Diagnosis and outcome of subcortical cystic leucomalacia.
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Three children who had suffered prolonged hypotension or severe asphyxia and who subsequently developed cystic subcortical leucomalacia are reported. This condition fits into the spectrum of perinatal ischaemic brain disease but the diagnosis in life has not previously been reported. Aetiological factors and neurodevelopmental outcome, which was poor in all cases, are discussed. (+info)
Blood thiamin concentrations in bovine polioencephalomalacia.
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Thiamin concentrations were determined by the thiochrome method in blood from 16 cattle with polioencephalomalacia (PEM) or other apparent central nervous disorders. The mean blood total thiamin concentration of the five cattle with PEM (20.5 +/- 5.1 microg/100 ml blood) was not significantly different from concentrations in the cattle with the other disorders, despite evidence of a thiamin diphosphate deficiency reported in cattle with PEM. (+info)
Morphologic variations in periventricular leukomalacia.
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Periventricular leukomalacia (PVL) usually is manifested as discrete foci of coagulation necrosis of the deep periventricular white matter in the human neonatal brain. During the examination of the brains of 116 infants utilizing an oil red O technic on gelatin-embedded frozen sections, 25 cases of PVL were found with typical foci of coagultion necrosis. Three morphologic varieties of the lesion could be demonstrated. In the first type, rather than being restricted to the periventricular zone, the discrete necrotic foci extended throughout the entire zone of cerebral white matter, even out to just beneath the cortex. The subcortical lesions appeared of short duration, whereas older lesions were always present nearer the ventricle. The second type of lesion presented as linear, some-what serpentine zones of coagulation necrosis radiating into the cerebral white matter. A third type of lesion consisted of a variegated irregular coagulation necrosis which was poorly delineated from more normal tissue. Diffuse pallor of the white matter, the nature of which is still not clear, was associted with the more severe lesions. Although the pathogenesis of PVL is unknown, it is suggested that these new varieties of PVL beyond the discrete periventricular foci of necrosis would be more apt to result in a diffuse loss of white matter and hence mental retardation if the child should survive. (+info)
Polioencephalomalacia associated with canine distemper virus infection.
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Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus. (+info)
Polioencephalomalacia in the dog.
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Disturbance of cerebral blood flow from causes such as meningitis, thromboembolic disease and atherosclerosis was considered an important factor in the pathogenesis of polioencephalomalacia in 25 dogs. In dogs with polioencephalomalacia of undetermined cause, the distribution of lesions in neocortex and paleocortex suggested a change of neuronal metabolism secondary to cerebral anoxia/ischemia. Five dogs with canine distemper infection had bilateral necrosis of the hippocampus and pyriform cortex. Convulsions, central visual impairment and hemiparesis were the most prominent neurologic signs. (+info)
Polioencephalomalacia in white-tailed deer (Odocoileus virginianus) in Saskatchewan.
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Polioencephalomalacia similar to that in domestic ruminants was diagnosed in two wild white-tailed deer (Odocoileus virginianus) with abnormal behaviour in Saskatchewan. (+info)
Subacute necrotizing encephalomyelopathy. Its relationship to central pontine myelinolysis.
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Clinical and neuropathological features of a case of subacute necrotizing encephalomyelopathy are discussed and compared with the features of central pontine myelinolysis. A hypothesis is offered relating the two diseases to a common aetiological factor. (+info)
Thiamin and niacin in the rumen.
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Thiamin analogs, produced in the rumen by thiaminase I, in the presence of a cosubstrate appear to be responsible for the central nervous system disorder, polioencephalomalacia (PEM). For PEM to occur, an analog must be produced that inhibits an essential thiamin-requiring reaction, and results from a cosubstrate present in the rumen. In high concentrate diets, thiaminase I is produced by rumen microbes. However, PEM can also be caused by thiaminase I of plant origin. Based on physical characteristics and cosubstrate specificity, the thiaminase I enzymes produced by Bacillus thiaminolyticus and Clostridium sporogenes appear to be different from the enzyme produced by the rumen. Because niacin and certain antihelmentics are thiaminase I cosubstrates, they should be used cautiously. Supplementary niacin increased microbial protein synthesis in vitro and in vivo, and was more effective with urea than soybean meal. Supplementary niacin (5 to 6 g X cow-1 X d-1) increased milk production in postpartum cows but not in those in mid-lactation, and in cows fed soybean meal but not in those fed urea. We believe the heating of soybean meal during commercial processing decreased the availability of niacin for rumen protozoa. Supplementary niacin for postpartum cows increased blood glucose, decreased blood ketones and reduced the incidence of ketosis. Niacin flow to the small intestine and its absorption from the small intestine increased with niacin supplementation. Supplemental niacin prevented the postpartum decrease in red blood cell niacin observed in control cows. (+info)