On the Functional State of Central Vestibular Structures in Monoaural Symptomatic Tinnitus Patients (BEAM-VbEP Study)

Clinical evidence suggests that over-excitation or disinhibition of structures in the brain occurs in tinnitus patients.(1,2) Brain electrical activity mapping of vestibular evoked potentials (BEAM-VbEP method) provides an electrophysiologic approach of quantification of function in brain cortex. The effect of tinnitus on the BEAM-VbEP image was examined in two groups of acoustic tumor patient Group A (n = 24) reported tinnitus and Group B (n = 22) did not. Statistically significant differences in the VbEP parameters have been identified between the two groups. The amplitude of the III/IV peak-to-peak component elicited by the rotation to the affected side, is higher (P < 0.05) in the tinnitus group than in the non-tinnitus group. Latencies of the late VbEP components (III, IV, and V) are shorter. In subgroup III, latency was 317.9 +/- 37.5 ms in the tinnitus group versus 335.5 +/- 30.9 ms in non-tinnitus group (p < 0.05); subgroup IV's component of 437.1 +/- 35.4 ms versus 470.9 +/- 43.5 ms ( p < 0.01), V 622.1 +/- 32.6 versus 655.5 +/- 46.6 ms (p < 0.05). Amplitude mapping of the most prominent VbEP component, subgroup III, demonstrates a well expressed negativity shift of the evoked brain electrical activity. The character of the electrophysiologic VbEP changes in the group of tinnitus patients is irritative. We consider the above described BEAM-VbEP images in tinnitus patients to reflect an electrophysiologic correlative of a state of cortical disinhibition, caused by either hyperactive or hypersensitive neural structures. Tinnitus is an aberrant perception of sound unrelated to an external source of acoustic stimulation; a dysynchrony within the auditory system.(3-5) Does tinnitus originate from hyperactive nerve fibers in the cochlea or is it a consequence of overexcited or disinhibited brain structures?(6,7) This basic question still has no acceptable solution. One working hypothesis is that tinnitus represents periodic or aperiodic excitation in the spontaneous activity of hair cells or nerve fibers originating from a restricted place on the basilar membrane.(8) In most clinical cases, the complaint of tinnitus is an accompanying symptom of other central or peripheral disorders (cerebrovascular and circulatory diseases, acoustic neuromas, sudden hearing loss, intoxication, side effects of drugs, among others which frequently cause various degrees of hearing loss with a corresponding decrease in the spontaneous activity of the auditory nerve.)(9,10) Thus, one could imagine such cases of tinnitus can be caused by some abnormal form of spontaneous activity in the central nervous system. Such considerations influenced us to evaluate the functional state of the brain in patients in whom tinnitus is the chief complaint. The method used in this study is the BEAM-VbEP method. This approach for vestibular stimulation and recording is suggested by the original concept of Shulman and colleagues,(5,11) that in some cases tinnitus can originate at the site of vestibular dysfunction. Furthermore, the BEAM-VbEP method provides data restricted not only to vestibular brain centers and pathways, but also to a much broader perspective to sensory pathways and associative cortical areas.