DIAGNOSIS:
Hypoxic-Ischemic Encephalopathy
The T2W images (Figs. 1, 2) show diffuse, bilaterally symmetrical increased signal in the cerebral cortex and cerebellar folia, as well as the basal ganglia and thalami. The diffusion-weighted images (Figs. 3, 4) show corresponding diffusion restriction in both cerebral and cerebellar hemispheres, basal ganglia and thalami, consistent with cytotoxic edema. The spectroscopy images (Figs. 6, 7) show inverted doublet of lactate at 1.33 ppm with decreased NAA and Cr
These findings are highly suggestive of hypoxic-ischemic encephalopathy.
1) Hypoxic ischemic encephalopathy (HIE) is due to global injury to the brain secondary to perfusion / oxygenation disturbances.
2) Common causes – hypotension, cardiac arrest, neonatal asphyxia, strangulation, smothering, aspiration, drowning, CO inhalation.
3) Patterns of HIE:
a) Cortical border zone infarcts.
b) Deep white matter infarcts (penetrating artery watershed zone).
c) Cortical pseudolaminar necrosis.
d) Predominantly deep gray nuclei.
4) MR spectroscopy
- Has a role in e arly evaluation of white matter injury- increase in lactate and decreased NAA before standard imaging sequences become abnormal.
- Elevated lactate is seen in the first few hours after ischemic injury. If present after 24 hours, lactate is good indicator of permanent brain injury.
- Decrease in NAA, Cr, Cho, myoinositol, NAA/cho.
- Increase in glutamine & glutamate.
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PubMed References for Hypoxic-Ischemic Encephalopathy
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