Pathogenesis and Prevention of Pontosubicular Necrosis

Abstract

Perinatal pontosubicular neuron necrosis (PSN) has similar characteristics to apoptosis, such as karyorrhexis, cellular atrophy and little glial reaction. In PSN pathogenesis, the developmental discrepancy between neurons exhibiting late maturation and vessels showing an early increase in the basis pontis and subiculum may predispose fetuses and neonates to PSN. Ischemia, hyperoxygenemia, hypocarbia and hypoglycemia have been reported to be causal factors. Apoptotic neurons are associated with activation of caspase-3, and remaining neurons are accompanied by growth factors in glial cells. Nestin, which is abundant in multipotential stem cells, is reactivated in cells surrounding the subacute and chronic lesions. Thus, local plasticity may be activated both in necrotic and apoptotic cell death, and the period of regeneration is important for the treatment of PSN.