In neonatal HIE, energy depletion in neurons and glial cells causes decreased re-uptake of glutamate which leads to increased extracellular glutamate. The distribution of the lesions in the putamen, thalamus, and peri-Rolandic cerebral cortex is related to intrinsic vulnerability of these areas to energy failure. One potentially important link among these areas is their interconnection by excitatory circuits ⁽¹¹⁾. Thus, overactivity in these excitatory pathways could contribute to spreading of the lesions via synapses. The corticospinal tract and corpus callosum may be involved in these pathways.

DWI and ADC maps often depict acute or subacute ischemic lesions in the corpus callosum, internal capsule and white matter when conventional MRI and CT are normal or only show subtle abnormalities (Figure 4) ⁽¹²⁾. MRS may be more sensitive to the presence of HIE than DWI by showing elevated lactate and glutamate/glutamine peaks, and decreased NAA peak^(13,14).

Figure 4. A 6-day-old boy with HIE due to perinatal asphyxia

A. On T2WI, the gray-white matter delineation is partially unclear. The corpus callosum appears high signal intensity.

B, C. DWI shows diffuse hyperintensity with decreased ADC in the corpus callosum, internal capsule, thalamus and white matter. This distribution is presumably related to overactivity of excitatory pathways.