scholarly journals Substantia Nigra Abnormalities Provide New Insight on the Neural Mechanisms Underlying the Sleep-Arousal Phase Dysfunctions in Sudden Infant Death Syndrome

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142096269 ◽  
Author(s):  
Anna M. Lavezzi ◽  
Riffat Mehboob ◽  
Graziella Alfonsi ◽  
Stefano Ferrero
Keyword(s):  
Substantia Nigra ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Great Part ◽  
Pathological Finding ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Sleep Arousal

The purpose of this study was to research possible developmental alterations of the substantia nigra (SN) in sudden infant death syndrome (SIDS), a syndrome frequently attributed to arousal failure from sleep. Brain stems of 46 victims of sudden infant death, aged from 1 to about 7 months (4 to 30 postnatal weeks), were investigated. Twenty-six of these cases were diagnosed as SIDS, due to the lack of any pathological finding, while the remaining 20 cases in which the cause of death was determined at autopsy served as controls. Maternal smoking was reported in 77% of SIDS and 10% of controls. Histopathological examination of the SN was done on 5-µm-thick sections of caudal midbrain stained with both hematoxylin-eosin and Klüver-Barrera. Densitometry, immunohistochemistry and histochemistry were applied to highlight the neuronal concentration, the tyrosine hydroxylase (TH) expression, and the presence of neuromelanin (NM) in this structure. Hypoplasia of the pars compacta portion of the SN was observed in 69% of SIDS but never in controls; TH expression was significantly higher in controls than in SIDS; and NM was observed only in 4 infants of the control group but not in SIDS. A significant correlation was found between SIDS, hypoplasia/low neuronal density, low TH expression in the pars compacta, and maternal smoking. Because the SN pars compacta, being the major dopamine brain center, controls many functions, including the sleep-arousal phase, its alterations, especially concurrently with smoking exposure, may contribute to explain the pathogenesis of SIDS that occur in the great part of cases at awakening from sleep.

scholarly journals Neurobiological Alterations Of The Substantia Nigra In Sudden Infant Death Syndrome

2020 ◽  
Author(s):  
Anna Lavezzi ◽  
Riffat Mehboob ◽  
Graziella Alfonsi ◽  
Stefano Ferrero
Keyword(s):  
Tyrosine Hydroxylase ◽  
Substantia Nigra ◽  
Infant Death ◽  
Maternal Smoking ◽  
Histopathological Examination ◽  
Pathological Finding ◽  
Sudden Infant Death ◽  
Substantia Nigra Pars Compacta ◽  
Control Group ◽  
Sudden Infant

Abstract Background - The purpose of this study was to research possible morphological and functional alterations of the substantia nigra in SIDS. Methods - Brainstems of 46 victims of sudden infant death, aged from 1 to 7 months, were investigated. Twenty-six of these cases were diagnosed as SIDS, due to the lack of any pathological finding, while the remaining 20 cases, in which the cause of death was determined at autopsy, served as controls. Maternal smoking was reported in 10% of controls and 77% of SIDS. Histopathological examination of the substantia nigra was done on midbrain 5-µm-thick sections stained with hematoxylin-eosin and Klüver-Barrera. Densitometry, immunohistochemistry and histochemistry were applied to highlight the neuronal concentration, the expression of tyrosine hydroxylase and neuromelanin, respectively. Results - Hypoplasia of the pars compacta of the substantia nigra was observed in SIDS but not in controls. Tyrosine hydroxylase expression in the substantia nigra was significantly higher in controls than in SIDS. Neuromelanin was observed as dark granules only in 4 infants of the control group but never in SIDS. A significant correlation was found between hypoplasia/low neuronal density, low tyrosine hydroxylase expression in the substantia nigra pars compacta and maternal smoking. Conclusion - The substantia nigra pars compacta, that is the main dopamine center in the brain, is involved in the control of many functions, including the sleep-arousal phase, and hence, its structural and/or functional alterations may explain the pathogenesis of SIDS, that often occurs during sleep. This study also indicates that maternal smoking can may have strongly influenced the SN altered development. Trial registration – not applicable for this study

