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婴儿猝死综合征:病因学的最新进展与新观点

Sudden infant death syndrome: an update and new perspectives of etiology.

作者信息

Rubens Daniel, Sarnat Harvey B

机构信息

Department of Anesthesia, University of Washington, Seattle Children's Hospital, Seattle, WA, USA.

出版信息

Handb Clin Neurol. 2013;112:867-74. doi: 10.1016/B978-0-444-52910-7.00008-8.

Abstract

Sudden infant death syndrome (SIDS) is a condition in which an infant, usually in the early postnatal period and nearly always before 6 months of age, dies during sleep for unexplained reasons and the standard autopsy fails to disclose an etiology. Various physiological explanations of risk factors include the prone sleeping position, overheating by excessive bundling, viral upper respiratory tract infections, parental smoking at home, and birthing injury resulting in an insult to the inner ear and central chemoreceptor zone, an immaturity that involves CO2 chemoreceptors that regulate respiratory control. Neuropathological studies and theories implicate: (1) hypoplasia or defective transmitter function in the medullary arcuate nucleus, a derivative of the rhombencephalic lip of His; (2) synaptic or receptor immaturity of the nucleus of the fasciculus solitarius, the "pneumotaxic center"; and (3) functional impairment of the serotonergic raphé nuclei of the pontine and medullary ventral median septum and other serotonergic neurons of the brainstem. Additional neurological risk factors for SIDS include perinatal neuromuscular diseases, infantile epilepsies or status epilepticus, and genetic metabolic encephalopathies.

摘要

婴儿猝死综合征(SIDS)是指婴儿通常在出生后早期,几乎总是在6个月龄之前,于睡眠中因不明原因死亡,且标准尸检未能揭示病因的一种情况。对风险因素的各种生理学解释包括俯卧睡眠姿势、过度包裹导致过热、病毒性上呼吸道感染、父母在家吸烟以及分娩损伤导致内耳和中枢化学感受器区域受损,这是一种涉及调节呼吸控制的二氧化碳化学感受器的不成熟状态。神经病理学研究和理论涉及:(1)延髓弓状核发育不全或递质功能缺陷,该核是His菱脑唇的衍生物;(2)孤束核(“呼吸调整中枢”)的突触或受体不成熟;(3)脑桥和延髓腹侧正中隔的5-羟色胺能中缝核以及脑干其他5-羟色胺能神经元的功能损害。SIDS的其他神经学风险因素包括围产期神经肌肉疾病、婴儿癫痫或癫痫持续状态以及遗传代谢性脑病。

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