Brain Injury in the Preterm Infant: New Horizons for Pathogenesis and Prevention.
Brain Injury in the Preterm Infant: New Horizons for Pathogenesis and Prevention.
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DOI：
10.1016/j.pediatrneurol.2015.04.006
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发表时间：
2015-09
影响因子：
3.8
通讯作者：
Back SA
中科院分区：
文献类型：
--
作者：
Back SA
早产儿存活下来时，会出现较轻微的运动和认知障碍，这似乎与以大脑灰质和白质为目标的细胞成熟过程中的广泛紊乱有关。虽然早产儿的大脑在以前是破坏性病变的高风险，但早产儿幸存者现在通常表现出较轻的损伤，这与异常的再生和修复反应有关，导致大脑生长减少。脑白质生长受损与髓鞘形成障碍有关，髓鞘形成障碍是由髓鞘形成前少突胶质细胞（preOLs）的急性死亡引发的，但随后是preOLs的快速再生，无法正常成熟为髓鞘细胞。尽管未成熟神经元比成熟神经元更能抵抗细胞死亡，但它们在树突乔木和突触的成熟过程中表现出广泛的紊乱，这进一步导致大脑生长受损。因此，更轻微的脑损伤涉及到修复机制的中断，其中神经元和前ols在神经回路发育的关键窗口期未能完全成熟。这些最近认识到的不同形式的脑灰质和白质发育异常提出了新的诊断挑战，并提出了新的治疗策略来促进大脑的生长和修复。
Preterm neonates are surviving with a milder spectrum of motor and cognitive disabilities that appear to be related to widespread disturbances in cell maturation that target cerebral gray and white matter. Whereas the preterm brain was previously at high risk for destructive lesions, preterm survivors now commonly display less severe injury that is associated with aberrant regeneration and repair responses that result in reduced cerebral growth. Impaired cerebral white matter growth is related to myelination disturbances that are initiated by acute death of pre-myelinating oligodendrocytes (preOLs), but are followed by rapid regeneration of preOLs that fail to normally mature to myelinating cells. Although immature neurons are more resistant to cell death than mature neurons, they display widespread disturbances in maturation of their dendritic arbors and synapses, which further contributes to impaired cerebral growth. Thus, even more mild cerebral injury involves disrupted repair mechanisms in which neurons and preOLs fail to fully mature during a critical window in development of neural circuitry. These recently recognized distinct forms of cerebral gray and white matter dysmaturation raise new diagnostic challenges and suggest new therapeutic strategies to promote brain growth and repair.