Leviton Alan, Gressens Pierre
Department of Neurology, Children's Hospital Boston, Boston, MA, USA.
Trends Neurosci. 2007 Sep;30(9):473-8. doi: 10.1016/j.tins.2007.05.009. Epub 2007 Aug 31.
Extremely low-gestational-age newborns have a prominently increased risk of brain dysfunctions attributed to white-matter damage, which is thought to result from the vulnerability of the oligodendrocyte. This white-matter damage now appears to be accompanied by cerebral-cortex and deep-gray-matter abnormalities, including excess apoptosis without replacement and the impairment of surviving neurons and resulting interference with synaptogenesis and connectivity. Recent advances in corticogenesis suggest that neurons migrate from the germinative zones through the white matter to the cortex when the white matter is most vulnerable and perhaps is being injured. Advances in developmental neuroscience also suggest that the excitotoxic and inflammatory processes that probably contribute to white-matter damage are also able to damage developing neurons. Together, these advances support the untested hypothesis that white-matter damage in the preterm newborn is accompanied by the death of neurons as they migrate through the dangerous minefield of white matter undergoing injury.
极低孕周新生儿因白质损伤而出现脑功能障碍的风险显著增加，白质损伤被认为是由少突胶质细胞的脆弱性所致。现在看来，这种白质损伤还伴有大脑皮质和深部灰质异常，包括过度凋亡且无替代、存活神经元受损以及由此对突触发生和连接的干扰。皮质发生学的最新进展表明，当白质最脆弱且可能正在受到损伤时，神经元从生发区穿过白质迁移至皮质。发育神经科学的进展还表明，可能导致白质损伤的兴奋性毒性和炎症过程也能够损伤发育中的神经元。这些进展共同支持了一个未经证实的假说，即早产新生儿的白质损伤伴随着神经元在穿过正在遭受损伤的危险白质“雷区”时的死亡。
