2001 Fiscal Year Final Research Report Summary
A Study on the changes of latency and amplitude of brainstem auditory evoked potentials due to cochlear nerve injury: an analysis of their correlations
| Project/Area Number |
12470281
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Hirosaki University |
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Principal Investigator |
SUZUKI Shigeharu Hirosaki University, Neurosurgery, Professor, 医学部, 教授 (30004708)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMAMURA Norihito Hirosaki University, Neurosurgery, Assistant, 医学部, 助手 (40312491)
SEKIYA Tetsuji Hirosaki University, Neurosurgery, Associate Professor, 医学部, 助教授 (70154656)
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| Project Period (FY) |
2000 – 2001
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| Keywords | cochlear nerve / nerve degeneration / hearing disturbence / cerebellopontine angle / surgery |
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| Research Abstract |
Intraoperative monitoring of brainstem auditory evoked potentials (BAEP) has been widely utilized to reduce the incidence of postoperative hearing disturbance due to cerebellopontine angle manipulations. The prolongation of wave V of BAEP is usually used as a criterion to warn the surgeons to modify their surgical maneuvers. However, it is not known whether all neuropathological changes are avoided if BAEP latency intraoperatively returns to the baseline level or some neuropathological changes "silently" occur even if BAEP normalizes. The aim of this study was to experimentally clarify this point that would be important for the long-term prognosis of patients' hearing.
The cerebellopontine angle portion of the auditory nerve was quantitatively compressed in the rats and reversible prolongation of BAEP latency was reproduced just as it occurs during surgery in humans. Twenty-four hours after the compression, the auditory nerve was removed for β-APP immunostaining to investigate the degree of axonal injury. The results of the present study disclosed that axonal injury occurred even in the cases where the intraoperative normalization of prolonged wave IV (equivalent to wave V in humans) latency had been obtained. Therefore, the interpretation of BAEP changes based only on the prolongation of the latency of BAEP was not enough to prevent the auditory nerve from developing morphological changes. Changes in the amplitude of wave V of BAEP appears to be more sensitive than its latency change as an intraoperative indicator for axonal injury in the auditory nerve.
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