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We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months. |
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basal ganglia,lesion of
basal ganglia,lesion,bilateral
cardiac arrest
cardiac arrest and resuscitation
CAT scan,false negative
cerebral cortex
coma
cortical infarction
encephalopathy
encephalopathy,anoxic
encephalopathy,post anoxic
gray matter
hypotension,systemic
hypoxic encephalopathy
laminar necrosis,cortical
MRI
MRI,abnormal
myoclonus
striatum,lesion of
striatum,lesion of,bilateral
white matter disease
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