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A dominant sigmoid sinus with either diverticulum or dehiscence (SS-Div/SS-Deh) is a common cause of pulsatile tinnitus (PT). For PT originating from SS-Div/SS-Deh, an etiology-specific and secure reconstruction using firm materials is vital for optimal outcomes. As a follow-up to our previous reports on transmastoid SS resurfacing or reshaping for SS-Div/SS-Deh, this study aimed to evaluate the long-term results of transmastoid resurfacing/reshaping. We retrospectively reviewed 20 PT patients who were diagnosed with SS-Div/SS-Deh, underwent transmastoid resurfacing/reshaping, and were followed up for more than 1 year postoperatively. For PT, immediate and long-term changes (> 1 year) in loudness and annoyance were analyzed using the visual analog scale (VAS). Additionally, pre and postoperative objective measurements of PT using transcanal sound recording and spectro-temporal analysis (TSR-STA), imaging results, and audiological findings were comprehensively analyzed. Significant improvements in PT were sustained or enhanced for > 1 year (median follow-up period: 37 months, range: 12–54 months). On TSR-STA, both peak and root mean square amplitudes decreased after surgery. Also, the average pure-tone threshold at 250 Hz improved after surgery. Thus, our long-term follow-up data confirmed that the surgical management of PT originating from SS-Div/SS-Deh is successful with regard to both objective and subjective measures.

Summary: Background: The aberrant brain network that gives rise to the phantom sound of tinnitus is believed to determine the effectiveness of tinnitus therapies involving neuromodulation with repetitive transcranial magnetic stimulation (rTMS) and sound therapy utilizing tailor-made notch music training (TMNMT). To test this hypothesis, we determined how effective rTMS or TMNMT were in ameliorating tinnitus in patients with different functional brain networks. Methods: Resting-state functional MRI was used to construct brain functional networks in patients with tinnitus (41 males/45 females, mean age 49.53±11.19 years) and gender-matched healthy controls (22 males/35 females, mean age 46.23±10.23 years) with independent component analysis (ICA). A 2 × 2 analysis of variance with treatment outcomes (Effective group, EG/Ineffective group, IG) and treatment types (rTMS/TMNMT) was used to test the interaction between outcomes and treatment types associated with functional network connections (FNCs). Findings: The optimal neuroimaging indicator for responding to rTMS (AUC 0.804, sensitivity 0.700, specificity 0.913) was FNCs in the salience network-right frontoparietal network (SN-RFPN) while for responding to TMNMT (AUC 0.764, sensitivity 0.864, specificity 0.667) was the combination of FNCs in the auditory network- salience network (AUN-SN) and auditory network-cerebellar network (AUN-CN). Interpretation: Tinnitus patients with higher FNCs in the SN-RFPN is associated with a recommendation for rTMS whereas patients with lower FNCs in the AUN-SN and AUN-CN would suggest TMNMT as the better choice. These results indicate that brain network-based measures aid in the selection of the optimal form of treatment for a patient contributing to advances in precision medicine. Funding: Yuexin Cai is supported by Key R&D Program of Guangdong Province, China (Grant No. 2018B030339001), National Natural Science Foundation of China (82071062), Natural Science Foundation of Guangdong province (2021A1515012038), the Fundamental Research Funds for the Central Universities (20ykpy91), and Sun Yat-Sen Clinical Research Cultivating Program (SYS-Q-201903). Yu-Chen Chen is supported by Medical Science and Technology Development Foundation of Nanjing Department of Health (No. ZKX20037), and Natural Science Foundation of Jiangsu Province (No. BK20211008).

Introduction: It was previously demonstrated that tinnitus due to profound unilateral hearing loss can be treated by the use of electrical stimulation via a cochlear implant (CI) with long-lasting positive effects. In cases where patients are not suitable for cochlear implantation due to aplasia/hypoplasia, cochlear malformations etc., an auditory brainstem implant (ABI) may be a solution. While auditory performance with ABI is well investigated, it is currently unknown whether stimulation through ABI also renders tinnitus reduction in patients with incapacitating tinnitus. The current case study reports on the subjective tinnitus perception during a 5-year follow-up period. In addition, a first H215O PET imaging study in an ABI patient is carried out revealing underlying neural substrates of tinnitus. Methods: A 56-year-old male single-sided deaf patient with incapacitating tinnitus received an ABI after insufficient auditory performances and only minor tinnitus reduction with CI. Audiological follow-up was carried out during a 5-year follow-up period comprising pure-tone audiometry, speech-in-quiet testing, speech-in-noise testing, tinnitus questionnaires (tinnitus questionnaire and numeric rating scale) and the HISQUI19 questionnaire. To investigate the neural substrates of tinnitus in this subject, H215O PET tomography scans were acquired in three different conditions: 1) ABI switched off which was considered as the resting-state measurement rendering the loudest possible tinnitus for the patient (ABI OFF); 2) ABI switched on causing a small suppression of tinnitus due to electrical stimulation (ABI ON); 3) ABI switched on and 70 dB SPL white noise presented directly to the external audio processor through a direct audio cable providing the maximum tinnitus suppression for the patient (NOISE). Results: Subjectively the patient reported a significant tinnitus reduction after implantation which remained stable over time with a decrease in tinnitus questionnaire from grade 4 to grade 2 and a 50% reduction in the numeric rating scale (from 8 to 4) during the 5-year period. Comparing the ABI OFF and ABI ON conditions, significant increase in regional cerebral blood flow (rCBF) was observed in brain areas involved in the salience network showing already suppression of tinnitus only by electrical stimulation in the absence of auditory stimuli. The NOISE condition showed relatively decreased rCBF in the insula (as well as in the orbitofrontal cortex) as compared with the ABI OFF condition. Abnormally activated areas comprising the salience network may have been significantly suppressed by the NOISE condition both by acoustic and electrical stimulations of the auditory pathway. Moreover, the NOISE condition showed significantly decreased rCBF in the parahippocampus as compared with the ABI OFF condition. This finding supports the idea of distinct tinnitus generators depending on the amount of hearing loss. Conclusion: The reduction of tinnitus in the current ABI subject may be attributable to partial peripheral reafferentation-induced deactivation of the parahippocampus-based tinnitus generator as well as the salience network. Further validation is required by the use of a follow-up study with a larger number of subjects.

Objective To discuss the possible pathophysiologic mechanism of pulsatile tinnitus (PT) perception due to high jugular bulb with bony dehiscence (HJBD) and its improvement after the dehiscent jugular bulb (JB) resurfacing using bone cement, and to describe the efficacy of an objective measure of PT using transcanal sound recording and spectro-temporal analysis (TSR/STA). Study design Retrospective case series study. Setting A university-based, tertiary care cancer center. Patients Three PT patients with HJBD. Main outcome measure(s) All patients underwent transtympanic resurfacing after the source of PT was confirmed by temporal bone imaging and TSR/STA. Improvement of symptom and the changes in the TSR/STA were analyzed. Results In the first case, a revision operation was performed due to slightly improved but persistent PT after initial resurfacing with bone pate and a piece of conchal cartilage. Revision transtympanic JB resurfacing was performed in this case using bone cement, and PT resolved immediately after the surgery. In the second and third cases, PT resolved completely, or was much abated, immediately after transtympanic resurfacing with bone cement. The TSR/STA also revealed improvement of PT. The median follow-up duration was 28 months, and all three patients remained asymptomatic or much improved compared with their preoperative status. Conclusions Transtympanic resurfacing with bone cement, reinforcing the dehiscent JB to reduce focal turbulent flow, is a simple and effective surgical treatment option in patients with PT due to HJBD. In patients with HJBD, the objective measurement of PT by TSR/STA may be of help in selecting appropriate surgical candidates and objective evaluation of the treatment outcome.

