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Query: UMLS:C0728731 (prematurity)
7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain injury in premature infants is of enormous public health importance because of the large number of such infants who survive with serious neurodevelopmental disability, including major cognitive deficits and motor disability. This type of brain injury is generally thought to consist primarily of periventricular leukomalacia (PVL), a distinctive form of cerebral white matter injury. Important new work shows that PVL is frequently accompanied by neuronal/axonal disease, affecting the cerebral white matter, thalamus, basal ganglia, cerebral cortex, brain stem, and cerebellum. This constellation of PVL and neuronal/axonal disease is sufficiently distinctive to be termed "encephalopathy of prematurity". The thesis of this Review is that the encephalopathy of prematurity is a complex amalgam of primary destructive disease and secondary maturational and trophic disturbances. This Review integrates the fascinating confluence of new insights into both brain injury and brain development during the human premature period.
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PMID:Brain injury in premature infants: a complex amalgam of destructive and developmental disturbances. 1908 19

A 36-year-old primigravida with a history of temporal lobe epilepsy presented at 25 weeks of pregnancy with generalized tonic clonic seizures. The clinical picture was confused with eclampsia because of rising blood pressure and proteinuria. Clinical investigations, which included a lumbar puncture, were carried out to rule out an infective cause for the seizures. A computed tomography of the brain was performed for evidence of intracranial hemorrhage. The patient was intubated and ventilated in the intensive care unit. The labile blood pressure settled in 2 days, and the transient heavy proteinuria also resolved after 3 days. Eclampsia would have warranted operative delivery of the preterm fetus with the attendant problems of prematurity. Delivery would have been hazardous in such an acutely unwell patient. The management also would have required magnesium sulfate with its potential for toxicity. Transient proteinuria may occur in status epilepticus. The blood pressure can be labile during epileptic seizures and, in the absence of an intracranial hemorrhage, generally settles without treatment after control of the seizures. This case highlights the importance of differentiating eclampsia in a patient with known epilepsy that may also mask other disease entities such as intracranial hemorrhage, meningitis, or encephalopathy. We have also discussed the importance of various signs associated with eclampsia and their clinical significance. The differential diagnosis of seizures in pregnancy are broad as symptoms of the various disease entities including eclampsia, intracranial hemorrhage, status epilepticus, meningitis, stroke overlap creating a dilemma in an acute emergency. We present a case whereby the clinical picture of status epilepticus was confused with eclampsia because of the presence of a rising blood pressure and proteinuria.
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PMID:Proteinuria in status epilepticus or eclampsia; a diagnostic dilemma. 1949 73

Neonatal hypoxic-ischemic encephalopathy (HIE) is a common cause of long-term neurological disability in children. Despite advances in supportive care, no treatments for HIE are available at present. The potential use of stem/progenitor cell therapies for neuroprotection or regeneration of the damaged adult brain has been evaluated in several preclinical studies, and the most promising results are now being tested in clinical trials. In recent years, the use of stem/progenitor cell transplantation in animal models of HIE has also been evaluated in several laboratories. It was shown that human umbilical cord blood mononuclear cells and mesenchymal stem/progenitor cells may have a therapeutic potential through multiple mechanisms acting locally in the central nervous system and possibly in peripheral organs of hypoxic-ischemic animals. Neural stem/progenitor cells (NSCs) have also been transplanted in animal models of HIE, migrating long distances to ischemic brain areas and differentiating into neurons. The results of these studies have raised important questions that must be addressed before these findings can be translated to the bedside. In this review, we give a critical overview of the different studies published up to now, and we discuss the endogenous regenerative potential of NSCs of the newborn brain when challenged by an HIE insult. We also discuss the use of cell therapies for the encephalopathy of prematurity.
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PMID:Cell therapy for neonatal hypoxic-ischemic encephalopathy. 1991 1

The role of the cerebral cortex in the cognitive deficits in preterm survivors is poorly understood. Periventricular leukomalacia (PVL), the key feature of encephalopathy of prematurity, is characterized by periventricular necrotic foci and diffuse gliosis in the surrounding cerebral white matter. Here, we tested the hypothesis that reductions in the density of layer I neurons and/or pyramidal neurons in layers III and/or V are associated with PVL, indicating cortical pathology potentially associated with cognitive deficits in long-term survivors. In controls (23 gestational weeks to 18 postnatal months) (n = 15), a lack of significant differences in pyramidal density among incipient Brodmann areas suggested that cytoarchitectonic differences across functional areas are not fully mature in the fetal and infant periods. There was a marked reduction (38%) in the density of layer V neurons in all areas sampled in the PVL cases (n = 17) compared to controls (n = 12) adjusted for postconceptional age at or greater than 30 weeks, when the six-layer cortex is visually distinct (P < 0.024). This may reflect a dying-back loss of somata complicating transection of layer V axons projecting through the necrosis in the underlying white matter. This study underscores the potential role of secondary cortical injury in the encephalopathy of prematurity.
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PMID:The cerebral cortex overlying periventricular leukomalacia: analysis of pyramidal neurons. 2033 17

