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

Survivors of premature birth have a predilection for perinatal brain injury, especially to periventricular cerebral white matter. Periventricular white matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia) and diffuse myelination disturbances. Recent neuroimaging studies support that the incidence of periventricular leukomalacia is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary but not sufficient to generate the initial injury that leads to PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. There has been substantial recent progress in the understanding of the cellular and molecular pathogenesis of PWMI. The oligodendrocyte progenitor is a key target for preventive strategies to reduce ischemic cerebral white matter injury in premature infants.
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PMID:Maturation-dependent vulnerability of perinatal white matter in premature birth. 1726 26

Laryngeal sensitivity in the newborn has been a subject of great interest for both researchers and clinicians for a number of years. From a clinical standpoint, laryngeal sensitivity is essential for both preventing foreign substances from entering into the lower airway and for finely tuning upper airway resistance. However, heightened reflexes originating from the laryngeal receptors in newborns and infants, due to neural immaturity, can lead to potentially dangerous cardiorespiratory events. The latter have been linked to apneas of prematurity, apparent life-threatening events, and sudden infant death syndrome (SIDS). From a physiological standpoint, many mechanisms pertaining to reflexes originating from laryngeal receptors are yet to be fully understood. This short review is an attempt to summarize current knowledge on laryngeal sensitivity and its potential consequences upon control of breathing abnormalities encountered within the first weeks of life.
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PMID:Laryngeal sensitivity in the neonatal period: from bench to bedside. 1758 53

During the past four decades major advances in the management of premature infants have led to progressive reduction in mortality. During this period mortality in very low birth weight infants (VLBW, <1500 grams and <30 weeks gestation age) has decreased, and more than 50% of infants less than 24 weeks gestation age now survive, increasing the population of VLBW infants in intensive care nursery environments. Thyroid function in these infants is characterized by decreased TSH and T4 responses to parturition, low serum total T4 and TSH levels and variable free T4 concentrations during the first 2-4 postnatal weeks of life. These features reflect a state of transient hypothalamic-pituitary or central hypothyroidism. There is a high prevalence of morbidity in these infants, as well, often associated with further reductions in serum total T4, T3, TBG and TSH concentrations and variable levels of free T4 and reverse T3, resembling the non-thyroidal illness (NTI) syndrome in adults. The etiologic roles of thyroid system immaturity and NTI in the transient hypothyroxinemia of prematurity (THOP) and the impact of THOP on the subsequent neurological deficits in VLBW infants remains unclear. Several thyroxine supplementation trials have been conducted with inconclusive results. Further studies are planned or in progress.
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PMID:Thyroid function and dysfunction in premature infants. 1764 79

Periventricular white matter (PVWM) injury is the leading cause of neurologic disability in survivors of prematurity. To address the role of ischemia in PVWM and cerebral cortical injury, we hypothesized that immaturity of spatially distal vascular 'end zones' or 'border zones' predisposes PVWM to greater decreases in cerebral blood flow (CBF) than more proximal structures. We quantified regional CBF with fluorescently labeled microspheres in 0.65 gestation fetal sheep in histopathologically defined three-dimensional regions by post hoc digital dissection and coregistration algorithms. Basal flow in PVWM was significantly lower than in gyral white matter and cortex, but was equivalent in superficial, middle, and deep PVWM. Absolute and relative CBF (expressed as percentage of basal) did not differ significantly during ischemia or reperfusion between PVWM, gyral white matter, or cortex. Moreover, CBF during ischemia-reperfusion was equivalent in three adjacent PVWM levels and was not consistent with the magnitude of severity of PVWM injury, defined by TUNEL (terminal deoxynucleotidyltransferase-mediated dUPT nick end labeling) staining. However, the magnitude of ischemia was predicted by the severity of discrete cortical lesions. Hence, unlike cerebral cortex, unique CBF disturbances did not account for the distribution of PVWM injury. Previously defined cellular maturational factors, thus, appear to have a greater influence on PVWM vulnerability to ischemic injury than the presence of immature vascular boundary zones.
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PMID:Cerebral blood flow heterogeneity in preterm sheep: lack of physiologic support for vascular boundary zones in fetal cerebral white matter. 1809 57

Apnea, defined as cessation of breathing resulting in pathological changes in heart rate and oxygen saturation, is a common occurrence especially in preterm neonates. It is due to immaturity of the central nervous system (apnea of prematurity) or secondary to other causes such as metabolic disturbances etc. Secondary causes of apnea should be excluded before a diagnosis of apnea of prematurity is made. Methylxanthines and continuous positive airway pressure form the mainstay of treatment. Mechanical ventilation is reserved for apnea resistant to the above therapy. An approach to the management of apnea in neonates is described.
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PMID:Apnea in the newborn. 1824 37

Apnea of prematurity (AOP) remains a major clinical problem in present day neonatology that warrants frequent evaluations and imposes challenges in therapeutic strategies. Although the pathogenesis of AOP is poorly understood, it is probably a manifestation of physiologic immaturity of breathing control rather than a pathologic disorder. Immature breathing responses to hypoxia, hypercapnia and exaggerated inhibitory pulmonary reflexes in preterm infants might also contribute to the occurrence or severity of AOP. Recent data suggest a role for genetic predisposition. Although typically resolve with maturation, the role of bradycardia and desaturation episodes associated with AOP in the development of sleep disorder breathing and neurodevelopmental delay needs further clarification. Pharmacological treatment with methylxanthines and CPAP remain the mainstay for treatment of AOP. However, recent studies have implicated central inhibitory neuromodulators including prostaglandins, GABA and adenosine in its pathogenesis, the fact that might provide future specific targets for treatment. This review will summarize new insights involving these issues as well as others involving the pathogenesis, treatment strategies and consequences of apnea in premature infants.
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PMID:Neonatal apnea: what's new? 1878 Mar 39