Along with phantom pain, tinnitus, a phantom auditory perception occurring in the absence of an external acoustic stimulus, is one of the most representative phantom perceptions that develops in subjects with decreased peripheral sensory input. Although tinnitus is closely associated with peripheral hearing loss (HL), it remains unclear why only some individuals with HL develop tinnitus. In this study, we investigated the differences between 65 HL with tinnitus (HL‐T) and 104 HL with no tinnitus (HL‐NT) using a resting‐state electroencephalography data‐based volume entropy model of the brain network, by comparing the afferent node capacities, that quantify the contribution of each node to the spread of information, of all Brodmann areas. While the HL‐T group showed increased information flow in areas involved in Bayesian inference (the left orbitofrontal cortex, the left subgenual anterior cingulate cortex, and the left ventrolateral prefrontal cortex) and auditory memory storage (the right hippocampus/parahippocampus), the HL‐NT group showed increased afferent node capacity in hub areas of the default mode network (DMN; the right posterior cingulate cortex and the right medial temporal gyrus). These results suggest that the balance of activity between the Bayesian inferential network (updating missing auditory information by retrieving auditory memories from the hippocampus/parahippocampus) and DMN (maintaining the “silent status quo”) determines whether phantom auditory perception occurs in a brain with decreased peripheral auditory input., Although tinnitus is closely associated with peripheral hearing loss (HL), it remains unclear why only some individuals with HL develop tinnitus. We have found that the balance of activity between the Bayesian inferential network (updating missing auditory information by retrieving auditory memories from the hippocampus/parahippocampus) and DMN (maintaining the “silent status quo”) determines whether phantom auditory perception occurs in a brain with decreased peripheral auditory input.

Tinnitus has traditionally been considered an otologic disorder; however, recent advances in auditory neuroscience have shifted investigations toward the brain. The Bayesian brain model explains tinnitus as an auditory phantom percept. According to the model, the brain works to reduce environmental uncertainty, and thus the absence of auditory information due to hearing loss may cause auditory phantom percepts, i.e., tinnitus. As in animal studies, our recent human observational study revealed the absence of ipsilesional tinnitus in subjects with congenital single-sided deafness, suggesting that auditory experience is a prerequisite for the generation of tinnitus. Prompted by anecdotal cases, we hypothesized that subjects with acquired hearing loss would not develop tinnitus if their duration of auditory experience was not sufficiently long. We retrospectively enrolled 22 subjects with acquired asymmetric hearing loss and unilateral tinnitus in better ear (TBE). Twenty-two hearing threshold-matched controls with tinnitus in worse ear (TWE) were selected from our database of tinnitus patients. All 22 TBE subjects reported that their acquired hearing loss developed before the age of 20, and the reported duration of auditory deprivation in the ear without tinnitus in the TBE group was significantly longer than that of the TWE group. In other words, the TBE group with limited auditory experience in the worse ear did not develop tinnitus in the worse ear while subjects with enough auditory experiences in the worse ear developed ipsilesional tinnitus in the TWE group. These preliminary results support our hypothesis that both auditory experience itself, and an individually variable critical duration of auditory deprivation, are prerequisites for the generation of tinnitus.

Tinnitus has traditionally been considered an otologic disorder; however, recent advances in auditory neuroscience have shifted investigations toward the brain. The Bayesian brain model explains tinnitus as an auditory phantom percept. According to the model, the brain works to reduce environmental uncertainty, and thus the absence of auditory information due to hearing loss may cause auditory phantom percepts, i.e., tinnitus. As in animal studies, our recent human observational study revealed the absence of ipsilesional tinnitus in subjects with congenital single-sided deafness, suggesting that auditory experience is a prerequisite for the generation of tinnitus. Prompted by anecdotal cases, we hypothesized that subjects with acquired hearing loss would not develop tinnitus if their duration of auditory experience was not sufficiently long. We retrospectively enrolled 22 subjects with acquired asymmetric hearing loss and unilateral tinnitus in better ear (TBE). Twenty-two hearing threshold-matched controls with tinnitus in worse ear (TWE) were selected from our database of tinnitus patients. All 22 TBE subjects reported that their acquired hearing loss developed before the age of 20, and the reported duration of auditory deprivation in the ear without tinnitus in the TBE group was significantly longer than that of the TWE group. In other words, the TBE group with limited auditory experience in the worse ear did not develop tinnitus in the worse ear while subjects with enough auditory experiences in the worse ear developed ipsilesional tinnitus in the TWE group. These preliminary results support our hypothesis that both auditory experience itself, and an individually variable critical duration of auditory deprivation, are prerequisites for the generation of tinnitus.

Just as the human brain works in a Bayesian manner to minimize uncertainty regarding external stimuli, a deafferented brain due to hearing loss attempts to obtain or “fill in” the missing auditory information, resulting in auditory phantom percepts (i.e., tinnitus). Among various types of hearing loss, sudden sensorineural hearing loss (SSNHL) has been extensively reported to be associated with tinnitus. However, the reason that tinnitus develops selectively in some patients with SSNHL remains elusive, which led us to hypothesize that patients with SSNHL with tinnitus (SSNHL-T) and those without tinnitus (SSNHL-NT) may exhibit different cortical activity patterns. In the current study, we compared resting-state quantitative electroencephalography findings between 13 SSNHL-T and 13 SSNHL-NT subjects strictly matched for demographic characteristics and hearing thresholds. By performing whole-brain source localization analysis complemented by functional connectivity analysis, we aimed to determine the as-yet-unidentified cortical oscillatory signatures that may reveal potential prerequisites for the perception of tinnitus in patients with SSNHL. Compared with the SSNHL-NT group, the SSNHL-T group showed significantly higher cortical activity in Bayesian inferential network areas such as the frontopolar cortex, orbitofrontal cortex (OFC), and pregenual anterior cingulate cortex (pgACC) for the beta 3 and gamma frequency bands. This suggests that tinnitus develops in a brain with sudden auditory deafferentation only if the Bayesian inferential network updates the missing auditory information and the pgACC-based top-down gatekeeper system is actively involved. Additionally, significantly increased connectivity between the OFC and precuneus for the gamma frequency band was observed in the SSNHL-T group, further suggesting that tinnitus derived from Bayesian inference may be linked to the default mode network so that tinnitus is regarded as normal. Taken together, our preliminary results suggest a possible mechanism for the selective development of tinnitus in patients with SSNHL. Also, these areas could serve as the potential targets of neuromodulatory approaches to preventing the development or prolonged perception of tinnitus in subjects with SSNHL.

