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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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