Maturation-dependent vulnerability of perinatal white matter in premature birth

Maturation-dependent vulnerability of perinatal white matter in premature birth
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DOI:
10.1161/01.str.0000254729.27386.05
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发表时间:
2007-02-01
期刊:
影响因子:
8.3
通讯作者:
McClure, Melissa M.
McClure, Melissa M.
中科院分区:
医学1区
文献类型:
--
作者:
Back, Stephen A.;Riddle, Art;McClure, Melissa M.

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早产的幸存者有围产期脑损伤的倾向,特别是脑室周围的脑白色物质。脑室周围白色物质损伤(PWMI)是早产儿脑损伤的最常见原因,也是慢性神经系统疾病的主要原因。慢性PWMI的范围包括局灶性囊性坏死病变(脑室周围白质软化)和弥漫性髓鞘形成障碍。最近的神经影像学研究支持脑室周围白质软化的发病率正在下降,而局灶性或弥漫性非囊性损伤正在成为主要的病变。在相当数量的婴儿中,PWMI似乎是由脑血流的扰动引起的,这反映了血管系统的解剖和生理不成熟。缺血性脑白色物质易受明显的自由基介导的损伤,特别是针对少突胶质细胞谱系的未成熟阶段。新出现的实验数据支持心室周围白色物质明显缺血是必要的,但不足以产生导致PWMI的初始损伤。PWMI在早产期间发生的发育偏好似乎与易感少突胶质祖细胞的出现时间和区域分布有关。少突胶质祖细胞的损伤可能通过破坏髓鞘形成少突胶质细胞的成熟而导致PWMI的发病。最近在PWMI的细胞和分子发病机制的理解方面取得了实质性进展。少突胶质细胞祖细胞是减少早产儿缺血性脑白色物质损伤的预防策略的关键目标。(中风。2007;38[第2部分]:724-730。
Survivors of premature birth have a predilection for perinatal brain injury, especially to periventricular cerebral white matter. Periventricular white matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia) and diffuse myelination disturbances. Recent neuroimaging studies support that the incidence of periventricular leukomalacia is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary but not sufficient to generate the initial injury that leads to PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. There has been substantial recent progress in the understanding of the cellular and molecular pathogenesis of PWMI. The oligodendrocyte progenitor is a key target for preventive strategies to reduce ischemic cerebral white matter injury in premature infants. (Stroke. 2007;38[part 2]:724-730.)