As the human brain works in a Bayesian manner to minimize uncertainty toward external stimuli, the deafferented brain may generate tinnitus in an attempt to fill in missing auditory information, e.g. due to hearing loss. However, not everybody with hearing loss develops tinnitus. Understanding the differences between people with hearing loss who develop tinnitus versus those who do not offers a unique opportunity to unravel critical brain areas involved in the generation of a phantom sound. In this study, we compared resting-state quantitative electroencephalography between hearing loss patients with (HL-T) and without tinnitus (HL-NT) to identify cortical oscillatory signatures that may reveal prerequisites for the selective development of tinnitus in subjects with hearing loss. We enrolled 65 subjects with HL-NT and 65 subjects with HL-T whose tinnitus handicap inventory scores were16 (grade 1) to minimize the bias induced by distress-induced cortical activity changes. Subjects in the HL-T and HL-NT groups were matched in terms of the bilateral hearing threshold (0.25-8 kHz) using nearest neighbor method. Compared to the HL-NT group, the HL-T group showed significantly higher activity in the right parahippocampus for the beta 1 frequency band, in the left inferior parietal lobule (IPL) for the beta 2 frequency band, and in the right IPL for the beta 3- and gamma frequency bands. Functional connectivity analyses revealed that the HL-T group had significantly higher connectivity than the HL-NT group between both parahippocampal gyri and the right IPL for the delta frequency band, and between the left posterior cingulate cortex (PCC) and right IPL for the beta 2 frequency band. These results suggest that tinnitus may be perceived only if auditory memory stored in the parahippocampus is actively linked to the IPL-based "circuit breaker" system and the circuit breaker signal is connected to the PCC-based default mode network (DMN). Thus, when the circuit breaker system regards tinnitus secondary to peripheral deafferentation as a salient event and then the DMN regards tinnitus as a norm, subjects with hearing loss may consciously perceive tinnitus. The results of this study further refine the recently proposed Bayesian model and decipher the neurobiological mechanism of the selective development of tinnitus in subjects with hearing loss.

Although hearing aids (HAs) are sometimes efficacious in abating tinnitus, the precise mechanism underlying their effect is unclear and predictors of symptom improvement have not been determined. Here, we examined the correlation between the amount of tinnitus improvement and pre-HA quantitative electroencephalography (qEEG) findings to investigate cortical predictors of improvement after wearing HAs. QEEG data of thirty-three patients with debilitating tinnitus were retrospectively correlated with the percentage improvements in tinnitus handicap inventory and the numerical rating scale scores of tinnitus. Activation of brain areas involved in the default mode network (DMN; inferior parietal lobule, parahippocampus, and posterior cingulate cortex) were found to be a negative predictor of improvement in tinnitus-related distress after wearing HAs. In addition, higher pre-HA cortical power at the medial auditory processing system or higher functional connectivity of the lateral/medial auditory pathway to the DMN was found to serve as a positive prognostic indicator with regard to improvement of tinnitus-related distress. In addition, insufficient activity of the pre-treatment noise canceling system tended to be a negative predictor of tinnitus perception improvement after wearing HAs. The current study may serve as a milestone toward a pre-HAs prediction strategy for tinnitus improvements in subjects with hearing loss and severe tinnitus.

To treat motor and psychiatric disorders, transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS) are world-widely in use in clinics. We combined these two types of neuromodulation technique to increase the effective response of a single session of neuromodulation in subjective tinnitus. Experimental groups with 80 tinnitus subjects consisted of four different treatment groups which are tDCS, tDCS with sham TMS, tDCS-TMS and TMS group. Subjects were given 1.5mA tDCS on the bi-frontal area and TMS stimulated contralateral single side of temporo-parietal cortex with 200 pulses at 1Hz stimulation. Comparing pre-treatment questionnaire scores to post-treatment questionnaire scores, all 4 groups showed statistically significant improvements. Although there was no significant difference among group comparison, the largest mean difference was shown in the combined group, especially for tinnitus intensity and tinnitus-related distress. Responders in the combined group were the highest for VAS intensity, maximum 80% of twenty subjects. To summarize, dual-neuromodulation responders could consist of responders of frontal tDCS and temporal TMS. In addition, abnormal activity in the frontal or temporal area of the responders is presumed to be modulated by treatment and will be suggested as the target areas in future studies.

Thalamocortical dysrhythmia (TCD) is a model proposed to explain divergent neurological disorders. It is characterized by a common oscillatory pattern in which resting-state alpha activity is replaced by cross-frequency coupling of low- and high-frequency oscillations. We undertook a data-driven approach using support vector machine learning for analyzing resting-state electroencephalography oscillatory patterns in patients with Parkinson’s disease, neuropathic pain, tinnitus, and depression. We show a spectrally equivalent but spatially distinct form of TCD that depends on the specific disorder. However, we also identify brain areas that are common to the pathology of Parkinson’s disease, pain, tinnitus, and depression. This study therefore supports the validity of TCD as an oscillatory mechanism underlying diverse neurological disorders., Thalamocortical dysrhythmia has been proposed to occur in a number of neurological and psychiatric disorders. Here, the authors use a data-driven approach to demonstrate thalamocortical dysrhythmia occurs in individuals with Parkinson’s disease, neuropathic pain, tinnitus, and depression.

One of the most intriguing questions in neuroscience is to understand the mechanism of information transfer between different brain areas. Recently, network theory has gained traction and is at the forefront of providing a possible explanation to not only the mechanism of information transfer but also in the identification of different neuropathologies. The perception of a phantom ringing in the ear called tinnitus, similar to other neuropathologies, has been shown to be accompanied by aberrant functional connectivity between different brain areas. Although, there have been independent studies showing that specific groups of areas encode individual symptoms of tinnitus, there has not been one study to show that tinnitus is the unified percept of distinguishable subnetworks encoding different behavioral aspects. This study combines resting-state functional connectivity obtained from the source-localized electroencephalography of 311 tinnitus patients and 264 controls, and a k-fold cross-validation machine learning algorithm to develop a predictive model that verifies the presence of behaviorally specific, spatiotemporally overlapping subnetworks in tinnitus. This reorganization is found to be exclusive to tinnitus, even when compared to physiologically similar disorders such as chronic pain, with each behavioral symptom having a unique oscillatory signature. This frequency-specific transmission of information, called multiplexing, enables different types of information to be carried between two brain regions through the same anatomical connection. In addition to understanding the efficient compensation mechanism of the brain in the presence of multisymptom disorders, the exclusivity of the prediction model presents an encouraging possibility for an objective neural marker for tinnitus.

Although tinnitus retraining therapy (TRT) based on Jastreboff's classical neurophysiological model is efficacious in most patients, its effects on the cortical activity changes responsible for the improvement of tinnitus are still unclear. In this study, we compared pre- and post-TRT resting-state quantitative electroencephalography (rs-qEEG) findings to identify power changes that could explain TRT-induced improvements. Thirty-seven patients with severe tinnitus were enrolled in the study, and rs-qEEG data recorded before the initial TRT sessions and 6 months after TRT were compared. In addition, associations between the changes in qEEG and percentage improvements in Tinnitus Handicap Inventory (THI) scores and numeric rating scale (NRS) scores of tinnitus loudness and tinnitus perception were examined. The mean THI score decreased significantly 6 months after the initial TRT session. Also, significant improvements were observed 6 months after the initial TRT session compared with the pre-treatment scores in NRS loudness, distress, and perception. As compared with the pre-TRT status, post-TRT 6 months status showed significantly decreased powers in the left primary and secondary auditory cortices for the gamma frequency band. Changes in the alpha 1 frequency band power in the right insula and orbitofrontal cortex (OFC) appeared to be positively correlated with the percentage changes in NRS distress. These results suggested that TRT improved tinnitus-related distress by reducing the power of the top-down autonomic response modulator or peripheral physiological responses to emotional experiences. That is, TRT induced habituation via modulation of functional connections between the auditory system and the limbic and autonomic nervous systems. Our results confer additional basis for understanding the neurophysiological model and the newly suggested integrative model of tinnitus by De Ridder et al. (2014) in the context of the long-term efficacy of TRT.

