A survey of the temporal bone collection at the Massachusetts Eye and Ear Infirmary reveals 21 cases that meet the criterion for the clinical diagnosis of presbycusis. It is evident that the previously advanced concept of four predominant pathologic types of presbycusis is valid, these being sensory, neural, strial, and cochlear conductive. An abrupt high-tone loss signals sensory presbycusis, a flat threshold pattern is indicative of strial presbycusis, and loss of word discrimination is characteristic of neural presbycusis. When the increments of threshold loss present a gradually decreasing linear distribution pattern on the audiometric scale and have no pathologic correlate, it is speculated that the hearing loss is caused by alterations in the physical characteristics of the cochlear duct, and the loss is identified as cochlear conductive presbycusis. It is clear that many individual cases do not separate into a specific type but have mixtures of these pathologic types and are termed mixed presbycusis. About 25% of all cases of presbycusis show none of the above characteristics and are classified as indeterminate presbycusis.

Objective: To determine the effect on hearing and balance symptoms following singular neurectomy (SN) for benign paroxysmal positional vertigo (BPPV) in the ampullary recess of the posterior semicircular canal. Research Design: The charts of 242 patients with chronic disabling BPPV who were treated with SN over a 29-year period (1972–2001) were reviewed. The results on relief of BPPV and hearing function were recorded. A subset of 16 patients where the posterior ampullary recess was entered to expose the SN is described in detail with regard to an effect on hearing and balance. Results: A total of 252 SN were performed in 242 patients. Ten patients underwent bilateral SN sequentially; the remaining 232 patients had unilateral SN. The ages of the patients ranged from 21 to 86 years, with a mean at 57 years. The female:male ratio was 174:68. Complete relief of BPPV was achieved in 244 patients (96.8%), incomplete relief in 3 (1%), and no relief in 5 (2%). Sensorineural hearing loss (SNHL) occurred in 9 patients (3.7%). A subset of 16 patients in whom the ampullary recess was opened during SN ranged in age from 21 to 79 years, with a mean at 56 years. The female:male ratio was 12:4, with right and left sides divided almost equally. Relief of BPPV was achieved in all 16 patients with no loss of hearing function. Five patients complained of a fistula response postoperatively (31%). The fistula response resolved by 6 months postoperatively in all 5 patients. Conclusions: SN is effective in relief of BPPV with little risk of SNHL (3.7%). The risk of SNHL is not increased when the posterior ampullary recess must be entered in order to transect the singular nerve. A positive fistula response may be present temporarily in almost one third of these patients.

One hundred twenty-six patients who were treated with labyrinthectomy (81 patients) or vestibular neurectomy (45) between the years 1979 and 1994 were reviewed. The cause for vertigo in 124 of the 126 patients was Meniere's disease (89 patients), labyrinthitis (15), delayed endolymphatic hydrops (8), vestibular neuritis (7), and failed labyrinthectomy (5). In the remaining 2 patients, a normal labyrinth was sacrificed to fistulize a petrous apex cyst. Both procedures were equally effective in relieving vertigo (labyrinthectomy 98.8%; neurectomy 97.8%), but the length of hospitalization, length of disability before return to work, and cost were twice as great with vestibular neurectomy than with labyrinthectomy. More patients exhibited prolonged ataxia following neurectomy (5 patients) than after labyrinthectomy (2). Vestibular neurectomy was associated with several complications: reversible facial paresis (15 patients), meningitis (1), cerebrospinal fluid leak (1), and epidural hematoma (1). Labyrinthectomy was complicated by postoperative hyponatremia in 1 patient. Selective vestibular neurectomy preserved hearing in 32 (82%) of 39 patients. Criteria for recommending either ablation procedure are discussed. The incidence of sequential involvement of the contralateral ear was 1.5%.

We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.

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