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Biomedical subjects

L R Ment

Publications and source records attributed to L R Ment.

At least 55 records · Page 3Linked to original sources

Cerebral thromboembolic disease in pediatric and adult inflammatory bowel disease: case report and review of the literature.

Cerebral and retinal vascular disease are rare complications of inflammatory bowel disease. Most reports are of adult patients, with only seven instances described in children. The eighth case, a 14-year-old boy with ulcerative colitis and cerebral venous thrombosis is reported in whom the diagnosis was confirmed by magnetic resonance imaging. The adult and pediatric literature is also reviewed.

Adolescent↗

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

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Randomized low-dose indomethacin trial for prevention of intraventricular hemorrhage in very low birth weight neonates.

We admitted 36 preterm neonates (600 to 1250 gm birth weight) with normal 6-hour echoencephalograms to a randomized, placebo-controlled prospective trial to determine whether a low dose of indomethacin would prevent germinal matrix or intraventricular hemorrhage and permit adequate urinary output. Between the sixth and tenth postnatal hours, indomethacin (0.1 mg/kg) or placebo was administered intravenously every 24 hours for a total of three doses. Cardiac ultrasound studies to assess the status of the ductus arteriosus were performed at 6 postnatal hours and on day 5. Urinary output, serum electrolytes, serum indomethacin levels, and renal and clotting functions were monitored. No differences in birth weight, gestational age, or Apgar scores were noted between the two groups of infants. Two indomethacin-treated infants and three infants given placebo had significant urinary output difficulties, requiring that the study medication be withheld. Of 19 infants given indomethacin, two had germinal matrix or intraventricular hemorrhage, in comparison with 8 of 17 infants given saline solution (p = 0.02). Of the infants who had a left-to-right patent ductus arteriosus shunt before treatment, 64% of the indomethacin-treated and 33% of the saline solution-treated infants no longer had a patent ductus arteriosus on day 5. Ductal status appeared unrelated to the development of germinal matrix or intraventricular hemorrhage.

Cerebral Hemorrhage↗

Beagle pup model of brain injury: regional cerebral blood flow and cerebral prostaglandins.

Asphyxia is the most common cause of severe brain injury in very young children, and frequently results in lesions of the periventricular white matter in addition to other neuropathological changes. This study examines the effects of asphyxia on regional cerebral blood flow (rCBF) and the role of prostaglandins (PG's) in its control in the newborn beagle pup. Pups were anesthetized, tracheotomized, paralyzed, artificially ventilated, and randomly assigned to two groups: asphyxial insult produced by discontinuing ventilatory support, and no insult. Experiments for carbon-14-iodoantipyrine autoradiographic determination of rCBF and regional cerebral PG determination were performed on separate groups of pups. These studies demonstrated a significant increase in cortical gray PGE2 levels at a time when rCBF was significantly impaired in response to severe asphyxial insult. No such increase was noted in the periventricular white matter zones.

Animals↗

Cassette electroencephalography in the evaluation of neonatal seizures.

Three-channel cassette electroencephalographic (EEG) recording for up to 24 hours was obtained from 37 neonates with clinically diagnosed or suspected seizures but no seizure activity on routine EEG. EEG seizures were recorded in seven patients, five of whom had experienced clinical seizures in the 24 hours prior to cassette EEG recording. EEG seizures were detected in only one of nine neonates with recurring clinical episodes believed unlikely to be seizures and in only one of 18 without recent clinical events. Cassette EEG can enhance the detection and differentiation of seizures in neonates with persistent clinical episodes but is of low yield otherwise.

Apnea↗

The electrocardiogram in preterm infants with intraventricular hemorrhage and apnea.

