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

Asphyxial seizures occurred in 89 of 101,829 infants born alive at term (0.87/1000) in three large maternity hospitals from January 1980 to December 1984. These seizures were significantly associated with antenatal complications, primiparity, and prolonged pregnancy. Meconium staining of the amniotic fluid was also associated with asphyxial seizures, but there were high false positive (11%) and false negative (50%) rates. Fifteen of the infants who had seizures died (18%) and 21 (25%) were handicapped at 1 year. Outcome was most successfully predicted by the way the infant was feeding at 1-2 weeks. All infants taking more than half their estimated requirements by mouth at 1 week were normal, and those still being fed by tube at 2 weeks were handicapped.
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PMID:Neonatal seizures: the Dublin Collaborative Study. 317 66

A review of 46 perinatal deaths was conducted using a 1982 to 1985 regional perinatal network database of 6701 delivered postdate (greater than or equal to 42 weeks gestation) infants. Perinatal mortality (6.9 per 1000 births) increased as gestational age advanced beyond 42 weeks, and was higher in young teenagers or mothers with some additional antenatal complications, such as hypertension. Meconium staining of the amniotic fluid, low Apgar scores, low birthweight, congenital malformations, and neonatal complications, including pneumothorax, meconium aspiration, and seizures, were associated with perinatal death.
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PMID:Postdate pregnancies: a review of 46 perinatal deaths. 365 Nov 86

The authors used the compounds 2-methyl-3)2-phenyl-3-methyl tetrahydroxasino)-propiophenone hydrochloriad (code PsI) and 1-phenoxycarboxy-1-phenyl-2-methyl-3 (2-phenyl-3-methyl-tetrahydroxasino-propan hydrochlorid(code P3) and carried out the following studies: influence of tripamine, corasol and strichnine seizures 1-phenoxycarboxy--1-phenyl-2-methyl--3 (2-phenyl--3-methyl-tetrahydroxasino) propar hydrochlor (Code P8) in white mice, effect on the hypertensive action of reserpine in white rats, investigations on the analeptic action in urethanized cats as well as on the analgetic effect, examined both by the test of "hot plate" and the method of Hendreshot-Forsaith. The examined compounds, administered in a dose of 1/6 of LD50, showed analgetic effect weaker than that of the preparations Morphinum hydrochloricum and Analigin, but their analeptic effect was less manifested that of of corasol. Similar to MAO-inhibitor-oproniazid although in smaller degree the compound PS1 potentiated tripamine seizures and inverted the hypotensive effect of Reserpine into hypertensive.
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PMID:[Pharmacological studies of 2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propiophenone hydrochloride and 1-phenoxycarboxy-1-phenyl-2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propane hydrochloride compounds]. 610 91

Passage of meconium in utero is a serious neonatal disorder carrying high morbidity and mortality. Role of planned team approach with aggressive intrapartum suctioning and intensive neonatal management was studied to evaluate its impact on neonatal morbidity and mortality. Meconium Stained Amniotic Fluid (MSAF) was found amongst 7.4% of all deliveries and among these 238 (10.5%) babies developed meconium aspiration syndrome (MAS). Ninety five per cent babies with MSAF were born at > 36 weeks of gestation and 76% were more than 2.5 kg. Passage of thick and thin meconium was seen in 44 and 56% respectively. Passage of thick meconium was significantly associated with severe asphyxia and carried a bad prognosis with increased risk of development of meconium aspiration syndrome, hypoxic schemic encephalopathy, seizures and pulmonary air leak syndrome. Aggressive team approach was responsible for lowering the mortality to 7.7%.
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PMID:Management of meconium stained amniotic fluid: a team approach. 840 22

We conducted a prospective cohort study of 323 consecutively born very low birth weight infants (< or = 1499 gm) to determine any association between prenatal cocaine exposure and (1) intracranial ultrasonographic abnormalities and (2) other adverse perinatal outcomes. The infants were assigned to either a cocaine-exposed group (n = 86) or a cocaine-nonexposed group (n = 146) on the basis of combined detection methods for prenatal maternal cocaine abuse including maternal history, maternal and infant urine immunoassay (Emit), and meconium analysis (high-performance liquid chromatography and gas chromatography-mass spectrometry). Ninety-one infants were not assigned because of early death before complete testing (n = 80) or missed tests (n = 11). The detected incidence of cocaine exposure in the assigned population was 37% (86/232). Meconium testing with high-performance liquid chromatography and gas chromatography-mass spectrometry was the sole means of detection in 30% (26/86) of cases. The cocaine-nonexposed infants did not differ from the cocaine-exposed infants in the incidence of intraventricular hemorrhage (36% vs 35%), grades III and IV intraventricular hemorrhage (14% vs 14%), or periventricular leukomalacia (4% vs 2%). Adverse outcomes increased by cocaine exposure were abruptio placentae (8% vs 18%; p = 0.046), surgical ligation of a patent ductus arteriosus (1% vs 7%; p = 0.02), and seizures (5% vs 17%; p = 0.004). We conclude that prenatal cocaine exposure does not increase the incidence or severity of intracranial hemorrhage or periventricular leukomalacia but does increase the risk of abruptio placentae, surgical ligation of a patent ductus arteriosus and seizures in very low birth weight infants.
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PMID:Risk of intracranial hemorrhage and other adverse outcomes after cocaine exposure in a cohort of 323 very low birth weight infants. 844 Nov 3

