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Background: Although many studies have suggested that air cells may play an important role in sigmoid sinus diverticulum and/or dehiscence (SSDD)-induced pulsatile tinnitus (PT), the exact effects remain unclear. This study aims to quantitatively investigate the effect of different degrees of pneumatization of temporal bone on sound transmission from the sigmoid sinus to the tympanic cavity., Methods: In the clinical study, 25 patients were enrolled to measure the sound intensity and frequency of SSDD-induced PT. In the experimental study, sound inputs at different frequencies at the dehiscent sigmoid plate were measured and compared among realistic object models of different degrees of pneumatization, when sound intensity in the tympanic cavity was fixed as the level of the PT sound intensity sensed by patients., Results: The sound intensity sensed by PT patients was 34.0 ± 13.0 dB SPL, which represented the sound intensity in the tympanic cavity transmitted from the dehiscent sigmoid plate. In the experimental study, when sound received in the tympanic cavity was fixed at 34 dB SPL, the mean inputs of sound intensity at the dehiscent sigmoid plate were 46.9, 46.2, 45.2, 47.1, 57, 57.4, and 74.1 dB SPL in a hypo-pneumatized model; 42.6, 43, 41.5, 43.2, 47.3, 58.2, and 78.8 dB SPL in a moderately pneumatized model; 52.6, 52.8, 48.1, 61, 64.2, 82.4, and >87.3 dB SPL in a well-pneumatized model; and 47.2, 46.2, 45.4, 49.4, 54.9, 66.6, and 77.7 dB SPL in hyper-pneumatized model, with increased sound frequencies (125-8000 Hz). The mean sound transmission distances were 41.7 mm, 45.2 mm, 47.6 mm, and 48.4 mm in successively better pneumatized models., Conclusion: Sound reduces while passing through air cells and attenuation is lowest in the moderately pneumatized temporal bone, followed by the hypo- and hyper-pneumatized temporal bones, and the highest in the well-pneumatized temporal bone. Lower-frequency sound attenuation (≤1000 Hz) is less than that of higher-frequency sound (>1000 Hz).

Previous studies have found a link between tinnitus and cognitive impairment, even leading to dementia. However, the mechanisms underlying this association are not clear. The purpose of this study was to explore intrinsic network changes in tinnitus and hearing loss patients with cognitive disorders. We included 17 individuals with bilateral idiopathic tinnitus, hearing loss, and cognitive impairment (PA) and 21 healthy controls. We identified resting-state networks (RSNs) and measured intra-network functional connectivity (FC) values via independent component analysis (ICA). We also evaluated correlations between RSNs and clinical characteristics. Compared with the healthy controls, the PA group showed decreased connectivity within the ventral attention network, dorsal attention network (DAN), visual network, left frontoparietal network, right frontoparietal network, sensorimotor network, and increased connectivity within the executive control network. MoCA (Montreal Cognitive Assessment) scores were negatively correlated with the FC values for left calcarine within the DAN. We identified abnormal intrinsic connectivity in several brain networks, mainly involving cognitive control, vision, sensorimotor function, and the cerebellum, in tinnitus patients with cognitive impairment. It may be possible to use the FC strength of the left calcarine within the DAN as an imaging marker to predict cognitive impairment in tinnitus patients. [ABSTRACT FROM AUTHOR]