephalomalacia. The first patient was 3 years old when she died with malnutrition and superimposed infection. A cortical infarct had been caused by an old thrombus in a small artery. The second case was a 9-year-old girl who had old encephalomalacia in the pineal region after extirpation of a pineoloma. The third patient was a 22-year-old man who had a cortical infarct from an embolus associated with chronic rheumatic endocarditis. Granules of hemosiderin had accumulated within the perikaryon of many astrocytes and other phagocytes in all cases, and in a few neurons in the second instance. Review of the literature reveals that cytoplasmic accumulation of particulate matter has been described infrequently with regard to neuroepithelial derivatives. Our findings indicate that astrocytes and neurons as well as derivations of mesenchyme may act as phagocytes of old blood.

Adult↗

PubMed2024

Identification of a novel intronic variant in COL4A2 gene associated with fetal severe cerebral encephalomalacia and subdural hemorrhage.

BACKGROUND: Genetic variants in COL4A2 are less common than those of COL4A1 and their fetal clinical phenotype has not been well described to date. We present a fetus from China with an intronic variant in COL4A2 associated with a prenatal diagnosis of severe cerebral encephalomalacia and subdural hemorrhage. METHODS: Whole exome sequencing (WES) was applied to screen potential genetic causes. Bioinformatic analysis was performed to predict the pathogenicity of the variant. In in vitro experiment, the minigene assays were performed to assess the variant's effect. RESULTS: In this proband, we observed ventriculomegaly, subdural hemorrhage, and extensive encephalomalacia that initially suggested cerebral hypoxic-ischemic and/or hemorrhagic lesions. WES identified a de novo heterozygous variant c.549 + 5G > A in COL4A2 gene. This novel variant leads to the skipping of exon 8, which induces the loss of 24 native amino acids, resulting in a shortened COL4A2 protein (p.Pro161_Gly184del). CONCLUSION: Our study demonstrated that c.549 + 5G > A in COL4A2 gene is a disease-causing variant by aberrant splicing. This finding enriches the variant spectrum of COL4A2 gene, which not only improves the understanding of the fetal neurological disorders associated with hypoxic-ischemic and hemorrhagic lesions from a clinical perspective but also provides guidance on genetic diagnosis and counseling.

Female↗

PubMed1975

Silent acute pancreatitis with encephalomalacia mimicking hepatic coma.

A very rare case of acute pancreatitis with concurrent encephalomalacia and ascites mimicking hepatic coma is described. The possibliity that the pancreatitis was caused by the administration of chlorothiazide in a diabetic patient is suggested as possible etiology. It is emphasized that when a cirrhotic patient develops coma, the possibility of painless,silent pancreatitis with encephalomalacia as well as hepatic coma should be considered in the differential diagnosis.

Acute Disease↗

PubMed1979

Multiple cystic encephalomalacia of infancy: computed tomographic findings in two cases with associated intracerebral calcification.

Two initially healthy infants developed acute encephalopathic illnesses characterized by stupor, seizures, cerebrospinal fluid (CSF) erythrocytic and monocytic pleocytosis, increased CSF protein, and decreased CSF glucose and progression to chronic decerebration. In one case, herpes simplex virus was recovered from cutaneous lesions. The initial computed tomography (CT) scan revealed widespread subcortical increased attenuation with further increase after contrast medium injection and patchy areas of decreased attenuation in the deep cerebral white matter. Subsequent CT scans demonstrated progressive cortical calcifications and persistence of low attenuation areas. Autopsy revealed multiple cystic encephalomalacia. The second infant had similar clinical, CSF, and CT findings but remains in a chronic decerebrate state at 14 months of age. The CT abnormalities seen in these patients have not been encountered in any of 13 other infants with the clinical diagnosis of meningitis or encephalitis. Multiple cystic encephalomalacia of infancy is a rare condition with a uniformly bleak prognosis. Computed tomography may prove useful in the early diagnosis, thereby aiding clinicians in counseling and in the acute and long-term management of patients with this lesion.

Brain Diseases↗

PubMed1979

[Encephalomalacia in partridges, quails and pheasants raised in warrens].

With the introduction of industrial methods of breeding game animals, resp., birds in confinement some new diseases have arisen, such as encephalomalacia. Due to its peculiar character this disease was first referred to as B-complex avitaminosis, respective therapeutic measures being taken. Recent studies have ruled out avitaminosis, and the disease is now confirmed as encephalomalacia. In the case of partridges, rock partridges, and pheasants some drop was found of the levels of vitamin E and selenium. Accordingly, vitamtin E and selenium therapy produced a rapid curative effect.