We reviewed the clinical characteristics and treatment outcomes of patients with glomus tympanicum tumors (GTTs) presenting with pulsatile tinnitus (PT). We explored whether transcanal sound recording-spectro-temporal analysis (TSR-STA) usefully evaluated changes in PT. The medical records of 13 patients who underwent surgical removal of GTTs were reviewed retrospectively. Two patients underwent preoperative endovascular embolization. Changes in PT, pre- and postoperative audiometry data, TSR-STA results, and clinical outcomes were evaluated. PT was the chief complaint in eight patients (61.5%) and resolved immediately after surgical intervention in all. Two patients exhibited ipsilateral, pseudo-low-frequency hearing loss (PLFHL); surgical GTT removal elicited postoperative improvements in the ipsilesional low-frequency hearing thresholds. Five patients underwent TSR-STA using previously described methods. TSR-STA revealed definite rise-and-fall patterns; surgical tumor removal abated this pattern in one patient, but, for the other four, the patterns did not change greatly post-intervention. Thus, GTT-related PT can be treated successfully (via surgical GTT removal) without complications. In selected cases, preoperative embolization reduces intraoperative hemorrhage. In PT patients with PLFHL, a detailed otoendoscopic examination of the middle ear is required to rule out a GTT. TSR-STA may usefully (and objectively) assess postoperative improvements in GTT-related PT.

OBJECTIVE A dominant sigmoid sinus with focal dehiscence or thinning (DSSD/T) of the overlying bony wall is a commonly encountered, but frequently overlooked, cause of vascular pulsatile tinnitus (VPT). Also, the pathophysiological mechanism of sound perception in patients with VPT remains poorly understood. In the present study, a novel surgical method, termed transmastoid SS-reshaping surgery, was introduced to ameliorate VPT in patients with DSSD/T. The authors reviewed a case series, analyzed the surgical outcomes, and suggested the pathophysiological mechanism of sound perception. The theoretical background underlying VPT improvement after transmastoid SS-reshaping surgery was also explored. METHODS Eight patients with VPT that was considered attributable to DSSD/T underwent transmastoid SS-reshaping surgery between February 2010 and February 2015. The mean postoperative follow-up period was 9.5 months (range 4–13 months). Transmastoid SS-reshaping surgery featured simple mastoidectomy, partial compression of the SS using harvested cortical bone chips, and reinforcement of the bony SS wall with bone cement. Perioperative medical records, imaging results, and audiological findings were comprehensively reviewed. RESULTS In 7 of the 8 patients (87.5%), the VPT abated immediately after surgery. Statistically significant improvements in tinnitus loudness and distress were evident on numeric rating scales. Three patients with preoperative ipsilesional low-frequency hearing loss exhibited postoperative improvements in their low-frequency hearing thresholds. No major postoperative complications were encountered except in the first subject, who experienced increased intracranial pressure postoperatively. This subsided after a revision operation for partial decompression of the SS. CONCLUSIONS Transmastoid SS-reshaping surgery may be a good surgical option in patients with DSSD/T, a previously unrecognized cause of VPT. Redistribution of severely asymmetrical blood flow, reinforcement of the bony SS wall with bone cement to reconstruct a soundproof barrier, and disconnection of a problematic sound conduction route via simple mastoidectomy silence VPT.

Although frequently classified as "objective tinnitus," in most cases vascular pulsatile tinnitus (VPT) is not equal to objective tinnitus because it is not easy to objectively document VPT. The present study was conducted to develop a novel transcanal sound recording and spectrotemporal analysis method for the objective and differential diagnosis of VPT.A case series with a control group.Tertiary referral center.Six VPT subjects with radiological abnormalities and six normal controls.The method was tested based on recordings obtained from the ipsilateral external auditory canal (EAC) using an insert microphone with the subject's head in four different positions. The recorded signals were first analyzed in the time domain, and short-time Fourier transform was performed to analyze the data in the time-frequency domain.From the temporal analysis, the ear canal signals recorded from the VPT subjects exhibited large peak amplitudes and periodic structures, whereas the signals recorded from the control subjects had smaller peak amplitudes and weaker periodicity. From the STA represented by two-dimensional spectrograms and three-dimensional waterfall diagrams, all of the VPT subjects demonstrated pulse-synchronous acoustic characteristics that were representative of their respective presumptive vascular pathologies, whereas the control subjects did not display such characteristics.The present diagnostic approach may provide additional information regarding the origins of VPT cases as well as an efficient and objective diagnostic method. Furthermore, this approach may aid in the determination of appropriate imaging modalities, treatment planning, and evaluation of treatment outcomes.

The mechanism of tinnitus suppression after cochlear implantation (CI) in single-sided deafness (SSD) is not fully understood. In this regard, by comparing pre-and post-CI quantitative electroencephalography (qEEG), we explored cortical changes relevant to tinnitus improvement. In SSD patients who underwent CI, qEEG data were collected: (1) before CI, (2) 6 months post-operatively with CI-on, and (3) 30 min after CI-off and source-localized cortical activity/functional connectivity analyses were performed. Compared to the pre-operative baseline, the CI-on condition demonstrated significantly decreased activity in the right auditory-and orbitofrontal cortices (OFC) for the delta frequency band as well as decreased connectivity between the auditory cortex/posterior cingulate cortex for the delta/beta2 bands. Meanwhile, compared to the CI-off condition, the CI-on condition displayed decreased activity in the right auditory cortices/OFC for the delta band, and in bilateral auditory cortices, left inferior frontal cortex/OFC for the gamma band. However, qEEG analyses showed no significant differences between the CI-off and baseline conditions. CI induced overall decreased cortical activity and functional connectivity. However, judging from no differences between the CI-off and baseline conditions, CI-induced cortical activity and functional connectivity changes are not by cortical plastic changes, but by dynamic peripheral reafferentation.

Background: Quantitative electroencephalography (qEEG) is effective when used to analyze ongoing cortical oscillations in cochlear implant (CI) users. However, localization of cortical activity in such users via qEEG is confounded by the presence of artifacts produced by the device itself. Typically, independent component analysis (ICA) is used to remove CI artifacts in auditory evoked EEG signals collected upon brief stimulation and it is effective for auditory evoked potentials (AEPs). However, AEPs do not reflect the daily environments of patients, and thus, continuous EEG data that are closer to such environments are desirable. In this case, device-related artifacts in EEG data are difficult to remove selectively via ICA due to over-completion of EEG data removal in the absence of preprocessing. New methods: EEGs were recorded for a long time under conditions of continuous auditory stimulation. To obviate the over-completion problem, we limited the frequency of CI artifacts to a significant characteristic peak and apply ICA artifact removal. Results: Topographic brain mapping results analyzed via band-limited (BL)-ICA exhibited a better energy distribution, matched to the CI location, than data obtained using conventional ICA. Also, source localization data verified that BL-ICA effectively removed Cl artifacts. Comparison with existing method: The proposed method selectively removes Cl artifacts from continuous EEG recordings, while ICA removal method shows residual peak and removes important brain activity signals. Conclusion: Cl artifacts in EEG data obtained during continuous passive listening can be effectively removed with the aid of BL-ICA, opening up new EEG research possibilities in subjects with Cls. (C) 2015 Elsevier B.V. All rights reserved.

