[Leukomalacia and subsequent brain status in relation to intensive neonatal care].
Leucomalacia or white matter necrosis is one of the major aspects of neonatal encephalopathies, especially in the premature baby. These necroses are found mainly in the deep periventricular white matter of the "semi-oval centre". Characteristically, they are ischaemic and their anatomical and histological progress is rapid: coagulation necrosis with rapid axonal fragmentation followed by polymorphic cellular reaction with glial cells and macrophages. Regeneration in the minor forms consists of glyosis process in severe forms; multiple cavities appear in a few weeks. Physiopathogenic hypotheses put forward are related to: 1 -- the very anatomic aite: special tissue and terminal arteries, 2 -- onset of myelinization process, 3 -- associated clinical and biological lesions such as hypoxia, acidosis and hypotention. These lesions are symptom-free during the neonatal period. One of us suggested in 1962 that these could be the anatomical basis of spastic monoplegia or diplegia (LITTLE's disease). All motor cerebral sequelae have disappeared since 10 years. This is particularly significant mainly in the case of spastic diplegia of the former premature baby under 2500 g. This decrease coincides with improvement in neonatal care, especially correction of hypoxia, acidosis and cardiovascular collapse. These findings seem to support the pathogenic hypotheses.
[Leukomalacia and subsequent brain status in relation to intensive neonatal care]. Leucomalacia or white matter necrosis is one of the major aspects of neonatal encephalopathies, especially in the premature baby. These necroses are found mainly in the deep periventricular white matter of the "semi-oval centre". Characteristically, they are ischaemic and their anatomical and histological progress is rapid: coagulation necrosis with rapid axonal fragmentation followed by polymorphic cellular reaction with glial cells and macrophages. Regeneration in the minor forms consists of glyosis process in severe forms; multiple cavities appear in a few weeks. Physiopathogenic hypotheses put forward are related to: 1 -- the very anatomic aite: special tissue and terminal arteries, 2 -- onset of myelinization process, 3 -- associated clinical and biological lesions such as hypoxia, acidosis and hypotention. These lesions are symptom-free during the neonatal period. One of us suggested in 1962 that these could be the anatomical basis of spastic monoplegia or diplegia (LITTLE's disease). All motor cerebral sequelae have disappeared since 10 years. This is particularly significant mainly in the case of spastic diplegia of the former premature baby under 2500 g. This decrease coincides with improvement in neonatal care, especially correction of hypoxia, acidosis and cardiovascular collapse. These findings seem to support the pathogenic hypotheses.