Seizures, hypoxic‐ischemic brain injury, and intraventricular hemorrhage in the newborn

Hill, Alan; Volpe, Joseph J.

doi:10.1002/ana.410100202

Cited by 122 publications

(38 citation statements)

References 83 publications

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“…The "watershed" pattern of neuronal damage seen in this study, with damage greatest in the parasagittal cortex, is very similar to that seen in some asphyxiated term infants (13) and in the fetal sheep after transient cerebral ischemia (7). This supports the suggestion that impaired cerebral blood flow is critical in provoking and localizing neuronal injury (14)(15)(16).…”

Section: Discussionsupporting

confidence: 85%

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

et al. 1992

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ABSTRACT. Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebial histologic and electrophysiologic changes after as~hvxia in chronicallv instrumented late-gestation fetal sheep: We reduced uteiine blood flow to an ascending aortic blood oxygen content < 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA% region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult ( r = 0.75, p < 0.005) but not with the degree of hypoxia.No other factor was independently predictive, but, when considered separately, pH ( r = 0.54; p < 0.05) and loss of intensity of the EEG ( r = 0.61, p < 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to ~7 . 0 in six of eight fetuses with damage, whereas it remained >7.0 in five of six without damage ( p < 0.05).We conclude that severe intrauterine asphyxia for periods of 30 to 120 min can cause predominant parasagittal neuronal death and that this is associated with hypotension, severe metabolic acidosis, and suppression of EEG during the insult. These data are consistent with the suggestion that impairment of cerebral perfusion is a critical event in localizing cerebral damage during perinatal asphyxia. to the degree of cerebral damage (5, 6). Indeed, there remains considerable controversy regarding the factors that contribute to perinatal hypoxic ischemic encephalopathy. We therefore examined the histologic and electrophysiologic changes associated with asphyxia due to uterine artery occlusion of varying duration in fetal sheep. MATERIALS AND METHODSPregnant sheep from 1 19 to 128 d of gestation (term is 147 d) were instrumented under 2% halothane anesthesia with an adjustable occluder, made from Teflon-lined cardiac catheterization introducers and catheters, around the maternal common uterine artery. The ovarian arteries were ligated just proximal to the ovaries to prevent anastomotic perfusion. The fetus was then instrumented as previously described (7, 8). Polyvinyl catheters were inserted into fetal ascending aortic arteries and the amniotic cavity. Two pairs of shielded stainless steel recording electrodes were placed over the parietal dura, 10 mm lateral to bregma, and 5 mm and 15 mm anterior. In seven fetuses, a pair of stimulating electrodes was also placed 15 mm lateral and 10 mm anterior to bregma. Electrocardiographic electrodes were placed s.c. over the shoulders. In the fir...

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Section: Discussionsupporting

confidence: 85%

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

et al. 1992

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“…The se are topi cs of major clinical relevance since seizures in the neon ate are frequ entl y manifested by apnea and cyanosis (2).…”

Section: Meth Odsmentioning

confidence: 99%

31P Nuclear Magnetic Resonance Study of the Effect of Hypoxemia on Neonatal Status Epilepticus

et al. 1986

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METH ODSbolic perturbat ion imp osed by hypoxia, by seizures during normoxia, and by seizures during hypoxia. The se are topi cs of major clinical relevance since seizures in the neon ate are frequ entl y manifested by apnea and cyanosis (2).In measuring cerebral metabolic state , we employed high resolution 31P_NMRspectroscopy, a powerful technique for noninvasi ve, sequential measurement of brain energy change s in vivo (6-9). These in vivo measur ements were corro borated by in vitro determ inati on of brain metabolite concentratio ns. Systemic changes. Experiments were carri ed out in neonatal(1-to 10-day old) mongrel dogs as previously described (8). Halothane (0.5-3.0%) in oxygen was administered to allow tracheostom y. Haloth ane was then discontinued and the animals were paral yzed with pan curonium (0.2 ml admi nistered intraperitoneally) and mechanically ventilated with a gas mixture of 30% O2/7 0% N20 . In add ition to the use of nitrou s oxide for analgesia, all sites of incision were infiltrated with local anesthetic (xylocaine, 1%). The femoral art eries were catheterized to continuously monitor blood pressure and to anaerobically withdraw sampl es for determination of blood gases. The femoral vein was cath eterized to allow infusion of dru gs. Wounds were periodically infiltrated with xylocaine.Carbon dioxide tensions were normalized (PC0 2, 30-40 mm Hg) by adju sting minute ventilation. Thereafter, ventilator settings were not changed. Animals who had abno rmal acid-base statu s (base deficit> 5 mm ol HC0 3 / liter) were not entered into the study. Following a 30-min normalization period, animals were randomly assigned to one of four stud y groups: control group , hypoxia group, seizure-normox ia or seizure-hypoxia group. Th e durat ion of hypoxia, seizure, or seizure and hypoxia was 45 min. Animals in the hypoxia group or seizure-hypoxia group were ventilated with a gas mixtu re containing 8% O 2 / 92% N2• Animals in the contro l group or seizure-norm oxia group were ventilated with a gas mixtu re consisting of 30% O 2 / 70% N20. Seizures were induced in the seizure-normo xia and seizurehypoxia group s with an intravenous infusion of the 'Y amino but yric acid blocking agent , bicuc ulline (Sigma Co.), 2 mg/kg intravenou sly. Animals in the contro l and hypoxia groups received an equ ivalent volume of 0.9% saline intravenously.Blood gases were measured with a Radiom eter microblood gas analyzer. Plasma glucose levels were measured using a Beckm an G lucose Analyzer II; plasma lactate levels were measured spectrophotometrically using standard enzymatic anal yses (10). Plasma catech olamine concentratio ns were determined by radioenzymati c analysis (1 1).Cerebral phys iology. Th e EEG was continuo usly recorded with scalp electrodes and a Beckman polygraph ic recorder. An auto-58 1 Abbreviations 3IP_NM R, phosphorus-31 nuclear magnetic resonance CBF, cerebral blood flow PCr, phosphocreatine ABSTRACf. Prolonged neonatal seizures are often accompanied or exacerbated by hypoxemia. To determine the e...

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“…Cooke (2) and Milligan (20) have reported increases in the cerebral blood flow index in infants with hypercarbia and volume expansion who subsequently developed intraventricular hemorrhage. Similarly, others (13,24) have noted increased cerebral blood flow velocity in neonates with seizures prior to the development of intraventricular hemorrhage.…”

Section: Discussionmentioning

confidence: 74%

“…Numerous studies (6,8,9,13,14,(16)(17)(18)23) have correlated events known to alter cerebral blood flow, such as hypercarbia, volume expansion, and pneumothoraces, with intraventricular homorrhage. Cooke (2) and Milligan (20) have reported increases in the cerebral blood flow index in infants with hypercarbia and volume expansion who subsequently developed intraventricular hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Neuronal Development and Related Histochemistry

Inomata

Nasu

Tomiyasu

et al. 1989

Acta Histochem. Cytochem

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Seizures, hypoxic‐ischemic brain injury, and intraventricular hemorrhage in the newborn

Cited by 122 publications

References 83 publications

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

31P Nuclear Magnetic Resonance Study of the Effect of Hypoxemia on Neonatal Status Epilepticus

Neuronal Development and Related Histochemistry

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