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KERATITIS NEUROPARALYTICACORNEAL LESIONS FOLLOWING OPERATIONS FOR TRIGEMINAL NEURALGIA
C. L. PANNABECKER, M.D.
Arch Ophthal. 1944;32(6):456-463.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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Degenerative changes in the cornea following lesions of the trigeminal nerve have long been observed and are well known. Magendie demonstrated them experimentally in 1924 and postulated the presence of specific trophic nerve fibers in the trigeminal nerve, the function of which was to regulate the metabolism of the tissues. Since Magendie's time many other etiologic theories have been presented, the important factors which have been emphasized being vasomotor disturbance, trauma and desiccation.
The concept of trophic fibers has now been generally rejected, but some control of cellular activity by the sensory nerves is recognized. Thus, Duke-Elder expressed the belief that lack of normal peripheral antidromic activity causes disturbance in metabolism and is the chief etiologic factor in neuroparalytic keratitis. It is also admitted that vasomotor disturbance, trauma and desiccation are of importance as secondary factors.
The outstanding characteristic of all cases of this disease is anesthesia of the cornea,
. . . [Full Text PDF of this Article]
Author Affiliations
ANN ARBOR, MICH.
From the Department of Ophthalmology, University Hospital.
Footnotes
Read before the Section on Ophthalmology at the Ninety-Fourth Annual Session of the American Medical Association, Chicago, June 14, 1944.
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