Apnea, Hypoxemia, and Aborted Sudden Infant Death Syndrome

PEDIATRICS ◽  
1978 ◽  
Vol 62 (5) ◽  
pp. 686-691
Author(s):  
June P. Brady ◽  
Ronald L. Ariagno ◽  
John L. Watts ◽  
Steven L. Goldman ◽  
Fe M. Dumpit
Keyword(s):  
Heart Rate ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Total Duration ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Nasal Catheter ◽  
End Tidal

To find out whether there is any relationship between the ventilatory response to hypoxia and the sudden infant death syndrome (SIDS), we studied the effects of mild induced hypoxia (PIO2, 120 mm Hg = 17% oxygen) in 16 infants aged 2 weeks to 6 months. Eight had recurrent apneic spells (apnea group) (five had aborted SIDS and three had recurrent apnea in the intensive care nursery) and eight were "well" preterm infants about to fly in a pressurized airplane (PIO2, 120 mm Hg) (control group). Mean birth weights were 2,245 and 1,400 gm and mean gestational ages were 35 and 30 weeks. Postconceptual ages (41.8 and 41.3 weeks) were almost identical. Heart rate was obtained from an ECG, and respiratory rate and pattern were obtained from a pneumogram. In addition, end-tidal PCO2 and PN2 or PO2 were obtained with a nasal catheter and gas analyzers. In the apnea group with inhalation of 17% oxygen, we observed an increase in periodic breathing and an increase in both rate and total duration of respiratory pauses. In the control group there were no significant changes. Heart rate and PCO2 did not change in either group. Our findings suggest that infants prone to apnea may have unique respiratory responses to mild induced hypoxia.

Maternal Smoking and Pulmonary Neuroendocrine Cells in Sudden Infant Death Syndrome

PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Airway Epithelium ◽  
Maternal Smoking ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Sudden Infant ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells

Background. Maternal smoking is a well-recognized risk factor for sudden infant death syndrome (SIDS), but the precise mechanism is unknown. We tested a hypothesis that maternal smoking affects pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs), which are innervated PNEC clusters and presumed airway chemoreceptors. Methods. Lung sections from infants who died of SIDS and whose mothers smoked during pregnancy (n = 22), infants who died of SIDS and whose mothers were nonsmokers (n = 17), and age-matched control infants (n = 15) who died of other causes were immunostained for bombesin (a PNEC and NEB marker) and assessed morphometrically. Results. The frequency of PNEC (the percentage of airway epithelium immunoreactive for bombesin) was increased up to twofold in the lungs of infants who died of SIDS (7.7 ± 0.4%) compared with controls (4.9 ± 0.4%), as was the frequency (40 ± 3.5 vs 23 ± 3.7/cm2) and size (748 ± 46.5 vs 491 ± 25.8,µm2) of NEBs. In infants who died of SIDS and who were born to smoking mothers, PNEC frequency was increased significantly compared with that in those born to nonsmoking mothers, but the frequency and size of NEBs were not significantly different between the two groups. Conclusion. Our findings suggest that maternal smoking potentiates hyperplasia of the PNEC system in the lungs of infants who die of SIDS and that a dysfunction of these cells may contribute to the pathophysiology of SIDS.

