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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non- sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increase wtih development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia which is a stimulator of the immune response, while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock--a feature of SIDS.
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PMID:Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens. 1079 Jul 32

SIDS is almost invariably sleep-related. Viable syndrome aetiology must be compatible with its many epidemiologically diverse risk factors, each of which directly or indirectly associates with the creation of psychological and/or physiological infant stress, and the subsequent disruption of normal, contented sleep. During essential deep 'rebound' recovery sleep, arousal ability and upper airway muscle tone decrease further to that in normal sleep, with subsequent upper airway obstruction. When stress impact causes sufficient sleep disruption and physiological fatigue, a failure to arouse and so restore sufficient tone to overcome such obstruction results in sudden, unexpected death. SIDS has therefore many causes which share a final lethal mechanical pathway. Evidence is presented for obstructive apnoea during sleep as being the primary syndrome death mode, for sleep disruption, reduced arousal ability, and infant stress in SIDS, and for risk factor association with the creation of this stress. Specific infant vulnerability in the first 6 months of life to stress predominantly related to total dependency on a carer for gratification of need, and to obstructive sleep apnoea due to normal anatomical, physical, and respiratory immaturity, including rapid physiological fatigue, and peaks in sleep and thermal stress vulnerability, are discussed. Further reasons for the limited age period of SIDS, and for reduced neonatal risk, are given. Prone sleeping risk can relate to positional airway obstruction during normal sleep without prior infant stress. Much of SIDS aetiology appears to concern factors related to socio-economic deprivation and subsequent sub-optimal infant care.
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PMID:Infant stress and sleep deprivation as an aetiological basis for the sudden infant death syndrome. 1117 74

Developmental studies on neurotransmitters and their receptors in sudden infant death syndrome (SIDS) infants and controls are reviewed, including comparison between the prone and supine positions at death. In SIDS infants, there are an increase of glial fibrillary acidic protein (GFAP)-positive astrocytes in the brainstem, an increase of substance P (SP) in the medulla and pons, a decrease of tyrosine hydroxylase (TH)-positive catecholaminergic neurons in the ventrolateral medulla (VLM), and vagal nuclei in the medulla oblongata and basal ganglia, a decrease of tryptophan hydroxylase (TrH)-positive serotonergic neurons in the periaqueductal gray matter (PAG), and decreases of 5-hydroxytryptamine 1A (5-HT1A) and 5-HT2A receptor immunoreactivities in the VLM and vagal nuclei in the medulla oblongata. These findings may be the result of chronic or repeated hypoxia and at the same time suggest hypofunction or immaturity of cardiorespiratory regulation. In contrast, 5-HT1A and 5-HT2A receptor immunoreactivities are increased in the PAG of SIDS infants. These increased immunoreactivities may reflect delayed neuronal maturation or a developmental abnormality of the nocicetive reaction of cardiorespiratory and arousal control in SIDS. Also, there are no differences of brainstem gliosis and catecholaminergic neuron changes between the prone and supine positions. Therefore, these changes may be predisposing factors for SIDS.
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PMID:Developmental neurotransmitter pathology in the brainstem of sudden infant death syndrome: a review and sleep position. 1235 Mar 1

The annual report of the Regional Infant and Child Mortality Review Committee (RICMRC) is attached. This Committee has as its mission the review of infant and child death so that information can be transformed into action to protect young lives. The Committee review area in 2001 included South Dakota's Minnehaha, Turner, Lincoln, Moody, Lake, and McCook counties. In 2001 there were no deaths in this region due to Sudden Infant Death Syndrome (SIDS), however, there was one death due to positional asphyxia that represents the hazards of soft bedding and prone sleeping. In addition to this case, there were seven other deaths due to injury mostly representing immaturity in driving various vehicles. These data reflect the need to remain vigilant in the public campaign to promote "back to sleep" and safe sleeping environments for infant. The RICMRC invites other communities to join in its efforts to review deaths to prevent potential life-threatening hazards to children in their local environs.
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PMID:The 2001 annual report of the Regional Infant and Child Mortality Review Committee. 1244 88

Recently, quantitative abnormalities in neuronal populations derived from the rhombic lip (inferior olive nucleus of the brain stem and external granular layer of the cerebellum) have been reported in victims of the sudden infant death syndrome (SIDS). In this study we examined the arcuate nucleus (ARCn) of 35 SIDS victims and 25 controls, to determine neuronal abnormalities involving this nucleus in SIDS. Computer-assisted cell evaluation was made on sections stained with hematoxylin and eosin to study the neuronal dimensions (nuclear and cytoplasmic area, nuclear/cytoplasmic ratio), the form factor and the density of reactive astrocytes. There was a significant reduction of the neuronal area (nuclear and cytoplasmic) in SIDS victims compared with controls. The neuronal populations of SIDS victims had a significantly higher form factor, index of immaturity. The SIDS victims were divided into two groups on the basis of ARCn development: 18 SIDS-A cases with a well-developed ARCn and 17 SIDS-B cases with severe bilateral hypoplasia. The results of our research indicate that the developmental defect is characterized by a reduction in size of the ARC neurons and by neuronal depletion. In SIDS the ARCn has the histomorphological features of neuronal immaturity, and there is a marked reduction of all quantitative cell parameters and lower astrocytes density with respect to controls. On the basis of the morphometric results of the arcuate neuronal populations, we hypothesize that infants whose neurons have failed to reach full maturity are at risk for SIDS because they are unable to develop appropriate cardioventilatory control.
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PMID:Delayed neuronal maturation of the medullary arcuate nucleus in sudden infant death syndrome. 1368 Feb 77

