| Project/Area Number |
15591836
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | St.Marianna University School of Medicine |
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Principal Investigator |
OCHI Kentaro St.Marianna University School of Medicine, Department of Otolaryngology, Assistant Professor, 医学部, 講師 (20214158)
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| Co-Investigator(Kenkyū-buntansha) |
OYAKE Daisuke St.Marianna University School of Medicine, Department of Otolaryngology, Assistant, 医学部, 助手 (00367343)
剱持 睦 聖マリアンナ医科大学, 医学部, 助手 (10257397)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | cochlear destruction / vestibular nerve / single unit / amikacin / loud sound / vestibular evoked myogenic potential / 前庭性誘発筋電位 / 音響外傷 |
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| Research Abstract |
The purpose of this study was to examine the underlying mechanisms of vestibular evoked myogenic potential(VEMP) by performing single unit recording from vestibular nerve in response to the loud sound after total destruction of cochlea Firstly, we tried to destruct cochlea by administration of aminoglycoside. One month after intramuscularly administration of amikacin at the dose 450 mg/kg for 14 days, action potential was still recorded. Then we increased dosage from 450 mg/kg to 900 mg/kg. The cochlea was completely destructed after 1 month, however acoustic stimuli induced no response at the maximum sound intensity. This suggests that the administration of amikacine induced destruction not only cochlea but also vestibule. We tried to determine the appropriate dosage which destruct cochlea without destruct vestibule. Although we applied two additional dosages of 450 mg/kg and 700 mg/kg, we failed to decide appropriate dosage.
Secondary, we tried to destruct cochlea by loud sound. Animals were exposed to the white noise at the intensity of 115 dB for 12hours, compound action potential was still recorded and this suggests that the cochlea was not destructed. Thirdly, we evaluated the effects of tinnitus inducing drugs (salicylate and quinine) on both cochlea and auditory cortex. Either intra-venous administration of salicylate or intramuscular administration of quinine induced no marked change in spontaneous activity in the primary auditory cortex. The effects of drugs on the spontaneous activity in the cochlear nerve were not confirmed. We reported the changes in CAP adaptation in experimentally induced endolymphatic hydrops.
We also performed clinical study and reported the VEMP pattern who suffered from Ramsay Hunt syndrome, acute sensorineural hearing loss, vestibular neuritis, and narrow internal auditory canal. In addition, the effect of age on VEMP was reported.
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