Specific Imaging Findings. The findings in Hypoxic Ischemic Encephalopathy (HIE) are variable and depend on brain maturity, severity and duration of insult, and timing of imaging studies. In moderate-to-severe HIE at term, the central gray matter is the most frequently affected with lesions in the lentiform nuclei and thalami, typically adjacent to the posterior limb of the internal capsule (PLIC). Cortical abnormalities are characteristically found in the perirolandic area. These lesions are T1 hypointense and T2 hyperintense in the acute phase (first 2 days), becoming T1 hyperintense after 3–5 days. An early sign is the loss PLIC on conventional MR sequences. The most reliable sign of HIE, which also remains for a long time, is the reversal of normal PLIC T1 hyperintensity compared to the adjacent lentiform nucleus and thalamus. In severe and prolonged HIE at term, there is diffuse brain swelling and edema, usually sparing the basal ganglia, brainstem, and cerebellum. The lesions rapidly evolve by cavitation, developing into multicystic encephalopathy. In mild HIE, typical MRI features are characterized by parasagittal lesions involving vascular boundary zones (watershed injury pattern). Diffusion imaging shows corresponding bright DWI signal and reduced apparent diffusion coefficient (ADC) values in the first 24 h. These abnormalities peak at 3–5 days and pseudonormalize by about the end of the first week. MR spectroscopy demonstrates lactate peak in the affected regions. A glutamine-glutamate (Glx) peak may also be elevated.
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