[Influence of a CNS pathology on the electrocochleography response]
- PMID: 7810323
[Influence of a CNS pathology on the electrocochleography response]
Abstract
This study analyzed 73 electrocochleographic recordings made in children with a normal hearing threshold, selected retrospectively from 1563 recordings made between 1973 and 1990. The aim of the study was to check the original findings for any correlation between the various response parameters which might be indicative of a pathological condition. Compound action potential (AP) latency and amplitude, presynaptic summation potential (SP) and cochlear microphonic (CM) amplitudes and AP rapid adaptation behavior were calculated and recordings were associated with clinical information on aetiologic diagnosis, otoscopic examination, impedance measurement data and the finding of any central nervous system (CNS) pathology. The trend of the amplitudes as a function of the intensity of all three potentials (input-output functions), CM and SP in particular, demonstrated unexpected scattered values especially towards the high intensities. This was found correlated to the presence of CNS pathology. The comparison between the two groups (with vs without CNS pathology) with the aid of the Student's t-test proved statically significant, especially for CM and SP amplitudes while rather less so for AP amplitude. In particular, all CM and SP amplitude values outside the confidence intervals (calculated as 95% of normal cases) revealed CNS pathology. It has been suggested that the influence of the CNS on cochlear function is due to a disturbed function of the olicocochlear bundle, which is known to have an inhibitory effect on cochlear dynamics; furthermore, there is also proof that it can be activated regardless of any ipso-and/or contra-lateral acoustic stimulation. The effects observed on the electrocochleography in cases with CNS disorders would thus be explained by an interruption of the olivocochlear bundle at the CNS level or a disruption of the CNS mechanism capable of controlling its activation.
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