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Biomedical subjects

C C Duncan

Publications and source records attributed to C C Duncan.

At least 55 records · Page 3Linked to original sources
PubMed1987

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1986

Petit mal epilepsy: a review and integration of recent information.

Petit mal (absence) epilepsy remains one of the most enigmatic of neurological disorders, and there is no widely accepted theory of its etiology. This review covers some of the current issues concerned with the disorder, including treatment and prognosis, neurochemical research, behavioral and psychophysiological effects of wave-spiked discharges, and EEG studies of seizure control. With respect to treatment, although effective drug therapy (valproic acid, ethosuximide) exists for the "pure" form of absence epilepsy, other forms, in which there is an admixture of grand mal seizures, are less amenable to pharmacotherapy. Moreover, the frequency of fatal hepatic toxicity following valproic acid therapy has been estimated at 1 in 20,000. With respect to prognosis, follow-up studies indicate that many patients do not outgrow the disorder but continue to suffer absence seizures well into adulthood. In recent years, there has been considerable research on the neurochemical basis of absence epilepsy. Current theories, including those that implicate gamma-aminobutyric acid, catecholamines, and "endogenous" epileptogens, are summarized; and requirements for an experimentally induced animal model of absence epilepsy are discussed. The majority of behavioral studies of the disorder have concerned the effects of petit mal-type discharges on sensory and cognitive processes. Some of these studies are reviewed; and recent work bearing on these issues, involving event-related brain potentials, is presented. Our review concludes with a discussion of research aimed at the development of electrophysiologically based approaches to the reduction of seizure frequency in patients with absence epilepsy.

Adolescent↗
PubMed1985

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↗
PubMed1985

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↗
PubMed1985

Human eastern equine encephalitis. Electron microscopic study of a brain biopsy.

An electron microscopic study was done on brain biopsy tissue from an eight-month-old female with acute eastern equine encephalitis diagnosed by indirect immunofluorescence. Rare clusters of round virions were found almost exclusively in the extracellular space. All virions observed had spiked envelopes, and their sizes averaged approximately 55 nm. Also found were rare enveloped virions along with degenerate organelles in a membrane-bound structure in the cytoplasm of macrophages. Intracytoplasmic development of virions was not found. Tubuloreticular complexes were seen in the endothelial cells and macrophages. This is the first report of an electron microscopic study on biopsy material from a case of human eastern equine encephalitis. It will extend the usefulness of brain biopsy in the diagnosis of acute encephalitis.

Astrocytes↗
PubMed1985

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↗