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Biomedical subjects

M Dambska

Publications and source records attributed to M Dambska.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

[Neuropathological analysis of 8 cases of clinically diagnosed Reye syndrome].

Authors discuss the possible etiopathogenesis of Reye syndrome (RS) on the base of eight own cases presented in this paper and others previously described. The febrile infection was observed on the beginning of the disease in all actually analysed cases and was followed by symptoms of acute damage of liver and brain. The central nervous system lesions present the changes increasing with time from brain oedema to the necrosis of nerve tissue. The oedematous changes could be recognized as a principal cause of unconsciousness and even of coma in RS. When the etiology of RS remain unknown the clinico-pathological observations of such cases incline to formulate three questions: Is an genetically conditioned background necessary which facilitate toxic or infectious factors to induce the RS? Is the etiology of RS only genetically conditioned? Is an specific viral infection the cause of RS?

Brain↗
PubMedDate not supplied

Anomalies of cerebral structures in acranial neonates.

Eleven cases of newborns with acrania and macroscopically diagnosed anencephaly were neuropathologically examined. They presented changes in which 1 group corresponded to the diagnosis of aprosencephaly. In the second group, the development of prosencephalic structures was more advanced. The pathomechanism of the observed anomalies was analyzed in relation to data provided by molecular-genetic classification of nervous system malformations, but that did not exclude the influence of eventual extrinsic factors.

Abnormalities, Multiple↗
PubMedDate not supplied

Brainstem lesions in the course of chronic fetal asphyxia.

We present a neuropathological study of brainstem involvement during the neonatal period, under the influence of prolonged fetal asphyxia. The investigation was performed on 20 brains of premature and mature newborns, who died in the course of chronic asphyxia. Ischemic cell change, neuronal loss and gliosis were present in the brainstem of all infants. Two topographic patterns of brainstem lesions in chronic anoxic encephalopathy were distinguishable in the newborns. The neurons of the cranial nerve nuclei were more severely damaged in the group of premature newborns. More severe lesions of the reticular formation were found in the group of mature newborns. The topography of brainstem damage seems to be dependent on the maturity of CNS structures at the time of injury.

Brain Diseases↗