Animals↗

PubMedDate not supplied

[E-vitamin activity of vitamin E derivatives with experimental encephalomalacia in chicks].

When adding pharmacopoeian alpha-tocopherylacetate, short-chain alpha-tocopherylacetate, alpha-tocopherylquinine, short-chain alpha-tocopherylquinone and alpha-tocopheronolactone to E-avitaminotic rations pharmacopoeian alpha-tocopherylacetate and alpha-tocopheronolactone manifest the highest E-vitamin activity in preventing encephalomalacia in chickens. The action of alpha-tocopheronolactone is not directly associated with changes in the content of vitamin E and ubiquinone in the brain and liver tissues. All the studied derivatives are effective in increasing resistance of erythrocytes to osmotic hemolysis. The data obtained evidence for a nonspecific function of vitamin E in preventing alimentary encephalomalacia in chickens as well as for the absence of disturbances in ubiquinone metabolism under conditions of the E-hypovitaminosis experimental model.

Animals↗

PubMed1978

Avian encephalomalacia in Barbados, West Indies: a description of spontaneous field cases with feed analyses.

The clinical, necropsy and histopathological findings in four natural outbreaks of encephalomalacia are reported. Feed analyses implicated low levels of vitamin E as the probable cause of the condition. Treatment with vitamin E has proved to be very effective. The instability of vitamin E in animal feed ingredients during long periods of shipment into the Caribbean may be important in the pathogenesis of the disease.

Animal Feed↗

PubMed1978

Multicystic encephalomalacia of infancy: clinico-pathological report of 7 cases.

Clinical follow up and complete neuropathological examination was made on seven cases of multicystic encephalomalacia of infancy. Etiological factors were carefully studied in all the cases. They consisted of prenatal injuries presenting as a cord prolapse, in 3 cases; prolonged labour with marked cyanosis; abdominal trauma during gestation, and various maternal infections at different stages of pregnancy. Pathological interest is centred on the variable involvement of different areas of the brain, generally sparing the cerebellum and brain stem, and being minimal or absent in the occipito-temporal areas. This distribution may be explained by a different effect of the "causal agency" on these different areas, or by a different capacity of these regions to react against injury. Among the etiological factors reviewed in the literature, the anoxic theory appears the most probable, as there was a close parallelism between lesions and vascular areas, mainly the carotid and vertebro-basilar systems.

Asphyxia Neonatorum↗

PubMed1979

Multicystic encephalomalacia in liveborn twin with a stillborn macerated co-twin.

Computed tomography showed multiple cystic lesions in the brains of three infants with cerebral palsy. Each patient was the product of a twin pregnancy with a stillborn, macerated co-twin. In two patients angiography was performed and suggested that the cystic lesions were multicystic encephalomalacia due to perinatal arterial occlusion.

Arterial Occlusive Diseases↗

PubMedDate not supplied

[Urinary uropepsin activity in patients with encephalomalacia as an index of the activity of the hypothalamo- hypophyseal-adrenal axis].

The determinations were carried out in 25 patients with thrombotic encephalomalacia. The changes in 24-hour urine uropepsin activity were studied after administration of metopirone and dexamethasone. The uropepsin activity in a sample of 24-hour urine was determined by the method of West, Ellis and Scott. A statistically significant fall of uropepsin activity was observed in 24-hour urine after metopirone, with a rise in the activity of this enzyme after dexamethasone administration.

Aged↗

PubMed1979

[Electron microscopic findings in the skeletal musculature of broilers with nutritional encephalomalacia].

Sings of myopathy were recorded by means of electron microscopy from the skeletal muscles of 20 broiler chickens, aged five and six weeks and suffering from spontaneous nutritional encephalomalacia. Focal deposits of osmiophilic, granular or amorphous matter, intermixed also with membrane fragments and condensed to homogenous osmiophilic bodies, were found quite often in the sarcoplasm. Those deposits were interpreted as lipoproteid complexes (pigmentation due to vitamin E deficit). Also observed were degenerative disorders of compensatory reactions of membraneous fibre organelles (sarcoplasmic reticulum, mitochondria) as well as decomposition of myofibrils and fibre hyalinization. Fibre regeneration and vascular damage occurred less often. Pathogenetically, the changes are interpreted particularly with regard to a membrane-stabilising anti-oxidant action of vitamin E and compared to the selenium-dependent myopathies of ruminants from which primary myofibrillar damage was recordable but no pigment accumulation.

Animals↗

PubMed1975