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RICHARD MONROE BERGLAND, M.D.

AMA Arch Neurol. 1960;2(3):260-265.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Myelin, the phospholipid surrounding the axon, has been intimately correlated with nervous function and is adversely affected in almost all neurological diseases.

Gasser,¹ in 1927, described A, B, and C fibers and made mathematical correlations between the diameter of the myelin sheath and conduction velocity. Since then, other neurophysiologists have made similar correlations.^* However, specific clinical correlations between demyelinating processes and functional losses have not been forth-coming.

It is the purpose of this paper to point out recent observations pertaining to the genesis of myelin, to report some of the more basic correlations between function (conduction) and form (myelin), and to suggest possible clinical applications.

Background

Conduction velocity has been shown to increase during embryonic development,³ and this change has been directly related to the increase in myelin. Most of these reports have concerned the nerve trunks of rather mature animals, where myelination is well under . . . [Full Text PDF of this Article]

Author Affiliations
New York

Footnotes
Submitted for publication Aug. 14, 1959.

Besides the myelin sheath diameter-conduction velocity correlations of Gasser, other anatomical parameters have been similarly correlated with conduction velocity. Among these are the axon diameter,2,3 the internodal length,3-5 the myelin sheath thickness,6 and the relative concentration of lipid in myelin.7

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