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Results for “ENCEPHALOMALACIA”

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At least 595 records · Page 33Linked to original sources
PubMed1996

Leukoencephalomalacia and hemorrhage in the brain of rabbits gavaged with mycotoxin fumonisin B1.

Two of five pregnant rabbits gavaged with purified fumonisin B1 at 1.75 mg/kg/day died, one after 9 and one after 13 doses. Microscopic examination revealed focal small hemorrhages in cerebral white matter in both animals, with malacia and hemorrhage also present in the hippocampus of one. The lesions were bilateral. Both animals also had marked degeneration of renal tubule epithelium and of hepatocytes. Apoptosis was the dominant degenerative change in kidney and liver. Fumonisin is known to cause leukoencephalomalacia and hemorrhage in equines, but CNS changes associated with exposure to fumonisins apparently have not been reported in other species. This preliminary observation in rabbits is reported to alert other investigators of a potential model of the disease in equines, as well as for investigation of potential mechanisms of toxicity to the CNS.

Animals↗
PubMed1980

Chronic Leigh Disease: a genetic and biochemical study.

The large family of a 21-year-old man who died of Leigh disease was investigated for evidence of neurological abnormalities and presence of the adenosine triphosphate-thiamine diphosphate phosphoryltransferase inhibitor factor. Of 217 persons (seven generations) included in the pedigree, 68 were examined neurologically and biochemically. Fourteen (20%), 5 of whom had abnormal neurological findings, were found to excrete the inhibitor factor. Clinical manifestations varied from severe neurological affliction to subtle deficits. A chronic relapsing course was frequently encountered, with exacerbations occurring in association with apparent metabolic stress. Parental consanguinity was identified in the propositus as well as in other family members with neurological abnormalities. Males and females were affected, and no vertical transmission of the trait was found. These multigenerational data suggest that Leigh disease in adults is inherited in an autosomal recessive manner and has variable degrees of expression with a wide spectrum of neurological manifestations.

Adult↗
PubMed1981

Seizures, hypoxic-ischemic brain injury, and intraventricular hemorrhage in the newborn.

The review deals with neonatal seizures, perinatal hypoxic-ischemic brain injury, and neonatal intraventricular hemorrhage. neonatal seizures are the most prominent signals of the largest number of neonatal neurological disorders. The convulsive phenomena may be subtle. The predominant etiological process is hypoxic-ischemic encephalopathy. Prognosis is related primarily to the neurological disease responsible for the seizures. Treatment may be specific for the underlying disorder (e.g., glucose or calcium) or less specific (i.e., therapy with anticonvulsant drugs). Prompt control of the seizures is important to avoid brain injury secondary to the effects of the seizures on ventilation, perfusion, and brain metabolism. Hypoxic-ischemic encephalopathy in the newborn most often is a consequence of intrauterine asphyxia. Diagnosis depends primarily on recognition of the clinical syndrome but also on a variety of neurodiagnostic techniques, including radionuclide and CT brain scans. Prognosis is estimated best by a combination of clinical analysis and specialized neurodiagnostic studies. management is based principally on vigorous support, particularly of ventilation and perfusion, maintenance of adequate glucose influx, and control of seizures. Intraventricular hemorrhage is the most common type of neonatal intracranial hemorrhage. The neuropathology is characterized by bleeding from capillaries of the subependymal germinal matrix. Secondary rupture of the ependymal lining then causes intraventricular hemorrhage. Pathogenesis relates to the anatomy of the germinal matrix, the distribution and regulation of cerebral blood flow, and the structure and vulnerability of periventricular capillaries. Precise diagnosis requires a brain imaging procedure; portable, real-time ultrasound is the preferred approach for critically ill infants. Prognosis relates to the severity of the hemorrhage as well as any preceding hypoxic-ischemic insults and the subsequent occurrence of hydrocephalus. Choice of therapy for posthemorrhagic ventricular dilatation depends upon severity and rapidity of progression and ranges from close observation only to ventriculoperitoneal shunting.

