 | Anthony P MarmarouShow email addressDepartment of Neurosurgery, Virginia Commonwealth University, 1101 E. Marshall St., 23298, Richmond, VA, USA | Division of Neurosurgery (A.M.), Medical College of Virginia, ... |
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Anthony P Marmarou:Expert Impact
Concepts for whichAnthony P Marmarouhas direct influence:Brain edema,Traumatic brain injury,Brain injury,Head injury,Intracranial pressure,Severe head injury,Brain tissue,Secondary insult.
Anthony P Marmarou:KOL impact
Concepts related to the work of other authors for whichfor which Anthony P Marmarou has influence:Traumatic brain injury,Intracranial pressure,Brain edema,Decompressive craniectomy,Cerebrospinal fluid,Severe tbi,Cerebral blood flow.
KOL Resume for Anthony P Marmarou
| Year | |
|---|---|
| 2012 | Department of Neurosurgery, Virginia Commonwealth University, 1101 E. Marshall St., 23298, Richmond, VA, USA |
| 2011 | Division of Neurosurgery (A.M.), Medical College of Virginia, Richmond, Virginia. Erasmus Medical Center, Department of Virginia Commonwealth University Medical Center, Department of Neurosurgery, Richmond, Virginia From the Sandra and Malcolm Berman Brain & Spine Institute (N.N.), Department of Neurosurgery, Sinai Hospital of Baltimore, Baltimore, MD; Departments of Neurosurgery and Neurology (N.N., P.M.K., W.C.Z., N.M., K.L., D.F.H.), Johns Hopkins University School of Medicine, Baltimore, MD; the Sandra and Malcolm Berman Brain & Spine Institute (M.A.W.), Department of Neurology, Sinai Hospital of Baltimore, Baltimore, MD; Department of Neurology (S.T.), Mount Sinai Medical Center, New York, NY; Department of Neurosurgery (R.B.), University of Miami, Miami, FL; Departments of Neurology and Neurological Surgery (S.A.M.), Columbia University College of Physicians & Surgeons, New York, NY; Departments of Neurology and Neurological Surgery (W.C., D.R.), Wayne State University, Detroit, MI; Department of Neurosurgery (R.N.), North Shore University Hospital and LIJ Medical Center, Philadelphia, PA; Department of Neurosurgery (S.H.), University of Minnesota, Minneapolis, MN; Department of Neurology and Psychiatry (S.C.F.), Saint Louis Medical Center, St. Louis, MO; Department of Neurosurgery (M.Z.), University of Cincinnati College of Medicine, Cincinnati, OH; Neuronetics (D.B.), Malvern, PA; Section of Neurosurgery (I.A.), University of Chicago Pritzker School of Medicine, Chicago, IL; American Brain Injury Consortium (A.M.), Richmond, VA. |
| 2010 | 3Department of Neurosurgery, Virginia Commonwealth University Medical Center, Richmond, Virginia |
| 2009 | From the Department of Public Health, Center for Medical Decision Making (BR, HFL, EWS), Erasmus MC, Rotterdam, The Netherlands; the Department of Neurosurgery (BR, AIRM), University Hospital Antwerp, Belgium; the Department of Neurosurgery (JL, AM), Virginia Commonwealth University, Richmond, Virginia, U.S.A.; and the Division of Community Health Sciences (IB, GSM, JW, GDM), University of Edinburgh, Scotland. Department of Neurosurgery, Virginia Commonwealth University Medical College of Virginia Campus, Richmond, VA, USA |
| 2008 | Department of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA, USA From Montefiore Medical Center (S.S., C.O., S.L.M.), Albert Einstein College of Medicine, Bronx, NY; Columbia University (D.C.H., E.B.), New York, NY; Children’s Memorial Research Center (D.R.N., L.G.E.), Feinberg School of Medicine, Northwestern University, Chicago, IL; Virginia Commonwealth University (J.M.P., A.M.), Richmond; Duke University Medical Center (D.V.L.), Durham, NC; and Eastern Virginia Medical School (L.M.F.), Norfolk. |
| 2007 | Department of Neurosurgery, Virginia Commonwealth University Medical Center, Richmond, Virginia. |
| 2006 | Departments of Neurosurgery and Radiology, Virginia Commonwealth University Medical College of Virginia Campus, Richmond, Virginia |
| 2005 | Division of Neurosurgery, Medical College of Virginia Commonwealth University, Richmond, Virginia, USA Department of Neurosurgery, Virginia Commonwealth University Medical Center, Richmond, Virginia |