Recent studies have suggested that hyperacusis, an abnormal hypersensitivity to ordinary environmental sounds, may be characterized by certain resting-state cortical oscillatory patterns, even with no sound stimulus. However, previous studies are limited in that most studied subjects with other comorbidities that may have affected cortical activity. In this regard, to assess ongoing cortical oscillatory activity in idiopathic hyperacusis patients with no comorbidities, we compared differences in resting-state cortical oscillatory patterns between five idiopathic hyperacusis subjects and five normal controls. The hyperacusis group demonstrated significantly higher electrical activity in the right auditory-related cortex for the gamma frequency band and left superior parietal lobule (SPL) for the delta frequency band versus the control group. The hyperacusis group also showed significantly decreased functional connectivity between the left auditory cortex (AC) and left orbitofrontal cortex (OFC), between the left AC and left subgenual anterior cingulate cortex (sgACC) for the gamma band, and between the right insula and bilateral dorsal anterior cingulate cortex (dACC) and between the left AC and left sgACC for the theta band versus the control group. The higher electrical activity in the SPL may indicate a readiness of “circuit-breaker” activity to shift attention to forthcoming sound stimuli. Also, because of the disrupted salience network, consisting of the dACC and insula, abnormally increased salience to all sound stimuli may emerge, as a consequence of decreased top-down control of the AC by the dACC and dysfunctional emotional weight attached to auditory stimuli by the OFC. Taken together, abnormally enhanced attention and salience to forthcoming sound stimuli may render hyperacusis subjects hyperresponsive to non-noxious auditory stimuli.

Introduction Auricular Arteriovenous Malformation of the external ear is a rarely encountered disease; in particular, arteriovenous malformation arising from the auricle, with spontaneous bleeding, has seldom been reported. Objective In the current study, we report an unusual case of late-onset auricular arteriovenous malformation originating from the posterior auricular artery that was confirmed by computed tomographic angiography. The case was successfully managed by pre-surgical intravascular embolization followed by total lesion excision. Prompted by this case, we also present a scoping review of the literature. Methods A case of a 60 year-old man with right auricular arteriovenous malformation treated in our tertiary care center, and 52 patients with auricular arteriovenous malformation described in 10 case reports and a retrospective review are presented. Auricular arteriovenous malformation can manifest as swelling of the ear, pulsatile tinnitus, pain, and/or bleeding. On physical examination, a pulsatile swelling and/or a tender mass is evident. When arteriovenous malformation is suspected, the lesions should be visualized using imaging modalities that optimally detect vascular lesions, and managed via embolization, mass excision, or auricular resection. Effectiveness of the various diagnostic methods used and the treatment outcomes were analyzed. Results Various imaging modalities including Doppler sonography, computed tomographic angiography, magnetic resonance angiography, and/or transfemoral cerebral angiography were used to diagnose 38 cases reported in the literature. In another 15 cases, no imaging was performed; treatment was determined solely by physical examination and auscultation. Of the total of 53 cases, 12 were not treated (their symptoms were merely observed) whereas 20 underwent therapeutic embolization. In total, 32 patients, including 1 patient who was not treated and 10 with persistent or aggravated arteriovenous malformation after previous embolization, underwent mass excision or auricular resection depending on the extent of the lesion. No major postoperative complication was recorded. The postoperative follow-up duration varied from 1 month to 19 years, and only one case of unresectable, residual cervicofacial arteriovenous malformation was recorded. Conclusion Auricular arteriovenous malformation is a rarely encountered disease, but should be suspected if a patient presents with a swollen ear and pulsatile tinnitus. Appropriate imaging is essential for diagnosis and evaluation of the extent of disease. As embolization affords only relatively poor control, total surgical removal of the vascular mass is recommended.

Although neurovascular compression of the cochlear nerve (NVC-C) presenting as typewriter tinnitus is a discrete disease category, verified diagnostic criteria are lacking. We sought to refine the diagnostic criteria for NVC-C by reference to a relatively large case series. The medical records of 22 NVC-C patients were retrospectively reviewed. Psychoacoustic characteristics, the results of diagnostic work-up (including audiovestibular neurophysiological tests and radiological evaluations), and the initial treatment response to carbamazepine were investigated. All subjects described their tinnitus as a typical “typewriter” or “staccato” sound. Of the 22 subjects, 11 (50%) had histories of vertiginous spells, but none had ipsilesional hearing loss. Vestibular function tests in 11 subjects tested revealed only 2 (18.2%) isolated cervical vestibular evoked myogenic potential abnormalities. Radiological comparisons of the symptomatic and asymptomatic sides, regarding the type of the vascular loop and neurovascular contact, revealed no significant differences. However, all 22 subjects exhibited immediate and marked responses to short-term carbamazepine treatment. Meticulous history-taking in terms of the psychoacoustic characteristics and the response to initial carbamazepine, are more reliable diagnostic clues than are radiological or neurophysiological data in NVC-C subjects. Therefore, the typical psychoacoustic characteristics and the response to initial carbamazepine should be included in the diagnostic criteria.

Recent studies have adopted the Bayesian brain model to explain the generation of tinnitus in subjects with auditory deafferentation. That is, as the human brain works in a Bayesian manner to reduce environmental uncertainty, missing auditory information due to hearing loss may cause auditory phantom percepts, i.e., tinnitus. This type of deafferentation-induced auditory phantom percept should be preceded by auditory experience because the fill-in phenomenon, namely tinnitus, is based upon auditory prediction and the resultant prediction error. For example, a recent animal study observed the absence of tinnitus in cats with congenital single-sided deafness (SSD; Eggermont and Kral, Hear Res 2016). However, no human studies have investigated the presence and characteristics of tinnitus in subjects with congenital SSD. Thus, the present study sought to reveal differences in the generation of tinnitus between subjects with congenital SSD and those with acquired SSD to evaluate the replicability of previous animal studies. This study enrolled 20 subjects with congenital SSD and 44 subjects with acquired SSD and examined the presence and characteristics of tinnitus in the groups. None of the 20 subjects with congenital SSD perceived tinnitus on the affected side, whereas 30 of 44 subjects with acquired SSD experienced tinnitus on the affected side. Additionally, there were significant positive correlations between tinnitus characteristics and the audiometric characteristics of the SSD. In accordance with the findings of the recent animal study, tinnitus was absent in subjects with congenital SSD, but relatively frequent in subjects with acquired SSD, which suggests that the development of tinnitus should be preceded by auditory experience. In other words, subjects with profound congenital peripheral deafferentation do not develop auditory phantom percepts because no auditory predictions are available from the Bayesian brain.