Preeclampsia (PE) is associated with 3 main risks for the fetus: perinatal death, intrauterine growth restriction (IUGR), preterm birth. Perinatal mortality is increased in infants with IUGR or asphyxia. Conversely, mortality and morbidity associated with preterm birth are not altered by PE without IUGR or asphyxia. Very preterm infant with IUGR are exposed to high risk of prolonged respiratory insufficiency. Neurological complications of prematurity are not more frequent in infants born to mothers with PE. Nevertheless birth asphyxia, (i.e. placental abruption) is associated with impaired neurological out-come especially in infants with neonatal encephalopathy. Long term outcome of infants born to mothers with PE is strongly correlated to gestational age. IUGR increases the risk of hypertension and metabolic syndrome in adulthood. Acute fatty liver of pregnancy can by caused by a fetal fatty-acid oxidation disorder.
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PMID:[Prognosis in newborns after mother's preeclampsia]. 2047 88

The hypothalamic-pituitary-adrenal (HPA) axis is essential for maintaining homeostasis in the fetus and newborn. A proportion of extremely preterm infants suffer from transient adrenocortical insufficiency of prematurity. Although these infants have suboptimal adrenocortical response to stress in the first week of life, the HPA axis adapts rapidly, and most exhibit an adequate response by day 14. An attenuated cortisol response in preterm infants might be protective against intracranial bleeding. Severe hypoxic-ischemic encephalopathy is a potent stimulus to the HPA axis. Chronic intrauterine hypoxemia can up-regulate the setpoint of the HPA axis and augments adrenal steroidogenic production, resulting in sustained elevation of circulating cortisol levels.
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PMID:Effect of stress on the hypothalamic-pituitary-adrenal axis in the fetus and newborn. 2123 4

Neonatal brain injury, caused by perinatal hypoxia-ischemia and extreme prematurity, remains a great challenge for prevention and treatment. There is no effective treatment for term hypoxic-ischemic encephalopathy (HIE) except hypothermia which by itself does not afford complete neuroprotection. Erythropoietin (EPO), a pleiotropic cytokine, has neuroprotective effects in a series of neonatal experimental models and recent clinical trials of HIE. However, the mechanisms, dosing, and the toxicity of EPO in these settings are inconsistently reported. This review will focus on the possible mechanisms, recent clinical advances and potential complications of EPO used in research and the clinic. In addition, optimal dose and administrative routes of EPO, and novel EPO mimetics will be discussed.
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PMID:Erythropoietin for neonatal brain injury: opportunity and challenge. 2127 66

Periventricular leukomalacia (PVL) is the prototypic lesion in the encephalopathy of prematurity. Although PVL is identified by targeting cerebral white matter (WM), neuropathological and MRI studies document gray matter (GM) loss in cortical and subcortical structures. This study aimed to investigate the distribution of GM changes in children with a history of premature birth and PVL. Voxel-based morphometry was used to examine regional GM abnormalities in 22 children with a history of preterm birth and PVL. Preterms with PVL were compared with 22 terms and 14 preterms without PVL of similar GA and birth weight. GM and WM global volumetric volumes were found to decrease in comparison with both control groups. Regional GM volume abnormalities were also found: compared with their term peers, preterm children with PVL showed several regions of GM reduction. Moreover, PVL differed from preterms without PVL in the medial temporal lobe bilaterally, thalamus bilaterally, and caudate nuclei bilaterally. In addition, in our preterm sample with PVL, birth weight showed a statistical significant correlation with decreased GM regions. In conclusion, the voxel-based morphometry methodology revealed that PVL per se does involve GM reductions.
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PMID:Gray matter volume decrements in preterm children with periventricular leukomalacia. 2138 51

When asked to address the above question, findings that appeared to be among the most relevant included (1) interventions in the delivery room directed at supporting the physiological transition from intrauterine to extrauterine life rather than actively intervening in it; (2) recent data suggesting that keeping extremely low-gestational age neonates at a pulse oximeter saturation (SpO(2)) of 91-95% would increase their chances of survival compared with aiming for lower SpO(2) values; (3) using caffeine citrate in infants <1250 g with apnoea of prematurity improves neurodevelopmental outcome; (4) injecting antivascular epithelial growth factor into the vitreous seems to be an effective treatment for retinopathy of prematurity and (5) moderate hypothermia for perinatal hypoxic-ischaemic encephalopathy increases the likelihood of survival without neurological impairment. Here, data that support these recent changes in approach will be presented and discussed.
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PMID:What are the main research findings during the last 5 years that have changed my approach to clinical practice? 2186 86

The preterm birth has been increasing for the last decade. With the development of neonatal intensive care techniques, the survival rate of preterm infants is increased markedly. However, the brain of preterm infants is so vulnerable to injury that preterm brain injury has become an enormous public health problem. Hypoxia-ischemia and infection/inflammation are two main perinatal risk factors causing premyelinating oligodendrocyte and cortical neuron injury. Encephalopathy of prematurity is characterized by diffuse white matter injury and neuronal/axonal disruption, leading to neurological disabilities such as cognitive impairment and cerebral palsy. The advancement in imaging techniques, especially magnetic resonance imaging, provides more information for preterm brain injury and brain development, which contributes to the diagnosis and follow-up of the preterm infants. This article reviews the progress in encephalopathy of prematurity in order to open a new window to prophylaxis and management of this disease.
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PMID:[Progress in encephalopathy of prematurity]. 2200 Apr 27


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