Retronasal and orthonasal olfactory function in relation to olfactory bulb volume in patients with posttraumatic loss of smell

OBJECTIVE: The aims of this study were to evaluate olfactory function with orthonasal and retronasal testing in patients with posttraumatic olfactory loss and to investigate the relation between residual olfactory function and olfactory bulb (OB) volume. METHOD: A retrospective study of 25 patients with posttraumatic olfactory loss was performed. Orthonasal olfactory function was assessed with the Sniffin' Sticks test kit; retronasal olfactory function was assessed with intraorally applied odors. Magnetic resonance imaging was used to determine OB volume and cortical damage in the frontal and temporal areas. RESULTS: The main outcomes of the present study were the demonstration of a correlation between olfactory function and OB volume, which was more pronounced for retronasal than for orthonasal olfactory function; retronasal olfactory function was most affected in the patients with the most extensive cerebral damage and was least compromised in patients without such damage; OB volumes were smaller in patients with parosmia compared with those without; and the presence of parosmia was clearly associated with the presence of cerebral damage. CONCLUSION: The data confirm that OB volume is an indicator of olfactory function but, interestingly, in this study, it is largely determined by retronasal olfactory sensitivity. In addition, these results emphasize the role of higher cortical centers in olfactory function, and especially in parosmia, which may, at least in some cases, be related to lesions in the fronto-orbital and anterior temporal cortices. It would be of interest to investigate OB volume further in relation to the prognosis of the disorder.     

Ensemble spontaneous activity in the guinea-pig cochlear nerve

Spectral analysis of electrical noise recorded from the round window (RW) of the cochlea is referred to as the ensemble spontaneous activity (ESA) of the cochlear nerve. The ESA is considered to represent the summed spontaneous activity of single fibers of the auditory nerve and changes in the spectral characteristics of the ESA have been observed in humans with tinnitus. Experiments were undertaken to determine the relationship of the ESA to auditory neurotransmission. The ESA consisted of energy centered at approximately 900 Hz, similar to the spectral peak of single auditory neuron discharges. The amplitude of the ESA was correlated with good auditory sensitivity in the 12-30 kHz region of the cochlea. Constant pure tones of 12-22 kHz suppressed the ESA reducing its amplitude in a frequency and intensity dependent manner implying that the ESA recorded at the RW is generated or dominated by neurons in the basal region of the cochlea. The ESA was significantly suppressed by round window perfusion of the P2X receptor agonist adenosine 5'-O-(3-thiotriphosphate) (ATPgammaS) (10 mM) the glutamate receptor antagonist 6-7-dinitroquinoxaline-2,3-dione (DNQX) (1 mM), and the sodium channel antagonist tetrodotoxin (TTX) (20 microM). Following intravenous furosemide injection (40 mg/kg) reduction and recovery of the ESA correlated with similar changes in the endocochlear potential (EP). Following DNQX and ATPgammaS an additional spectral peak at 200 Hz was often observed. This peak has been postulated to be a correlate of tinnitus in humans but had not previously been observed in a guinea-pig model of tinnitus. These data confirm the spectral characteristics of the ESA in guinea-pigs and show it is dependent on the sensitivity of the auditory nerve and intact auditory neurotransmission. In addition these experiments support the view that the ESA represents summed spontaneous neural activity in the cochlea and provide a platform for studies of the influence of ototoxic compounds on the spontaneous neural outflow of the cochlea as a model of tinnitus.     

Characteristics of tinnitus with or without hearing loss: Clinical observations in Sicilian tinnitus patients

Objective

To analyze the clinical characteristics of tinnitus both in normal hearing subjects and in patients with hearing loss.

Methods

The study considered 312 tinnitus sufferers, 176 males and 136 females, ranging from 21 to 83 years of age, who were referred to the Audiology Section of the Department of Bio-technology of Palermo University. The following parameters were considered: age, sex, hearing threshold, tinnitus laterality, tinnitus duration, tinnitus measurements and subjective disturbance caused by tinnitus. The sample was divided into two groups: Group 1 (G1) subjects with normal hearing; Group 2 (G2) subjects with hearing loss.

