Myelin pp 337-367 | Cite as

Pathophysiology of Conduction in Demyelinated Nerve Fibers

  • J. M. Ritchie


Charcot (1877) first described demyelination as the major pathological lesion in the multiple sclerosis (MS) over 100 years ago, and the clinical signs and symptoms of this disease have been attributed to this anatomical defect. Demyelination is also a common sequela of a multitude of other conditions, many of which initially affect other components of white matter, in particular blood vessels, glia, and axons. Furthermore, myelin may be secondarily damaged by neoplasia, trauma, infarct necrosis, abscess, edema, anoxia, and hemorrhage, and it may also be altered following degeneration of the overlying cortex. There are, however, a significant number of diseases of the central nervous system (CNS) and peripheral nervous systems (PNS) in which myelin itself appears to be primarily and selectively affected (see Chapter 9). But despite extensive neuropathological and neurological information, it is probably fair to say that until about 20 years ago, little was known about the electrophysiology of these demyelinating diseases or about the structure and function of normal myelinated axons and related elements. In the decade that followed, a considerable amount was learned, primarily about pharmacological aspects and the electrophysiology of normal and demyelinated nerve fibers. Along with this development, the clinical electrophysiology of demyelinating diseases has been explored with increasing care.


Multiple Sclerosis Conduction Velocity Demyelinating Disease Conduction Block Compound Action Potential 
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© Springer Science+Business Media New York 1984

Authors and Affiliations

  • J. M. Ritchie
    • 1
  1. 1.Department of PharmacologyYale University School of MedicineNew HavenUSA

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