A competing risk model of sudden infant death syndrome incidence in two US birth cohorts

2001 ◽  
Vol 138 (5) ◽  
pp. 661-667 ◽  
Author(s):  
Harold A. Pollack ◽  
John G. Frohna
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Risk Model ◽  
Sudden Infant Death ◽  
Competing Risk ◽  
Sudden Infant ◽  
Birth Cohorts ◽  
Competing Risk Model

Evolution and significance of the triple risk model in sudden infant death syndrome

2016 ◽  
Vol 53 (2) ◽  
pp. 112-115 ◽  
Author(s):  
Jade Spinelli ◽  
Lyndsey Collins-Praino ◽  
Corinna Van Den Heuvel ◽  
Roger W Byard
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Risk Model ◽  
Sudden Infant Death ◽  
Sudden Infant

Neuropathological Developments in Sudden Infant Death Syndrome

2018 ◽  
Vol 21 (6) ◽  
pp. 515-521 ◽  
Author(s):  
Fiona M Bright ◽  
Robert Vink ◽  
Roger W Byard
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Risk Model ◽  
Sudden Infant Death ◽  
Reproducible Research ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Integrated Network ◽  
Neurokinin 1 ◽  
Medullary Nuclei

A wide variety of neuropathological abnormalities have been investigated in infants who have died of sudden infant death syndrome (SIDS). Issues which detracted from early studies included failure to use uniform definitions of SIDS and lack of appropriately matched control populations. Development of the triple risk model focused attention on the concept of an inherent susceptibility to unexpected death in certain infants, with research demonstrating a role for the neurotransmitter serotonin within the brainstem. However, it now appears that neuropathological abnormalities in SIDS infants are more complex than a simple serotonergic deficiency in certain medullary nuclei but instead could involve failure of an integrated network of neurochemical transmitters in a variety of subcortical locations. The following overview examines recent research developments looking particularly at the potential role of the peptide neurotransmitter substance P and its neurokinin-1 receptor in multiple nuclei within the brainstem, asymmetry and microdysgenesis of the hippocampus, and decreased orexin levels within dorsomedial, perifornical, and lateral levels in the hypothalamus. Whether such research will lead to identifiable biomarker for infants at risk of SIDS is yet to be established. Use of standardized and consistent methods of classifying and categorizing infant deaths will be pivotal in generating reproducible research results.

scholarly journals Is Shock a Key Element in the Pathology of Sudden Infant Death Syndrome (SIDS)?

2008 ◽  
Vol 11 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Jane Blood-Siegfried ◽  
Margaret T. Bowers ◽  
Marcia Lorimer
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Risk Model ◽  
Critical Time ◽  
Sudden Infant Death ◽  
Developed Countries ◽  
Autonomic Response ◽  
Sudden Infant ◽  
Cardiorespiratory Control ◽  
Sleeping Position

In developed countries, sudden infant death syndrome (SIDS) is the most common cause of death for infants between 1 month and 1 year of age. The etiology of SIDS is likely to be multifactorial, and current paradigms often describe three overlapping elements of risk. Those elements are a critical developmental period, a vulnerable infant, and one or more exogenous stressors. In the triple-risk model, SIDS infants are described as having an underlying vulnerability in cardiorespiratory control in the central nervous system during a critical period when autonomic control is developing. This vulnerability might affect the response to exogenous stressors, including prone sleeping position, hypoxia, and increased carbon dioxide. In the common bacterial hypothesis and fatal triangle, the focus is on the stressors. In the first, a combination of common respiratory infections can cause SIDS in an infant during a developmentally vulnerable period. This theory also includes 3 factors of vulnerability: a genetic predisposition, a vulnerable developmental age, and infectious stressors. In the fatal triangle theory, infection, inflammation, and genetics each play a role in triggering a SIDS fatality. From our work in an animal model, we have found that rat pups die from a combination of infectious insults during a critical time of development. This is exacerbated by perinatal nicotine exposure, a condition shown to alter the autonomic response in exposed offspring. We are proposing that shock and cardiovascular collapse is a key element that links these theories.

Sudden Infant Death Syndrome: Police Can Make a Difference

1998 ◽  
Author(s):  
Linda Esposito ◽  
Larry Minda ◽  
Claire Forman
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant
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