To determine the relationship of electrocardiographic changes to both intraventricular hemorrhage (IVH) and neonatal apnea, continuous electrocardiographic monitoring, serial electrocardiograms, and cranial echoencephalograms were obtained on 41 consecutive preterm neonates with birth weight below 1,250 g. Nineteen patients (46%) were diagnosed as having an IVH within the first postnatal week. Six patients died while still requiring mechanical ventilation. Of the 35 surviving infants, 21 experienced apnea. Though the QRS axis was significantly different in the two groups, in both groups it was within the normal range. Of note, 69% of those surviving neonates with IVH experienced apnea, while 53% of those surviving without IVH had apnea. Unlike adult patients with subarachnoid hemorrhage, there are no characteristic electrocardiographic changes in preterm neonates with IVH. Therefore, the neonatal electrocardiogram could not be used to predict neonatal apnea. Continuous electrocardiographic monitoring was useful in detecting transient arrhythmias and episodes of bradycardia in apneic infants. Infants with IVH appeared to be at higher risk for neonatal apnea than their non-IVH peers. The authors stress the importance of continuous electrocardiographic monitoring in all preterm neonates at risk for IVH.

Apnea↗

Beagle puppy model of perinatal cerebral insults. Cerebral blood flow changes and intraventricular hemorrhage evoked by hypoxemia.

Asphyxia, with its attendant hypoxemia, is by far the most common cause of neonatal cerebral infarction, and frequently results in lesions of the parieto-occipital white matter in addition to other neuropathological changes. This study examines the effects of hypoxemia on regional cerebral blood flow (CBF) in the newborn beagle pup. The animals were anesthetized, underwent a tracheotomy, and were paralyzed. Pups were randomly divided into two groups: one group was subjected to hypoxemia produced by altering the oxygen concentration in the inspired air, and the other received no insult. In the hypoxemic pups, the pO2 was 13.1 +/- 2.1 mm Hg (mean +/- standard deviation). Autoradiographic determinations of CBF were performed by the carbon-14-iodoantipyrine technique 15 minutes after randomization. Significant increases in CBF were found throughout the brains of the hypoxemic pups. The CBF was increased to cortical and central gray regions and to frontal and temporal white matter but was unchanged in the parietal white matter, one of the classic sites of radiological and neuropathological injury in neonates with perinatal asphyxia. An unexpected finding was the increased incidence of germinal matrix and/or intraventricular hemorrhages in the hypoxemic pups.

Animals↗

Beagle puppy model of perinatal cerebral infarction. Regional cerebral prostaglandin changes during acute hypoxemia.

Perinatal cerebral infarction, or stroke, is a not uncommon finding in newborns who survive after intensive care. Asphyxia, with its component parts hypoxemia and hypotension, represents the most common cause of perinatal cerebral infarction and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated regional alterations in cerebral blood flow (CBF) in response to hypoxemic insult. This work examines the effects of hypoxemia on regional cerebral prostaglandin levels in the developing brain, since some observers believe that local CBF is controlled in part by prostaglandins. In this study, newborn beagle pups were anesthetized, subjected to tracheotomy and artificially ventilated to maintain normoxemia and normocarbia. Mean arterial blood pressure (MABP) was continuously monitored by means of an indwelling catheter and transducer, and craniectomies were performed. When the pups were physiologically stabilized, they were randomly assigned to receive acute hypoxemic insult (pO2 14.0 +/- 1.55 mm Hg, mean +/- standard deviation) accomplished by altering the oxygen concentration in the inspired air) or to receive no insult (mean pO2 84.3 +/- 13.0 mm Hg). Fifteen minutes following stable hypoxemic or normoxic conditions, all pups underwent in vivo freezing of the intracranial contents under anesthesia followed by rapid sacrifice. No significant differences were noted between the MABP, pH, or pCO2 values for the control and hypoxemic pups during the experimental period. Regional cerebral prostaglandin data demonstrated a significant increase in prostaglandin (PG)E2 in the gray matter of hypoxemic pups when compared to the normoxic controls (p less than 0.02). No significant differences were noted for 6-keto-PGE1 alpha, the stable metabolite of prostacyclin, or thromboxane (TX)B2, the stable metabolite of TXA2, in the gray matter. In addition, although 6-keto-PGE1 alpha was significantly lower in the periventricular white matter of the hypoxemic pups (p less than 0.05), there were no changes in the white matter in either PGE2 or TXA2. This regional differential synthesis of PGE2 in response to hypoxemic insult may explain the relative failure of CBF to the periventricular white matter and thus the neuropathological alterations attributed to it.

