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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