We retrospectively analyzed the clinical records of 137 patients who were treated at our clinic for acute low-tone sensorineural hearing loss of unknown cause over a period of 8 years. The analyses of the clinical records indicated the following clinical characteristics: female preponderance; peak incidence during the fourth decade of life; frequent accompanying tinnitus, sensation of ear fullness, and/ or autophony; suspicion of bilateral involvement; and association with autonomic imbalance. The hearing in most of the patients completely recovered, but some selected patients experienced fluctuating hearing loss or progression to Meniere's disease. Our results suggest that a subgroup of patients with severe initial hearing loss should be carefully followed up, although it is difficult to predict the outcome of this disorder.

The temporal bone pathology of a 71-year-old man with bilateral sensorineural hearing loss and facial paralysis caused by diffuse metastatic leptomeningeal carcinomatosis is described. The origin of this malignant disease was an extremely rare entity, a transitional cell carcinoma of the renal pelvis. Histopathologic study of the temporal bone demonstrated that tumor cells filled the internal auditory meatus, infiltrated into the Rosenthal's canals, and reached the scala tympani of the basal turn of the bilateral cochleas. The vestibulocochlear nerve and facial nerve trunks in the internal auditory meatus had been destroyed by the bilateral tumor invasion. Case reports of temporal bone metastases of leptomeningeal carcinomatosis published since 1965 were reviewed. In leptomeningeal carcinomatosis, it is suggested that tumor cells infiltrate the internal auditory meatus of both ears simultaneously from the cerebrospinal fluid, involving the seventh and eighth nerve trunks, and then cause bilateral sensorineural hearing loss and facial paralysis.

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Histopathological observation of celloidin serial sections of the chinchilla middle ear after treatment with propylene glycol disclosed the development of severe inflammation of the middle ear mucosa and tympanic membrane, papillary proliferation of the epidermis of the tympanic membrane and external auditory meatus, and retraction and adhesion of the tympanic membrane. The findings for the tympanic membrane, impedance testing and histopathological examination suggested that there were two types of acquired cholesteatoma formation, probably with a difference in the pathogenesis. In one type, the proliferated epidermal layer of the tympanic membrane penetrated into the middle ear cavity making tympanic perforations. In the other type, there was progressive retraction of the tympanic membrane forming a retraction pocket. We discuss the two different patterns of cholesteatoma development.