| 2004 | Department of Neurosurgery, VCU-MCV Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia. |
| 2003 | Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, P.O. Box 950508, 23298-0508, Richmond, Virginia, USA |
| 2002 | Division of Neurosurgery, Virginia Commonwealth University, Richmond, Virginia, USA |
| 2001 | Division of Neurosurgery, Medical College of Virginia, Campus of Virginia Commonwealth University, Richmond, Virginia |
| 2000 | Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA. |
| 1999 | From the Divisions of General/Trauma Surgery (B.H.S., G.L.B., H.J.S., C.R.B., J.P.H.) and Neurosurgery (A.P.M., M.R.B.), Department of Surgery, Medical College of Virginia of Virginia Commonwealth University, Richmond, Virginia. Presented at the 28th Annual Meeting of the Western Trauma Association, February 22-28, 1998, Lake Louisa, Alberta, Canada. Address for reprints: Harvey J. Sugerman, MD, Box 980519, Medical College of Virginia, Richmond, VA 23298-0519. Division of Neurosurgery, Medical College of Virginia. Virginia Commonwealth University, Richmond, USA |
| 1998 | Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Sanger Hall, 1101 E. Marshall St., Box 980508, 23298-0508, Richmond, Virginia, USA Medical College of Virginia/VCU. BH Saggi, MD. HJ Sugerman, MD. Richmond, VA. |
| 1997 | Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University Division of Neurosurgery, MCV Station Hll, Room 8004a, 1101 E Marshal St., P.O.Box 508, 23298, Richmond, VA, USA |
| 1996 | From the Divisions of General/Trauma Surgery (G.L.B., P.C.R., C.R.B., H.J.S.) and Neurosurgery (A.M.), Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia. This work was supported by the US Army Medical Research and Development Command under Contract No. DAMD17-93-C-3106. The views, opinions, and findings contained in this report are those of the authors and should not be construed as an official Department of the Army position, policy, or decision unless so designated by other documentation. Presented at the 55th Annual Meeting of the American Association for the Surgery of Trauma, September 27-30, 1995, Halifax, Nova Scotia, Canada. Address for reprints: Harvey J. Sugerman, MD, David M. Hume Professor of Surgery, Department of General/Trauma Surgery, Medical College of Virginia, Box 980519, MCV Station, Richmond, Virginia 23298-0519. Medical College of Virginia, Richmond, USA. |
| 1995 | Division of Neurosurgery and Toxicology School of Medicine Medical College of Virginia Richmond, Virginia 23298–0631 |
| 1994 | Division of Neurosurgery, Medical College of Virginia, MCV Station, Box 508, 23298, Richmond, VA, USA |
| 1993 | Division of Neurosurgery, Medical College of Virginia, USA Ist Dept. Anesthesia & Intensive Care - Hospital of Parma, Via Abbeveratoia, 14, 43100, Parma, Italy Medical College of Virginia, Richmond, Virginia |
| 1992 | Division of Neurosurgery, Medical College of Virginia, Richmond, Virginia Traumatic Coma Data Bank, Biometry and Field Studies Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MarylandUSA |
| 1991 | Department of Neurosurgery, Medical College of Virginia, Richmond, Virginia |
| Concept | World rank |
|---|---|
| dwi mabp | #1 |
| edema adc | #1 |
| icp bradycor | #1 |
| neurochemical damage | #1 |
| hypoxemia series | #1 |
| patients tham | #1 |
| icp placebos polyethylene | #1 |
| kidney current trial | #1 |
| combination cellular component | #1 |
| edema simulator | #1 |
| hypotension neuronal injury | #1 |
| iap headaches | #1 |
| iii baer | #1 |
| supplemental prognostic | #1 |
| trauma coupled | #1 |
| random translational motion | #1 |
| induced aqp4 | #1 |
| cpp major influence | #1 |
| defective autoregulation pvi | #1 |
| patients intact autoregulation | #1 |
| contribution icp | #1 |
| dural sinus pressure | #1 |
| pathophysiology brain edema | #1 |
| fod measurement | #1 |
| edema formation models | #1 |
| pma brain edema | #1 |
| reduced pvi | #1 |
| formation asdh | #1 |
