Iron accumulation in the basal ganglia following severe ischemic-anoxic insults in children.

Increased iron deposition is described in four children following severe ischemic-anoxic insult and subsequent resuscitation. All cases demonstrated on T2-weighted magnetic resonance images areas of hypointensity in the basal ganglia, thalami, and white matter that were attributed to iron deposition. Associated areas of hyperintensity were also seen in the periventricular and subcortical white matter, and these were attributed to gliosis. In one case calcium deposition was also present within the areas of hypointensity. These findings suggest that after anoxic-ischemic damage, normal axonal transportation of brain iron can no longer occur. This may lead to increased accumulation of iron centrally at the sites of iron uptake in the basal ganglia and in the white matter. Additional iron deposition may occur more rapidly due to direct injury by lipid peroxidation degradation products catalyzed by iron.