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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There were 17 survivors of severe neonatal respiratory distress treated with IPPV for more than 24 hours (36-520 hrs, mean duration of IPPV 6 days) followed into the second year of life. 11 of these young children were physically and neurologically normal. 3 were developmentally retarded (3 months or more), 2 had neurological defects without mental subnormality. These defects (Hemiplegia and Diplegia) were correlated with low gestational ages (32 and 33 weeks respectively) 1 child was severely defective. This one was treated because of apnea caused by seizures in postmaturity syndrome (44 weeks gestation). The overall incidence of defects was 3/17 (= 17%).
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PMID:[Development after respiratortreatment during the newborn period (author's transl)]. 94 49

Over a period of one year, 16,365 consecutively live born neonates were prospectively studied for evidence of birth asphyxia using the requirement of greater than one minute of positive pressure ventilation for identifying infants suffering from birth asphyxia. Asphyxia occurred in 2.8% of all neonates. Multivariate analysis of high risk factors associated with increased risk of asphyxia showed that low birth weight was the most significant predictor of asphyxia: asphyxia occurred in 68% of infants of less than 1,000 g birth weight and decreased to 1.2% in infants of 3-4 kg birth weight. Perinatal risk factors associated with a higher incidence of asphyxia include: postmaturity, birth weight (less than or equal to 2.5 kg) and with the presence of maternal and/or obstetric complications. The impact of asphyxia on neonatal mortality was most pronounced in more mature infants and the mortality was increased 3 fold in infants of less than 34 week gestation and greater than 27 fold for infants greater than 38 week gestation. Of the asphyxiated neonates, intrauterine growth retardation, fetal macrosomia, hypothermia, hyaline membrane disease, seizures, hypoglycemia and hyponatremia were significantly associated with an increased risk of death.
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PMID:Perinatal risk factors in birth asphyxia: relationship of obstetric and neonatal complications to neonatal mortality in 16,365 consecutive live births. 262 78

The dramatic reduction in perinatal morbidity and mortality over the last decade has not been accompanied by any diminution in the incidence of cerebral palsy. We investigated retrospectively the relationship of certain perinatal events to the subsequent development of cerebral palsy in 75 infants. Cerebral palsy occurred in association with acute intrapartum asphyxia in 8% and traumatic delivery in 11%. Thirty-five percent of cases were associated with chronic fetal distress, defined by a unique fetal heart rate (FHR) pattern consisting of a normal baseline rate with persistently absent variability and mild variable decelerations with overshoot. This pattern was found frequently in association with postmaturity, meconium staining, intrauterine growth retardation, and neonatal seizures. Acid-base studies, when available, did not reveal acidosis. Twenty-seven percent of the cases involved a combination of chronic fetal distress, acute intrapartum fetal asphyxia, and/or traumatic delivery. We postulate that antenatal intermittent umbilical cord compression secondary to oligohydramnios results in repetitive transient central nervous system ischemia, insufficient to cause death, but resulting in a characteristic FHR pattern and impaired neurologic development. If these data are confirmed, this FHR pattern may be an important marker for the development of subsequent neurologic handicap or other adverse outcome.
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PMID:Perinatal antecedents of cerebral palsy. 270 35

This investigation is, to our knowledge, the first population-based case-control study of prenatal, perinatal, and postnatal risk factors for generalized tonic-clonic seizures (GTCS). The clinical diagnosis of GTCS was confirmed through the independent review of the complete medical history of potential cases by three neurologists. All subjects with onset of GTCS before age 30 who were residents of Rochester, Minnesota at time of diagnosis between 1935 and 1979, and who were born in this community, were included (N = 53). Two controls were matched to each patient, and for both patients and controls, the unique records-linkage system for residents of Rochester was used to obtain information about possible risk factors. A history of convulsions in the mother, febrile seizures, and head trauma were significantly more common in cases than in controls. However, factors previously suggested such as: advanced age of the mother, previous miscarriages, gestational toxemia or eclampsia, bleeding during the index pregnancy, low birth weight, asphyxia, or postmaturity were not confirmed. Based on the present and previous studies, we suggest that different types of seizures have different risk factors and should, therefore, be investigated separately.
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PMID:Risk factors for generalized tonic-clonic seizures: a population-based case-control study in Rochester, Minnesota. 361 51

Seven patients, six boys and one girl, ranging in age from 2 years 7 months to 5 years 6 months at first contact, presented with severe language delay and dysphasic errors. They were found to have markedly abnormal EEGs despite the fact that only two of the children had had febrile seizures. The EEG abnormalities consisted to spike-wave or sharp wave discharges in focal or bilateral synchronous fashion, and were not affected by anticonvulsants. The children had normal motor development and no dysmorphic features. Results of neurological examinations were normal. CT and isotope scans were unrevealing. Intelligence, measured by a non-verbal scale, was normal. The authors suggest that an electrophysiological disturbance was the underlying cause of both the language deficits and the EEG abnormalities. The remarkably frequent occurrence of postmaturity (five of the seven cases) suggests that perinatal events may be an etiological factor.
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PMID:Development dysphasia and electroencephalographic abnormalities. 617 37