SPECIFIC CHANGES IN HUMAN BRAIN FOLLOWING REPERFUSION AFTER CARDIAC-ARREST

被引:103
作者
FUJIOKA, M
OKUCHI, K
SAKAKI, T
HIRAMATSU, KI
MIYAMOTO, S
IWASAKI, S
机构
[1] NARA MED UNIV,DEPT NEUROSURG,KASHIHARA,NARA,JAPAN
[2] NARA MED UNIV,DEPT EMERGENCY & CRIT CARE MED,KASHIHARA,NARA,JAPAN
[3] NARA MED UNIV,DEPT RADIOL,KASHIHARA,NARA,JAPAN
关键词
CEREBRAL ISCHEMIA; TRANSIENT; HEART ARREST; HEMORRHAGE; MAGNETIC RESONANCE IMAGING; REPERFUSION;
D O I
10.1161/01.STR.25.10.2091
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose Very few reports are available on serial changes in human brain after cardiac arrest. The primary objective of this study is to investigate sequential neuroradiological changes in patients remaining in a persistent vegetative state following resuscitation after cardiac arrest. Methods We repeatedly studied eight vegetative patients resuscitated from unexpected out-of-hospital cardiac arrest using computed tomographic (CT) scanning and high-held magnetic resonance (MR) imaging at 1.5 T. Results In seven of the eight patients, CT scans obtained between days 2 and 6 featured symmetrical low-density lesions in the bilateral caudate, lenticular, and/or thalamic nuclei. These ischemic lesions were persistently of low density on serial CT scans. In these seven patients, MR images demonstrated what were thought to be hemoglobin degradation products derived from minor hemorrhages localized in the bilateral basal ganglia, thalami, and/or substantia nigra. Diffuse brain edema in the acute stage and diffuse brain atrophy in the chronic stage were consistent neuroradiological findings. No abnormal enhanced lesions were demonstrated by CT scans. Conclusions The most characteristic findings on high-field MR images were symmetrical lesions in the bilateral basal ganglia, thalami, and/or substantia nigra with specific changes suggestive of minor hemorrhages that were not evident on CT scans. We speculate that these minor hemorrhages result from diapedesis of red blood cells in these regions during the reperfusion period through the endothelium disrupted by ischemia-reperfusion insult.
引用
收藏
页码:2091 / 2095
页数:5
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