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Medline Plus Health Information
*Brain Diseases
*Hypoglycemia

(Stroke. 1997;28:584-587.)
© 1997 American Heart Association, Inc.


Articles

Specific Changes in Human Brain After Hypoglycemic Injury

Masayuki Fujioka, MD; Kazuo Okuchi, MD; Ken-Ichiro Hiramatsu, MD; Toshisuke Sakaki, MD; Syouji Sakaguchi, MD; Yoshinobu Ishii, MD

From the Departments of Neurosurgery (M.F., K.O., K.-I.H., T.S.) and Radiology (S.S.), Nara Medical University, and Department of Medicine, Keioh Hospital (Y.I.), Nara, Japan.

Correspondence to Masayuki Fujioka, MD, Department of Neurosurgery, Emergency and Critical Care Medical Center, Nara Prefectural Nara Hospital, 1-30-1, Hiramatsu-cho, Nara, 631, Japan. E-mail RXL00203{at}niftyserve.or.jp

Background and Purpose Very few reports are available on serial changes in the human brain after severe hypoglycemic injury. The aim of this study was to investigate sequential neuroradiological changes in brains of patients after hypoglycemic coma compared with those after cardiac arrest previously studied with the same methods.

Methods We repeatedly studied CT scans and MR images obtained at 1.5 T in four vegetative patients after profound hypoglycemia associated with diabetes mellitus.

Results 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 images 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.

Conclusions 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 that 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.


Key Words: brain injuries • diabetes mellitus • heart arrest • hypoglycemia • magnetic resonance imaging




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