Kotlarek F, Sturm K W, Zeumer H, Brüll D
Klin Padiatr. 1982 Sep-Oct;194(5):335-42. doi: 10.1055/s-2008-1033834.
200 premature and mature neonates with clinical evidence of hypoxia or traumatic encephalopathy were examined by cranial computerized tomography (CT) during the first two weeks postnatally. The findings were compared with those in a "control group" consisting of 14 neonates with extraneural malformations. Cerebral hemorrhages were easily identified by their high density, in CT images. Bilateral areas of lowered density within the periventricular white matter, however, could not always be attributed to irreversible tissue damage prior to about 14 days after the hypoxic event in term newborns, and in preterm infants even later. During this early period of life an apparent decrease of periventricular density was regularly observed that must not be mistaken for a pathological change. In two cases persistent periventricular areas of decreased density were caused by neuropathologically verified foci of incomplete leucomalacia.
200例有缺氧或创伤性脑病临床证据的早产和足月新生儿在出生后两周内接受了头颅计算机断层扫描(CT)检查。将这些结果与由14例患有神经外畸形的新生儿组成的“对照组”的结果进行比较。脑出血在CT图像中因其高密度而易于识别。然而,对于足月儿,在缺氧事件发生后约14天之前,以及对于早产儿甚至更晚的时候,脑室周围白质内双侧密度降低区域并不总是可归因于不可逆的组织损伤。在生命的这个早期阶段,经常观察到脑室周围密度明显降低,这绝不能被误认为是病理变化。在两例病例中,持续的脑室周围密度降低区域是由神经病理学证实的不完全性脑白质软化灶引起的。