Nakamura Y, Okudera T, Hashimoto T
Department of Pathology, St. Mary's Hospital, Kurume-shi, Japan.
J Neuropathol Exp Neurol. 1994 Nov;53(6):582-9. doi: 10.1097/00005072-199411000-00005.
Arterial and venous structures in the deep white matter of the developing brain were examined by postmortem angiography. About the anterior horn, body and trigon of the lateral ventricle, ventriculopetal arteries reached the deep white matter and branched out to form an abundant network of small arterioles (hypervascular zone) particularly in premature brain, thus indicating the tentative border zone between ventriculofugal and petal arteries not to be hypovascular. A deep draining group of medullary veins converged at different zones in the deep white matter, becoming large to form a large converging zone, and finally drained into a subependymal vein. A fan-shaped draining area of the converging group of veins corresponded well to the area of periventricular leukomalacia (PVL) with the edema and hemorrhage. About the occipital horn and inferior horn of the lateral ventricle, transcerebral veins were abundant and PVL was rarely seen. The pathogenesis of PVL could not be fully explained by border zone infarct. An alternative pathogenesis of PVL is considered the following: 1) circulatory disturbance of the deep draining group of veins occurs, 2) edema with or without venous hemorrhage follows, 3) edema fluid and hemorrhage compress abundant arterioles in the deep white matter with 4) consequent coagulation necrosis.
通过尸检血管造影术对发育中大脑深部白质的动脉和静脉结构进行了检查。在侧脑室的前角、体部和三角区附近,向心性动脉到达深部白质并分支形成丰富的小动脉网络(高血管区),尤其是在早产儿脑中,这表明离心性动脉和向心性动脉之间的暂定边界区并非低血管区。一组深部引流髓静脉在深部白质的不同区域汇聚,逐渐变粗形成一个大的汇聚区,最终引流至室管膜下静脉。静脉汇聚组的扇形引流区域与伴有水肿和出血的脑室周围白质软化(PVL)区域高度对应。在侧脑室枕角和下角附近,经脑静脉丰富,很少见到PVL。PVL的发病机制不能完全用边界区梗死来解释。PVL的另一种发病机制如下:1)深部引流髓静脉组发生循环障碍,2)随后出现伴有或不伴有静脉出血的水肿,3)水肿液和出血压迫深部白质中丰富的小动脉,4)继而发生凝固性坏死。