The hearing loss in Ménière disease usually precedes the first attack of vertigo but it may appear later. Episodic deafness without vertigo has been called cochlear Ménière syndrome. As already mentioned, with recurrent attacks, there is a saltatory progressive unilateral hearing loss (in most series only 10 percent of cases involve both ears, but Baloh places the figure closer to 30 percent). Early in the disease, deafness affects mainly the low tones and fluctuates in severity; actually, tones below 500 Hz are affected early on, and this loss is not evident to the patient. Without measurable fluctuations in pure-tone audiometric thresholds, the diagnosis is left uncertain. Later the fluctuations cease and high tones are affected. Speech discrimination is relatively preserved. The attacks of vertigo usually cease when the hearing loss is complete but there may be an interval of months or longer before this occurs. Audiometry reveals a sensorineural type of deafness, with air and bone conduction equally depressed. Provided that deafness is not complete, loudness recruitment can be demonstrated in the involved ear (see earlier).
During an acute attack of Ménière disease, rest in bed is effective treatment, as the patient can usually find a position in which vertigo is minimal. The antihistaminic agents—cyclizine and meclizine, or transdermal scopolamine—are useful in the more protracted cases. Promethazine is an effective vestibular suppressant, as is trimethobenzamide (given in 200-mg suppositories), which also suppresses nausea and vomiting. For many years, a low-salt diet in combination with ammonium chloride or potassium and diuretics has been used in the treatment of Ménière disease, but the value of this regimen has never been established. The same is true for dehydrating agents such as oral glycerol and more recently introduced calcium channel blockers. Mild sedative drugs may help the anxious patient between attacks. The administration of corticosteroids was at one time popular but they have never been proven effective; transtympanic irrigation with dexamethasone is still practiced by some otologists but neither of these approaches is currently popular.
If the attacks are very frequent and disabling, permanent relief can be obtained by surgical means. Destruction of the labyrinth should be considered only in patients with strictly unilateral disease and who have reached the point of complete or nearly complete loss of hearing. In patients with bilateral disease or significant retention of hearing, the vestibular portion of the eighth nerve can be sectioned. Currently, an endolymphatic–subarachnoid shunt is the operation favored by some surgeons, and selective destruction of the vestibule by a cryogenic probe or transtympanic injection of gentamicin is favored by others. Decompression of the eighth cranial nerve, by separating it from an adjacent vessel, as suggested by Janetta (1984), is still a controversial measure and probably better suited to the treatment of sustained and disabling but unexplained vertigo, rather than the treatment of Ménière disease. The decision to undertake any surgical procedure must be tempered by the fact that a majority of the patients, who are middle-aged, stabilize spontaneously in a few years.