| pvi baer | #1 |
| dopamine cortical contusion | #1 |
| normal pressure‐volume | #1 |
| lactate severe diffuse | #1 |
| primary brain lesion | #1 |
| 1 animals mortality | #1 |
| cortical surface albumin | #1 |
| brain energy depletion | #1 |
| rapid evacuation series | #1 |
| hartmann experimental models | #1 |
| contributor brain | #1 |
| secondary insult model | #1 |
| sham trauma | #1 |
| edema cats | #1 |
| rapid absorption water | #1 |
| 41 mhz relationship | #1 |
| brain tissue production | #1 |
| percussion model | #1 |
| data 1 animals | #1 |
| head injury models | #1 |
| tham treated animals | #1 |
| 66 mm hg | #1 |
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Prominent publications by Anthony P Marmarou
Cerebral blood flow and metabolism in severely head-injured children. Part 1: Relationship with GCS score, outcome, ICP, and PVI.
[ PUBLICATION ]
The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow ("CBF15"), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average ...
| Known for Gcs Score | Cerebral Blood Flow | Patients Hyperemia | Cbf Icp | Severely Head |
Production and clearance of lactate from brain tissue, cerebrospinal fluid, and serum following experimental brain injury.
[ PUBLICATION ]
Lactate dynamics in the brain, cerebrospinal fluid (CSF), and serum were studied in 20 chloralose-anesthetized cats following fluid-percussion trauma. Brain lactate and brain tissue pH were measured by hydrogen-1 and phophorus-31 magnetic resonance spectroscopy. The CSF, arterial, and cerebrovenous serum lactate levels as well as serum glucose concentration were quantified. In the six sham-operated control animals, brain, CSF, cerebrovenous, and arterial lactate levels as well as brain ...
| Known for Brain Tissue | Cerebrospinal Fluid | Lactate Csf | Severe Trauma | Normal Values |
Magnetic resonance imaging-monitored acute blood-brain barrier changes in experimental traumatic brain injury.
[ PUBLICATION ]
The authors posit that cellular edema is the major contributor to brain swelling in diffuse head injury and that the contribution of vasogenic edema may be overemphasized. The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury and to what extent barrier permeability is affected by the secondary insults of hypoxia and hypotension. The BBB disruption was quantified and visualized using T1-weighted magnetic ...
| Known for Brain Barrier | Magnetic Resonance | Hypoxia Hypotension | Animals Trauma | Closed Head Injury |
Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow.
[ PUBLICATION ]
Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of ...
| Known for Blood Pressure | Severe Head | Icp Patients | Autoregulation Cerebral | Volume Brain |
Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury.
[ PUBLICATION ]
The objective of this study was to use diffusion-weighted magnetic resonance imaging (DWI) to help detect the type of edema that develops after experimental trauma and trauma coupled with hypotension and hypoxia (THH). Reduction in the apparent diffusion coefficients (ADCs) is thought to represent cytotoxic edema. In a preliminary series of experiments, the infusion edema model and middle cerebral artery occlusion models were used to confirm the direction of ADC change in response to ...
| Known for Cytotoxic Edema | Trauma Hypoxia | Intracranial Pressure Icp | Pressure Brain | Secondary Insult |
Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.
[ PUBLICATION ]
The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late ...
| Known for Cellular Edema | Brain Swelling | Weighted Imaging | Increase Adc | Control Animals |
Neuroprotective Effect of Hypothermia on Neuronal Injury in Diffuse Traumatic Brain Injury Coupled With Hypoxia and Hypotension
[ PUBLICATION ]
It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley ...
| Known for Neuronal Injury | Hypoxia Hypotension | Secondary Insult | Animals Trauma | Neurons Rats |
Posttraumatic ventriculomegaly: hydrocephalus or atrophy? A new approach for diagnosis using CSF dynamics.
