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In all patients, consecutive CT scans showed symmetrical, persistent low-density lesions with transient enhancement in the caudate and lenticular nuclei and transient enhancement in the cerebral cortex 7 to 14 days after onset. Serial MR im ages consistently revealed symmetrical lesions of persistent hyperintensity and hypointensity on T1- and T2-weighted images, respectively, in the caudate and lenticular nuclei, cerebral cortex, substantia nigra, and/or hippocampus from 8 days to 12 months after onset. Repeated MR images revealed specific lesions in the bilateral basal ganglia, cerebral cortex, substantia nigra, and hippocampus, which suggests the particular vulnerability of these areas to hypoglycemia in the human brain. We speculate th at the localized lesions represent tissue degeneration, including some combination of selective neuronal death, proliferation of astrocytic glial cells, paramagnetic substance deposition, and/or lipid accumulation. The absence of localized hemorrhages on MR images in hypoglycemic encephalopathy is in marked contrast to the presence of regional minor hemorrhages in postischemic-anoxic encephalopathy. |
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basal ganglia
basal ganglia,lesion of
CAT scan
CAT scan,abnormal
caudate nucleus
caudate nucleus,lesion of
coma
hippocampus
hypoglycemia
hypoglycemic coma
lenticular nucleus,lesion of
MRI
MRI,abnormal
MRI,CAT scan compared to
MRI,high signal intensity of basal ganglia
MRI,serial
persistent vegetative state
prognosis
striatum,lesion of
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