Results

Among the patients considered, 115 have normal hearing while 197 have a hearing deficit. There is a slight predominance of males respect to females that is more evidenced in G2 (61.42% of males vs. 38.58% of females). The highest percentage of tinnitus results in the decades 41–50 for G1 and >70 for G2 with a statistically significant difference between the two groups (P < 0.0001).The hearing impairment results in most cases of sensorineural type (74.62%) and limited to the high frequencies (58.50%), moreover the 72.10% of the patients with SNHL had a high-pitched tinnitus while the 88.37% of the patients high-frequency sensorineural hearing loss had a high-pitched tinnitus (P < 0.0001). As for the subjective discomfort, the catastrophic category resulted most representative among subjects with normal hearing with a statistically significant difference between the two groups but no significant correlation was found between the level of tinnitus intensity and the tinnitus annoyance confirming the possibility that tinnitus discomfort is elicited by a certain degree of psychological distress as anxiety, depression, irritability and phobias that do not allow the phenomenon of the ‘habituation’.

Conclusion

This work, according to literature data, suggests that the hearing status and the elderly represent the principal tinnitus related factors; moreover tinnitus characteristics differ in the two groups for tinnitus pitch. There is, in fact, a statistically significant association between high-pitched tinnitus and high-frequency SNHL suggesting that the auditory pathway reorganization induced by hearing loss could be one of the main source of the tinnitus sensation.     

Clinical presentation of qualitative olfactory dysfunction

Many patients with olfactory dysfunction not only experience quantitative reduction of olfactory function, but also suffer from distorted olfactory sensations. This qualitative dysfunction is referred to as parosmia (also called troposmia) or phantosmia, with the major difference that distorted olfactory sensations are experienced in the presence or absence of an odor, respectively. Our clinical observations corroborate the literature in terms of a general underestimation of the incidence of olfactory distortions. Based on selected cases we try to show that olfactory distortions exhibit a large variance in their clinical appearance. Further, emphasis is placed on the fact that only a detailed and directed history of the patient can provide cues to the correct diagnosis.     

Inhibitory neurotransmission in animal models of tinnitus: maladaptive plasticity

Tinnitus is a phantom auditory sensation experienced by up to 14% of the United States population with a smaller percentage experiencing decreased quality of life. A compelling hypothesis is that tinnitus results from a maladaptive plastic net down-regulation of inhibitory amino acid neurotransmission in the central auditory pathway. This loss of inhibition may be a compensatory response to loss of afferent input such as that caused by acoustic insult and/or age-related hearing loss, the most common causes of tinnitus in people. Compensatory plastic changes may result in pathologic neural activity that underpins tinnitus. The neural correlates include increased spontaneous spiking, increased bursting and decreased variance of inter-spike intervals. This review will examine evidence for chronic plastic neuropathic changes in the central auditory system of animals with psychophysically-defined tinnitus. Neurochemical studies will focus on plastic tinnitus-related changes of inhibitory glycinergic neurotransmission in the adult dorsal cochlear nucleus (DCN). Electrophysiological studies will focus on functional changes in the DCN and inferior colliculus (IC). Tinnitus was associated with increased spontaneous activity and altered response properties of fusiform cells, the major output neurons of DCN. Coincident with these physiologic alterations were changes in glycine receptor (GlyR) subunit composition, its anchoring/trafficking protein, gephyrin and the number and affinity of membrane GlyRs revealed by receptor binding. In the IC, the primary afferent target of DCN fusiform cells, multi-dimensional alterations in unit-spontaneous activity (rate, burst rate, bursting pattern) were found in animals with behavioral evidence of chronic tinnitus more than 9 months following the acoustic/cochlear insult. In contrast, immediately following an intense sound exposure, acute alterations in IC spontaneous activity resembled chronic tinnitus-related changes but were not identical. This suggests that long-term neuroplastic changes responsible for chronic tinnitus are likely to be responsible for its persistence. A clear understanding of tinnitus-related plasticity in the central auditory system and its associated neurochemistry may help define unique targets for therapeutic drug development.     

A study on the prognostic significance of qualitative olfactory dysfunction

We investigated the frequency and prognostic significance of qualitative olfactory dysfunction (parosmia, phantosmia) in a retrospective patient based study. A total of 392 patients with impairment of olfaction were tested at least two times for their olfactory function using the “Sniffin’ Sticks”. The mean interval between the first and the last test was 11 months. At the first visit 34% of all patients reported parosmia. Parosmia was most frequent in patients with postinfectious olfactory loss (56%), and less frequent in idiopathic, posttraumatic, sinunasal disease with frequencies of 10, 14, and 28%, respectively. In contrast, only 12% of all patients had phantosmias, with no significant differences between the patient groups. Improvement of olfactory function was found in 23% of all patients (n = 90). Pre-existing parosmia or phantosmia had no significant effect on recovery rate. Regarding qualitative olfactory dysfunction, 29% of those patients reporting parosmia reported relief of this symptom after an average of 12 months, whereas 53% of phantosmic patients lost phantosmia during the observation period. Although it has been suggested that olfactory distortion s could be regarded as an indicator of early recovery of decreased olfactory sensitivity, the current data indicate that occurrence of parosmia or phantosmia has little prognostic value. Phantosmia disappears at a faster rate than parosmia. These insights into qualitative olfactory dysfunction are regarded to be significant in the counseling of patients with olfactory loss.     

