The common causes are otosclerosis, otitis media, and trauma. Of the various types of progressive conductive deafness, otosclerosis is the most frequent, being the cause of about half the cases of bilateral (but not necessarily symmetrical) deafness that have their onset in early adult life, usually in the second or third decade. A predilection to otosclerosis is transmitted as an autosomal dominant trait with variable penetrance. Pathologically, it is characterized by an overgrowth of labyrinthine capsular bone around the oval window, leading to progressive fixation of the stapes. The remarkable advances in microotologic surgery designed to mobilize or replace the stapes and to reconstruct the ossicular chain, have greatly altered the prognosis in this disease; significant improvement in hearing can now be achieved in the majority of patients.
The use of antibiotic drugs has markedly reduced the incidence of purulent otitis media, both the acute and chronic forms, which in former years were common causes of conductive hearing loss in children. Repeated attacks of serous otitis media are, however, still an important cause of this type of deafness.
Fractures of the temporal bone, particularly those in the long axis of the petrous pyramid, may damage middle ear structures; frequently there is bleeding into the middle ear as well, and a ruptured tympanic membrane. Transverse fractures through the petrous pyramid are more likely to damage both the cochlear–labyrinthine structures and the facial nerve. Other diseases of the temporal bone—such as Paget disease, fibrous dysplasia, and osteopetrosis—may impair hearing by compression of the cochlear nerve. It should be noted that rupture of the tympanic membrane, as for example from blast injury does not cause much hearing loss; in the case of a blast, the cause of reduced hearing is cochlear damage.
This has many causes. The common high-frequency sensorineural type of hearing loss in the aged (presbycusis) is probably a result of neuronal degeneration, that is, progressive loss of spiral ganglion neurons (Suga and Lindsay). Explosions or intense, sustained noise in certain industrial settings or from gun blasts or even rock music may result in a high-tone sensorineural hearing loss from cochlear damage. Certain antimicrobial drugs (namely, the aminoglycoside group and vancomycin) damage cochlear hair cells and, after prolonged use, can result in severe hearing loss. If these drugs have been used to treat bacterial meningitis, it may be difficult to determine whether the antibiotic or the infection is the cause. A variety of other commonly used drugs are ototoxic, including certain neurotoxic cancer chemotherapies, especially platinum containing drugs, usually in a dose-dependent fashion (see Nadol). Quinine and acetylsalicylic acid may impair sensorineural function transiently.