The annual report of the Regional Infant and Child Mortality Review Committee (RICMRC) is attached. This Committee has as its mission the review of infant and child death so that information can be transformed into action to protect young lives. The 2002 review area includes South Dakota's Minnehaha, Turner, Lincoln, Moody, Lake, McCook, and Union counties. In 2002 there was one death in this region due to SIDS, plus one infant death due to positional asphyxia that illustrates the hazards of soft bedding and prone sleeping. These data reflect the need to remain vigilant in the public campaign to promote "back to sleep" and safe sleeping environments for infants. There were four other deaths due to accidental injury, mostly representing immaturity in driving various vehicles. In 2002 there were two child abuse homicides, and three teenage suicides. The RICMRC invites other communities to join in its efforts to review deaths to prevent potential life-threatening hazards to children in their local environs.
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PMID:The 2002 annual report of the Regional Infant and Child Mortality Review Committee. 1473 38

We used Statistics Canada's linked stillbirth, live birth and infant death files to assess the risks of adverse pregnancy outcomes among Inuit and North American Indian vs. other ethnic women in Quebec, 1985-97 (1 125 462 singleton births). Mother tongue was used to define ethnicity, with the largest French language group as the reference. Main outcome measures are adjusted odds ratios (AOR) for preterm birth, small-for-gestational-age (SGA), stillbirth, neonatal and postneonatal death controlled for maternal age, education, marital status, parity, infant sex, community size, and community-level random effects using multilevel logit models. Inuit women had higher risks of preterm birth (AOR = 1.49, 95% CI [1.25, 1.78]) and immaturity-related infant mortality (AOR = 3.03 [1.36, 6.74]), while Indian women did not. Infants of Inuit (AOR = 0.39 [0.31, 0.49]) and Indian (AOR = 0.27 [0.24, 0.31]) women had substantially lower risks of SGA. Elevated risks of stillbirth were observed among Indian women [AOR = 1.53 (1.09, 2.15)], and of postneonatal death among both Inuit (AOR = 4.45 [2.74, 7.22]) and Indian (AOR = 1.86 [1.28, 2.70]) infants. Both Inuit and Indian infants had much higher risks of sudden infant death syndrome (SIDS) and infection-related mortality. Although the absolute risks of adverse outcomes declined from 1985-87 to 1995-97, the relative disparities between aboriginal and non-aboriginal women changed little over this period. We conclude that Inuit and Indian women have different risk profiles for adverse pregnancy outcomes, and that prevention of preterm birth among Inuit women, and of SIDS and infection-related infant mortality in both aboriginal groups, are important targets for future research and intervention.
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PMID:Risks of adverse pregnancy outcomes among Inuit and North American Indian women in Quebec, 1985-97. 1473 46

Apnoea is common in the newborn period and especially in preterm newborns. Bradycardia and desaturation of oxyhaemoglobin typically occur with apnoea. These abnormalities reflect an immature cardiorespiratory system and resolution of this immaturity can be expected within a predictable time frame. Infants who have apnoea in the newborn period are thought not to be at higher risk for sudden infant death syndrome (SIDS). Whether apnoea episodes are associated with a higher incidence of long-term handicap for these infants is not yet clear.
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PMID:Clinical correlates, natural history and outcome of neonatal apnoea. 1505 Feb 13

The mechanisms underlying respiratory system immaturity in newborns have been investigated, both in vivo and in vitro, in humans and in animals. Immaturity affects breathing rhythmicity and its modulation by suprapontine influences and by afferents from central and peripheral chemoreceptors. Recent research has moved from bedside tools to sophisticated technologies, bringing new insights into the plasticity and genetics of respiratory control development. Genetic research has benefited from investigations of newborn mice having targeted deletions of genes involved in respiratory control. Genetic variability may govern the normal programming of development and the processes underlying adaptation to homeostasis disturbances induced by prenatal and postnatal insults. Studies of plasticity have emphasized the role of neurotrophic factors. Improvements in our understanding of the mechanistic effects of these factors should lead to new neuroprotective strategies for infants at risk for early respiratory control disturbances, such as apnoeas of prematurity, sudden infant death syndrome and congenital central hypoventilation syndrome.
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PMID:Development of respiratory control: evolving concepts and perspectives. 1594 76

This article intends to show how the cerebellum, a structure ordinarily not considered in mediating breathing or cardiovascular control, may play a critical role in compensatory responses particularly to hypoxic insults occurring pre and/or postnatally and thus may be involved in the sudden unexplained perinatal and infant death. Besides the ontogenesis of the cerebellar cortex in man, we reported alterations of biopathological features (neuronal immaturity, altered apoptotic programs, negative expression of somatostatin and EN2 gene, intense c-fos expression positivity, astrogliosis) in the cortex and in the dentate nucleus of the 63% of sudden deaths, and only in 10% of the controls. The correlation of these results with the mother's smoking habit was highly significant. Therefore, we support the hypothesis, already expressed in previous studies on brainstem, of a close relation between maternal cigarette smoking and a wide range of morpho-physiological defects of the brain, leading to unexplained sudden death in stillbirths, newborns, and Sudden Infant Death Syndrome (SIDS) victims.
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PMID:Alterations of biological features of the cerebellum in sudden perinatal and infant death. 1690 Jun 66


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