L
Labe C. Scheinberg
Researcher at Albert Einstein College of Medicine
Publications - 87
Citations - 11350
Labe C. Scheinberg is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Multiple sclerosis & Cerebral edema. The author has an hindex of 35, co-authored 87 publications receiving 11153 citations. Previous affiliations of Labe C. Scheinberg include Icahn School of Medicine at Mount Sinai & Saint Barnabas Medical Center.
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Journal ArticleDOI
New diagnostic criteria for multiple sclerosis: guidelines for research protocols.
Charles M. Poser,Donald W. Paty,Labe C. Scheinberg,W I McDonald,F A Davis,George C. Ebers,Kenneth P. Johnson,William A. Sibley,Donald H. Silberberg,Wallace W. Tourtellotte +9 more
TL;DR: Today there is a need for more exact criteria than existed earlier in order to conduct therapeutic trials in multicenter programs, to compare epidemiological surveys, to evaluate new diagnostic procedures, and to estimate the activity of the disease process in MS.
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Fatigue in Multiple Sclerosis
TL;DR: Multiple sclerosis fatigue appears to be a distinct clinical entity, often disabling, that can be distinguished from normal fatigue, affective disturbance, and neurologic impairment.
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On the presence of Ia-positive endothelial cells and astrocytes in multiple sclerosis lesions and its relevance to antigen presentation.
TL;DR: The presence of Ia molecules on some endothelial cells and astrocytes in MS brain tissue suggests a role in antigen presentation perhaps relevant to the initiation and perpetuation, respectively, of the inflammatory process.
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Factors associated with unemployment of patients with multiple sclerosis
TL;DR: The employment status of 79 male and 233 female multiple sclerosis patients was evaluated by interview to identify the relationship between degree of disability and employment status and other determinants of employment status.
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Tropical spastic paraparesis: a model of virus-induced, cytotoxic T-cell-mediated demyelination?
TL;DR: It is postulated that cytotoxic T cells, either directly or via cytokines, induce lysis of the myelin sheath and subsequently the axon, resulting in a mixed picture of demyelination and axonal loss with secondary tractal degeneration.