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围产期缺氧缺血性脑病的新概念

New concepts in perinatal hypoxia ischemia encephalopathy.

作者信息

Scafidi Joseph, Gallo Vittorio

机构信息

Department of Neurology, Children's National Medical Center, 111 Michigan Avenue, NW, Washington, DC 20010, USA.

出版信息

Curr Neurol Neurosci Rep. 2008 Mar;8(2):130-8. doi: 10.1007/s11910-008-0021-2.

DOI:10.1007/s11910-008-0021-2
PMID:18460281
Abstract

This article summarizes recent insights into perinatal hypoxic-ischemic brain injury in the neonate. Before effective treatments can be offered, diagnosis, timing, and an understanding of the pathogenesis are imperative. The analysis of appropriate animal models is also summarized in this review. These models have provided interesting evidence that after hypoxia ischemia, progenitor cells in the postnatal brain are stimulated to generate new neurons and oligodendrocytes. The role of these newly generated cells is unclear, and mechanisms of migration and survival are currently being elucidated. A discussion of more recent imaging techniques, such as diffusion tensor imaging, is provided. This allows for improved understanding of the microstructural organization of white matter and how this is altered by hypoxic-ischemic injury. Neuroprotection with hypothermia is now occurring in full-term neonates that meet clinical criteria; however, specific therapies such as inhibition of non-N-methyl-D-aspartate receptors may offer improved outcomes by targeting specific pathways and populations of cells.

摘要

本文总结了近期对新生儿围产期缺氧缺血性脑损伤的见解。在提供有效治疗之前,诊断、时机把握以及对发病机制的了解至关重要。本综述还总结了对合适动物模型的分析。这些模型提供了有趣的证据,表明缺氧缺血后,出生后脑内的祖细胞会被刺激产生新的神经元和少突胶质细胞。这些新生成细胞的作用尚不清楚,目前正在阐明其迁移和存活机制。本文还讨论了诸如扩散张量成像等更新的成像技术。这有助于更好地理解白质的微观结构组织以及缺氧缺血性损伤如何改变这种组织。符合临床标准的足月儿目前正在接受低温神经保护治疗;然而,诸如抑制非N - 甲基 - D - 天冬氨酸受体等特定疗法可能通过针对特定途径和细胞群体提供更好的治疗效果。

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Perinatal hypoxic/ischemic brain injury induces persistent production of striatal neurons from subventricular zone progenitors.围产期缺氧/缺血性脑损伤诱导脑室下区祖细胞持续产生纹状体神经元。
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