Long-Lasting forward Suppression of Spontaneous Firing in Auditory Neurons: Implication to the Residual Inhibition of Tinnitus

Tinnitus is the perception of a sound that has no external source. Sound stimuli can suppress spontaneous firing in auditory neurons long after stimulus offset. It is unknown how changes in sound stimulus parameters affect this forward suppression. Using in vivo extracellular recording in awake mice, we found that about 40 % of spontaneously active inferior colliculus (IC) neurons exhibited forward suppression of spontaneous activity after sound offset. The duration of this suppression increased with sound duration and lasted about 40 s following a 30-s stimulus offset. Pure tones presented at the neuron’s characteristic frequency (CF) were more effective in triggering suppression compared to non-CF or wideband noise stimuli. In contrast, non-CF stimuli often induced forward facilitation. About one third of IC neurons exhibited shorter suppression durations with each subsequent sound presentation. These characteristics of forward suppression are similar to the psychoacoustic properties of residual inhibition of tinnitus: a phenomenon of brief (about 30 s) suppression of tinnitus observed in tinnitus patients after sound presentations. Because elevated spontaneous firing in central auditory neurons has been linked to tinnitus, forward suppression of this firing with sound might be an underlying mechanism of residual inhibition.     

Central auditory speech test findings in individuals with subjective idiopathic tinnitus

This study reports central auditory speech test performance of 25 consecutive patients with subjective idiopathic tinnitus of the severe disabling type. A preliminary study of 14 individuals who had subjective idiopathic tinnitus and complained of difficulty in hearing and understanding revealed a high incidence of abnormal central auditory speech test performance (71%), despite satisfactory peripheral hearing. The results (1) identify objectively for the first time that tinnitus affects specific components of the auditory pathway; (2) provide a basis for monitoring methods of tinnitus control; and (3) provide a basis for understanding "the interference effect" and problem of communication difficulties in patients with tinnitus of the severe disabling type.     

A biochemical model of peripheral tinnitus

Subjective tinnitus may be defined as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an externally evoking auditory stimulus. Tinnitus can be caused or exacerbated by one or more of five forms of stress. We propose and provide evidence supporting a model that explains, but is not limited to, peripheral (cochlear) tinnitus. In this model, naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes. In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear N-methyl-D-aspartate (NMDA) receptors. This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds. It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism. Finally, the proposed excitatory interactions of dynorphins and glutamate at NMDA receptors need not be restricted to the auditory periphery.     

Olfactory function and olfactory bulb volume in patients with postinfectious olfactory loss

OBJECTIVE: The study aimed to investigate whether the degree of postinfectious olfactory loss is reflected in volume of the olfactory bulb (OB). STUDY DESIGN: Retrospective study of 26 patients with postinfectious olfactory loss. MATERIALS AND METHODS: Olfactory function was assessed with the "Sniffin' Sticks" test kit, and the magnetic resonance imaging study focused on OB volume and the olfactory sulcus. RESULTS: The study revealed that 1) OB volume varies with regard to olfactory function, 2) OB volume decreases with duration of olfactory loss, and 3) patients with parosmia had smaller OB volumes than patients who did not report such smell distortions, although their overall olfactory function was not significantly different from each other. CONCLUSION: The study emphasizes that OB volume is a gauge of olfactory function.     

Tinnitus suppression by electrical promontory stimulation (EPS) in patients with sensorineural hearing loss

