Cerebral dysfunction after chronic hypoxia in children

O'Dougherty, Margaret; Wright, Francis S.; Loewenson, Ruth B.; Torres, Fernando

doi:10.1212/wnl.35.1.42

Cited by 63 publications

(32 citation statements)

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“…An increased frequency of such disabilities has also been reported in low-and verylow-birth-weight infants in the absence of cerebral palsy or other major handicaps [19]. Similar behavioral disabilities are evident in children exposed to chronic early postnatal hypoxia resulting from congenital heart defects [16], although, to our knowledge, behavioral assessments of children whose mothers underwent a laparoscopic procedure during gestation have not been conducted. Overall, this result is disturbing because it suggests that the physiologic effects of maternal pneumoperitoneum, as previously reported in fetal sheep [17], may manifest as postnatal neurologic impairment.…”

Section: Discussionmentioning

confidence: 68%

Early postnatal behavior deficits after maternal carbon dioxide pneumoperitoneum during pregnancy

et al. 2003

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Section: Discussionmentioning

confidence: 68%

Early postnatal behavior deficits after maternal carbon dioxide pneumoperitoneum during pregnancy

et al. 2003

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“…Certain heart defects, however, are repaired later in life, prolonging the hypoxic status. A significant negative correlation between age of corrective surgery (for cyanotic heart defects) and IQ scores has been shown, suggesting that longer periods of chronic hypoxia may reduce intelligence (O'Dougherty, 1983;O'Dougherty, 1985). Another advantage of surgery on neonates is the lower incidence of postoperative seizures in neonates than in older infants (Newburger et al, 1993).…”

Section: Age At Repairmentioning

confidence: 99%

Neurocognitive Consequences of Surgically Corrected Congenital Heart Defects: A Review

et al. 2006

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With advances in surgical procedures, neuropsychological assessment after congenital heart defects and pre, peri- and/or postoperative predictors of adverse outcome has become an important focus in research. We aim to summarize neuropsychological sequelae associated with different types of congenital heart defects, critically review the methodology used in more than 20 empirical studies that were retrieved from biomedical electronic search engines, and identify possible directions for future research. Despite the lack of adequate control groups and long-term studies, there seem to be some cognitive deficits. The largest group of children with isolated congenital heart defects present with normal intellectual capacities. However, they tend to show language deficits and motor dysfunction. Although performances on memory tasks are good, unambiguous conclusions concerning their attentional and executive functioning are still lacking. Serious behavioral problems are not an issue. In addition to a detailed description of the (neuro) psychological consequences of pediatric cardiac surgery, an overview of the predictors of the cognitive defects is provided.

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“…In children with CHD, long-term studies using standardized tests of academic achievement have demonstrated lower scores compared with the controls [54]. Multiple risk factors such as chronic hypoxia, anesthesia, and potentially low cerebral blood flow during cardiopulmonary bypass may be responsible for these learning disabilities [35][36][37].…”

Section: Introductionmentioning

confidence: 99%

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

Raman

Tkáč

Ennis

et al. 2005

Developmental Brain Research

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The cognitive deficits observed in children with cyanotic congenital heart disease suggest involvement of the developing hippocampus. Chronic postnatal hypoxia present during infancy in these children may play a role in these impairments. To understand the biochemical mechanisms of hippocampal injury in chronic hypoxia, a neurochemical profile consisting of 15 metabolite concentrations and 2 metabolite ratios in the hippocampus was evaluated in a rat model of chronic postnatal hypoxia using in vivo 1 H NMR spectroscopy at 9.4 T. Chronic hypoxia was induced by continuously exposing rats (n = 23) to 10% O 2 from postnatal day (P) 3 to P28. Fifteen metabolites were quantified from a volume of 9-11 Al centered on the left hippocampus on P14, P21, and P28 and were compared with normoxic controls (n = 14). The developmental trajectory of neurochemicals in chronic hypoxia was similar to that seen in normoxia. However, chronic hypoxia had an effect on the concentrations of the following neurochemicals: aspartate, creatine, phosphocreatine, GABA, glutamate, glutamine, glutathione, myoinositol, N-acetylaspartate (NAA), phosphorylethanolamine, and phosphocreatine/creatine (PCr/Cr) and glutamate/glutamine (Glu/Gln) ratios ( P b 0.001 each, except glutamate, P = 0.04). The increased PCr/Cr ratio is consistent with decreased brain energy consumption. Given the well-established link between excitatory neurotransmission and brain energy metabolism, we postulate that elevated glutamate, Glu/Gln ratio, and GABA indicate suppressed excitatory neurotransmission in an energy-limited environment. Decreased NAA and phosphorylethanolamine suggest reduced neuronal integrity and phospholipid metabolism. The altered hippocampal neurochemistry during its development may underlie some of the cognitive deficits present in human infants at risk of chronic hypoxia. D 2005 Elsevier B.V. All rights reserved.Theme: Other systems of the CNS Topic: Brain metabolism and blood flow

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Cerebral dysfunction after chronic hypoxia in children

Cited by 63 publications

References 0 publications

Early postnatal behavior deficits after maternal carbon dioxide pneumoperitoneum during pregnancy

Early postnatal behavior deficits after maternal carbon dioxide pneumoperitoneum during pregnancy

Neurocognitive Consequences of Surgically Corrected Congenital Heart Defects: A Review

In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus

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