Both invasive and non-invasive neuromodulation of the dorsolateral prefrontal cortex (DLPFC) are capable of suppressing tinnitus loudness. Repetitive transcranial magnetic stimulation (rTMS) of the DLPFC has an add-on effect for auditory cortex (AC) rTMS in improving tinnitus-related distress. We aimed to investigate whether TMS and rTMS of the DLPFC is capable of reducing tinnitus loudness and what mechanism might be involved. Two TMS studies targeting the right DLPFC were performed. Study 1 investigated 44 tinnitus patients who underwent either 1 or 10 Hz real or sham TMS (200 pulses at 80% motor threshold). In Study 2 we performed rTMS (10 sessions of 600 pulses) in responders of study 1. Changes on the visual analog scale (VAS) loudness were evaluated. All patients underwent a pre-TMS electroencephalography: differences in functional connectivity between responders and non-responders were evaluated using sLORETA. Only 1 Hz TMS was capable of significantly reducing tinnitus loudness for 11 patients with a mean suppression of 39.23%. RTMS for these 11 patients yielded a 21% improvement in VAS loudness, and in 7 of 11 rTMS was successful, with, a mean suppression of 27.13%. The responders were characterized by a difference in lagged linear connectivity in the theta band among the DLPFC, anterior cingulate cortex (ACC), parahippocampus and AC. In summary, 1 H, TMS and rTMS of the right DLPFC can transiently reduce the perceived tinnitus loudness mediated via functional connections between the DLPFC and a network consisting of the ACC, parahippocampus and AC. (C) 2013 Elsevier Inc. All rights reserved.

Notwithstanding successful reduction of tinnitus after cochlear implantation (CI) in patients with single-sided deafness (SSD) in recent studies, neither the exact mechanism of suppression nor the predictors of the amount of improvement are fully understood yet. We collected quantitative electroencephalography (qEEG) data from nine SSD patients who underwent CI for tinnitus management. By correlating the degree of improvement in tinnitus intensity and tinnitus-related distress with preoperative source-localized qEEG findings and comparing qEEG findings of patients with marked improvement after CI with those with relatively slight improvement with regard to source-localized activity complimented by connectivity analysis, we attempted to find preoperative predictors of tinnitus improvement. Our results showed increased activities of the auditory cortex (AC), posterior cingulate cortex (PCC) and increased functional connectivity between the AC and PCC as negative prognostic factors for the reduction of tinnitus intensity after CI in patients with SSD. Also, relatively increased activity of the right dorsolateral prefrontal cortex and decreased connectivity between distress-related areas such as the orbitofrontal cortex/parahippocampus and sensory-perception areas such as the AC/precuneus were found in patients with relatively slight improvement in tinnitus-related distress as compared with those with marked improvement. The current study suggests that preoperative cortical oscillations can be applied to predict post-CI tinnitus reduction in patients with SSD. (C) 2013 Elsevier B.V. All rights reserved.

Although hyperacusis, a hyperresponsiveness to non-noxious auditory stimuli, is a sound-evoked symptom, possible resting-state pathologic oscillations in hyperacusis brain have never been explored. By comparing 17 tinnitus participants with hyperacusis (T+H+) and 17 without hyperacusis (T+H-), we aimed to explore characteristic resting-state cortical activity of hyperacusis. The T+H+ and T+H- groups, strictly matched for all tinnitus sound characteristics to exclude tinnitus-related cortical changes, were compared using resting-state electroencephalography source-localized activity complemented by functional connectivity analyses. Correlation analysis revealed that hyperacusis questionnaire score was positively correlated with the orbitofrontal cortex (OFC) beta power, the right auditory cortex (AC) alpha1 power, and the dorsal anterior cingulate cortex (dACC) beta1 power. Compared to the T+H- group, the T+H+ group demonstrated increased beta power in the dACC and OFC, and increased alpha power in the right AC. Region of interest analyses including 17 normal controls further confirmed that these differences originated solely from relatively increased power of the T+H+ group, not from a relative power decrease of the T+H- group. Also, the T+H+ group showed increased connectivity between the OFC/dACC and the AC as compared to the T+H- group. The beta power increase in the OFC/dACC may indicate increased resting-state vigilance in tinnitus patients with hyperacusis. In addition, increased alpha power in the AC may reflect an adaptive top-down inhibition against sound stimuli probably mediated by the increased beta power of the OFC. The OFC/dACC, also frequently found to be activated in analogous diseases such as allodynia/hyperalgesia, may compose a hyperresponsiveness network.

Pulsatile tinnitus (PT) is often an initial presenting symptom of dural arteriovenous fistula (dAVF), but it may be overlooked or diagnosed late if not suspected on initial diagnostic work-up. Here, we assess anatomical features, treatment outcomes, and clinical implications of patients with PT due to dAVF. Of 220 patients who were diagnosed with dAVF between 2003 and 2014, 30 (13.6%) presented with only PT as their initial symptom. The transverse-sigmoid sinus (70.0%) was the most common site, followed by the hypoglossal canal (10.0%) and the middle cranial fossa (6.7%) on radiologic evaluation. Regarding venous drainage patterns, sinus or meningeal venous drainage pattern was the most common type (73.3%), followed by sinus drainage with a cortical venous reflux (26.7%). PT disappeared completely in 21 (80.8%) of 26 patients who underwent therapeutic intervention with transarterial embolization of the fistula, improved markedly in 3 (11.5%), and remained the same in 2 (7.7%). In conclusion, considering that PT may be the only initial symptom in more than 10% of dAVF, not only otolaryngologists but also neurologists and neurosurgeons should meticulously evaluate patients with PT. In most cases, PT originating from dAVF can be cured with transarterial embolization regardless of location and venous drainage pattern.

BACKGROUND AND PURPOSE: Typewriter tinnitus, a symptom characterized by paroxysmal attacks of staccato sounds, has been thought to be caused by neurovascular compression of the cochlear nerve, but the correlation between radiologic evidence of neurovascular compression of the cochlear nerve and symptom presentation has not been thoroughly investigated. The purpose of this study was to examine whether radiologic evidence of neurovascular compression of the cochlear nerve is pathognomonic in typewriter tinnitus. MATERIALS AND METHODS: Fifteen carbamazepine-responding patients with typewriter tinnitus and 8 control subjects were evaluated with a 3D T2-weighted volume isotropic turbo spin-echo acquisition sequence. Groups 1 (16 symptomatic sides), 2 (14 asymptomatic sides), and 3 (16 control sides) were compared with regard to the anatomic relation between the vascular loop and the internal auditory canal and the presence of neurovascular compression of the cochlear nerve with/without angulation/indentation. RESULTS: The anatomic location of the vascular loop was not significantly different among the 3 groups (all, P > .05). Meanwhile, neurovascular compression of the cochlear nerve on MR imaging was significantly higher in group 1 than in group 3 (P = .032). However, considerable false-positive (no symptoms with neurovascular compression of the cochlear nerve on MR imaging) and false-negative (typewriter tinnitus without demonstrable neurovascular compression of the cochlear nerve) findings were also observed. CONCLUSIONS: Neurovascular compression of the cochlear nerve was more frequently detected on the symptomatic side of patients with typewriter tinnitus compared with the asymptomatic side of these patients or on both sides of control subjects on MR imaging. However, considering false-positive and false-negative findings, meticulous history-taking and the response to the initial carbamazepine trial should be regarded as more reliable diagnostic clues than radiologic evidence of neurovascular compression of the cochlear nerve.

