Prevention of benign paroxysmal positional vertigo with vitamin D supplementation: A randomized trial.

OBJECTIVE: To assess the effect of vitamin D and calcium supplementation in preventing recurrences of benign paroxysmal positional vertigo (BPPV). METHODS: We performed an investigator-initiated, blinded-outcome assessor, parallel, multicenter, randomized controlled trial in 8 hospitals between December 2013 and May 2017. Patients with confirmed BPPV were randomly assigned to the intervention (n = 518) or the observation (n = 532) group after successful treatment with canalith repositioning maneuvers. The primary outcome was the annual recurrence rate (ARR). Patients in the intervention group had taken vitamin D 400 IU and 500 mg of calcium carbonate twice a day for 1 year when serum vitamin D level was lower than 20 ng/mL. Patients in the observation group were assigned to follow-ups without further vitamin D evaluation or supplementation. RESULTS: The intervention group showed a reduction in the ARR (0.83 [95% confidence interval (CI), 0.74-0.92] vs 1.10 [95% CI, 1.00-1.19] recurrences per 1 person-year) with an incidence rate ratio of 0.76 (95% CI, 0.66-0.87, p < 0.001) and an absolute rate ratio of -0.27 (-0.40 to -0.14) from intention-to-treat analysis. The number needed to treat was 3.70 (95% CI, 2.50-7.14). The proportion of patients with recurrence was also lower in the intervention than in the observation group (37.8 vs 46.7%, p = 0.005). CONCLUSIONS: Supplementation of vitamin D and calcium may be considered in patients with frequent attacks of BPPV, especially when serum vitamin D is subnormal. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that for patients with BPPV, vitamin D and calcium supplementation reduces recurrences of BPPV.

Increased parietal circuit-breaker activity in delta frequency band and abnormal delta/theta band connectivity in salience network in hyperacusis subjects.

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.

The efficacy and safety of systemic injection of Ginkgo biloba extract, EGb761, in idiopathic sudden sensorineural hearing loss: a randomized placebo-controlled clinical trial.

Steroids are currently the most frequently accepted agents for idiopathic sudden sensorineural hearing loss (ISSNHL). However, the therapeutic effect of steroids is not always satisfactory. In this pilot study, we evaluated whether systemic treatment with Ginkgo biloba extract (EGb761) has an additive therapeutic effect in patients receiving a systemic steroid due to ISSNHL. A multicenter, randomized, double-blind clinical trial was performed. Fifty-six patients with ISSNHL were allocated to either EGb761 or placebo. In both groups, methylprednisolone was administered for 14 days. EGb761 was infused intravenously for 5 days in the EGb761 group, while the same amount of normal saline was infused in the placebo group. For the efficacy evaluation, pure-tone audiometry, speech audiometry, tinnitus handicap inventory (THI) and short form-36 health (SF-36) survey outcomes were obtained before administration and on days 3, 5, 14 and 28 of administration. Twenty-four patients in each group completed the study protocol. There was no difference in hearing loss between the two groups before treatment. At day 28, air conduction threshold values in the placebo and EGb761 groups were 34.63 ± 28.90 and 23.84 ± 25.42 dB, respectively (p = 0.082). Speech discrimination scores in the placebo and EGb761 groups were 69.17 ± 40.89 and 87.48 ± 28.65 %, respectively (p = 0.050). THI and SF-36 scores in the placebo and EGb761 groups were similar. Although a combination of steroid and EGb761 for initial treatment did not show better pure tone threshold, compared with steroid alone, speech discrimination was significantly improved in combination therapy. Further studies will be needed to know if addition of EGb761 actually improves the outcome of ISSNHL treatment.

Contralateral suppression of distortion-product otoacoustic emissions: a potential diagnostic tool to evaluate the vestibular nerve.

The amplitude of distortion-product otoacoustic emission (DPOAE) is suppressed in one ear when the contralateral ear is subjected to sound stimulation. Contralateral suppression of DPOAE is the phenomenon resulted by the efferent cochlear innervation on the outer hair cells via medial olivocochlear bundle (MOCB) and inferior vestibular nerve. We assumed that DPOAE would not be suppressed by contralateral sound stimulation in patients with vestibular nerve lesion as long as the specific pathway conveying that efferent innervation is affected. To test this hypothesis, we compared the amount of DPOAE contralateral suppression in patients with vestibular neuritis and healthy controls. Twenty healthy volunteers without hearing loss and vestibulopathy, and 13 patients with vestibular neuritis were recruited. DP audiogram was measured without contralateral sound stimulation and then with contralateral sound stimulation (70 dB HL of 2 kHz narrow band noise, NBN). The suppression value of DPOAE was evaluated according to the f2 frequency and was defined as the amount of DPOAE suppression: An-Ao, where An represents the DPOAE amplitude in the presence of contralateral NBN, and Ao represents the DPOAE amplitude in the absence of NBN. Cervical vestibular evoked myogenic potential (cVEMP) was performed in some patients with vestibular neuritis. The suppression values of DPOAE were compared between groups and were analyzed according to the results of cVEMP. The amount of suppression of DPOAE during contralateral sound stimulation was significantly reduced in the patient group compared to control at the f2 frequencies of 1257, 1587, and 2002 Hz (P=0.045, P<0.001, P=0.009, respectively). However, the results of contralateral suppression of DPOAE were not consistent with the results of cVEMP in this study. Efferent cochlear innervation was affected in vestibular neuritis. Evaluation of contralateral suppression of DPOAE can be a potential diagnostic tool to evaluate the functional integrity of the vestibular nerve. Further studies are necessary to clarify this mechanism.