Acute Disease↗

Randomized indomethacin trial for prevention of intraventricular hemorrhage in very low birth weight infants.

We admitted 48 preterm neonates (600 to 1250 gm birth weight, normal 6-hour echoencephalograms) to a randomized prospective indomethacin or placebo trial for the prevention of neonatal intraventricular hemorrhage. Beginning at 6 postnatal hours, indomethacin or placebo was administered intravenously every 12 hours for a total of five doses. Cardiac ultrasound studies to assess the status of the ductus arteriosus were performed at 6 postnatal hours and on day 5. Urinary output, serum electrolytes, and renal and clotting functions were monitored. No differences in birth weight, gestational age, Apgar scores, or ventilatory needs were noted between the two groups. Six infants given indomethacin had intraventricular hemorrhage, compared to 14 control infants (P = 0.02). The indomethacin-treated group had significant decreases in serum prostaglandin values 30 hours after the initiation of therapy. The overall incidence of patent ductus arteriosus was 82% at 6 postnatal hours; 84% of the indomethacin-treated infants experienced closure of the ductus, compared to 60% of the placebo-treated patients. Closure of the ductus was not related to incidence of intraventricular hemorrhage. We speculate that indomethacin may provide some protection against neonatal intraventricular hemorrhage by acting on the cerebral microvasculature.

6-Ketoprostaglandin F1 alpha↗

Early childhood developmental follow-up of infants with GMH/IVH: effect of methylxanthine therapy.

Theophylline, aminophylline, and caffeine are methylxanthines frequently used in the treatment of idiopathic apnea of prematurity. These agents alter both cerebral blood flow and metabolism and are frequently administered to small preterm neonates, many of whom have experienced germinal matrix and/or intraventricular hemorrhage (GMH/IVH) and thus may suffer underlying disturbances of both cerebral blood flow and metabolism. Our data demonstrate that infants with GMH/IVH required methylxanthine therapy in the neonatal period more often than their nonhemorrhage peers. Because the combined presence of GMH/IVH and methylxanthine therapy may compound the potential for adverse effects in these infants, we analyzed the neurodevelopmental outcome of 73 very-low-birthweight neonates at 18 months corrected age with respect to the presence of GMH/IVH and neonatal methylxanthine therapy. Though further studies are needed, we cautiously conclude that the 18-month Bayley mental score demonstrates no harmful effects of neonatal methylxanthine therapy on cognitive functioning.

Apnea↗

Cranial asymmetry and lambdoid synostosis in a sibship.

In craniosynostosis, as in all congenital diseases, the interaction of hereditary and neonatal environmental factors can be separated only in rare cases. Four siblings with an asymmetry of the posterior right portion of the skull are presented. The youngest of the four suffered from severe cyanotic congenital heart diseases and secondarily suffered from ischemic/hypoxic cerebral injury. This child had complete synostosis of the right lambdoid and posterior sagittal sutures by the age of 5 1/2 months. The cranial asymmetry was less pronounced in each of the older children and was nearly undetectable in the oldest, a 7 1/2-year-old girl. True synostosis was not present in any of the older siblings. It is suggested that an autosomal-dominant hereditary condition caused a hypotrophic mesenchymal relationship of occipitotemporal ontogenesis. This condition was compensated for through childhood by the molding effect of the brain in the older three siblings. The systemic disease and delayed cerebral growth in the youngest probably led to the complete picture of craniosynostosis.

Adult↗