No abstract

In examining 181 patients (327 ears) with sensorineural hearing loss of unknown etiology and 25 people (50 ears) with normal hearing by high-resolution computed tomography (CT), the image of the large vestibular aqueduct (VA) was defined as being a visible large aperture (> or = 4 mm), and small distance between vestibule and traceable part of the VA nearest to the vestibule (> or = 1 mm). The large VA was found in 13 patients (23 ears, 7.0%); it was relatively frequent following hypoplastic cochlea (33 ears, 10.1%) in all the inner ear anomalies detected. In patients with large VA, high-frequency hearing was affected more than low frequency, and history of sudden hearing loss was observed frequently (61% of ears with large VA), which was found to be triggered by characteristic episodes such as minor head trauma, etc. Those clinical features were observed more in those without cochlear anomaly than in those accompanying cochlear anomaly. Pathogenesis of sensorineural hearing loss and characteristic fluctuation of hearing in those patients are discussed.

To investigate the relationship between motor and sensory speech center, cortical activity was examined using PET while normal subjects perceived their own voice which sounded different to the articulated one. The results showed significant activation in the superior temporal gyri with absence of activity in the supplementary motor area (SMA). In a previous study we found significant activation in SMA with no activity in the superior temporal gyrus when normal subjects simply vocalized. Thus, two different cortical pathways for vocalization were delineated: programmed pathway in SMA, and pathway with auditory verbal feedback. The former is thought to be the mature system in the adult, and the latter may be related to speech acquisition.

No abstract

To investigate the effect of unilateral deafness on central auditory mechanisms, we examined patients with unilateral deafness of various durations. Auditory evoked magnetic fields (AEF) were recorded using a whole-head neuromagnetometer. In patients who had unilateral deafness for more than 3 weeks, the average N100m latency in the ipsilateral hemisphere did not differ from that in the contralateral hemisphere. In addition, in some patients with congenital or early onset deafness, the equivalent current dipole (ECD) moment was larger in the ipsilateral hemisphere than in the contralateral hemisphere. These findings suggest that unilateral deafness may cause reorganization of the central auditory pathway. They also suggest that central auditory pathway in adults has some plasticity, though not as much as in childhood.