National Post-Perinatal Infant Mortality and Cot Death Study, Scotland 1981-82

Arneil, Gavin C.; Gibson, A. A. M.; McIntosh, Helen; Brooke, Hazel; Harvie, Ann; Patrick, W.

doi:10.1016/s0140-6736(85)91273-5

Cited by 34 publications

(9 citation statements)

References 1 publication

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“…There was a shift in the mean maternal age nationally at delivery for the four years of our study compared with the mean age during a previous Scottish study 20. Mothers were, on average, older during the later study (72% ≥25 in 1992-5 v 30% in 1981-2.)…”

Section: Discussioncontrasting

confidence: 47%

Case-control study of sudden infant death syndrome in Scotland, 1992-5

Brooke

Gibson

Tappin

et al. 1997

BMJ

203

138

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Section: Discussioncontrasting

confidence: 47%

Case-control study of sudden infant death syndrome in Scotland, 1992-5

Brooke

Gibson

Tappin

et al. 1997

BMJ

203

138

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“…This analysis has confirmed many of the clinical characteristics previously reported in SIDS cases [3,4], Before discussing these findings, however, it is important to recall that the number of SIDS cases examined is very small. In agreement with previous stud ies, a younger maternal age [5,6], increased number of teenage mothers, [7,8], close spacing of pregnancies [9] and a history of smoking during pregnancy [6] were found more frequently in the SIDS cases.…”

Section: Discussionsupporting

confidence: 86%

Pre- and Perinatal Clinical Characteristics of Infants Who Suffer Sudden Infant Death Syndrome

1987

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In a population-based study, clinical and physiological data were collected in the neonatal period on 7,496 full-term (≥ 37 weeks) infants of birthweights > 2.50 kg born in 3 hospitals. The sample excluded a small number of infants who were born with severe illnesses from which there was no period of recovery before death in the neonatal period. Twenty-seven of the infants had died by the time all of the population had passed their third birthday. Twenty-one of these cases died suddenly and unexpectedly, and in 13 there was no adequate explanation for death (sudden infant death syndrome – SIDS). Pre- and early postnatal clinical data on the infants who had died were compared to a randomly selected sample of 478 survivors. This analysis showed that the infants who suffered SIDS showed similar clinical characteristics to those previously reported. Unlike the SIDS group, however, the prenatal histories of the non-SIDS deaths were similar to controls, showing no evidence of a sub-optimal intra-uterine environment.

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“…Several risk factors for SIDS relate to the mother and pregnancy, including prematurity, low birth weight, prenatal and postnatal cigarette smoke exposure (Schoendorf et al 1992; Haglund 1993; Blair et al 1996; Fleming et al 1996; MacDorman et al 1997; Wisborg et al 2000; Anderson et al 2005; Mitchell et al 2006) and prenatal alcohol ingestion (Scragg et al 1993; Alm et al 1999; Iyasu et al 2002; Kinney et al 2003; Klug et al 2003; Duncan et al 2008b). There is also a male bias in SIDS with twice as many boys than girls dying of SIDS (Froggatt et al 1968; Beal 1972; Stewart 1975b; Arneil et al 1985; Millar et al 1993). Likewise, there is a noted ethnic disparity with significantly increased SIDS rates among African American infants and Native American infants (Mathews et al 2002).…”

Section: The Sudden Infant Death Syndromementioning

confidence: 99%

Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome

Paterson

Hilaire

Weese‐Mayer

2009

Respiratory Physiology & Neurobiology

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Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant less than 12 months of age that occurs during sleep and remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. It is the leading cause of postneonatal mortality in the developed world. The cause of SIDS is unknown, but is postulated to involve impairment of brainstem-mediated homeostatic control. Extensive evidence from animal studies indicates that serotonin (5-HT) neurons in the medulla oblongata play a role in the regulation of multiple aspects of respiratory and autonomic function. A subset of SIDS infants have several abnormalities in medullary markers of 5-HT function and genetic polymorphisms impacting the 5-HT system, informing the hypothesis that SIDS results from a defect in 5-HT brainstem-mediated control of respiratory (and autonomic) regulation. Here we review the evidence from postmortem human studies and animal studies to support this hypothesis and discuss how the pathogenesis of SIDS is likely to originate in utero during fetal development.

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National Post-Perinatal Infant Mortality and Cot Death Study, Scotland 1981-82

Cited by 34 publications

References 1 publication

Case-control study of sudden infant death syndrome in Scotland, 1992-5

Case-control study of sudden infant death syndrome in Scotland, 1992-5

Pre- and Perinatal Clinical Characteristics of Infants Who Suffer Sudden Infant Death Syndrome

Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome

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