[ PUBLICATION ]
Cerebrospinal fluid (CSF) dynamics were correlated to the changes in ventricular size during the first 3 months posttrauma in patients with severe head injury (Glasgow Coma Scale score < or = 8, 75 patients) to distinguish between atrophy and hydrocephalus as the two possible causes of posttraumatic ventriculomegaly. Using the bolus injection technique, the baseline intracranial pressure (ICP), pressure volume index, and resistance for CSF absorption (R0) provided a three-dimensional ...
| Known for Csf Dynamics | Posttraumatic Ventriculomegaly | Ventricular Size | Normal Pressure | Hydrocephalus Atrophy |
A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure
[ PUBLICATION ]
OBJECTIVES: To determine the effect of acutely increased intra-abdominal pressure on pleural pressure, intracranial pressure, and cerebral perfusion pressure, and to clarify the relationship between these parameters.
DESIGN: Nonrandomized, controlled study.
SETTING: Laboratory at a university medical center.
SUBJECTS: Yorkshire swine, weighing 15 to 20 kg.
INTERVENTIONS: Anesthetized, ventilated swine had a balloon inserted into the peritoneal cavity and catheters placed for measurement ...
| Known for Intracranial Pressure | Increased Intra | Mm Hg | Peritoneal Cavity | Cerebral Venous |
Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries.
[ PUBLICATION ]
OBJECT: The edema associated with brain swelling after traumatic brain injury (TBI) has been thought to be vasogenic in origin, but the results of previous laboratory studies by the authors have shown that a cellular form of edema is mainly responsible for brain swelling after TBI. In this study the authors used magnetic resonance (MR) imaging techniques to identify the type of edema that occurs in patients with TBI.
METHODS: Diffusion-weighted MR imaging was used to evaluate the ...
| Known for Brain Swelling | Cellular Edema | Patients Tbi | Adc Values | Water Content |
N-Acetylaspartate Reduction as a Measure of Injury Severity and Mitochondrial Dysfunction Following Diffuse Traumatic Brain Injury
[ PUBLICATION ]
N-Acetylaspartate (NAA) is considered a neuron-specific metabolite and its reduction a marker of neuronal loss. The objective of this study was to evaluate the time course of NAA changes in varying grades of traumatic brain injury (TBI), in concert with the disturbance of energy metabolites (ATP). Since NAA is synthesized by the mitochondria, it was hypothesized that changes in NAA would follow ATP. The impact acceleration model was used to produce three grades of TBI. Sprague-Dawley ...
| Known for Atp Naa | Injury Severity | Severe Tbi | Traumatic Brain | Secondary Insult |
Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 +/- 5.0 mm Hg and PaO2 at 122 +/- 18 mm Hg (mean +/- standard deviation). The mean Glasgow Coma Scale score on ...
| Known for Ventricular Csf | Severe Head | Lactic Acidosis | Poor Outcome | Lactate Concentration |
The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination ...
| Known for Brain Injury | Hyperventilation Tham | Pcr Ratio | Resonance Spectroscopy | Systemic Buffering Agents |
A new model of diffuse brain injury in rats. Part II: Morphological characterization.
[ PUBLICATION ]
A new model producing diffuse brain injury, without focal brain lesions, has been developed in rats. This has been achieved by allowing a weight of 450 gm to fall onto a metallic disc fixed to the intact skull of the animal which is supported by a foam bed. Two levels of injury were examined by adjusting the height of the falling weight to either 1 m or 2 m. Two groups of animals were studied. Group 1 animals were separated into three subgroups: 10 received a 1-m weight drop, 58 received ...
| Known for Diffuse Brain Injury | New Model | Brain Stem | Cerebral Cortex | 1 Animals |
Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial.
[ PUBLICATION ]
There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a ...
| Known for Prolonged Hyperventilation | Randomized Clinical Trial | Cerebral Vasoconstriction | Closed Humans | 12 Months |