Objective In patients with pulsatile tinnitus (PT), physical examination such as auscultation with head position change or digital compression over the ipsilateral jugular vein provides physicians with important information. However, objective diagnosis of PT is sometimes limited because 1) audible bruit is absent on auscultation in some patients, 2) abnormal vascular structures found in radiologic evaluation is not always pathognomonic because they can be found in asymptomatic subjects as well, and 3) although an objective diagnostic tool using transcanal sound recording has recently been introduced, special equipment is needed. In this regard, recent studies that have reported ipsilateral low-frequency hearing loss (LFHL) on pure-tone audiometry (PTA) in some patients with PT, and its recovery after successful management, prompted us to conduct a retrospective observational study on the characteristics of the audiometric profile, the association between the audiometric profile and radiologic findings, and pre- and posttreatment changes in low-frequency hearing thresholds in PT patients. We tested two hypotheses: PT patients with marked vascular pathologies located close to the cochlea may show ipsilateral pseudo-LFHL (PLFHL) because of the masking effects of the PT itself, and their PLFHL may disappear if their vascular pathology is successfully managed by surgical or endovascular intervention. Study design Retrospective case review. Setting Tertiary referral center. Patients A total of 85 PT subjects who underwent both audiologic and radiologic examinations. Main outcome measure All patients' pre- and posttreatment PTA thresholds and radiologic findings were analyzed. By comparing the LFHL (an ipsilateral hearing threshold greater than 10 dB HL at both 250 and 500 Hz or greater than 20 dB HL at either 250 or 500 Hz compared with the contralateral side) group and a non-LFHL group with regard to the incidence of vascular structural abnormalities, we evaluated the incidence of abnormal vascular structures in the head and neck between the LFHL and non-LFHL groups. In addition, by comparing pre- and posttreatment PTA thresholds of seven PT patients with ipsilateral LFHL, we further evaluated the changes in low-frequency hearing thresholds and their role as an objective sign for diagnosis and outcome evaluation. Results Of 85 patients, 22 (25.9%) presented with ipsilateral LFHL. Compared with patients without this condition, patients with ipsilateral LFHL showed a significantly higher rate of abnormal vascular structure. In addition, most of the radiologic abnormalities found in the LFHL group were highly suspicious causative lesions that are responsible for the perception of PT according to the previous literature. In eight PT patients with ipsilateral LFHL who underwent both pre- and posttreatment audiograms, the average posttreatment pure-tone threshold at 250 Hz showed significant improvement compared with the pretreatment threshold. Conclusion PT patients presenting with ipsilateral LFHL have higher possibility of having a discrete vascular pathology near the cochlea on radiologic evaluation. As ipsilateral LFHL improves in most patients after treatment, LFHL in patients with PT may be PLFHL because of the masking effects of the pulsatile sound, and the changes in the low-frequency thresholds may be applicable for objective diagnosis and evaluation of the effects of the treatment.

Although tinnitus retraining therapy (TRT) is efficacious in most patients, the exact mechanism is unclear and no predictor of improvement is available. We correlated the extent of improvement with pre-TRT quantitative electroencephalography (qEEG) findings to identify neural predictors of improvement after TRT. Thirty-two patients with debilitating tinnitus were prospectively enrolled, and qEEG data were recorded before their initial TRT sessions. Three months later, these qEEG findings were correlated with the percentage improvements in the Tinnitus Handicap Inventory (THI) scores, and numeric rating scale (NRS) scores of tinnitus loudness and tinnitus perception. The THI score improvement was positively correlated with the pre-treatment activities of the left insula and the left rostral and pregenual anterior cingulate cortices (rACC/pgACC), which control parasympathetic activity. Additionally, the activities of the right auditory cortices and the parahippocampus, areas that generate tinnitus, negatively correlated with improvements in loudness. Improvements in the NRS scores of tinnitus perception correlated positively with the pre-TRT activities of the bilateral rACC/pgACC, areas suggested to form the core of the noise-canceling system. The current study supports both the classical neurophysiological and integrative models of tinnitus; our results serve as a milestone in the development of precision medicine in the context of TRT.

In tinnitus, PET and other functional imaging modalities have shown functional changes not only in the auditory cortex but also in nonauditory regions such as the limbic, frontal, and parietal areas. Nonetheless, disparities in task dimension among studies, low statistical power due to small sample size, and the intrinsic uncertainty of a modality that measures activity indirectly limit the comprehensive understanding of the results from PET studies. These difficulties prompted us to undertake a metaanalysis of PET studies on tinnitus using a coordinate-based technique (activation-likelihood estimation) to retrieve the most consistent activation areas across different task dimensions and to compare the results with those from other imaging modalities. Methods: We performed 2 activation-likelihood estimation metaanalyses on data from 10 studies with 56 foci in which we examined the contrast between tinnitus individuals and controls and the difference in activation between sound stimuli and resting state in tinnitus individuals. Results: The studies show that the most consistently activated regions in tinnitus subjects, compared with controls, were the left primary and bilateral secondary auditory cortices, left middle and bilateral inferior temporal gyri, left para-hippocannpal area, left geniculum body, left precuneus, right anterior cingulate cortex, right claustrum, right middle and inferior frontal gyri, and right angular gyrus. The relatively activated area under sound stimuli, compared with resting state, in tinnitus subjects was the secondary auditory cortex. Our study reconfirms the findings of previous quantitative electroencephalography or magnetoencephalography studies because most of the 14 brain areas with significant activation found in our metaanalysis replicate these earlier data. Our results suggest that the areas described in the tinnitus network are solidly replicable regardless of the applied functional imaging technique. Conclusion: This study proves that PET is a useful modality for tinnitus research and solidifies human tinnitus research itself by confirming previously described brain areas involved in the generation and maintenance of tinnitus.

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Objective Although vascular pulsatile tinnitus (VPT) has been classified as “objective”, VPT is not easily recognizable or documentable in most cases. In response to this, we have developed transcanal sound recording (TSR) and spectro-temporal analysis (STA) for the objective diagnosis of VPT. By refining our initial method, we were able to apply TSR/STA to post-treatment outcome evaluation, as well as pre-treatment objective diagnosis. Methods TSR was performed on seven VPT patients and five normal controls before and after surgical or interventional treatment. VPT was recorded using an inserted microphone with the subjects placed in both upright and supine positions with 1) a neutral head position, 2) head rotated to the tinnitus side, 3) head rotated to the non-tinnitus side, and 4) a neutral position with ipsi-lesional manual cervical compression. The recorded signals were analyzed in both time and time-frequency domains by performing a short-time Fourier transformation. Results The pre-treatment ear canal signals of all VPT patients demonstrated pulse-synchronous periodic structures and acoustic characteristics that were representative of their presumptive vascular pathologies, whereas those the controls exhibited smaller peaks and weak periodicities. Compared with the pre-treatment signals, the post-treatment signals exhibited significantly reduced peak- and root mean square amplitudes upon time domain analysis. Additionally, further sub-band analysis confirmed that the pulse-synchronous signal of all subjects was not identifiable after treatment and, in particular, that the signal decrement was statistically significant at low frequencies. Moreover, the post-treatment signals of the VPT subjects revealed no significant differences when compared to those of the control group. Conclusion We reconfirmed that the TSR/STA method is an effective modality to objectify VPT. In addition, the potential role of the TSR/STA method in the objective evaluation of treatment outcomes in patients with VPT was proven. Further studies incorporating a larger sample size and more refined recording techniques are warranted.

