BIOCHEMISTRY and molecular biology have developed into sophisticated sciences of increasing importance in the understanding of disease processes. It has become obvious that biochemical alterations play a role in certain types of deafness, for it has not been possible to find morphological alterations to explain the functional deficits existing in some ears.1
It is well known that a certain number of patients with clinical otosclerosis develop sensorineural, as well as conductive, hearing loss. Light microscopic studies of the temporal bones from patients with otosclerosis have failed, however, to demonstrate an anatomical lesion to explain this associated sensorineural deafness. Statistically, it has been stated that patients with otosclerosis develop sensorineural hearing losses at the same frequency as the aging population.2 One concept recently advanced is that stiffening of the basilar membrane may explain the descending bone-conduction curves often observed in otosclerosis.1
There have been several reports indicating
SILVERSTEIN H, SCHUKNECHT HF. Biochemical Studies of Inner Ear Fluid in Man: Changes in Otosclerosis, Meniere's Disease, and Acoustic Neuroma. Arch Otolaryngol. 1966;84(4):395–402. doi:10.1001/archotol.1966.00760030397003
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