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回顾过去 30 年我们对脑血管发育和围生期脑损伤发病机制的认识。

A history of our understanding of cerebral vascular development and pathogenesis of perinatal brain damage over the past 30 years.

机构信息

Yanagawa Institute for Developmental Disabilities, International University of Health and Welfare, Fukuoka, Japan.

出版信息

Semin Pediatr Neurol. 2009 Dec;16(4):226-36. doi: 10.1016/j.spen.2009.09.004.

DOI:10.1016/j.spen.2009.09.004
PMID:19945657
Abstract

This article reviews our studies focusing on cerebral vascular development, the pathogenesis of subependymal/intraventricular hemorrhage (SEH/IVH), periventricular leukomalacia (PVL), and pontosubicular neuron necrosis (PSN). Their pathogenesis consists of predisposing developmental and causal factors. SEH/IVH may be caused by reperfusion or overperfusion following ischemia in the subependymal germinal matrix with characteristic vasculature. The cause of PVL is multifactorial (ie, ischemia and inflammation), predisposed by the maturational status of the vasculature and oligodendroglia in the white matter. Focal PVL is ischemic necrosis, and diffuse PVL or white matter injury may include cytotoxic damage. PSN has an apoptotic character, and may be induced by ischemic and oxidative stress on specific immature neurons. Further studies on preventive and therapeutic measures are necessary in clinical, pathologic, and experimental fields. The monitoring and control methods of brain hemodynamics and cellular stability should be more developed to prevent brain damages.

摘要

这篇文章回顾了我们在脑血管发育、室管膜下/脑室内出血(SEH/IVH)、脑室周围白质软化(PVL)和浦肯野细胞神经元坏死(PSN)发病机制方面的研究。其发病机制包括易患的发育和因果因素。SEH/IVH 可能是由于脑室内下生发基质缺血后再灌注或过度灌注引起的,具有特征性的血管。PVL 的病因是多因素的(即缺血和炎症),易患因素包括血管和白质少突胶质细胞的成熟状态。局灶性 PVL 是缺血性坏死,弥漫性 PVL 或白质损伤可能包括细胞毒性损伤。PSN 具有凋亡特征,可能是由于特定未成熟神经元的缺血和氧化应激引起的。在临床、病理和实验领域有必要进一步研究预防和治疗措施。应该进一步开发脑血流动力学和细胞稳定性的监测和控制方法,以预防脑损伤。

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