Neurochemical Alterations in Sudden Unexplained Perinatal Deaths-A Review.

Nazeer Muhammad,Javeria Amin,Hasnain Javed,Naseer Ahmed,Nargis Bibi,Riffat Mehboob,Syed Amir Gilani,Muhammad Sharif

doi:10.3389/fped.2018.00006

Abstract

Sudden unexpected perinatal collapse is a major trauma for the parents of victims. Sudden infant death syndrome (SIDS) is unexpected and mysterious death of an apparently healthy neonate from birth till 1 year of age without any known causes, even after thorough postmortem investigations. However, the incidence of sudden intrauterine unexplained death syndrome (SIUDS) is seven times higher as compared with SIDS. This observation is approximated 40–80%. Stillbirth is defined as death of a fetus after 20th week of gestation or just before delivery at full term without a known reason. Pakistan has the highest burden of stillbirth in the world. This basis of SIDS, SIUDS, and stillbirths eludes specialists. The purpose of this study is to investigate factors behind failure in control of these unexplained deaths and how research may go ahead with improved prospects. Animal models and physiological data demonstrate that sleep, arousal, and cardiorespiratory malfunctioning are abnormal mechanisms in SIUDS risk factors or in newborn children who subsequently die from SIDS. This review focuses on insights in neuropathology and mechanisms of SIDS and SIUDS in terms of different receptors involved in this major perinatal demise. Several studies conducted in the past decade have confirmed neuropathological and neurochemical anomalies related to serotonin transporter, substance P, acetylcholine α7 nicotine receptors, etc., in sudden unexplained fetal and infant deaths. There is need to focus more on research in this area to unveil the major curtain to neuroprotection by underlying mechanisms leading to such deaths.

Highlights

In the first year of life, the most frequent type of death is “Crib death,” “Cot death” commonly termed as “sudden infant death syndrome” (SIDS)
Mild level of respiratory viral infection was observed by investigators in cases of sudden death infants up to 80% [48]
Fetal growth restriction (FGR) is related with minimizing brain volume and altered structure, cortical volume, and decreased total myelination that deficits cells number

Summary

Introduction

In the first year of life, the most frequent type of death is “Crib death,” “Cot death” commonly termed as “sudden infant death syndrome” (SIDS). Among every 1,700–2,000 births approximately, one baby gets affected [1]. Numerous inherited abnormalities, such as morphological substrates for SIDS–sudden intrauterine unexplained death syndrome (SIUDS), were detected, mainly represented by variations of cardiac conduction system just like accessory pathway, abnormal resorptive degeneration, and hypoplasia/agenesis of the vital brainstem structures. Just some limited reviews have sufficiently analyzed the neurological substrates, albeit even subtle anomalies of the autonomic nervous system can measure the dysfunctions in the fundamental functions, prompting sudden and unexpected death [3, 4]. In-depth examination results, performed at the University of Milan, Lino Rossi Research Center, have added to recognize the area and the nature of these anomalies, normally observed in both SIUDS and SIDS. For example, alcohol, maternal smoking, and drug abuse are identified to be the potential contributors of SIUDS and SIDS [5] while environmental pollution such as insecticides and pesticides has been reported recently [6]

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