2004, Number 1
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ABSTRACTDespite recent advances in perinatal care resulting in reduced neonatal mortality, the incidence of cerebral palsy and/or mental retardation has not decreased. Perinatal hypoxia is one of the major causes of developmental disabilities. In India, perinatal asphyxia is a frequent pathological entity and causes approximately 20% of perinatal deaths. Nagdyman y cols. reported that one third of the children born with asphyxia showed an ischemichypoxic encephalopathy.
EEG recordings are very useful to evaluate hypoxic newborns. Depression of EEG activity shows a high correlation with neurological deterioration in infants. Many authors consider EEG to have prognostic value. Van Lieshou y cols. emphasized the correlation between EEG and clinical outcome, even to predict minor sequelae (adverse consequences).
Another important perinatal risk factor is prematurity. Periventricular-intraventricular haemorrhage and periventricular leukomalacia are serious forms of brain injury in the premature newborn and could be responsible for death or severe neurological sequelae in infancy. These injuries can also be detected by serial EEGs.
The present study has two goals: 1) to describe the neurological complications observed in a group of children with perinatal risk factors that were studied in our laboratory, and 2) to describe Computed Tomography findings consisting of generalized hypodensities, that we know to have been reported previously only in subjects with cardiac arrest.
We studied 34 newborn infants from the Materno-Infantil and General Hospitals from Querétaro. All had a history of perinatal risk factors, the majority with moderate to severe asphyxia (25 cases). In 22 infants CT scans were obtained and 14 were examined by transfontanellar ultrasonography with doppler. In 23 infants EEGs were recorded, and in 16 of them, serial EEGs were obtained.
Important CT hypodensities of the cortical gray matter, all of which also involved the white cortical matter, were observed in 7 infants. In these children the thalamus, the basal ganglia and the structures of the posterior fossa had normal density. These children showed consistently abnormal EEG activity with slow wave focus and paroxysmal activity.
In another six cases periventricular leukomalacia was observed. Two of these children also had other pathologies: one had a brain infarct and cerebellar atrophia, and the other one had an extended brain infarct. All the six children also showed enlarged lateral ventricles.
In many other children ventricle enlargement was seen, with concomitant EEG abnormalities including hemispheric asymmetries, paroxysmal activity and poorly characterized sleep waves.
The most characteristic observation in cranial ultrasonography was the enlargement of the interhemispheric sulcus that was frequently accompanied by EEG abnormalities.
We conclude that there are neurological complications that may be accompanied by structural abnormalities that may be very severe, and EEG abnormalities that are maintained for several months in the group of children studied with moderate to severe perinatal hypoxia. Our results emphasize the importance of preventing perinatal hypoxia and of early intense neurohabilitatory intervention in order to try to reduce its subsequent consequences.
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