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围产期缺氧缺血对早产儿脑干的损害。

Impairment of perinatal hypoxia-ischemia to the preterm brainstem.

机构信息

Children's Hospital, Shanghai Medical University, Shanghai, China.

出版信息

J Neurol Sci. 2009 Dec 15;287(1-2):172-7. doi: 10.1016/j.jns.2009.07.029. Epub 2009 Sep 6.

Abstract

Hypoxia-ischemia is a major perinatal problem that results in severe damage to the newborn brain. This study assessed functional integrity of the brainstem at term in preterm infants after perinatal hypoxia-ischemia to shed light on the influence of hypoxia-ischemia on the preterm brainstem. We recruited sixty-eight preterm infants after perinatal hypoxia-ischemia, ranging in gestation 28-35 weeks. Brainstem evoked response was studied at term age (37-42 weeks postconceptional age) with 91-910/s clicks using the maximum length sequence technique. Compared with healthy preterm infants, the preterm infants after perinatal hypoxia-ischemia showed a significant increase in I-V interval at very high rates 455 and 910/s of clicks (P<0.05, 0.05). III-V interval and III-V/I-III interval ratio also increased significantly at 455 and 910/s (P<0.05-0.01). The slope of III-V interval-rate function was significantly steeper than in the healthy preterm infants (P<0.05). Compared with normal term controls, the preterm infants after hypoxia-ischemia showed similar, but slightly more significant, abnormalities. The differences between the preterm infants after hypoxia-ischemia and the healthy preterm and term infants generally increased with increasing click rate. These results demonstrated that central components of brainstem auditory evoked response were abnormal at very high click rates in the preterm infants after perinatal hypoxia-ischemia. Click rate-dependent change in the more central part of the brainstem is also abnormal. Apparently, functional integrity of the brainstem, mainly in the more central part, is impaired. Hypoxic-ischemic damage to the preterm brainstem is unlikely to completely recover within a relatively short period after the insult, which is of clinical importance.

摘要

缺氧缺血是围生期的一个主要问题,可导致新生儿大脑严重受损。本研究旨在评估围生期缺氧缺血后早产儿足月时脑干的功能完整性,以阐明缺氧缺血对早产儿脑干的影响。我们招募了 68 名围生期缺氧缺血后的早产儿,胎龄 28-35 周。使用最大长度序列技术,在足月时(孕后 37-42 周)用 91-910/s 点击进行脑干诱发电位研究。与健康早产儿相比,围生期缺氧缺血后的早产儿在非常高的点击率 455 和 910/s 时,I-V 间期明显增加(P<0.05,0.05)。3-V 间期和 3-V/I-3 间期比在 455 和 910/s 时也显著增加(P<0.05-0.01)。3-V 间期-率函数的斜率明显比健康早产儿陡峭(P<0.05)。与正常足月对照组相比,缺氧缺血后的早产儿表现出相似但略为显著的异常。缺氧缺血后的早产儿与健康早产儿和足月婴儿之间的差异通常随着点击率的增加而增加。这些结果表明,围生期缺氧缺血后早产儿在非常高的点击率时,脑干听觉诱发电位的中枢成分异常。脑干更中心部分的点击率依赖性变化也是异常的。显然,脑干的功能完整性,主要是更中心部分,受损。在损伤后相对较短的时间内,缺氧缺血对早产儿脑干的损伤不太可能完全恢复,这具有临床重要意义。

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