OBJECTIVE: Almost 10-15% of the population suffer from chronic tinnitus. There are clinical indications that a 'pathological sound' may be induced by any level of the auditory pathways. Theraupeutical difficulties and many hypotheses about tinnitus and places from which they originate might indicate various methods of treatment. Electrostimulation tinnitus suppression was achieved by many authors from 22 (Graham, Hazell) to 87% (Portman). The aim of our study was to define the usefulness of electrostimulation in treatment of persistent noise induced cochlear lesion tinnitus (group I - 43 men) and compare the results with the non noise induced tinnitus group II (68 patients). METHODS: Otolaryngological and audiological examination of the patients was made before and after electrostimulation, and at 90 days. The stimulation system consisted of a prototype tinnitus suppressor, the active platino-iridium needle electrode and silver surface electrode located on the forehead. Transtympanal electrical stimulation was performed using positive polarity direct current. Parameters of electrical impulse were individually different and depended on tinnitus parameters and patients sensation. The current levels ranged from 20 to 600 microA and frequency ranged from 60 to 10000 Hz. Average time of EPS was 60 s. RESULTS: The control examination 90 days after stimulation in group I showed subjective improvement in 18 (41.9%) patients, 22 (51.2%) did not notice any change and tinnitus deteriorated in 3 (6.9%) of the patients. In the comparative group II improvement was occurred in 34 (50%) persons including 2 (17.6%) in whom tinnitus was abolished, in 30 (44.1%) tinnitus was unchanged and 4 (0.6%) became worse. In both groups our method did not have a destructive influence on hearing. Electrical stimulation to relieve tinnitus has been used for nearly 200 years, but it is unclear how electrical stimulation works to suppress tinnitus. CONCLUSION: In our opinion electrical stimulation by using positive DC changes the spontaneous activity of cochlear nerve fibres. According to our results it is suggested that the mechanism of beneficial effects is due to increased microcirculation in part of the auditory pathways. Poorer results in patients with noise induced tinnitus could be explained by greater damage of the cochlea outer hair cells. In our opinion EPS could be a method of treatment for persistent tinnitus in cases which fail to respond to other methods.     

PERIPHERAL HEARING LOSS CAUSES HYPEREXCITABILITY OF THE INFERIOR COLLICULUS

Growing evidence has been found to suggest that early development of the central auditory system is dependent on acoustic stimuli. Peripheral damage caused by noise exposure and ototoxic drugs can induce functional and anatomical changes along the auditory pathways. The inferior colliculus (IC) is a unique structure in the auditory system located between the primary auditory nuclei of the brainstem and the thala-mus. Damage to the IC inhibitory circuitry may affect central auditory processing and sound perception. Here, we review some of the striking electrophysiological changes in the IC that occur after noise exposure and ototoxic drug treatment. A common occurrence that emerges in the IC after peripheral damage is hyper-excitability of sound-evoked response. The hyperexcitability of the IC is likely related with reduced inhibi-tory response that requires normal peripheral inputs. Early age hearing loss can result in a long lasting in-creased susceptibility to audiogenic seizure which is related to hyperactivity in the IC evoked by loud sounds. Our studies suggest that hearing loss can cause increased IC neuron responsiveness which may be related to tinnitus, hyperacusis, and audiogenic seizure.     

Severe chemotherapy-induced parosmia

BACKGROUND: Smell and taste disorders are among the side effects of chemo- and radiotherapy. Although direct radionecrosis of the salivary glands and the taste buds might explain the chemosensory problems after radiotherapy, the olfactory and gustatory complaints seen after chemotherapy remain unexplained. The patients reporting olfactory symptoms rarely complain about qualitative olfactory disorders such as parosmia or phantosmia. Quantitative olfactory loss such as anosmia and hyposmia seem to be more frequent. METHODS: We present the case of a 63-year-old woman with chemotherapy-induced parosmia leading to severe nutrition and appetite problems resulting in a life-threatening weight loss. RESULTS: With the aid of a simple nose clip the parosmia could be abolished and oral food intake became possible again. Parosmia resolved gradually over an observation period of 9 months, in parallel to an increase of olfactory sensitivity. The patient progressively gained appetite and weight. CONCLUSION: Parosmia can occur as a severe and potentially life-threatening complication of chemotherapy. This rare presentation of parosmia illustrates the importance of olfactory testing with an adequate recognition of the underlying problem and a consecutive treatment.     

