Ictal and Interictal Electrographic Seizure Durations in Preterm and Term Neonates

Scher, Mark S.; Hamid, Marisha Y.; Steppe, Doris A.; Beggarly, Marquita E.; Painter, Michael J.

doi:10.1111/j.1528-1157.1993.tb02412.x

Cited by 170 publications

(93 citation statements)

References 10 publications

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“…Seizures were identified visually and defined as the concurrent appearance of sudden, repetitive, evolving stereotyped waveforms in the EEG signal lasting more than 10 seconds and of an amplitude greater than 20 mV. 23 Data were analyzed using SPSS 15.0 for windows (SPSS, Chicago, Il, USA) and JMP 8.0 (SAS Institute, Cary, NC, USA). For analysis of the recovery data after occlusion (from 1 to 168 hours post occlusion) the baseline period was taken as the mean of the 24 hours before occlusion.…”

Section: Methodsmentioning

confidence: 99%

Partial Neural Protection with Prophylactic Low-Dose Melatonin after Asphyxia in Preterm Fetal Sheep

Drury

Davidson

Bennet

et al. 2013

J Cereb Blood Flow Metab

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Melatonin is a naturally occurring indolamine with mild antioxidant properties that is neuroprotective in perinatal animals. There is limited information on its effects on preterm brain injury. In this study, 23 chronically instrumented fetal sheep received 25 minutes of complete umbilical cord occlusion at 101 to 104 days gestation (term is 147 days). Melatonin was administered to the ewe 15 minutes before occlusion (0.1 mg/kg bolus followed by 0.1 mg/kg per hour for 6 hours, n ¼ 8), or the equivalent volume of vehicle (2% ethanol, n ¼ 7), or saline (n ¼ 8), or maternal saline plus sham occlusion (n ¼ 8). Sheep were killed after 7 days recovery in utero. Fetal blood pressure, heart rate, nuchal activity, and temperature were similar between groups. Vehicle infusion was associated with improved neuronal survival in the caudate nucleus, but greater neuronal loss in the regions of the hippocampus, with reduced proliferation and increased ameboid microglia in the white matter (Po0.05). Maternal melatonin infusion was associated with faster recovery of fetal EEG, prolonged reduction in carotid blood flow, similar neuronal survival to vehicle, improved numbers of mature oligodendrocytes, and reduced microglial activation in the white matter (Po0.05). Prophylactic maternal melatonin treatment is partially protective but its effects may be partly confounded by ethanol used to dissolve melatonin. Keywords: asphyxia; brain; ethanol; melatonin; neuroprotection; preterm fetus INTRODUCTION Birth asphyxia is relatively common with preterm birth, and remains a significant cause of neonatal death and neurodevelopmental delay. 1 Excess free radical production during asphyxia and early reperfusion are associated with lipid peroxidation, nucleic acid damage, and mitochondrial dysfunction that promote cell death. 2 Melatonin is a naturally occurring indolamine involved in circadian rhythm, which also has antioxidant properties. 3,4 It readily crosses the human and ovine placentae making it an attractive option for prophylactic treatment of fetuses at high risk of perinatal hypoxia. 4 Melatonin given before and immediately after hypoxia-ischemia is neuroprotective in postnatal rodents. [5][6][7][8][9] Postnatally, high-dose (5 mg/kg per hour over 6 hours) melatonin given immediately after hypoxia-ischemia in term piglets augmented protection from therapeutic hypothermia on both magnetic resonance spectroscopy markers of anaerobic stress, and histopathology. 10 In contrast, there have been few studies of antenatal treatment and relatively limited large-animal evidence that prophylactic lowdose melatonin can protect against hypoxic-ischemic injury in the preterm fetus. In fetal sheep, Miller et al 11 showed that maternal prophylactic melatonin (1 mg total) given before 10-minute umbilical cord occlusion at term-equivalent was associated with reduced brain lipid peroxidation, neuronal death, microglial activation, and astrogliosis. 11,12 In preterm fetal sheep at 0.6 gestation (Term ¼ 147 days) fetal infusion of high-dose (20 mg/kg) J...

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Section: Methodsmentioning

confidence: 99%

Partial Neural Protection with Prophylactic Low-Dose Melatonin after Asphyxia in Preterm Fetal Sheep

Drury

Davidson

Bennet

et al. 2013

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…Seizures were identified visually from the raw EEG and defined as the concurrent appearance of sudden, repetitive, evolving stereotyped waveforms in the EEG signal lasting more than 10 s and of an amplitude greater than 20 μV (39). Physiological data were evaluated by ANOVA with time as a repeated measure (SPSS v15, SPSS, Chicago, IL) followed by one-way ANOVA post hoc test when a significant overall effect was found.…”

Section: Discussionmentioning

confidence: 99%

Limited predictive value of early changes in EEG spectral power for neural injury after asphyxia in preterm fetal sheep

et al. 2012

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“…Seizures were identified visually on the raw EEG record and defined as the concurrent appearance of sudden, repetitive, evolving stereotyped waveforms in the EEG signal lasting more than 10 secs and of an amplitude greater than 20 mV (Scher et al, 1993). Only episodes for which stable tPO 2 recordings were available were analyzed.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Oxygenation during Postasphyxial Seizures in Near-Term Fetal Sheep

González

Hunter

Bennet

et al. 2005

J Cereb Blood Flow Metab

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After exposure to asphyxia, infants may develop both prolonged, clinically evident seizures and shorter, clinically silent seizures; however, their effect on cerebral tissue oxygenation is unclear. We therefore examined the hypothesis that the increase in oxygen delivery during postasphyxial seizures might be insufficient to meet the needs of increased metabolism, thus causing a fall in tissue oxygenation, in unanesthetized near-term fetal sheep in utero (gestational age 12571 days). Fetuses were administered an infusion of the specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine, followed by 10 mins of asphyxia induced by complete umbilical cord occlusion. The fetuses then recovered for 3 days. Sixty-one episodes of electrophysiologically defined seizures were identified in five fetuses. Tissue PO 2 (tPO 2 ) did not change significantly during short seizures (o3.5 mins), 5.270.2 versus baseline 5.670.1 mm Hg (NS), but fell to 2.270.2 mm Hg during seizures lasting more than 3.5 mins (Po0.001). During prolonged seizures, cortical blood flow did not begin to increase until tPO 2 had begun to fall, and then rose more slowly than the increase in metabolism, with a widening of the brain to blood temperature gradient. In conclusion, in the immature brain, during prolonged, but not short seizures, there is a transient mismatch between cerebral blood flow and metabolism leading to significant cerebral deoxygenation.

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Ictal and Interictal Electrographic Seizure Durations in Preterm and Term Neonates

Cited by 170 publications

References 10 publications

Partial Neural Protection with Prophylactic Low-Dose Melatonin after Asphyxia in Preterm Fetal Sheep

Partial Neural Protection with Prophylactic Low-Dose Melatonin after Asphyxia in Preterm Fetal Sheep

Limited predictive value of early changes in EEG spectral power for neural injury after asphyxia in preterm fetal sheep

Cerebral Oxygenation during Postasphyxial Seizures in Near-Term Fetal Sheep

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