Toward a Deeper Understanding of Multiple Sclerosis Pathophysiology
MAY 30, 2015
MD Magazine staff
The MD Magazine Peer Exchange "Modifying the Course of Multiple Sclerosis in New Ways: The Latest Advances in Treatment" features a distinguished panel of physician experts discussing key topics in multiple sclerosis (MS) research and management, including the latest insights into MS pathophysiology, new medication options and their application in clinical practice, and more.
This Peer Exchange is moderated by Paul Doghramji, MD, who is a family physician at Pottstown Memorial Medical Center in Pottstown, PA, and medical director of Health Services at Ursinus College, in Collegeville, PA.
The panelists are:
- Fred D. Lublin, MD, FAAN, FANA, the Saunders Family Professor of Neurology and director of The Corinne Goldsmith Dickinson Center for Multiple Sclerosis, and co-chief editor of Multiple Sclerosis and Related Disorders at the Icahn School of Medicine at Mount Sinai
- Patricia K. Coyle, MD, professor of neurology, vice chair of Clinical Affairs, and director of MS Comprehensive Care Center
- Suhayl Dhib-Jalbut, MD, professor and chief of the Department of Neurology at Rutgers, Robert Wood Johnson Medical School
Dr. Lublin said “The nature of the inflammation may differ from early to late [stages of the disease] but no matter where you are in the stage of MS there is inflammation.”
He also noted that “we’ve come to understand that again in all phases of MS there’s a degenerative phase.” This differs from individual to individualâ€‘â€‘some people may be more demyelinating and other people more degenerativeâ€‘â€‘but there is degeneration very early on in the acute stages of MS and it increases as you go farther along in the course of the disease. “It’s thought at the present time to be the generator of the bulk of the serious disability that MS produces,” he said.
Lublin said a third thing about MS pathology that is becoming clearer is there is substantial neuronal loss associated with the disease. “We call this a white matter disease, we concentrate on oligodendrocytes and demyelination, remyelination, but there’s a considerable amount of both cortical and deep gray matter neuronal loss and we haven’t quite figured out where that fits into the pathologic process in terms of this causing that, whether it’s dying back or whether it’s an independent process,” he said.