Gabrielle M. de Courten‐Myers

University of Cincinnati

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Co-Authors

Ronald E. Myers

Thomas Jefferson University

Kenneth R. Wagner

Sandia National Laboratories

Marla Kleinholz

Veterans Health Administration

K. R. Wagner

Society of Interventional Radiology

Guohua Xi

University of Michigan–Ann Arbor

T. I. Mandybur

University of Cincinnati Medical Center

T Rabinowicz

University of Lausanne

Joseph P. Broderick

University of Cincinnati

Steven Rostad

RealNetworks (United States)

Lucy B. Rorke

University of Pennsylvania

Cooperative Institutions

University of Cincinnati

University of Cincinnati Medical Center

Cincinnati Children's Hospital Medical Center

University of Pennsylvania

Veterans Health Administration

Neurological Surgery

Sabin Vaccine Institute

The Ohio State University

University of California, Los Angeles

Yale University

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Hyperglycemic versus Normoglycemic Stroke: Topography of Brain Metabolites, Intracellular pH, and Infarct Size

Journal of Cerebral Blood Flow & Metabolism (1992)

Kenneth R. Wagner Marla Kleinholz Gabrielle M. de Courten‐Myers Ronald E. Myers

Hyperglycemia aggravates brain pathologic outcome following middle cerebral artery (MCA) occlusion in cats. We presently determined if hyperglycemia during occlusion leads to high lactic acid accumulations in the ischemic MCA territory. We measured brain metabolite concentrations in 14 MCA territory sites at 0.5 and 4 h following occlusion in hyper- (20 m M) and normoglycemic (5 m M) cats and correlated these results with previous brain pathologic findings. Hyper- versus normoglycemia during MCA occlusion resulted in significantly higher lactate concentrations in the ischemic territory and more numerous loci with lactates >17 μmol/g. At 0.5 h of occlusion, ATP levels were lower in normoglycemic cats, while at 4 h, ATP was similarly reduced (40%) in both glycemia groups. At 4 h, PCr was more reduced in hyperglycemics secondary to a greater brain tissue acidosis. Carbohydrate substrates at 0.5 h were more markedly depleted in normoglycemics, likely limiting lactate accumulation (34.3% versus only 5.0% of sites in hyperglycemics with glucose <0.5 μmol/g). Although lactate was markedly elevated at both 0.5 and 4 h in hyperglycemic ischemic territories, clip release at 4 versus 0.5 h yields a significantly poorer brain pathologic outcome. Correspondingly, intracellular pH, calculated from the creatine kinase equilibrium, was more markedly depressed at 4 than at 0.5 h of occlusion, demonstrating a time-dependent dissociation between tissue lactate and hydrogen ion accumulations. The present findings show that following MCA occlusion (a) hyperglycemia increases the magnitude and topographic extent of marked tissue lactic acidosis, (b) infarct size following 0.5 h of clip release correlates more closely with tissue acidosis than with lactate concentrations, (c) ischemic tissue ATP concentrations correlate poorly with infarct size, (d) normoglycemia limits lactate accumulation during focal ischemia because tissue glucose is depleted, and (e) early during ischemia, tissue buffering or antiport mechanisms may prevent marked increases in intracellular hydrogen ion activity.

Lactic acidosis

Intracellular pH

Creatine kinase

10.1038/jcbfm.1992.31

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Citations (105)

Delayed profound local brain hypothermia markedly reduces interleukin-1β gene expression and vasogenic edema development in a porcine model of intracerebral hemorrhage

Acta neurochirurgica. Supplementum (2006)

K. R. Wagner Shauna Beiler Christian R. Beiler J. M. Kirkman Kenneth R. Casey

Proinflammatory cytokine

Cerebral edema

Brain Edema

10.1007/3-211-30714-1_39

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Citations (54)

Plasma Infusions into Porcine Cerebral White Matter Induce Early Edema, Oxidative Stress, Pro-Inflammatory Cytokine Gene Expression and DNA Fragmentation: Implications for White Matter Injury with Increased Blood- Brain-Barrier Permeability

