TRATADO DE LIBRE COMERCIO PARA AMÉRICA DEL NORTE

The prevalence of SOAEs in the control group was 52%, which was in agreement with that previously reported for a normal population (30 -50%) (Probst et al., 1991), but lower than recently reported results by Penner and Zhang (1997) (62- 83%). This discrepancy between the studies may be explained by the differences in recording equipment and the methodology: in Penner and Zhang’s study SOAEs were directly recorded using Etymotic Research ER-10A microphone and analysed using “suitably tailored spectral responses”, while in this study click-synchronised SOAE were recorded and analysed using an IL088 Analyser. The prevalence of SOAEs in the tinnitus group

in toto was 53%, which was similar to that of the control group (52%). However, the consistent presence of SOAEs in the subgroup of subjects with head injury was notable and a 62% prevalence in patients with Meniere’s disease was higher than that normally expected, considering the age and elevated audiometric thresholds. In this latter group, the prevalence was higher despite the older age range (in the controls mean: 30± 4 years and in Meniere’s mean: 48±12 years), which, according to the normal age dependence, should have resulted in a reduction of SOAE prevalence. The low prevalence of SOAE in subjects with SNHL due to noise exposure (17.6%) is in agreement with even lower previously reported results (Probst et al., 1987; Penner, 1990). The SOAE reproducibility, indirectly proportional to the presence of "on-off' SOAE peaks, and directly proportional to “stable” SOAE peaks, was significantly lower in the tinnitus group, particularly in the subgroup tinnitus/normal hearing and tinnitus/head injury. The

relative frequency shift (rFs), representing the magnitude of SOAE frequency shifting in the two sessions, was significantly higher in the tinnitus group (0.59±0.9%) than in the control group (0.25±0.4%). Direct comparison of the data (rFs) in this study, with previously reported physiological shifting of SOAEs was not possible, due to the differences in instrumentation.

These results lead to the conclusion that the variability of SOAEs is, in a significant number of subjects, associated with the complaint of tinnitus.

SOAEs are, in general, thought to arise as a response to random perturbations in cochlear mechanics due to inherent irregularities in OHCs arrangement (Kemp, 1986). In normal subjects, in whom cochlear structural arrangement and functional capacity remain unchanged, and control mechanisms are well balanced, there is no reason for changes in SOAEs, and this is confirmed by the finding of stable SOAEs. These weak narrow-band signals, due to their continuous presence, are subject to perceptual adaptation, and are, therefore, inaudible. Conversely, the instability of SOAEs, as reported previously in some subjects with tinnitus (Penner et al., 1981; Bums and

Keefe, 1992), may lead to their audibility. Stable SOAEs and tinnitus may be present in

subjects in whom the process of adaptation is impaired, with consequent audibility of SOAEs. This may occur in stressful situations, which are well recognised to trigger or exacerbate tinnitus (Hinchcliffe and King, 1992).

Besides being perceived, and therefore being the direct cause of tinnitus [according to Penner, (1990), the 95% confidence limits for the prevalence SOAE-related tinnitus were

1% and 9.5%], SOAEs may be viewed as pathophysiological correlates of tinnitus.

Unstable SOAEs may correspond to the unstable cochlear mechanics due to some local causes, resulting from mutual interaction of multiple peaks, changes in the middle ear transfer properties, and various external (acoustic, mechanical) and internal factors. However, variable SOAEs, as mentioned above, may also reflect instability of the higher central nervous structures. The effect of the central auditory system on cochlear mechanics may be exerted through efferently induced mechanisms of electro-mechanical transduction (Zenner, 1986), which may alter the gain in the feedback loop of a cochlear amplifier, and further, the SOAE frequency spectrum. This may find support in the observation of significantly higher inter-session variability of the medial olivocochlear

suppression in patients with tinnitus in comparison with normal subjects, reported by Graham and Hazell (1994), which would correspond to the finding of unstable SOAEs. It could be speculated that abnormality/dysfunction in the higher auditory and other central structures may alter the control mechanisms of the cochlea, e.g. disinhibition of suppressive efferent function, leading to an increase in cochlear output, and consequently to the occurrence of unstable SOAE.

This "scenario" is supported by the SOAE findings in the tinnitus/head injury subgroup, which demonstrate the highest prevalence of SOAEs, the bilateral presence in all subjects, the largest number of SOAE spectral peaks and the most prominent relative frequency shift. These subjects had normal audiometric threshold levels, thus implying normal peripheral auditory function, so that SOAE findings could be suggestive of “undamped” cochlear activity, subsequent to central efferent disinhibition following head injury. The altered central auditory' activity, reflected in cochlear micromechanics, may provide a basis for the generation of tinnitus in this subgroup of patients. In addition to tinnitus, these patients with head injury also complained of hyperacusis, which is commonly described as an increased gain in auditory function, and the SOAE findings would, indeed, support this hypothesis.

The high SOAE prevalence and reduced reproducibility of SOAEs in subjects with Meniere’s disease may also be an indication of the involvement of the central nervous system mechanisms in the pathogenesis of this condition. It has been suggested (LePage, 1989) that dysfunction of the efferent medial olivocochlear system, through its capacity to modulate the osmotic forces internal to the OHCs, could lead to failure of local homeostasis, and Meniere’s disease. The presence of SOAE in Meniere’s disease may be an expression of a prolonged excitatory state of the cochlea, leading to an increase in spontaneous activity of auditory neurones and, subsequently, to tinnitus.

In conclusion, this study has shown that an increased variability of SOAEs is associated with the complaint of tinnitus in a significant number of subjects. This implies that variable SOAEs may be a pathophysiological correlate of tinnitus. SOAE may, therefore, be used as an objective indicator of the presence of tinnitus in a subset of subjects with recordable SOAEs, and the presence of variable SOAEs may increase the probability of a subject having tinnitus. On the basis of this study, a subject with tinnitus may be

considered 7.5 times more likely to have “on-off’ SOAEs or 3 times less likely to have “stable” SOAEs, and relative frequency shift greater than 0.3%, than a subject without tinnitus.

Additionally, the difference in the SOAE prevalence between tinnitus subjects observed

in toto and in the subgroups emphasises the importance of studying tinnitus in aetiologically homogeneous groups, to identify group-characteristics as a consequence of particular underlying mechanisms. The high prevalence of variable SOAEs may be suggestive of the involvement of central mechanisms in the generation of tinnitus, and thus SOAEs may provide an insight into the activity of higher auditory structures.