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ObjectivesMorphological studies on presbycusis, or age-related hearing loss, have been performed in several different strains of mice that demonstrate hearing loss with auditory pathology. The C57BL/6 (C57) mouse is a known model of early onset presbycusis, while the CBA mouse is characterized by relatively late onset hearing loss. We performed this study to further understand how early onset hearing loss is related with the aging process of the cochlea.MethodsWe compared C57 cochlear pathology and its accompanying apoptotic processes to those in CBA mice. Hearing thresholds and outer hair cell functions have been evaluated by auditory brainstem response (ABR) recordings and distortion product otoacoustic emission (DPOAE).ResultsABR recordings and DPOAE studies demonstrated high frequency hearing loss in C57 mice at P3mo of age. Cochlear morphologic studies of P1mo C57 and CBA mice did not show differences in the organ of Corti, spiral ganglion, or stria vascularis. However, from P3mo and onwards, a predominant early outer hair cell degeneration at the basal turn of the cochlea in C57 mice without definitive degeneration of spiral ganglion cells and stria vascularis/spiral ligament, compared with CBA mice, was observed. Additionally, apoptotic processes in the C57 mice also demonstrated an earlier progression.ConclusionThese data suggest that the C57 mouse could be an excellent animal model for early onset 'sensory' presbycusis in their young age until P6mo. Further studies to investigate the intrinsic or extrinsic etiologic factors that lead to the early degeneration of organ of Corti, especially in the high frequency region, in C57 mice may provide a possible pathological mechanism of early onset hearing loss.

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ObjectivesVascular tinnitus is the most common form of pulsatile tinnitus, particularly when the tinnitus corresponds with the pulse of patients. In this study, we reviewed the 10-year clinical data on vascular tinnitus of our tinnitus clinic to investigate the frequency of the underlying etiologies, to introduce a diagnostic protocol, and to evaluate the treatment outcomes.MethodsWe retrospectively collected the data of 57 patients who were diagnosed as vascular tinnitus between April 2001 and December 2011. Careful history taking, otoscopy, thorough physical examinations, audiometry, laboratory tests, as well as radiologic examinations were performed according to our diagnostic protocol to find the origin of pulsatile tinnitus. Treatment options were individualized based on the specific etiology, and the outcomes were assessed using patient's subjective reports at the follow-up interviews.ResultsHigh jugular bulb was the most common cause (47.4%) of vascular tinnitus, and venous hum was the next (17.5%). Dural arteriovenous fistula, intracranial aneurysm, atherosclerotic carotid artery disease, and hypertension were less common causes. Vascular tinnitus was alleviated in most patients after the appropriate treatment: surgical intervention, tinnitus retraining therapy, reassurance, and medications.ConclusionVascular tinnitus can be successfully diagnosed by the regular use of the suggested protocol. Many patients with vascular tinnitus have treatable underlying etiologies. Treatment of those etiologies or at least counseling about the tinnitus itself can benefit the patients with troublesome vascular tinnitus.

At 6 months after noise exposure, all mice in the experimental group had moderate hearing loss. Most of the RAM performances improved gradually within each group across five trials, probably due to learning effect. The HL group showed lower performance scores than the control group in several trial points in the RAM task. The contact time with the novel object was shorter in the HL group than in the control group.