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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Birth asphyxia is O2i CO2 exchange disorder during the labour, with consequent hypoxia and ischemia. The term "asphyxia" has been used unprecisely quite often. The most frequently used criteria for birth asphyxia have been: fetal bradycardia, meconium stained amniotic fluid, fetal acido-base status with umbilical artery pH value below 7.10, low Apgar score and need for endotracheal intubation. The correct Apgar score quantification depends on the examiner. Fetal acido-base status measured in umbilical artery could be useful biochemical parameter of birth asphyxia. Only if the fetal oxygen supply during the labour is severe and long enough disturbed, the neurological abnormalities will develop later. Our study has enrolled 70 children with various degree of motor impairment, detected during neonatal period and/or infancy. They have been followed up till 24 months chronological age for term neonates and 24 months corrected age for prematures. 34 children out of them have developed clear clinical signs of cerebral palsy. Birth asphyxia as a possible cause of cerebral palsy has been documented in 10 cases, e.g. 29.4%. The criteria for birth asphyxia have been low Apgar score, meconium stained amniotic fluid and clinical signs of hypoxic-ischemic encephalopathy. Fetal blood gas and acido-base measurements obtained from umbilical artery at delivery have been an important parameter of intrapartal asphyxia. Those measurements should be introduced as a routine method in our practice, in the cases of fetal heart deceleration, to asses the extent of fetal acidosis.
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PMID:[Birth asphyxia as a cause of cerebral palsy]. 1121 10

Hypoxic ischemia is a common cause of damage to the fetal and neonatal brain. Although systemic and cerebrovascular physiologic factors play an important role in the initial phases of hypoxic-ischemic injuries, the intrinsic vulnerability of specific cell types and systems in the developing brain may be more important in determining the final pattern of damage and functional disability. Excitotoxicity, a term applied to the death of neurons and certain other cells caused by overstimulation of excitatory, mainly glutamate, neurotransmitter receptors, plays a critical role in these processes. Selected neuronal circuits as well as certain populations of glia such as immature periventricular oligodendroglia may die from excitotoxicity triggered by hypoxic ischemia. These patterns of neuropathologic vulnerability are associated with clinical syndromes of neurologic disability such as the extrapyramidal and spastic diplegia forms of cerebral palsy. The cascade of biochemical and histopathologic events triggered by hypoxic ischemia can extend for days to weeks after the insult is triggered, creating the potential for therapeutic interventions.
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PMID:Neurobiology of hypoxic-ischemic injury in the developing brain. 1138 30

Hypoxic-ischemic injury to the prenatal and perinatal brain is a major contributor to morbidity and mortality to infants, often leading to mental retardation, seizures, and cerebral palsy. The susceptibility of the immature CNS to hypoxia-ischemia is largely dependent on the temporal and regional status of critical developmental processes, as well as on the regulation of cerebral blood flow and metabolism. The molecular and biochemical mechanisms of acute injury to the neonatal brain in experimental rodent and murine models of hypoxic-ischemic and ischemic injury, including disturbances of intracellular homeostasis, role of glutamate receptors, free radicals and transitional ions, as well as the modifying role of gene expression to cell death/survival will be reviewed in this chapter.
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PMID:Molecular and biochemical mechanisms of perinatal brain injury. 1148 16

Hypoxia-ischemia (HI) is a leading cause of white matter damage, a major contributor to cerebral palsy in premature infants. Preferential white matter damage is believed to result from vulnerability of the immature oligodendrocyte (the pro-OL) to factors elevated during ischemic damage, such as oxygen free radicals and glutamate. In order to determine whether pro-OLs undergo apoptotic death after HI, we analyzed periventricular white matter OLs in P7 rats 4, 12 and 24 h after HI to analyze the time course and mode of cell death. DNA fragmentation was seen at 12 and 24 h of recovery after HI, representing a 17-fold increase over control. In addition, caspase-3 activation was found in NG2+ pro-OLs at 12 h. Electron-microscopic analysis of cell death in the white matter revealed a transition from early necrotic deaths to hybrid cell deaths to classical apoptosis between 4 and 24 h of recovery from HI. The delayed time course of apoptosis in pro-OLs supports the feasibility of interventions to improve clinical outcomes for newborns surviving birth asphyxia.
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PMID:Perinatal hypoxia-ischemia induces apoptotic and excitotoxic death of periventricular white matter oligodendrocyte progenitors. 1159 21

Cerebral hypoxia/ischemia of the newborn has a frequency of 4/1,000 births and remains a major cause of cerebral palsy, epilepsy, and mental retardation. Despite progress in understanding the pathogenesis of hypoxic-ischemic injury, the data are incomplete regarding the mechanisms leading to permanent brain injury. Here we tested the hypothesis that cerebral hypoxia/ischemia damages stem/progenitor cells in the subventricular zone (SVZ), resulting in a permanent depletion of oligodendrocytes. We used a widely accepted rat model and examined animals at recovery intervals ranging from 4 h to 3 weeks. Within hours after the hypoxic-ischemic insult 20% of the total cells were deleted from the SVZ. The residual damaged cells appeared necrotic. During 48 h of recovery deaths accumulated; however, these later deaths were predominantly apoptotic. Many apoptotic SVZ cells stained with a marker for immature oligodendrocytes. At 3 weeks survival, the SVZ was smaller and markedly less cellular, and it contained less than 1/4 the normal complement of neural stem cells. The corresponding subcortical white matter was dysmyelinated, relatively devoid of oligodendrocytes and enriched in astrocytes. We conclude that neural stem cells and oligodendrocyte progenitors in the SVZ are vulnerable to hypoxia/ischemia. Consequently, the developmental production of oligodendrocytes is compromised and regeneration of damaged white matter oligodendrocytes does not occur resulting in failed regeneration of CNS myelin in periventricular loci. The resulting dysgenesis of the brain that occurs subsequent to perinatal hypoxic/ischemic injury may contribute to the cognitive and motor dysfunction that results from asphyxia of the newborn.
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PMID:Hypoxia/ischemia depletes the rat perinatal subventricular zone of oligodendrocyte progenitors and neural stem cells. 1159 26

