Harper Ronald M, Kinney Hannah C
Department of Neurobiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Curr Pediatr Rev. 2010 Feb 1;6(1):39-47. doi: 10.2174/157339610791317214.
Current evidence suggests that multiple neural mechanisms contribute to the fatal lethal event in SIDS. The processes may develop from a range of otherwise seemingly-innocuous circumstances, such as unintended external airway obstruction or accidental extreme flexion of the head of an already-compromised structure of the infant upper airway. The fatal event may occur in a sleep state which can suppress muscle tone essential to restore airway patency or exert muscle action to overcome a profound loss of blood pressure. Neural processes that could overcome those transient events with reflexive compensation appear to be impaired in SIDS infants. The evidence ranges from subtle physiological signs that appear very early in life, to autopsy findings of altered neurotransmitter, including serotonergic, systems that have extensive roles in breathing, cardiovascular regulation, and thermal control. Determination of the fundamental basis of SIDS is critical to provide biologic plausibility to SIDS risk reduction messages and to develop specific prevention strategies.
目前的证据表明，多种神经机制导致了婴儿猝死综合征（SIDS）中的致命事件。这些过程可能源于一系列看似无害的情况，例如意外的外部气道阻塞，或者婴儿上呼吸道结构本已受损时头部的意外过度弯曲。致命事件可能发生在睡眠状态，这种状态会抑制恢复气道通畅或施加肌肉作用以克服严重血压下降所必需的肌肉张力。在SIDS婴儿中，那些本可通过反射性补偿克服这些短暂事件的神经过程似乎受到了损害。证据涵盖了从生命早期就出现的细微生理迹象，到神经递质改变的尸检结果，包括在呼吸、心血管调节和体温控制中具有广泛作用的血清素能系统。确定SIDS的根本原因对于为降低SIDS风险的信息提供生物学合理性以及制定具体的预防策略至关重要。
