Development of Catecholaminergic Neurons and Substance P-Positive Nerve Fibers in the Brain Stem of Victims of Sudden Infant Death Syndrome

2015 ◽  
pp. 13-18
Author(s):  
Sachio Takashima ◽  
Hideo Yamanouchi ◽  
Laurence E. Becker
Keyword(s):  
Substance P ◽  
Brain Stem ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Nerve Fibers ◽  
Sudden Infant ◽  
Catecholaminergic Neurons ◽  
The Brain

Neuropathology of Early Sudden Infant Death Syndrome—Hypoplasia of the Pontine Kolliker-Fuse Nucleus: A Possible Marker of Unexpected Collapse during Skin-to-Skin Care

2018 ◽  
Vol 36 (05) ◽  
pp. 460-471 ◽  
Author(s):  
Anna Lavezzi ◽  
Stefano Ferrero ◽  
Beatrice Paradiso ◽  
Liliya Chamitava ◽  
Francesco Piscioli ◽  
...  
Keyword(s):  
Brain Stem ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Skin Care ◽  
Sudden Infant ◽  
Neonatal Deaths ◽  
Specific Finding ◽  
Skin To Skin ◽  
The Brain

Objective To find a possible pathogenetic mechanism of the early sudden infant death occurring in newborns during the skin-to-skin care (SSC), through the examination of neuronal centers regulating the vital activities. Study Design This is an in-depth examination of the brain stem in 22 healthy term newborns, suddenly died in the first hour of life without the identification of a cause at autopsy (early sudden infant death syndrome [eSIDS]), 12 of them concomitantly with SSC, and 10 with age-matched controls died of known pathology. Results Developmental alterations of neuronal structures of the brain stem were highlighted in 19 of the 22 eSIDS, but not in control. The hypoplasia of the pontine Kölliker-Fuse nucleus (KFN), an important respiratory center, was diagnosed at the histological examination, validated by morphometric quantifications, in 11 of the 12 eSIDS while they were placed on the mother's chest and in 2 of the 10 SSC unrelated neonatal deaths. Conclusion The delayed development of the KFN could represent a specific finding of eSIDS occurring during SSC. Therefore, it is necessary to point out that the SSC represents a further risk factor that must be added to others already known for sudden infant death syndrome. Then this practice needs appropriate monitoring strategies of the infant's conditions.

scholarly journals Genes regulating the serotonin metabolic pathway in the brain stem and their role in the etiopathogenesis of the sudden infant death syndrome

Genomics ◽  
2008 ◽  
Vol 91 (6) ◽  
pp. 485-491 ◽  
Author(s):  
Francesco Nonnis Marzano ◽  
Milena Maldini ◽  
Laura Filonzi ◽  
Anna Maria Lavezzi ◽  
Stefano Parmigiani ◽  
...  
Keyword(s):  
Brain Stem ◽  
Sudden Infant Death Syndrome ◽  
Metabolic Pathway ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
The Brain

scholarly journals Aquaporin-1 and aquaporin-9 gene variations in sudden infant death syndrome

2021 ◽  
Author(s):  
Siri Hauge Opdal ◽  
Linda Ferrante ◽  
Torleiv Ole Rognum ◽  
Arne Stray-Pedersen
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Brain Function ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Aquaporin 9 ◽  
Genes Encoding ◽  
External Risk ◽  
The Brain

AbstractSeveral studies have indicated that a vulnerability in the development and regulation of brain function is involved in sudden infant death syndrome (SIDS). The aim of this study was to investigate the genes encoding the brain aquaporins (AQPs) AQP1 and AQP9 in SIDS. The hypothesis was that specific variants of these genes are part of the genetic vulnerability predisposing infants to sudden unexpected death. The study included 168 SIDS cases with a median age of 15.5 (range 2–52) weeks and 372 adolescent/adult deceased controls with a median age of 44 (range 11–91) years. In the AQP1 gene, the rs17159702 CC/CT genotypes were found to be associated with SIDS (p = 0.02). In the AQP9 gene, the combination of a TT genotype of rs8042354, rs2292711 and rs13329178 was more frequent in SIDS cases than in controls (p = 0.03). In the SIDS group, an association was found between genetic variations in the AQP1 gene and maternal smoking and between the 3xTT combination in the AQP9 gene and being found lifeless in a prone position. In conclusion, this study adds further evidence to the involvement of brain aquaporins in SIDS, suggesting that specific variants of AQP genes constitute a genetic predisposition, making the infant vulnerable to sudden death together with external risk factors and probably other genetic factors.

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