Background Peripheral auditory deafferentation and central compensation have been regarded as the main culprits of tinnitus generation. However, patient-to-patient discrepancy in the range of the percentage of daytime in which tinnitus is perceived (tinnitus awareness percentage, 0 – 100%), is not fully explicable only by peripheral deafferentation, considering that the deafferentation is a stable persisting phenomenon but tinnitus is intermittently perceived in most patients. Consequently, the involvement of a dysfunctional noise cancellation mechanism has recently been suggested with regard to the individual differences in reported tinnitus awareness. By correlating the tinnitus awareness percentage with resting-state source-localized electroencephalography findings, we may be able to retrieve the cortical area that is negatively correlated with tinnitus awareness percentage, and then the area may be regarded as the core of the noise cancelling system that is defective in patients with tinnitus. Methods and Findings Using resting-state cortical oscillation, we investigated 80 tinnitus patients by correlating the tinnitus awareness percentage with their source-localized cortical oscillatory activity and functional connectivity. The activity of bilateral rostral anterior cingulate cortices (ACCs), left dorsal- and pregenual ACCs for the delta band, bilateral rostral/pregenual/subgenual ACCs for the theta band, and left rostral/pregenual ACC for the beta 1 band displayed significantly negative correlations with tinnitus awareness percentage. Also, the connectivity between the left primary auditory cortex (A1) and the rostral ACC, as well as between the left A1 and the subgenual ACC for the beta 1 band, were negatively correlated with tinnitus awareness percentage. Conclusions These results may designate the role of the rostral ACC as the core of the descending noise cancellation system, and thus dysfunction of the rostral ACC may result in perception of tinnitus. The present study also opens a possibility of tinnitus modulation by neuromodulatory approaches targeting the rostral ACC.

Recent findings regarding differences in tinnitus-related neural activity according to onset age have raised a question on possible onset age-related differences in neural substrates of distress. Hence we collected quantitative electroencephalography (qEEG) findings of 28 late-onset tinnitus (LOT) and 29 early-onset tinnitus (EOT) (mean onset age 52.3 and 29.0 years, respectively) participants. According to the tinnitus questionnaire (TQ) score grade, LOTs were then subdivided into 13 high distress (HD; TQ grade 3 or 4) and 15 low distress (LD; TQ grade 1 or 2), while EOTs into 14 HD and 15 LD. Compared to the EOT group, the LOT group demonstrated increased qEEG source-localized activity and functional connectivity primarily in the anterior cingulate cortex (ACC) and parahippocampus. In subgroup comparisons, the ACC was activated more in HD-LOT participants than in LD-LOT participants for the beta 1, beta 2 and gamma frequency bands, while the left orbitofrontal cortex and left dorsolateral prefrontal cortex were activated more in HD-EOT than in LD-EOT for the delta/beta and gamma frequency bands, respectively. Even with the same amount of tinnitus-related distress level, responsible neural substrates are different according to the onset age. These differences may be important for exploring different target areas of treatment according to tinnitus onset age, as well as for conducting similar studies on other pathologies, such as depression or pain.

While tinnitus can be interpreted as a simple or elementary form of auditory phantom perception, musical hallucinosis is a more complex auditory phantom phenomenon not only limited to sound perception, but also containing semantic and musical content. It most often occurs in association with hearing loss. To elucidate the relation between simple and complex auditory phantom percepts a source localized electroencephalography (EEG) study is performed. The analyses showed in both simple and complex auditory phantoms an increase in theta-gamma activity and coupling within the auditory cortex that could be associated with the thalamocortical dysrhythmia model. Furthermore increased beta activity within the dorsal anterior cingulate cortex and anterior insula is demonstrated, that might be related to auditory awareness, salience and its attribution to an external sound source. The difference between simple and complex auditory phantoms relies on differential alpha band activity within the auditory cortex and on beta activity in the dorsal anterior cingulate cortex and (para) hippocampal area. This could be related to memory based load dependency, while suppression within the primary visual cortex might be due the presence of a continuous auditory cortex activation inducing an inhibitory signal to the visual system. Complex auditory phantoms further activate the right inferior frontal area (right sided Broca homolog) and right superior temporal pole that might be associated with the musical content. In summary, this study showed for the first time that simple and complex auditory phantoms might share a common neural substrate but differ as complex auditory phantoms are associated with activation in brain areas related to music and language processing. (C) 2013 Elsevier Inc. All rights reserved.

Recent findings regarding different characteristics according to the age of tinnitus onset prompted us to conduct a study on the differences in tinnitus-related neural correlates between late-onset tinnitus (LOT; mean onset age, 60.4 years) and early-onset tinnitus (EOT; mean onset age, 29.7 years) groups. Hence, we collected quantitative electroencephalography findings of 29 participants with LOT and 30 with EOT, and from 59 controls. We then compared the results between the 2 groups and between the tinnitus groups and age- and sex-matched control groups using resting state electroencephalography source-localized activity and connectivity analyses. Compared with the EOT and older control groups, the LOT group demonstrated increased localized activity and functional connectivity in components of previously described tinnitus distress networks, and the default mode and intrinsic alertness networks, such as the prefrontal cortices, dorsal anterior cingulate cortex, and insula. The current findings of intrinsic differences in tinnitus-related neural activity between the LOT and EOT groups might be applicable for planning individualized treatment modalities according to age of onset. Moreover, differences with regard to the age of tinnitus onset might be a milestone for future studies on onset-related differences in other similar pathologies, such as pain or depression. (C) 2013 Elsevier Inc. All rights reserved.

Although transcranial direct current stimulation (tDCS) has already been used to manage tinnitus patients, paucity of reports and variations in protocols preclude a comprehensive understanding. Hence, we conducted a meta-analysis based on systemic review to assess effectiveness of tDCS in tinnitus management and to compare stimulation parameters. PubMed was searched for tDCS studies in tinnitus. For randomized controlled trials (RCTs), a meta-analysis was performed. A total of 17 studies were identified and 6 of them were included in the systemic review and 2 RCTs were included in the meta-analysis. Overall 39.5% responded to active tDCS with a mean tinnitus intensity reduction of 13.5%. Additionally, left temporal area (LTA) and bifrontal tDCS indicated comparable results. Active tDCS was found to be more effective than sham tDCS for tinnitus intensity reduction (Hedges'g=.77, 95% confidence interval 0.23–1.31). The efficacy of tDCS in tinnitus could not be fully confirmed by the current study because of the limited number of studies, but all studies included in the current systemic review and meta-analysis demonstrated significant tinnitus intensity improvement. Therefore, tDCS may be a promising tool for tinnitus management. Future RCTs in a large series regarding the efficacy as well as the comparison between LTA- and bifrontal tDCS are recommended.

Accompanying neurological symptoms and signs are diagnostic hallmarks of fourth nerve palsy (4NP) from an intra-axial lesion. Due to the proximity of the trochlear nucleus and fascicles to the inferior colliculus (IC), auditory symptoms including tinnitus may occur with an intra-axial 4NP. A 53-year-old man with hypertension and diabetes developed right 4NP with a sudden worsening of tinnitus. MRI disclosed an infarction involving the trochlear fascicle and IC in the left dorsal midbrain. Tinnitus may be a symptom indicating an intra-axial lesion causing a 4NP.