Sudden Infant Death Syndrome in a Twin: A Comparison of Sibling Histories

PEDIATRICS ◽  
1986 ◽  
Vol 78 (1) ◽  
pp. 146-150
Author(s):  
A. Kahn ◽  
D. Blum ◽  
M. F. Muller ◽  
L. Montauk ◽  
A. Bochner ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Clinical Risk Factor ◽  
Control Group ◽  
Sudden Infant ◽  
First Year ◽  
Control Infant ◽  
The Mean ◽  
First Year Of Life

To determine possible characteristics of infant victims of sudden death, we examined 114 items related to the pre- and postnatal histories of 42 pairs of twins one of whom died of sudden infant death syndrome (SIDS) leaving a surviving sibling. Interviews with the parents were conducted after the occurrence of SIDS, and the data were checked with records held by gynecologists and pediatricians. To evaluate the specificity of any factors, we studied a control group of 42 age- and sex-matched pairs of twins, both of whom survived the first year of life. Only 11 of 114 characteristics were significantly related to SIDS: future victims had a smaller weight and height at birth, stayed longer in the nursery, and followed a moving object with their eyes, had head control, and smiled at a later age than their surviving siblings. They also fatigued more often during feeding (11/42) and had reduced arm and neck tonus (9/42). They were described as longer sleepers than their surviving siblings. During sleep, some SIDS twins, but no surviving twin, were found to be cyanotic at least once or pale (4/42) and were repeatedly covered with abundant sweat (8/42). In the control group of normal twins, the occurrence of most of these characteristics was found with a frequency comparable to that seen in the SIDS infants; the specificity of these characteristics is thus considered doubtful. The mean birth weight and height were significantly greater in the control group, and no control infant had an episode of cyanosis or pallor or repeated episodes of profuse sweating observed during their sleep. It is concluded that, if further research validates the occurrence of night hyperhydrosis in some future SIDS victims, this symptom could be a clinical risk factor.

Smoking and the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 893-896 ◽  
Author(s):  
E. A. Mitchell ◽  
R. P. K. Ford ◽  
A. W. Stewart ◽  
B. J. Taylor ◽  
D. M. O. Becroft ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Risk Of Death ◽  
Increased Risk ◽  
Wide Range ◽  
Household Members ◽  
Control Study

Objective. Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. Methods. A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. Results. Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. Conclusion. Passive tobacco smoking is causally related to SIDS.

scholarly journals What risk factors for sudden infant death syndrome are preterm and term medically complex infants exposed to at home?

2020 ◽  
Author(s):  
Ian Mitchell ◽  
Daniel Y Wang ◽  
Christine Troskie ◽  
Lisa Loczy ◽  
Abby Li ◽  
...  
Keyword(s):  
Risk Factors ◽  
Respiratory Syncytial Virus ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Term Infants ◽  
Medical Complexity ◽  
Syncytial Virus

Abstract Objectives Risk factors for sudden infant death syndrome include premature birth, maternal smoking, prone or side sleeping position, sleeping with blankets, sharing a sleeping surface with an adult, and sleeping without an adult in the room. In this study, we compare parents’ responses on sleep patterns in premature and term infants with medical complexity. Methods Parents of children enrolled in the Canadian Respiratory Syncytial Virus Evaluation Study of Palivizumab were phoned monthly regarding their child’s health status until the end of each respiratory syncytial virus season. Baseline data were obtained on patient demographics, medical history, and neonatal course. Responses on adherence to safe sleep recommendations were recorded as part of the assessment. Results A total of 2,526 preterms and 670 term infants with medical complexity were enrolled. Statistically significant differences were found in maternal smoking rates between the two groups: 13.3% (preterm); 9.3% (term) infants (χ 2=8.1, df=1, P=0.004) and with respect to toys in the crib: 12.3% (term) versus 5.8% preterms (χ 2=24.5, df=1, P<0.0005). Preterm infants were also significantly more likely to be placed prone to sleep (8.8%), compared with term infants (3.3%), (χ 2=18.1, df=1, P<0.0005). Conclusion All the infants in this study had frequent medical contacts. There is a greater prevalence of some risk factors for sudden infant death syndrome in preterm infants compared to term infants with medical complexity. Specific educational interventions for vulnerable infants may be necessary.

Sign in / Sign up

Export Citation Format

Share Document