Contents of this section: Tinnitus and OAEs

        The generation of tinnitus is a topic of much scientific debate. For example the role of the cochlea in the generation of subjective tinnitus has been theorized to be related with the excitatory drift in the operating point of the Inner Hair Cells (See Eric LePage , chapter 11 in Mechanisms of Tinnitus, by Vernon and Moller editors, Longwood, 1995).

         On the other hand a recent study on brain imaging of the effects of lidocaine on tinnitus by Reyes et al has reached different conclusions on the main generation site of tinnitus. Using a single-blind placebo-controlled design, they mapped lidocaine related changes in neural activity, measured by regional cerebral blood flow (rCBF) with (15)O-H(2)O positron emission tomography. Intravenous lidocaine produced both increases and decreases in the loudness of tinnitus. The change in tinnitus loudness was associated with a statistically significant change in neural activity in the right temporal lobe in auditory association cortex. Decreases in tinnitus loudness resulted in larger changes in rCBF than increases. The unilateral activation pattern associated with tinnitus, in contrast with the bilateral activation produced by a real sound, suggests that tinnitus originates in the central auditory system rather than the cochlea.

        Despite the difficulty of localizing the site of tinnitus generation, a number of studies (Ceranic et al, 1995; 1998) has shown evidence that in Tinnitus patients OAEs are not normal or easily detectable at the tinnitus frequency region, even in subjects with normal hearing thresholds. It is very difficult to collect data from a large number of tinnitus subjects with and without hearing deficits. Conclusions from smaller group of patients should be considered with caution. It is interesting that there is enough anecdotal and not published (or in English MEDLINE journals) information related to the abnormalities of the OAE structure close to the tinnitus region. For example in a Chinese study (Liu B, Liu C, Song B. from the Beijing Institute of Otolaryngology, 1996) examining 306 ears with tinnitus (with and without hearing deficits) the following conclusions were made:

1. In these cases there was no correlation between the frequency of tinnitus and SOAE.

2. In 94.8% of sensorineural hearing loss with tinnitus the DPOAE-gram presented lower amplitude or was absent within the frequency range of elevated pure-tone-threshold.

3. In 59% of cases with normal hearing and tinnitus the amplitude of DPOAE at nearby frequencies of tinnitus was decreased and there was no SOAE detectable. At frequencies other than that of tinnitus, the amplitude of DPOAE was normal and SOAE could be recorded.

        In another study by Rosanowski et al (1997), the measurement of TEOAEs in groups of tinnitus patients (with or without hehearingeficits) treated with lidocaine did not give consistent results in either of the two groups. The Tinnitus measurement and audiometric masking could only be carried out in patients older than 10 years and showed non-reproducible results. The paper concluded that Otoacoustic emissions give no further information about the development and therapeutic outcome of the tinnitus.

         The relationship between SOAEs and subjective Tinnitus has not been found as statistically significant (Zurek, 1981; Penner and Burns 1987; Penner 1990, Ceranic et al, 1998a,b)and according to Penner (1990) only 4% of the tinnitus patients exhibit related SOAEs. In a recent study by Ceranic et al (1998b) the presence of tinnitus was related to a high variability (decreased incidence) of the recorded SOAEs.

        The above information suggests that it is still premature to conclude that OAEs provide an objective evidence of tinnitus, considering the number of variables at play and more research is required to elucidate these arguments.


Ceranic BJ, Prasher DK, Luxon LM. Tinnitus and Otoacoustic Emissions. Clinical Otolaryngology, 1995, 20,192-200.

Ceranic BJ, Prasher DK, Raglan E, Luxon LM.. Tinnitus after head injury: evidence from otoacoustic emissions. J Neurol Neurosurg Psychiatry 1998a Oct;65(4):523-9.

Ceranic BJ, Prasher DK, Luxon LM.. Presence of tinnitus indicated by variable spontaneous otoacoustic emissions. Audiol Neurootol 1998b Sep-Oct;3(5):332-44.

Penner MJ and Burns EM. The dissociation of SOAEs and Tinnitus.JSHR 1987, 30, 396-403.

Penner MJ . An estimate of the prevalence of tinnitus caused by SOAEs. Archives of Otoralyngology, Head and Neck Surgery, 1990, 116:418-423.

Reyes SA, Salvi RJ, Burkard RF, Coad ML, Wack DS, Galantowicz PJ, Lockwood AH. Brain imaging of the effects of lidocaine on tinnitus. Hear Res 2002 Sep;171(1-2):43-50

Rosanowski F, Hoppe U, Proschel U, Eysholdt U. Chronic tinnitus in children and adolescents. HNO 1997 Nov;45(11):927-32

Zurek P.. Spontaneous narrowband acoustic signals emitted by human ears. JASA 1981, 70: 446-450

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