Most often, subjective tinnitus signifies a disorder of the tympanic membrane, ossicles of the middle ear, inner ear, or eighth nerve. As already remarked, a majority of patients who complain of persistent tinnitus have some degree of deafness as well. Tinnitus that is localized to one ear and is described as having a tonal character (such as a ringing, bell-like, or like a high and steady musical tone) is particularly likely to be associated with impairment of cochlear or neural function. Tinnitus associated with sensorineural hearing loss of high frequency is often described as “chirping,” and that of low frequency as “whooshing” or blowing (Marion and Cevette). Tinnitus as a result of middle ear disease (e.g., otosclerosis) tends to be more constant than the tinnitus of sensorineural disorders; it is of variable intensity and lower pitch and is characterized by clicks, pops, and rushing sounds.
As remarked previously, the pitch of tinnitus associated with a conductive hearing loss is generally of low frequency (median frequency of 490 Hz, with a range of 90 to 1,450 Hz). That which accompanies sensorineural loss is higher (median frequency of 3,900 Hz, with a range of 545 to 7,500 Hz). This rule does not apply to Ménière disease, in which the tinnitus is usually described as a low-pitched whoosh, buzz, or roar (median frequency of 320 Hz, with a range of 90 to 900 Hz), thus resembling the tinnitus that accompanies a conductive rather than a sensorineural hearing loss (Nodar and Graham). The tinnitus of Ménière disease often fluctuates in intensity, like the hearing loss.
The mechanism of tonal tinnitus has not been established although a number of theories have been postulated. One supposition attributes tinnitus to an overactivity or disinhibition of hair cells adjacent to a part of the cochlea that has been injured. Other postulates a decoupling of hair cells from the tectorial membrane. Yet a third theory is based on the finding of an abnormal discharge pattern of afferent neurons, attributed to ephaptic transmission between nerve fibers that have been damaged by vascular compression (Møller).
Relief of unilateral tinnitus in certain selected cases has reportedly been achieved by vascular decompression of the eighth nerve in a manner comparable to hemifacial spasm, superior oblique myokymia, and some cases of trigeminal neuralgia (Jannetta). However, for most forms of tinnitus, there is little effective treatment (see the review by Lockwood et al). Many patients become reconciled to its presence once the benign nature of the disorder is explained to them. It is possible to fit some patients with a special audiologic instrument, like a hearing aid, that masks the tinnitus by delivering a sound of like pitch and intensity. Patients who are likely to benefit can be identified during the audiogram by noting improvement in tinnitus with the application of superimposed tones. Also, a hearing aid that improves audition may suppress or diminish tinnitus. Antiepileptic drugs and tocainide hydrochloride have been suggested as treatments, but have not been helpful in our experience. Some success in reducing the symptom has been achieved with small doses of amitriptyline at night. In extreme circumstances some groups have experimented with implanted stimulators on the temporal cortex.