Vascular, axonal and glial pathogenesis of periventricular leukomalacia in fetuses and neonates
Vascular, axonal and glial pathogenesis of periventricular leukomalacia in fetuses and neonates
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DOI：
10.1159/000054266
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发表时间：
2002-01-01
期刊：
影响因子：
--
通讯作者：
Itoh, M.
中科院分区：
文献类型：
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作者：
Takashima, S.;Hirayama, A.;Itoh, M.
早产儿脑室周围白质软化症（PVL）是脑性瘫痪和智力障碍的重要原因。在PVL的发病机制中，深白色物质中发育中的血管和分化中的胶质祖细胞都对缺血敏感，并且作为诱发因素非常重要。作为PVL的第一个体征出现的轴突肿胀见于胎儿和新生儿，继发于宫内感染的细胞活化也可能易患PVL。病因包括围产期脑灌注不足，这导致轴突损伤、谷氨酸释放、小胶质细胞中细胞因子和星形胶质细胞中神经生长因子的产生增加，以及最终神经元和少突胶质细胞的可塑性增加。PVL后细胞反应性如巢蛋白表达可能是确定治疗和康复有效时间的重要指标。版权所有（C）2002 S. Karger AG，巴塞尔。
Periventricular leukomalacia (PVL) in prematurely born infants is an important cause of cerebral palsy and intellectual impairment. In the pathogenesis of PVL, both the developing vasculature and differentiating glial progenitor cells within the deep white matter are susceptible to ischemia and very important as predisposing factors. Axonal swellings, which occur as the first signs of PVL, are found in fetuses as well as neonates, and cellular activation secondary to intrauterine infection may also predispose to PVL. Causal factors include cerebral hypoperfusion in the perinatal period, which leads to axonal damage, glutamate release, elevated production of cytokines in microglia and nerve growth factor in astrocytes, and finally an increased plasticity in neurons and oligodendrocytes. Cellular reactivities such as nestin expression following PVL may represent important indicators for determining the effective time for treatment and rehabilitation. Copyright (C) 2002 S. Karger AG, Basel.