Brain Ischemia↗
PubMed1982

Selective reduction of blood flow to white matter during hypotension in newborn dogs: a possible mechanism of periventricular leukomalacia.

The cerebrovascular response of newborn animals to hypotension has not been defined on a regional basis. Using an autoradiographic technique employing 14C-iodoantipyrine as indicator, we studied the cerebral physiological responses of newborn dogs to hypotension induced by exsanguination or by administration of Escherichia coli endotoxin. Regional cerebral blood flow (rCBF) to all gray matter structures was preserved, even at mean arterial pressures as low as 20 mm Hg. In contrast, rCBF to periventricular and occipital white matter decreased significantly during severe hypotension. The selective hypoperfusion of cerebral white matter during severe hypotension may provide a mechanistic explanation for the pathogenesis of periventricular leukomalacia.

Animals↗
PubMed1984

Acquired perinatal leukoencephalopathy.

Between 36 and 44 weeks after conception, telencephalic white matter in the newborn appears to be particularly vulnerable to insults that result in morphological disturbances. Available evidence indicates that this disorder (or group of disorders), named acquired perinatal leukoencephalopathy, reflects a decrease in blood flow through the distal vessels supplying paraventricular white matter and/or a metabolic disturbance produced by, or in response to, an infectious agent. Major advances in our understanding of the causes, mechanisms, and sequelae of acquired perinatal leukoencephalopathy may be made in the next decade because of improvement in brain imaging techniques, improved survival of high-risk babies, and relatively routine follow-up of these high-risk babies.

Brain↗
PubMed1990

Stroke in pediatric acquired immunodeficiency syndrome.

In a 4 1/2-year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.

Acquired Immunodeficiency Syndrome↗
PubMed1975

Diffuse reticulosis with leukomalacia.

A malignant lymphoproliferative disease with acute clinical course and selective clinical CNS involvement is described. The metastatic lesions in the brain are compared with a primary microglioma of the brain.

Blood Vessels↗
PubMed1986

Vitamin E and selenium participation in fatty acid desaturation. A proposal for an enzymatic function of these nutrients.

A critical review of the literature on the effects of vitamin E and selenium deficiences on unsaturated fatty acid metabolism reveals that some of these effects are inconsistent with the antioxidant hypothesis of these nutrients as their only biological function. On the basis of these data it is proposed that vitamin E and selenium play a role in the desaturation of n-3 and n-6 polyunsaturated fatty acids by participating in the microsomal electron transport chain and in a proposed peroxidase moiety of the desaturase complex, respectively. A re-interpretation of the experimental literature in terms of the proposed hypothesis is provided, with some suggestions to test its main tenets.

Animals↗
PubMed1988

Clinicopathological study of germinal matrix hemorrhage, pontosubicular necrosis, and periventricular leukomalacia in stillborn.

The occurrence of germinal matrix hemorrhage (GMH), pontosubicular necrosis (PSN), and periventricular leukomalacia (PVL) was evaluated in 58 stillborn, among whom 23 (40%) showed one or more lesions. A comparative study of neuropathological findings and obstetrical histories in stillborn beyond 26 weeks of gestation showed a greater frequency of damage when the pregnancies had been complicated. The pathogenesis of PSN is disputed. As PSN was found in stillborn (13 cases), hyperoxia is not an essential pathogenetic factor. PSN may represent a form of anoxic encephalopathy. However, PSN was found as an isolated lesion in an infant of a diabetic mother and in most cases of intrauterine growth retardation; hypoglycemia may therefore be involved in the pathogenesis. Ultrasound examinations of living neonates have indicated the prenatal occurrence of GMH in some cases, and our study opens the possibility that there is intrauterine involvement of PVL and PSN as well. Consequently, cerebral lesions diagnosed in newborn may have occurred in utero.

Encephalomalacia↗