Joseph Junewick, MD FACR
over 7 years ago
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Hypoxic ischemic injury
Heather Borders, MD
|Diagnostic Category: Vascular
|Created: over 5 years ago
|Updated: over 5 years ago
3 day old Term infant status post body cooling for history of placental abruption and hypoxic ischemic injury.
Severe hypoxic ischemic injury
Axial T1 weighted images demonstrate increased signal in the ventrolateral thalami and putamina. Diffusion weighted images demonstrate restricted diffusion in the ventrolateral thalami, putamina, hippocampi and paracentral region.
Severe asphyxial events in term neonates result in a primarily central pattern of injury involving the deep gray matter (putamina, ventrolateral thalami, hippocampi, dorsal brainstem, and lateral geniculate nuclei) and occasionally the perirolandic cortex. These areas of the brain are actively myelinating or contain the highest concentrations of NMDA receptors at term and are, therefore, the most susceptible to neonatal HII.
Diffusion-weighted images will demonstrate increased signal intensity in the region of the ventrolateral thalami and basal ganglia (particularly the posterior putamina), in the perirolandic regions, and along the corticospinal tracts.
Conventional T1- and T2-weighted MR images of injured areas may demonstrate hyperintensity on both T1- and T2-weighted images. Signal intensity changes can also be seen in the dorsal brainstem and hippocampi.
Suggested possible causes of T1 shortening include hemorrhage, calcification, lipid release from myelin breakdown, and even the paramagnetic effects of free radicals.
When bilateral basal ganglia lesions are seen in a neonate, the primary differential diagnostic considerations are underlying inborn errors of metabolism—especially mitochondrial disorders.
Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood Benjamin Y. Huang, MD, MPH and Mauricio Castillo, MD March 2008 RadioGraphics, 28, 417-439.