> Objective: To describe the perinatal characteristics of neurologically impaired infants with normal intrapartum fetal heart rate (FHR) patterns. Methods: In a registry of 300 neurologically impaired singleton term infants, a retrospective chart review was undertaken to analyze those patients with a normal intrapartum FHR pattern, i.e. reactive FHR pattern with a normal baseline rate throughout labor, and a subsequent finding of central nervous system impairment. Neonates with an abnormal intrapartum FHR pattern or a traumatic birth were excluded. In addition, the four criteria necessary for intrapartum asphyxia were as follows: arterial pH <7.00, Apgar score </=3 for 5 min, neonatal neurologic sequelae, such as seizures, and multiorgan system dysfunction. Infants were then categorized according to the timing of probable fetal injury. Results: Of the 300 infants in the registry, 24 (8%) neonates were identified. Six (25%) of these were considered postdates. Primary antenatal complications included early pregnancy bleeding (3 (13%)), cigarette and/or alcohol use (4 (17%)), and polyhydramnios (2 (8%)). Meconium was found in 12 patients (50%) during labor; of these, two (8%) patients had meconium aspiration syndrome and required extra corporeal membrane oxygenation (ECMO). None of the infants satisfied the four criteria for intrapartum asphyxia. Sixteen (67%) neonates were discharged with their mothers. The remaining eight neonates were admitted to the neonatal intensive care unit, and two (8%) neonatal deaths occurred due to meconium aspiration syndrome and sudden infant death syndrome. The long term neurologic outcome of the 22 survivors ranged from 3 to 14 years and included the following: developmental delay (10 (45%)), seizure disorder (7 (32%)), cerebral palsy (11 (50%)), and mental retardation (4 (17%)). None of these infants appeared to have been injured during labor. The probable timing of neurologic injury appeared to be early pregnancy (13 (54%)) or postnatally (11 (46%)). Conclusions: Infants who are later found to be neurologically impaired can have normal intrapartum FHR patterns during labor. These neurologic injuries seem to occur in early pregnancy or after birth. In the absence of fetal trauma, these findings suggest that a reactive intrapartum FHR pattern is not associated with intrapartum fetal asphyxia.
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PMID:Normal Fetal Heart Rate Pattern in the Brain-damaged Infant: A Failure of Intrapartum Fetal Monitoring? 968 57

Incidental reports suggest that antenatal treatment of pyridoxine dependent seizures (PDS) may improve neurodevelopmental outcome of affected patients. Two families with PDS are reported, both with two affected siblings. Antenatal treatment with pyridoxine was instituted during the second pregnancy in each family (50 and 60 mg daily from 3 and 10 weeks of gestation, respectively). Perinatal characteristics and neurodevelopmental outcome at 4 (Family A) and 12 (Family B) years of age were compared between the untreated and treated child within each family. Meconium-stained amniotic fluid was present in both first pregnancies and abnormal foetal movements were noticed in one. In the treated infants, pregnancy and birth were uncomplicated. In family A, postnatal pyridoxine supplementation prevented neonatal seizures. Both children in family A were hypotonic and started walking after 2 years of age; both had white matter changes on MRI, and the first child was treated for squint. IQ was 73 and 98 in the antenatally untreated and treated child, respectively. The second child in family B developed seizures on the seventh day, because pyridoxine maintenance therapy had not been instituted after birth. Seizures responded rapidly to pyridoxine supplementation. MRI showed large ventricles and a mega cisterna magna. IQ was 80 and 106 in the antenatally untreated and treated child respectively. Both children had normal motor development. These results suggest that antenatal pyridoxine supplementation may be effective in preventing intrauterine seizures, decreasing the risk of complicated birth and improving neurodevelopmental outcome in PDS.
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PMID:Antenatal treatment in two Dutch families with pyridoxine-dependent seizures. 1958 65