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婴儿猝死综合征的脑干研究

Brainstem research in sudden infant death syndrome.

作者信息

Kinney H C, Filiano J J

机构信息

Department of Neuroscience, Children's Hospital, Boston, Mass.

出版信息

Pediatrician. 1988;15(4):240-50.

PMID:3068663
Abstract

One of the leading hypotheses in SIDS research is that SIDS is due to a subtle defect in brainstem neural circuits which control respiration and/or cardiac stability during sleep. We review the rationale for the brainstem hypothesis and possible mechanisms of sleep-related sudden death. We also summarize the neuropathological studies in SIDS in the context of the neuroanatomy and neurochemistry of cardiorespiration and arousal. Quantitative abnormalities in brainstem reactive astrocytes (scar cells), dendritic spines, and neurotransmitter levels, and number of small myelinated vagal fibers have been reported in SIDS. The cause of these abnormalities is not known, nor is their relationship to each other or sudden death clear. Their complete elucidation, however, is perhaps the most compelling reason for continued SIDS brainstem research, since such abnormalities could be the critical clues necessary for solving SIDS.

摘要

婴儿猝死综合征(SIDS)研究中一个主要的假说认为,SIDS是由于脑干神经回路存在细微缺陷,这些神经回路在睡眠期间控制呼吸和/或心脏稳定性。我们回顾了脑干假说的基本原理以及与睡眠相关的猝死的可能机制。我们还在心肺呼吸和觉醒的神经解剖学及神经化学背景下总结了SIDS的神经病理学研究。已有报告称,SIDS患者脑干反应性星形胶质细胞(瘢痕细胞)、树突棘、神经递质水平以及小的有髓迷走神经纤维数量存在定量异常。这些异常的原因尚不清楚,它们彼此之间的关系以及与猝死的关系也不明确。然而,对它们的全面阐释可能是继续进行SIDS脑干研究的最令人信服的理由,因为这些异常可能是解决SIDS问题所需的关键线索。

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