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DOI: 10.1148/rg.26si065504
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RadioGraphics 2006;26:S159-S172
© RSNA, 2006

Neonatal Hypoxic-Ischemic Encephalopathy: Multimodality Imaging Findings1

Christine P. Chao, MD, Christopher G. Zaleski, MD and Alice C. Patton, MD

1 From the Department of Radiology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224 (C.P.C.); Department of Radiology, Nemours Children’s Clinic, Jacksonville, Fla (C.G.Z.); and Department of Radiology, Mayo Clinic, Rochester, Minn (A.C.P.). Presented as an education exhibit at the 2005 RSNA Annual Meeting. Received February 1, 2006; revision requested March 9 and received May 15; accepted May 24. All authors have no financial relationships to disclose. Address correspondence to A.C.P. (e-mail: patton.alice{at}mayo.edu).

Diffuse hypoxic-ischemic brain injury in the neonate results in neonatal hypoxic-ischemic encephalopathy (HIE). Because of differences in brain maturity at time of insult, severity of hypotension, and duration of insult, there are four distinct patterns of brain injury. Cranial ultra-sonography and computed tomography reveal periventricular leukomalacia, germinal matrix hemorrhage, and hydrocephalus. Magnetic resonance imaging is the most sensitive modality for evaluating the patterns of brain injury. In preterm neonates, mild hypotension causes periventricular injury; severe hypotension results in infarction of the deep gray matter, brainstem, and cerebellum. In term neonates, mild hypotension causes parasagittal cortical and subcortical injury; severe hypotension causes characteristic injury of the lateral thalami, posterior putamina, hippocampi, corticospinal tracts, and sensorimotor cortex. Prompt recognition of these imaging findings can help exclude other causes of encephalopathy, affect prognosis, and facilitate earlier (although mostly supportive) treatment.

© RSNA, 2006







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