Perinatal risk factors in children with serious motor and mental handicaps

Nelson, Karin B.; Broman, Sarah H.

doi:10.1002/ana.410020505

Cited by 93 publications

(34 citation statements)

References 8 publications

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“…The tonic phase was associated with apnea and urinary incontinence. The tonic posture and apneic episodes lasted for [3][4][5] min. Thereafter, tonic-clonic seizures commenced with associated swimming-like movements which continued until interrupted by another tonic or clonic fit.…”

Section: Institutional Approvalmentioning

confidence: 99%

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Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

et al. 1995

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Section: Institutional Approvalmentioning

confidence: 99%

“…On the othe~. hand, both published and unpublished experimental studies in immature animals of most, although not all, species have failed to demonstrate that even prolonged seizures (status epilepticus) lead to overt brain injury (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14] (see "Discussion").…”

mentioning

confidence: 99%

Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

et al. 1995

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“…The authors' previous study 59 of CBF following asphyxial insult of 15 minutes demonstrated profound decreases in flow to all cerebral regions examined. Based on the predictive value of a low 5-minute Apgar score 25 and the practical time of instituting life-saving support measures, 60 5 minutes of asphyxia followed by a 5-minute resuscitation phase were chosen for this experiment. Drug (i.e., nimodipine) was administered as soon as might be practically possible.…”

Section: A6a1mentioning

confidence: 99%

Beagle pup model of perinatal asphyxia: nimodipine studies.

Ment¹,

Stewart²,

Duncan³

et al. 1987

Stroke

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Calcium antagonists may be of significant benefit in the pharmacotberapy of cerebral ischemia, possibly by improving postischemic cerebral blood flow (CBF). This study evaluated the effects of the calcium antagonist nimodipine on CBF in a newborn beagle pup model of perinatal asphyxia lasting 5 minutes. Immediately after the asphyxia] episode, nimodipine (2 /ug/kg/min) or saline was infused for 10 minutes, following which [ u C]iodoantipyrine determinations of CBF were performed. In noninsulted pups, nimodipine caused both significant decreases in CBF to cortical and deep gray structures as well as a decrease in mean arterial blood pressure (MABP) (p < 0.05). In insulted pups, nimodipine similarly decreased MABP (p < 0.001) and CBF to cortical and deep gray matter regions. Nimodipine appeared to have no effect on arterial blood gases and EEG tracings in either insulted or noninsulted pups. Although nimodipine may be shown to improve neurologic outcome in asphyxiated newborn infants, the limits of this study do not show the mechanism to be that of improving CBF. 910 Hypoxic/ischemic insults are known to result in cerebral metabolic disturbances characterized by decreased concentrations of highenergy phosphate compounds and by increased cerebral lactate. Cerebral blood flow (CBF) falls, and secondary failure of the ion pump results in neuronal depolarization and calcium entry. This imbalance in intracellular calcium provokes the accumulation of free fatty acids, which in turn uncouples oxidative metabolism and produces additional neuronal permeability changes. "~1 4 In response to ischemic insult, calcium channel blockers have been reported to both act on vascular smooth muscle to increase CBF 1 " 315 and to block calcium influx at voltage-gated calcium channels to preserve neuronal integrity.16 " 18While much has been written about the efficacy of calcium antagonists in adult animal models of hypoxic/ischemic insult, little is known about the role of these agents in the response of the developing nervous system to such problems. 1920 Severe perinatal asphyxia, the classic hypoxic/ischemic insult of the newborn period, has been reported to occur in between 1 in 50 and 1 in 500 live births 21 Newborn beagle pups provide a good model for the study of the developing brain. Neuropathologic insults such as perinatal cerebral infarction and intraventricular hemorrhage may be produced by clinically relevant models and CBF may be determined. 3839The purpose of this study was to evaluate the effects of the calcium antagonist nimodipine on CBF in newbom beagle pups exposed to a clinically relevant model for perinatal asphyxia. To approximate clinical events, nimodipine was administered as an i.v. infusion after asphyxial insult. Materials and MethodsThe following studies were performed with the approval of the Yale University Committee on Animal Care.Newborn beagle pups (24-96 hours old) were lightly anesthetized with 20 mg/kg i.p. pentobarbital, tracheotomized after local 1% xylocaine infiltration, paralyzed with 1 mg/kg...

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“…35 We investigated the influence of the thromboxane synthesis inhibitor CGS 13080 on CBF and metabolism in newborn beagle pups exposed to perinatal asphyxia. Based on the predictive value of a low 5-minute Apgar score 36 and the practical time of instituting life-saving support measures, 37 5 minutes of asphyxia was chosen for these experiments. For saline-treated pups, insult produced marked increases in CBF to the medulla, midbrain, and pons; CBF fell in cortical gray structures.…”

Section: Discussionmentioning

confidence: 99%

Thromboxane synthesis inhibitor in a beagle pup model of perinatal asphyxia.

Ment

Stewart

Petroff

et al. 1989

Stroke

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During perinatal asphyxia, cerebral blood flow is markedly reduced in the gray and white matter of the telencephalon. Since previous work has implicated prostaglandins in the control of blood flow, we tested the hypothesis that a thromboxane synthesis inhibitor would improve cerebral blood flow and blunt the metabolic alterations that accompany asphyxia. Forty-three newborn beagles 2-7 days old were anesthetized, ventilated, and randomized to insult (5 minutes of asphyxia) or no insult and received treatment with either the thromboxane synthesis inhibitor CGS 13080 (CIBA-GEIGY Corp.) (0.06 mg/kg/hr i.v. infusion) or saline. Cerebral blood flow was measured in 25 pups. Pups received treatment 30 minutes before insult or no Insult. In pups randomized to insult and receiving saline, cerebral blood flow increased during insult in the medulla but decreased elsewhere. Pups randomized to insult and treated with thromboxane synthesis inhibitor had increased cerebral blood flow during insult in all cerebral regions studied. In addition, these pups experienced a significantly higher incidence of intraventricular hemorrhage than did pups randomized to insult and receiving saline. In other experiments with 18 pups, brain extracts were prepared for proton nuclear magnetic resonance spectral analysis of high-energy phosphorylated compounds and lactate levels. In pups exposed to insult and receiving saline, mean±SD phosphocreatine concentration fell from 1.9±0.1 to 0.4±0.1 mmol/kg, lactate concentration increased from 2.0±0.5 to 3.3±0.4 mmol/kg, and the calculated pH fell 0.8 units. There were no differences between groups. Our findings suggest that therapeutic strategies for perinatal asphyxia must extend beyond blood flow maintenance to methods that may reduce cerebral metabolic needs. We can then hope to prevent neuropathologic changes. (Stroke 1989;20:809-814)

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Perinatal risk factors in children with serious motor and mental handicaps

Cited by 93 publications

References 8 publications

Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

Beagle pup model of perinatal asphyxia: nimodipine studies.

Thromboxane synthesis inhibitor in a beagle pup model of perinatal asphyxia.

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