Teiji Tanahashi

A case of hearing loss due to bilateral temporal lobe infarction

A 40‐year‐old, right‐handed female showed cortical deafness and aphasia following a brain stroke. A CT scan showed that a low‐density area occupied both of the temporal lobes. In the basal ganglia and thalamus no lesions were observed. Results of audiological examination were as follows. (1) Pure‐tone audiometry revealed a mild bilateral hearing loss. An audiogram showed a type of C4 dip. (2) Bekesy audiometry showed that the thresholds were extremely unstable. (3) Speech audiometry showed very poor discrimination scores. (4) Discrimination of musical instruments was remarkably poor. (5) An aural reflex test showed normal responses. (6) The auditory brain‐stem response elicited by click stimuli was normal in pattern and latency. (7) Middle latency response was almost normal. Auditory function in the cochlea and the brain stem appeared to be almost intact, but cortical and/or subcortical damage of hearing function was suspected bilaterally. The conclusion from these data is that bilateral partial temporal ...

Fundamental observations for tinnitus

Changes in the spontaneous discharges of the auditory neuron in the cochlear nucleus were analyzed under various conditions. Young adult cats were anesthetized with pentobarbital, pentazocine, and diaxepam. Characteristic frequency, threshold, PST histogram, and the spontaneous discharge rate of each neuron were obtained before and following asphyxia. EEG, ECG, and blood gas content were also analyzed. Following asphyxia, lasting from 60–110 s, the spontaneous discharges increased markedly in ten neurons, but in five neurons, the increase was slight or nonexistent. The spontaneous discharge of the auditory neuron in the cochlear nucleus following asphyxia was temporarily suppressed by the administration of Lidocaine or Diltiazem. This effect was observed continuously for over 3 h. The dose effect was also examined.