Neuroradiology

Hypoxia, perinatal

When the hypoxic insult occurs late in the third trimester or in the perinatal or neonatal period of a full-term infant, the lesions are typically located in the grey matter, both deep grey matter nuclei and cortex, as well as the subcortical white matter. Acutely, these lesions may be difficult to see on MR, particularly on T2-weighted images. Chronically, on long TR images, there is often hyperintensity due to gliosis and/or cyst formation within the grey matter structures, most commonly involving the putamen and thalami. Acute cortical laminar necrosis may result in hypointensity of the cortical ribbon on long TR images, although contrast enhancement may be the most obvious finding on MR. When hypoxia is severe or prolonged in full-term neonates or infants (Fig.1), there may be a dramatic loss of supratentorial brain tissue resulting in cystic encephalomalacia of the cerebral hemispheres but relative preservation of cerebellum, brain stem and diencephalic structures. Cystic encephalomalacia can be seen on imaging studies as multiseptated fluid collections replacing brain parenchyma. In addition to these ischaemic lesions, haemorrhagic lesions, particularly in the basal ganglia, commonly occur in full-term infants with hypoxic ischaemic encephalopathy (HIE).

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Fig.1

a, b. Axial CT without contrast, 2 hours after respiratory arrest following extraction of bronchial foreign body; no significant changes are yet noted. c, d. MR, T2-weighted images, performed immediately after CT; hyperintensity of the basal ganglia and cortex, indicating intracellular accumulation of fluid due to anoxia. Initial hyperintensity of the white matter. e, f. Axial CT 24 hours later. Marked diffuse hypointensity of both cortex and white matter. The posterior fossa structures are relatively spared.
Hypoxia, perinatal, Fig.1 (a)
Hypoxia, perinatal, Fig.1 (b)
Hypoxia, perinatal, Fig.1 (c)
Hypoxia, perinatal, Fig.1 (d)
Hypoxia, perinatal, Fig.1 (e)
Hypoxia, perinatal, Fig.1 (f)