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Book contents

26 - Brainstem Neuropathology in Sudden Infant Death Syndrome

Published online by Cambridge University Press:  20 July 2018

Fiona M Bright
Affiliation:
School of Medicine, the University of Adelaide, Adelaide, Australia
Robert Vink
Affiliation:
Sansom Institute for Health Research, University of South Australia, Adelaide, Australia
Roger W Byard
Affiliation:
School of Medicine, The University of Adelaide, Adelaide, Australia and Florey Institute of Neuroscience and Mental Health, Victoria, Australia
Jodhie R. Duncan
Affiliation:
University of Melbourne
Roger W. Byard
Affiliation:
University of Adelaide
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Summary

Introduction

Sudden infant death syndrome (SIDS) has a complex and heterogeneous pathogenesis, with multiple abnormalities in a number of physiological functions and systems including neurological, cardiovascular, respiratory, gastrointestinal, nutritional, endocrine, metabolic, infectious, immunological, environmental, and genetic (1-7). Typically, without warning, an apparently healthy infant is found deceased sometime after being placed to sleep (8). there are many theories involving animal and human studies that have attempted to understand the pathophysiology of SIDS. Unfortunately, to date, there are no biomarkers available to aid in the prevention or definitive diagnosis of SIDS. the aim of much scientific research has been to determine the mechanisms of failure in SIDS infants that are undetectable prior to death and that remain just as unclear following death. While the precise cause of death in infants dying of SIDS has not been identified, there is considerable evidence that the syndrome results from a combination of circumstances involving [1] a cardiorespiratory challenge that occurs in [2] a neurologically compromised infant at [3] a specific period of postnatal development (3, 9, 10). The following chapter will focus on the failure of cardiorespiratory and autonomic control associated with neuropathology of the brainstem in SIDS.

An important step in understanding the complex pathophysiology of SIDS was the establishment of the Triple Risk Model, which successfully conceptualized the epidemiological, physiological, and neuropathological data associated with SIDS. the Triple Risk Model proposes three coinciding factors: [1] an underlying vulnerability of the infant; [2] a critical developmental period in homeostatic control that the infant is transitioning through; and [3] the application of an exogenous stressor/s such as an asphyxiating environment (11). the model implies that an infant may be most at risk of SIDS when all three factors are simultaneously present (8, 11). All three factors contribute to the risk of an adverse event that occurs suddenly in an otherwise “healthy” infant. therefore, consideration of the Triple Risk Model is of key importance to SIDS research, with the model providing a foundation upon which researchers can build in the generation of research hypotheses.

Type
Chapter
Information
SIDS Sudden Infant and Early Childhood Death
The past, the present and the future
, pp. 589 - 614
Publisher: The University of Adelaide Press
Print publication year: 2018

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