Sudden Unexpected Death in Infancy: Biological Mechanisms

Galland, Barbara; Elder, Dawn

doi:10.1016/j.prrv.2014.09.003

Cited by 12 publications

(9 citation statements)

References 67 publications

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“…Au cours des premiers mois, il peut donc exister un défaut d'ajustement autonomique responsable d'une réponse retardée ou inefficace à la bradycardie qui peut devenir symptomatique et dangereuse [4,5]. Cette dysautonomie peut être favorisée par des facteurs environnementaux [6,7].…”

Section: éTiologieunclassified

“…Cette entité regroupe les morts subites du nourrisson (MSN) qui sont des morts inattendues restant inexpliquées après une investigation approfondie (autopsie, analyse des circonstances de la mort et de l'histoire clinique antérieure [13]), mais aussi les morts expliquées par une pathologie aiguë et brutale, un accident, un traumatisme ou un empoisonnement [6]. Les nuances de ces définitions révèlent les enjeux actuels de la prise en charge des MIN : améliorer le nombre d'investigations postmortem et rendre disponibles des statistiques de mortalité fiables pour en comprendre et suivre les différentes causes.…”

Section: Définitionsunclassified

“…L'hypothèse du « triple modèle » développée par Kinney et Thach [16] stipule que trois facteurs concourent à la MIN : un âge critique ; des facteurs déclenchants comme l'exposition à des pathologies intercurrentes ou des facteurs environnementaux, cible des campagnes de prévention ; des facteurs de vulnérabilité qui donnent lieu actuellement à des travaux de recherche dans différents domaines, en particulier cardiaque, neurologique, métabolique, biochimique et génétique [6,17].…”

Section: Physiopathologieunclassified

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Malaise et mort inattendue du nourrisson : deux entités différentes

Naud

2015

Archives de Pédiatrie

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Section: éTiologieunclassified

Section: Définitionsunclassified

Section: Physiopathologieunclassified

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Malaise et mort inattendue du nourrisson : deux entités différentes

Naud

2015

Archives de Pédiatrie

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“…Failed autoresuscitation : animal studies have shown that cardiorespiratory, sleep, and arousal mechanisms are abnormal following exposure to risk factors associated with SIDS or in infants who later succumb to SIDS (11, 12). Although the exact cause of SIDS is unknown, immaturity of brain stem autonomic cardiorespiratory/thermoregulatory control and failure of autoresuscitation during sleep are significant determinants of survival (11, 12).…”

Section: Introductionmentioning

confidence: 99%

Microbiome–Gut–Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS—A Novel Hypothesis

Vijayakumar

Praveen

2017

Front. Pediatr.

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Sudden infant death syndrome (SIDS) continues to be a major public health issue. Following its major decline since the “Back to Sleep” campaign, the incidence of SIDS has plateaued, with an annual incidence of about 1,500 SIDS-related deaths in the United States and thousands more throughout the world. The etiology of SIDS, the major cause of postneonatal mortality in the western world, is still poorly understood. Although sleeping in prone position is a major risk factor, SIDS continues to occur even in the supine sleeping position. The triple-risk model of Filiano and Kinney emphasizes the interaction between a susceptible infant during a critical developmental period and stressor/s in the pathogenesis of SIDS. Recent evidence ranges from dysregulated autonomic control to findings of altered neurochemistry, especially the serotonergic system that plays an important role in brainstem cardiorespiratory/thermoregulatory centers. Brainstem serotonin (5-HT) and tryptophan hydroxylase-2 (TPH-2) levels have been shown to be lower in SIDS, supporting the evidence that defects in the medullary serotonergic system play a significant role in SIDS. Pathogenic bacteria and their enterotoxins have been associated with SIDS, although no direct evidence has been established. We present a new hypothesis that the infant’s gut microbiome, and/or its metabolites, by its direct effects on the gut enterochromaffin cells, stimulates the afferent gut vagal endings by releasing serotonin (paracrine effect), optimizing autoresuscitation by modulating brainstem 5-HT levels through the microbiome–gut–brain axis, thus playing a significant role in SIDS during the critical period of gut flora development and vulnerability to SIDS. The shared similarities between various risk factors for SIDS and their relationship with the infant gut microbiome support our hypothesis. Comprehensive gut-microbiome studies are required to test our hypothesis.

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“…The paper by Galland and Elder reviews biological mechanisms in this triple-risk framework [6]. Machaalani and Waters look specifically at brainstem abnormalities as a possible cause for the vulnerability, and/or failure to respond to an external stressor [7].…”

mentioning

confidence: 99%

SIDS symposium – A perspective for future research

Waters¹

2014

Paediatric Respiratory Reviews

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Sudden Unexpected Death in Infancy: Biological Mechanisms

Cited by 12 publications

References 67 publications

Malaise et mort inattendue du nourrisson : deux entités différentes

Malaise et mort inattendue du nourrisson : deux entités différentes

Microbiome–Gut–Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS—A Novel Hypothesis

SIDS symposium – A perspective for future research

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