Faculty Profile

Address:
710 W 168 Street
New York, NY 10032

Phone: 212-305-8389
Fax: 212-305-5796

rsm2@columbia.edu

Education and Training
M.D. 1988 University of San Francisco
Intern 1989 Cornell New York Hospital
Resident 1992 Columbia Presbyterian Medical Center
Fellow 1994 Columbia Presbyterian Medical Center


Affiliations

Stem Cell Consortium
Neurology

 

Randolph Marshall, M.D.
Associate Professor

Research Summary
Behavioral and physiologic investigation of early hemispheric ischemia in patients undergoing therapeutic carotid balloon test occlusions. Evaluation of visual-spatial dysfunction using behavioral and functional imaging methodologies.

Selected Publications:
1. Fitzsimmons BF, Marshall RS, Pile-Spellman J, Lazar RM. Neurobehavioral differences in superselective Wada testing with amobarbital versus lidocaine.
Am J Neuroradiol. 2003 Aug;24(7):1456-60.

2. Lazar RM, Fitzsimmons BF, Marshall RS, Mohr JP, Berman MF. Midazolam challenge reinduces neurological deficits after transient ischemic attack. Stroke. 2003 Mar;34(3):794-6.

3. Marshall RS, Rundek T, Sproule DM, Fitzsimmons BF, Schwartz S, Lazar RM. Monitoring of cerebral vasodilatory capacity with transcranial Doppler carbon dioxide inhalation in patients with severe carotid artery disease. Stroke. 2003 Apr;34(4):945-9.

4. Marshall RS, Lazar RM, Young WL, Solomon RA, Joshi S, Duong DH, Rundek T, Pile-Spellman J. Clinical utility of quantitative cerebral blood flow measurements during internal carotid artery test occlusions. Neurosurgery. 2002 May;50(5):996-1004; discussion 1004-5.

5. Lazar RM, Fitzsimmons BF, Marshall RS, Berman MF, Bustillo MA, Young WL, Mohr JP, Shah J, Robinson JV. Reemergence of stroke deficits with midazolam challenge. Stroke. 2002 Jan;33(1):283-5.

6. Marshall RS, Lazar RM, Pile-Spellman J, Young WL, Duong DH, Joshi S, Ostapkovich N. Recovery of brain function during induced cerebral hypoperfusion. Brain. 2001 Jun;124(Pt 6):1208-17.

Current Projects

1. Human Brain Function in Induced Cerebral Hypofusion
The overall goal for the project is to test assumptions about brain function and physiology at the onset of cerebral ischemia in humans. Specific aim 1 is to establish the time course of the onset and persistence of the clinical manifestations of early ischemia under known hemodynamic conditions. Specific aims 2 and 3 are to determine what hemodynamic and physiologic factors produce neurologic dysfunction during cerebral hypoperfusion, and Specific aim 4 is to use the behavioral and physiologic data from the cerebral hypoperfusion testing to predict risk for subsequent hemodynamic ischemia in those patients in whom permanent carotid artery occlusion is required.
National Institute of Neurological Disorders and Stroke
9/30/1999-2/29/2004

Honors and Awards

1995-2000 Clinical Investigator Development Award (NINDS)
1996 Clinical Trials Pilot Study Award, Columbia University

Committee, Council and Professional Society Memberships

American Academy of Neurology
Association for Research in Neurological and Mental Disease
American Heart Association, NY Chapter
American Heart Association Stroke Council

Keywords

cerebral ischemia /hypoxia, disease /disorder model, model design /development, pathologic process, stroke, attention, disease /disorder onset, disease /disorder proneness /risk, hemodynamics, method development, behavior test, clinical research, human subject, infrared spectrometry, ultrasound blood flow measurement

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