Summary: It has been well known for a number of years that placing a baby to sleep on their stomachs increases the risk of SIDS. Researchers report a developmental abnormality more prevalent in premature and male babies, may contribute to SIDS risk, in conjunction to the sleep position.
Source: University of Adelaide.
International research involving the University of Adelaide has uncovered a developmental abnormality in babies – especially in premature babies and in boys – that for the first time has been directly linked to cases of sudden infant death syndrome (SIDS).
Researchers believe this abnormality, in the brain’s control of head and neck movement, breathing, heartbeat and the body’s responses to deprivation of oxygen supply, could be the reason why some babies sleeping on their front are more at risk of SIDS.
The research was conducted by Dr Fiona Bright and Professor Roger Byard, Adelaide Medical School, University of Adelaide, in collaboration with Professor Hannah Kinney’s lab at Harvard Medical School and Boston Children’s Hospital.
The results of the study, which investigated 55 SIDS cases in the United States, are now published in the journal PLOS ONE.
“One of the reasons why SIDS is so devastating for families is that death often occurs with no warning and no obvious signs of illness,” says Dr Fiona Bright, Research Associate in the Adelaide Medical School, University of Adelaide, who conducted her work at Harvard and Adelaide as part of her PhD studies.
“While the exact cause of death in SIDS has not been identified, multiple studies have pointed to a subset of SIDS babies that are not entirely ‘normal’ before death. These infants all seem to have some form of underlying vulnerability, exposing them to increased risk.
“Our studies have now discovered a significant abnormality within key regions of the brainstem in SIDS babies, specifically in parts of the brainstem that control breathing and movements of the head and neck. This abnormality is directly linked to SIDS cases,” she says.
The abnormality is in the transmission in the brain of a neuro-peptide, known as “substance P”, and its binding with an associated neuroreceptor, “neurokinin-1” (NK1R). Until now, worldwide investigations of the role of substance P in SIDS have been inconsistent and inconclusive.
“Substance P and the NK1R neuroreceptor play a critical role in the brain’s control of the respiratory system, the cardiovascular system, and in how the body responds to hypoxia – that is, deprivation of oxygen at the cell level,” Dr Bright says.
“An infant with this abnormality is likely to have impaired respiratory and motor responses to life-threatening challenges during sleep. While they may be otherwise healthy looking, there is an inability for that child’s brain and body to respond appropriately to an event in which the child is deprived of oxygen in some way.”
Study supervisor Professor Roger Byard, Professor of Pathology at the University of Adelaide, says this abnormality is a key reason why it is more dangerous for babies to sleep on their front.
“We’ve known for many years that babies sleeping face down places them at greater risk of SIDS – now we have a much better understanding as to why,” Professor Byard says.
“If a child has this underlying vulnerability in its brain chemistry, and its breathing becomes compromised by sleeping on its front, that child is at greater risk of death because its body simply can’t respond in the normal way. The baby can’t lift its head, and its breathing and heartbeat will be compromised,” he says.
The study has shown that the abnormality in substance P is significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants.
“This demonstrated deficiency in substance P highlights that the problem in SIDS infants is much more complex than was once thought, and most likely involves the interactions of a number of chemicals, including serotonin,” Dr Bright says.
“Ultimately, we hope that future research could lead to the development of screening techniques or biomarkers to identify infants who may be at risk of SIDS,” she says.
This research was funded under a Fellowship established by the River’s Gift SIDS charity. River’s Gift was founded in 2011 by two devastated parents who were searching for answers around the sudden death of their healthy four-month-old son, River. River’s Gift has now evolved into a global movement, with fundraisers and supporters worldwide.
“The main objective of River’s Gift is to fund world-leading SIDS research, to make a major contribution to the discovery of a cure for this heart-breaking loss of life,” says River’s Gift General Manager Karl Waddell.
“We are excited about these latest research findings, which show tangible evidence as to the underlying cause of SIDS in a number of cases. We hope this research will eventually assist in the quest to stamp out SIDS,” he says.
Funding: River’s Gift SIDS charity funded the study.
Source: Monika Landgraf – University of Adelaide
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to University of Adelaide, Weth.
Original Research: Full open access research for “Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex” by Fiona M. Bright, Robert Vink, Roger W. Byard, Jhodie R. Duncan, Henry F. Krous, and David S. Paterson in PLOS ONE. Published online September 20 2017 doi:10.1371/journal.pone.0184958
[cbtabs][cbtab title=”MLA”]University of Adelaide “Now We Know Why Babies Shouldn’t Sleep Face Down.” NeuroscienceNews. NeuroscienceNews, 25 October 2017.
<https://neurosciencenews.com/sids-sleep-position-7811/>.[/cbtab][cbtab title=”APA”]University of Adelaide (2017, October 25). Now We Know Why Babies Shouldn’t Sleep Face Down. NeuroscienceNews. Retrieved October 25, 2017 from https://neurosciencenews.com/sids-sleep-position-7811/[/cbtab][cbtab title=”Chicago”]University of Adelaide “Now We Know Why Babies Shouldn’t Sleep Face Down.” https://neurosciencenews.com/sids-sleep-position-7811/ (accessed October 25, 2017).[/cbtab][/cbtabs]
Abstract
Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex
Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.
“Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex” by Fiona M. Bright, Robert Vink, Roger W. Byard, Jhodie R. Duncan, Henry F. Krous, and David S. Paterson in PLOS ONE. Published online September 20 2017 doi:10.1371/journal.pone.0184958
