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  Vol. 63 No. 4, April 1960 TABLE OF CONTENTS
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Pathogenesis of Paralysis of the Third Cranial Nerve

WILLIAM P. KEEFE, M.D.; C. WILBUR RUCKER, M.D.; JAMES W. KERNOHAN, M.D.

AMA Arch Ophthalmol. 1960;63(4):585-592.

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

Paralysis of the third cranial nerve presents a discouraging problem from a clinical standpoint, for too often, even after intensive investigation, the cause remains obscure.1 Even when a cause is found, the exact manner in which conduction through the nerve is interrupted remains uncertain.

In order to clarify the mechanism by which the third cranial nerve is interrupted and to establish the site of involvement in various diseases, we examined the brains of a number of patients seen at the Mayo Clinic who had exhibited impaired function of the nerve during life. We shall present a few representative examples of the more frequent causes of third-nerve paralysis.

Anatomic Aspects

To comprehend the pathogenesis of paralysis of the third cranial nerve, complete cognizance of its course and relationships is necessary. The oculomotor nerves extend from the midbrain into the orbits (Fig. 1a). They leave the midbrain between the cerebral . . . [Full Text PDF of this Article]


Author Affiliations

Rochester, Minn.

Mayo Clinic and Mayo Foundation; Fellow in Ophthalmology (Dr. Keefe); Section of Ophthalmology (Dr. Rucker) and Section of Pathologic Anatomy (Dr. Kernohan). The Mayo Foundation, Rochester, Minnesota, is a part of the Graduate School of the University of Minnesota.


Footnotes

Submitted for publication June 15, 1959.

Read at the meeting of the American Ophthalmological Society, Hot Springs, Virginia, May 28 to 30, 1959.



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