Current Neurovascular Research (2005)

Kenneth R. Wagner Christopher Dean Shauna Beiler David R. Bryan Benjamin Packard

Plasma infused into porcine cerebral white matter induces both acute interstitial and delayed vasogenic edema. Edematous white matter contains extracellular plasma proteins and rapidly induces oxidative stress as evidenced by increased protein carbonyl formation and heme oxygenase-1 induction. We tested the hypothesis that edematous white matter would also upregulate pro-inflammatory cytokine gene expression and develop DNA damage. We infused autologous plasma into the frontal hemispheric white matter of pentobarbital-anesthetized pigs. We monitored and controlled physiological variables and froze brains in situ at 1, 4 or 24 hrs. We determined edema volumes by computerassisted morphometry. We measured white matter protein carbonyl formation by immunoblotting, cytokine gene expression by standard RT-PCR methods and DNA fragmentation by agarose gel electrophoresis. White matter edema developed acutely (1 hr) after plasma infusion and increased significantly in volume between 4 and 24 hrs. Protein carbonyl formation also occurred rapidly in edematous white matter with significant elevations (3 to 4-fold) already present at 1 hr. This increase remained through 24 hrs. Pro-inflammatory cytokine gene expression was also rapidly increased at 1 hr post-infusion. Evidence for DNA fragmentation began at 2 to 4 hrs, and a pattern indicative of both ongoing necrosis and apoptosis was robust by 24 hrs. Plasma protein accumulation in white matter induces acute edema development and a cascade of pathochemical events including oxidative stress, pro-inflammatory cytokine gene expression and DNA damage. These results suggest that in diseases with increased blood-brain barrier (BBB) permeability or following intracerebral hemorrhage or traumatic brain injury, interstitial plasma can rapidly damage white matter.

Cerebral edema

Vascular permeability

10.2174/1567202053586785

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Citations (42)

Cerebral amyloid angiopathy and Alzheimer’s disease

Neurobiology of Aging (2004)

Gabrielle M. de Courten‐Myers

Neurocognitive

Stroke

Amyloid (mycology)

10.1016/j.neurobiolaging.2004.02.004

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Citations (28)

Title Page / Table of Contents / Abstracts

Pediatric Neurosurgery (1988)

Lisa Ford Gabrielle M. de Courten‐Myers T. I. Mandybur Ronald E. Myers Bruce B. Storrs

Table (database)

Table of contents

10.1159/000120380

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Citations (0)

Contributors

Elsevier eBooks (1984)

Matteo Adinolfí Eva Alberman Frederick C. Battaglia R.D.H. Boyd Fiona Broughton Pipkin

10.1016/b978-0-407-00366-8.50006-x

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The Human Cerebral Cortex: Gender Differences in Structure and Function

Journal of Neuropathology & Experimental Neurology (1999)

