Filiano J J, Kinney H C
Department of Neurology, Children's Hospital, Boston, Mass.
Biol Neonate. 1994;65(3-4):194-7. doi: 10.1159/000244052.
Neuropathologic studies in SIDS victims support the concept that they are not entirely 'normal' prior to death, but rather possess underlying vulnerabilities which put them at risk for sudden death. This concept forms a key link in a triple-risk model for the pathogenesis of SIDS proposed by us. According to this model, sudden death in SIDS results from the intersection of three overlapping factors: (1) a vulnerable infant; (2) a critical developmental period in homeostatic control, and (3) an exogenous stressor(s). An infant will die of SIDS only if he/she possesses all three factors; the infant's vulnerability lies latent until he/she enters the critical period and is subject to an exogenous stressor. According to this model, heterogeneous disorders may make the infant vulnerable to sudden death during the critical period, as potentially exemplified by two previously reported lesions in SIDS brains (arcuate nucleus hypoplasia and subtle hypomyelination). Nevertheless, the triple-risk model does not preclude the possibility that the majority of SIDS deaths will be explained by a single common pathway upon which multiple stressors impinge to produce sudden death during the critical period.
对婴儿猝死综合征(SIDS)受害者的神经病理学研究支持这样一种观点,即他们在死亡前并非完全“正常”,而是存在潜在的易损性,这使他们面临猝死风险。这一观点是我们提出的SIDS发病机制三重风险模型中的关键环节。根据该模型,SIDS中的猝死是由三个重叠因素的交集导致的:(1)易损婴儿;(2)内稳态控制的关键发育阶段;(3)一个或多个外源性应激源。只有当婴儿具备所有这三个因素时才会死于SIDS;婴儿的易损性处于潜伏状态,直到他/她进入关键阶段并受到外源性应激源的影响。根据该模型,异质性疾病可能会使婴儿在关键阶段易发生猝死,此前在SIDS大脑中报道的两种病变(弓状核发育不全和轻微髓鞘形成不足)可能就是例证。然而,三重风险模型并不排除这样一种可能性,即大多数SIDS死亡将由单一共同途径来解释,在关键阶段,多种应激源作用于该途径导致猝死。