Cerebral hypoxic-ischemic damage in the newborn: Cellular mechanisms and excitatory amino-acids involvement.

Brain damage from hypoxia-ischemia plays a major role in neonatal mortality and morbidity. Different lesional mechanisms have been proposed. The most recent hypothesis involves the excitatory amino acids, especially glutamate. In this review, arguments in favour of a glutamate involvement in the lesional process are presented, with particular attention to the consequences of glutamate fixation on post synaptic receptors, especially N-methyl-D-aspartate receptors. Alterations of the intracellular concentration of calcium may also play a role in the pathogenesis of hypoxic-ischemic lesions. A better understanding of the metabolic processes could lead to new therapeutic possibilities.