Gabrielle M. de Courten‐Myers

Most people are aware of subtle differences in cognitive functions between men and women. Psychometric tests confirm specific gender differences in a number of areas, the most robust being in spatial orientation and mathematical tasks which are better performed by males. Nonetheless, normal males and females perform comparably on intelligence tests and human brains lack sexual dimorphism on routine neuropathological exams—other than mean differences in weight and size. Even so, human brains demonstrate: 1) a sexually dimorphic nucleus in the hypothalamus with twofold neuronal numbers in males than in females; 2) the planum temporale/anterior Sylvian fissure on the left side are larger in males; 3) some studies reveal the posterior corpus callosum to be more bulbous in females while others fail to show this difference; and 4) a cytoarchitectural study demonstrates definite sexual dimorphism of cerebral cortex with significantly higher neuronal densities and neuronal number estimates in males and a reciprocal increase in neuropil/neuronal processes in female cortex as implied by the 2 sexes' similar mean cortical thicknesses. Such morphologic differences may provide the structural underpinning for the gender differences exhibited by the normal and diseased brain. Males manifest a higher prevalence of mental retardation and of learning disabilities than females which may reflect the male fetus' smaller overproduction of nerve cells. Such an inference is supported by the demonstration of 1) better functional recovery following early brain injury than after later insults, 2) substantially overproduced and secondarily reduced nerve cells in human cerebral cortex during gestation, 3) the demonstration of a similar neuronal production and a testosterone-dependent neuronal involution of the sexually dimorphic hypothalamic nucleus in rats, and 4) more cortical neurons present in the adult human male than female. If an overproduced nerve cell population is capable of compensating for pathologic nerve cell losses taking place during the process of neuronal involution, the magnitude of overproduced nerve cells may define the extent of the protection conveyed. Because male fetuses appear to involute fewer overproduced cortical neurons than females, this gender difference could explain in part the boys' greater functional impairments from early brain damage. Women, on the other hand, exhibit a higher incidence and prevalence of dementia than do men. Given the females' overall larger extent of cortical neuropil (neuronal processes) and lower neuronal numbers compared with men, any disease that causes neuronal loss could be expected to lead to more severe functional deficits in women due to their loss of more dendritic connections per neuron lost. In conclusion, superimposed on a strong background of functional and structural equality, human male and female cerebral cortex display distinct, sexually dimorphic features, which can begin to be linked to a complex array of gender-specific advantages and limitations in cognitive functions.

Sexual dimorphism

Planum temporale

Neuropil

Sex characteristics

Human brain

Cingulate cortex

10.1097/00005072-199903000-00001

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Citations (151)

FACTORS DEFINING HEMORRHAGIC BRAIN INFARCT DEVELOPMENT

Journal of Neuropathology & Experimental Neurology (1989)

Gabrielle M. de Courten‐Myers Marla Kleinholz J. A. Wolker K. R. Wagner R. E. Myers

10.1097/00005072-198905000-00061

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Citations (0)

Effect of nitric oxide syntase inhibition on cerebral blood flow and injury volume.

Stroke (1994)

Gabrielle M. de Courten‐Myers Ronald E. Myers

Stroke

10.1161/01.str.25.5.1082

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Citations (1)

Brain injury from marked hypoxia in cats: role of hypotension and hyperglycemia.

Stroke (1985)

Gabrielle M. de Courten‐Myers Satoshi Yamaguchi K. R. Wagner P. Ting Ronald E. Myers

The present study identifies several factors that govern brain pathologic response to marked hypoxia. None of 13 cats exposed to 25 minutes of marked hypoxia (FiO2 = 3.4%; PaO2 = 17 +/- 3 mm Hg, S.D.) that maintained mean arterial blood pressure (MABP) greater than 65 mm Hg were brain injured after reoxygenation and long term survival. In contrast, 12 of 13 exposed to the same hypoxia but that experienced reductions in MABP less than 45 mm Hg for 4 +/- 1 minutes developed a pattern of brain injury closely resembling that of humans surviving in a persistent vegetative state after cardiorespiratory arrest. Higher serum glucose and lactate concentrations and lower blood pH values significantly correlated with development of hypotension during hypoxia. Four of 8 cats exposed to 21 minutes of marked hypoxia followed by 4 minutes of 100% N2 breathing that also led to hypotension similarly developed brain injury. Among the hypoxic/hypotensive cats the magnitude of the hyperglycemic response to hypoxia as modulated by 0, 1, or 2 days of preexposure fasting, strongly correlated with occurrence and extent of brain damage. Peak cisterna magna CSF lactate concentrations 10 to 30 minutes into recovery distinguished those animals that remained brain-intact (less than 13 mM) from those that developed brain damage (greater than 15 mM) with 100% accuracy. Seven cats developed delayed cardiogenic shock 3 to 12 hours into the recovery period. This outcome was predicted by blood pH values less than 6.70 shortly after resuscitation while all 27 surviving cats exhibited values greater than 6.80.

Hypoxia

Cisterna magna

10.1161/01.str.16.6.1016

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Citations (44)