Developmental neuropathology and impact of perinatal brain damage. III: gray matter lesions of the neocortex.

摘要: The evolving neuropathology of primarily undamaged cortical regions adjacent to the injured site has been studied in 36 infants who survived a variety perinatally acquired encephalopathies (microgyrias, ulegyrias, multicystic encephalopathies, porencephalies, and hydranencephalies) later died unrelated causes. Their survival times range from hours, days, weeks, or months, several years. Ten these children developed epilepsy, 2 cerebral palsy, were neurologically mentally impaired. In all cases studied, cortex survives, retains its intrinsic vasculature, is capable continuing differentiation. However, postinjury development characterized by progressive alterations compatible with dysplasia that affects structural functional differentiation neurons, synaptic profiles, fiber distribution, glial elements, vasculature. profiles many neurons are transformed an increased number loci replace extrinsic ones vacated destruction afferent fibers. fibers layer I some Cajal-Retzius cells survive even severe lesions may be interconnecting have lost other type connections. Some undergo hypertrophy, acquire new morphologic features, achieve large size (meganeurons). Probably, meganeurons their hypertrophy partial endomitotic DNA and/or RNA reduplication (polyploidy). These not static but ongoing processes continue affect still developing eventually influence neurologic cognitive maturation affected children. This study proposes that, reorganization consequences (acquired dysplasia), rather than original lesion, represent main underlying mechanism pathogenesis ensuing neurological sequelae, such as, dyslexia, impairment, poor school performance.