Perinatal human hypoxia-ischemia vulnerability correlates with brain calcification

Deregulation of intracellular calcium homeostasis is widely considered as o ne of the underlying pathophysiological mechanisms of hypoxic-ischemic brai n injury. Whether this alteration can result in cerebral calcification was investigated in basal ganglia, cerebral cortex, and hippocampus of human pr emature and term neonates together with glial reaction, in all samples nona rteriosclerotic calcifications were observed, their number and size were ar ea-specific and increased in term neonates. Basal ganglia always presented the highest degree of calcification and hippocampus the lowest, located mai nly in the CA1 subfield. In all cases, neuronal damage was associated with astroglial reaction and calcium precipitates, with microglial reaction only in basal ganglia and cerebral cortex, and argues for the participation of excitatory amino acid receptors in hypoxia-ischemia damage. These data corr elate with hypoxia-ischemia vulnerability in the perinatal period. The clin ical relevance of these precipitates and the neuroprotective interest of no n-NMDA receptor manipulation are discussed in the light of our results. (C) 2001 Academic Press.