耳鸣大鼠NMDA受体亚型1、2A、2B的表达研究

目的研究耳鸣大鼠听皮层NMDA（N-甲基-D-天冬氨酸,N-methyl-D-aspartate）受体亚型1、2A、2B（NR1、NR2A、NR2B）的表达变化,从而推测其在耳鸣的发生中可能的作用机制。方法按照随机化原则将动物分成3组,每组9只：A组为耳鸣模型组、B组为生理盐水组、C组为空白对照组。A组通过腹腔注射水杨酸钠并用食物抑制法进行验证。造模成功后运用核酸荧光染料SYBR Green实时荧光定量PCR（Polymerase Chain Reaction,聚合酶链反应）方法检测NMDA受体三种亚型的表达情况。结果NR1在A组的表达显著低于C组（P〈0.05）,NR2A在A组的表达则显著高于C组（P〈0.05）,而A、C两组之间NR2B的表达差异比较无统计学意义（P〉0.05）。NMDA受体三种亚型B、C两组之间表达差异比较均无统计学意义（P〉0.05）。A组NR2A、NR2B与NR1表达量的比值较C组均增大。结论耳鸣大鼠听皮层NMDA受体调节亚基的调控作用增大,突触局部受体蛋白质合成改变,听皮层发生了与NMDA受体相关的可塑性变化,这可能是耳鸣产生的机制之一。     

A novel surgical treatment for long lasting unilateral peripheral parosmia: Olfactory cleft blocking technique

The treatment of qualitative olfactory disease is challenging. We aimed to treat parosmia using a new minimally invasive surgical technique-the olfactory cleft blocking technique- by preventing odorants from reaching the olfactory epithelium. A novel surgical procedure for blocking the anterior and inferior openings of the olfactory cleft was accomplished in a patient with unilateral persistent peripheral parosmia. The HRCT and endoscopy were performed preoperatively and postoperatively to evaluate the anatomical structure of the olfactory cleft. The T&T olfactometer was used to assess the preoperative and postoperative olfactory function. After surgery, the patient's parosmia disappeared. Endoscopic examination and CT scan showed complete obstruction of the anterior and inferior portions of the olfactory cleft. No recurrence was reported during a 2-year follow-up. No surgical complications were reported except olfactory loss in the operative nostril. For patients with long-term unilateral peripheral olfactory dysfunction, the olfactory cleft blocking technique seems a novel, simple, safe and effective treatment. Further studies are required with a larger number of patients in order to access success rate.     

阻塞性睡眠呼吸暂停低通气综合征患者听力学损害研究进展

阻塞性睡眠呼吸暂停低通气综合症(obstructive sleep apnea hypopnea syndrome,OSAHS)是一种常见的睡眠障碍性疾病,长期的呼吸暂停和低通气可引起不同程度的低氧血症及高碳酸血症,继发组织缺氧,最终导致多器官功能损害,其中包括第8对颅神经-听神经的损害.临床观察中也发现了部分OSAH...     

Neurochemistry of the peripheral and central auditory system after ototoxic drug exposure: implications for tinnitus

Platinum-containing drugs, such as cisplatin and carboplatin, are known to have ototoxic side effects causing hearing loss that may be accompanied by tinnitus. This study reviews recent studies on the ototoxicity of cisplatin and carboplatin and summarizes the effects of protective agents that may prevent hearing loss and tinnitus. The primary locus of ototoxicity is in the cochlea, but oxidative stress to the inferior colliculus has been reported recently with carboplatin. Enhanced spontaneous activity within the dorsal cochlear nucleus has been correlated with loss of outer hair cells in animal experiments using cisplatin. This may result from disinhibition of neurons within the dorsal cochlear nucleus caused by reduced input from spiral ganglion cells. Carboplatin may cause tinnitus by oxidative stress within the inferior colliculus or by loss of inhibition within the inferior colliculus resulting from cochlear damage. This could lead to compensatory gain and enhanced responses in neurons within the auditory cortex. Protective agents may prevent tinnitus by preventing damage to the cochlea, thereby obviating the development of disinhibition within central auditory pathways.     

Olfactory dysfunction and daily life

The objective of the present study was to investigate the hypothesis that subjects with parosmia suffer more in their daily life than patients who experience only quantitative olfactory loss. Two hundred five outpatients of the Smell and Taste Clinic and 25 healthy controls were included. The newly developed Questionnaire of Olfactory Disorders (QOD) was administered in combination with other psychometric tests (Beck Depression Inventory, Befindlichkeitsskala and the Short Form-36 Health Survey) along with an olfactory test (Sniffin Sticks). Results of the QOD were found to be an appropriate and valid measure of the impact of olfactory dysfunction on daily life. Patients with parosmia and quantitative olfactory dysfunction show higher rates of daily life complaints when compared to patients suffering from quantitative olfactory impairment only (QOD-PS: P=0.005). In addition, hyposmic and anosmic patients indicated significantly more complaints compared to patients with normosmia. Further, female patients seemed to suffer more from olfactory dysfunction than male patients. In conclusion, the assessment of the degree of qualitative olfactory dysfunction may be possible by the use of instruments based on questionnaires regarding daily life problems.     

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.