The Sudden Infant Death Syndrome in Hospitalized Babies

PEDIATRICS ◽  
1974 ◽  
Vol 54 (5) ◽  
pp. 644-646
Author(s):  
Donald R. Peterson ◽  
J. Bruce Beckwith ◽  
E. A. Benson

"If infants die because, while passing through a period of increased physiological vulnerability, some critical combination of intrinsic and extrinsic factors proves lethal, then it would be strange if death occurs only in the course of minor and not major illnesses. Is it possible that sudden unexplained death does happen in hospital, but is not recognized as such because the major diagnosis is judged to be the cause of death, or do the resuscitative measures which are readily available prevent it?" This provocative question, posed in an editorial in late 1971,1 drew a response from Raphael, who submitted rather convincing evidence of an instance of sudden unexplained infant death in a Canadian hospital.2

2004 ◽  
Vol 7 (2) ◽  
pp. 171-179 ◽  
Author(s):  
Anna Maria Lavezzi ◽  
Giulia Ottaviani ◽  
Gianmario Ballabio ◽  
Lino Rossi ◽  
Luigi Matturri

The parabrachial/Kölliker-Fuse complex has been defined, in different animal species, to lie in the dorsolateral part of the pontine tegmentum and to be subdivided into three well-defined regions: the medial parabrachial nucleus, the lateral parabrachial nucleus, and the Kölliker-Fuse nucleus. Experimental studies have shown that the parabrachial/Kölliker-Fuse complex is involved in a variety of functional activities and above all plays an important role in respiratory modulation. In human brainstem, the cytoarchitecture and physiology of this complex have not yet been fully characterized. The aim of the present study was to examine fetal and infant human brainstems in order to define the precise morphology of the three nuclei of the parabrachial/Kölliker-Fuse complex, and to determine whether this nervous center shows morphologic alterations in sudden infant death syndrome (SIDS) and in sudden intrauterine unexplained death (SIUD). In serial sections of 31 brain-stems of subjects aged from 32 gestational wk to 10 months of life, we studied, by morphologic and morphometric analyses, the cytoarchitecture and the extension of the three nuclei of the parabrachial/Kölliker-Fuse complex. All the morphometric parameters were very similar in SIUD and SIDS cases to those of the respective control group, as shown by the absence of significant statistical differences between the two fetus and infant groups. We observed that the features of both the lateral and the medial parabrachial nuclei are largely consistent with those reported in experimental studies. In contrast, the Kölliker-Fuse nucleus appears to be more developed in human beings than in other animal species, showing a greater extension and a more complex structure, as well as subdivision into two subnuclei (compactus and dissipatus).


2020 ◽  
Vol 134 (6) ◽  
pp. 2143-2147
Author(s):  
Jakob Matschke ◽  
Jan-Peter Sperhake ◽  
Nadine Wilke ◽  
Klaus Püschel ◽  
Markus Glatzel

Abstract Sudden infant death syndrome (SIDS) is the sudden unexpected death of an infant < 1 year of age that remains unexplained after comprehensive workup including complete autopsy and investigation of the circumstances of death. The triple risk hypothesis posits that SIDS results as a combination of both intrinsic and extrinsic factors on the background of a predisposing vulnerability. Neuropathological examination in the past has focussed mainly on the brainstem as the major player in respiratory control, where subtle findings have been linked to the chain of events leading to death in SIDS. The cerebellum has received less attention, probably due to an assumed negligible role in central cardiorespiratory control. We report four cases of SIDS in which neuropathological investigation revealed cerebellar heterotopia of infancy, a distinct malformation of the cerebellum, and discuss the potential impact of this condition on the aetiology and pathogenesis of SIDS.


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