Very low-birth-weight premature infants often suffer from a variety of respiratory problems, including respiratory distress syndrome (RDS), hypopnea and periodic breathing, and apnea. These conditions are likely related to immaturity of the respiratory centers; yet how respiratory rhythms originating from these centers, including their complexity, relate to demographic measures of prematurity remains largely unknown. In 39 neonates with mild RDS (22 males, 28 +/- 2 wk gestational age, 1,036 +/- 234 g body wt), we derived the univariate association between complexity of two respiratory rhythms [respiratory rate (RR) and tidal volume (Vt)] and postmenstrual age, gestational age, postnatal age, and weight at time of study. RR and Vt rhythm complexities were assessed using approximate entropy, sample entropy, base scale entropy, and forbidden words entropy estimated for 300 consecutive breaths determined from respiratory inductance plethysmography, irrespective of breathing effort rate or amplitude, collected during sleep while the neonates were exposed to nasal continuous positive airway pressure (4-6 cmH(2)O). RR and Vt exhibited increased complexity with increased maturity, but only in terms of base scale entropy and forbidden words entropy, which are based on pattern matching, rather than approximate entropy and sample entropy, which are based on conditional probabilities. Specifically, RR complexity as measured by forbidden word entropy increased with increasing weight (r = 0.502), postconceptional age (r = 0.423), and gestational age (r = 0.493). As measured by base scale entropy, RR complexity increased with increasing weight (r = 0.488) and postconceptional age (r = 0.390). Vt complexity, measured by base scale entropy, was greater with increased postnatal age (r = 0.428). Our results indicate that respiratory rhythms become more complex with increasing levels of maturity, as indicated by increased weight and several age parameters. This emphasizes the importance of the later weeks of gestation in the maturation of respiratory centers in the brain and suggests a promising use of entropy measures in exploring respiratory maturation in infants.
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PMID:Effect of weight and age on respiratory complexity in premature neonates. 1903 92

Retinopathy of prematurity (ROP) is a complex disease of the developing retinal vasculature in premature infants. Clinical manifestations range from mild, usually transient changes of the peripheral retina to severe progressive vasoproliferation, and potentally blinding retinal detachment. With better standards in premature units and with increased survival rate of low gestational age and low birth weight infants the incidence of ROP also increased. The incidence of ROP has been decreasing in developed countries over the past decade, and ROP has become potentially confined to immature neonates with birth weights less than 1000 grams in these countries. Prematurity and retinal immaturity are the major risk factors. Oxygenation, respiratory distress, apnea, bradycardia, hearth disease, infection, hypercarbia, acidosis, anemia, and the need for transfusion are thought by some to be contributory factors. All of the preterm babies with a birth weight under 1500 grams and a gestational age under 32 weeks should be followed for ROP.
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PMID:[Retinopathy of prematurity]. 1940 50

Obstructive lung diseases remain as important complications of preterm birth, usually attributed to a combination of lung immaturity, oxygen therapy and ventilator support. This is particularly true for low birth weight infants with severe respiratory neonatal disease; however, preterm infants that did not initially demonstrate significant respiratory neonatal disease also have reduced lung function when examined later in life, suggesting that prematurity alone could generate a persistent obstructive disease. Recent data have shown a significant reduction in maximal expiratory flows in healthy premature infants compared with control infants and reference values, when tested in the first months of life. Reduced expiratory flows were associated with male sex, low gestational age, smoking exposure and increased weight gain. The mechanism for this has not been determined and could result from smaller airways, a decrease in pulmonary elastic recoil secondary to abnormal alveolarisation of the lung parenchyma, as well as more compliant airways.
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PMID:Effect of preterm birth on airway function and lung growth. 1965 91

Intraventricular hemorrhage (IVH) is a major complication of prematurity. IVH typically initiates in the germinal matrix, which is a richly vascularized collection of neuronal-glial precursor cells in the developing brain. The etiology of IVH is multifactorial and is primarily attributed to the intrinsic fragility of the germinal matrix vasculature and the disturbance in the cerebral blood flow (CBF). Although this review broadly describes the pathogenesis of IVH, the main focus is on the recent development in molecular mechanisms that elucidates the fragility of the germinal matrix vasculature. The microvasculature of the germinal matrix is frail because of an abundance of angiogenic blood vessels that exhibit paucity of pericytes, immaturity of basal lamina, and deficiency of glial fibrillary acidic protein (GFAP) in the ensheathing astrocytes endfeet. High VEGF and angiopoietin-2 levels activate a rapid angiogenesis in the germinal matrix. The elevation of these growth factors may be ascribed to a relative hypoxia of the germinal matrix perhaps resulting from high metabolic activity and oxygen consumption of the neural progenitor cells. Hence, the rapid stabilization of the angiogenic vessels and the restoration of normal CBF on the first day of life are potential strategies to prevent IVH in premature infants.
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PMID:Intraventricular hemorrhage in premature infants: mechanism of disease. 1981 35


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