There is growing evidence that a large number of very low birth weight infants are exhibiting neurobehavioral problems in the absence of cerebral palsy at follow-up that has extended into school age and adolescence. Many clinical factors (ie, chronic lung disease, recurrent apnea and bradycardia, transient hypothyroxemia of prematurity, hyperbilirubinemia, nutritional deficiencies, glucocorticoid exposure), as well as stressful environmental conditions, including infant-provider interaction, constant noise, and bright light, may act in combination to impact on the developing brain, even in the absence of overt hemorrhage and/or ischemia. Any potential intervention strategy designed to prevent cognitive and behavioral problems has to account for the numerous biological and clinical conditions and/or interventions, as well as postdischarge social and environmental influences.
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PMID:Neurobehavioral deficits in premature graduates of intensive care--potential medical and neonatal environmental risk factors. 1173 57

In the premature infant, hypoxic-ischemic damage to the cerebral white matter [periventricular leukomalacia (PVL)] is a common and leading cause of brain injury that often results in chronic neurologic disability from cerebral palsy. The cellular basis for the propensity of white matter injury to occur in the developing brain and the greater resistance of the adult white matter to similar injury remains unknown. By using a neonatal rat model of hypoxic-ischemic injury, we found that the mechanism of perinatal white matter injury involved maturation-dependent vulnerability in the oligodendroctye (OL) lineage. The timing of appearance of late OL progenitors was the major developmental factor that accounted for the susceptibility of the neonatal white matter to injury. Late OL progenitors were the major OL lineage stage killed by apoptosis, whereas early OL progenitors and more mature OLs were highly resistant. The density of pyknotic late OL progenitors was significantly increased in the ischemic hemisphere (67 +/- 31 cells/mm2) versus the control hemisphere (2.2 +/- 0.4 cells/mm2; mean +/- SEM; p = 0.05), which resulted in the death of 72 +/- 6% of this OL stage. Surviving late OL progenitors displayed a reactive response in which an increase in cell density was accompanied by accelerated maturation to a P27/kip1-positive oligodendrocyte. Because we showed recently that late OL progenitors populate human cerebral white matter during the high risk period for PVL (Back et al., 2001), maturation-dependent vulnerability of OL progenitors to hypoxia-ischemia may underlie the selective vulnerability to PVL of the white matter in the premature infant.
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PMID:Selective vulnerability of late oligodendrocyte progenitors to hypoxia-ischemia. 1178 90

Cyclooxygenase-2 (COX-2) is known to be expressed in rat brain and up-regulated by ischemia. The administration of COX inhibitors before as well as soon after the ischemic insult reduces the extension of cerebral damage in rats. Overexpression of COX-2 has also been shown in the ischemic brain of adult human patients, while no information concerning COX-2 expression in neonatal ischemia is available. Intrapartum asphyxia and perinatal brain injury may result in cerebral palsy, mental retardation or epilepsy. COX-2 expression in the brain of neonates delivered after severe birth asphyxia was investigated using immunohistochemistry. Meningeal vessel walls of term and preterm babies widely expressed COX-2 immunoreactivity, as did periventricular large vessels in preterms. A number of brain cells (mature and immature cortical, periventricular and basal ganglia neurons, and oligodendrocytes of the cerebral white matter in brains from term neonates) also expressed COX-2. The present findings suggest that COX-2 may take part in enhancing neonatal brain damage via different mechanisms, such as those involving excitotoxicity and production of reactive oxygen species.
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PMID:Cyclooxygenase-2 immunoreactivity in the ischemic neonatal human brain. An autopsy study. 1184 93

Neuropathologic findings in stillbirths oftentimes provide insight into the specific mechanisms leading to death. Examination of the brains of stillborn infants may also identify pathophysiologic processes that result in prenatal brain injury in liveborn as well as stillborn infants and that lead to neurologic disorders in liveborn infants, such as cerebral palsy or the sudden infant death syndrome (SIDS). A variety of abnormalities are found in the brains of stillborns, the most common including cerebral white matter necrosis (periventricular leukomalacia) or gliosis, germinal matrix or intraventricular hemorrhage, cerebral infarcts, pontosubicular necrosis, and spinal cord or brainstem necrosis. The 2 major hypotheses that have been proposed for the pathophysiology of cerebral white matter injury in the perinatal period are hypoxia/ischemia and infection/cytokines as the basis for injury. The fetal brain may be selectively vulnerable to various insults at specific stages of development.
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PMID:Neuropathology associated with stillbirth. 1187 72

The infants' brain during the prenatal, perinatal and neonatal periods is susceptible to injury. Many problems in the perinatal period often result in bleeding, ischemia and other pathological changes in the infant brain. Which can subsequently cause cerebral palsy or developmental disorders. Unless they are discovered early and measures are taken, permanent brain damage may remain. Although neurological examinations at this stage is very difficult, it is very important to be familiar with neurological signs and assessment of extremely and very low birth weight infants and to discover early any abnormal findings of diseases such as neonatal asphyxia, intraventricular haemorrhage, periventricular leukomalacia, neonatal seizures and hydrocephalus.
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PMID:[Neurological signs and assessment of extremely and very low birth weight infants]. 1190 9


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