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Ion Channels and Neuronal Dysfunction in Multiple Sclerosis
Stephen G. Waxman, MD, PhD
Arch Neurol. 2002;59:1377-1380.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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What causes the signs and symptoms of multiple sclerosis (MS)? It is
almost axiomatic to regard MS as a demyelinating disorder in which axonal
conduction block, caused by loss of myelin, produces clinical deficits. In
addition, during the past few years, increased attention has focused on axonal
degeneration in MS. The available evidence suggests that demyelination provides
a structural correlate for relapsing-remitting disease while axonal degeneration,
which may be associated with atrophy of the brain and spinal cord, produces
nonremitting deficits.
Neurons, of course, are the ultimate mediators of nervous system function
and arbiters of neurologic status. Do surviving neurons in MS, nonatrophic
and with intact axons, exhibit abnormalities at the molecular level, more
subtle than axonal degeneration or neuronal atrophy? If so, are these abnormalities
inconsequential molecular oddities or do they contribute to neuronal injury
or perturb neuronal function? Among the molecules that make . . . [Full Text of this Article]
From the Department of Neurology and Paralyzed Veterans of America/Eastern
Paralyzed Veterans Association Neuroscience Research Center, Yale University
School of Medicine, New Haven, Conn, and Center for Restorative Neurology,
Veterans Affairs Hospital, West Haven, Conn.
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