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- W2404760485 abstract "We described a patient with delayed cerebral demyelination following a post-operatively hypoxic encephalopathy. A 65-year-old man, with a history of exposure to the atomic bomb at Hiroshima in 1945, suffered from hypoxia, hypotension and respiratory acidosis and became unresponsive 10 hours after a laminectomy for lumbar disc herniation, in December 1993. Following an emergent resuscitation, the patient had gradually recovered and could walk 2 weeks later. Three weeks after the insult, however, the patient developed an apallic state with frontal lobe signs. Except an increased level of myelin basic protein in the CSF, there were no other abnormal laboratory findings. Brain CTs showed a leukoaraiosis. MRI one month post-operation, demonstrated extensive high signal intensity areas in the cerebral white matter on T2-weighted image, and a gadolinium-enhanced spotty lesion in the right globus pallidus on T1-weighted image. Three months after the operation, the high signal intensity on T2-weighted image became more intensive and extensive, while the enhanced spotty lesion in the globus pallidus disappeared. The corpus callosum and cerebellar white matter were spared throughout the observation. The SPECT using 123I-IMP showed a hypoperfusion in the frontal lobe at 1 month. Three months later, the hypoperfusion areas extended to the whole cerebral and cerebellar cortices, relatively less affected in the motor area and basal ganglia. The patient had improved slightly over the next few months. We speculate that subclinical vulnerability in the white matter secondary to exposure to the atomic bomb, in addition to the incomplete prolonged hypoxia, hypotension and acidosis, caused selective cerebral demyelination in this patient." @default.
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- W2404760485 date "1995-01-01" @default.
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- W2404760485 title "[Sequential neuroimaging in a patient with delayed post-hypoxic leukoencephalopathy]." @default.
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