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Article
October 1960

An Investigation of Secondary Nerve Degeneration in Clinical Otosclerosis

Author Affiliations

Syracuse, N.Y.
Assistant Professor, Department of Otolaryngology, State University of New York College of Medicine, Syracuse, N.Y.

Arch Otolaryngol. 1960;72(4):425-430. doi:10.1001/archotol.1960.00740010435001
Abstract

There is quite general agreement that the hearing loss in clinical otosclerosis begins as the result of stapedial footplate fixation and is consequently expressed as an impairment of hearing by air conduction. Agreement is not as common concerning the ultimate involvement of cochlear function. Early clinical observations caused many writers1,6,10,11 to express the opinion that nerve degeneration is a secondary effect of the disease. Though the exact physiology or pathology of the process which involves the nerve has not been conclusively shown, it has been suggested that extension of the bony growth to the basal turn of the cochlea1 or toxic products of the otosclerotic growth10 may contribute to the onset of secondary nerve degeneration. Furthermore, it is often implied that the degeneration is related to duration of hearing loss and that fenestration surgery seems to retard or prevent the neural progression in the fenestrated ear.7,10

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