Abstract
OBJECTIVE: Microvascular compressions of the cochlear nerve can lead to tinnitus. The tinnitus initially is related to nonsynchronous signal transmission in the auditory nerve, neurophysiologically characterized by a peak II amplitude decrease. Chronic compression can lead to a focal demyelination, resulting in an increase in Iinterpeak latency I-III with tinnitus and frequency-specific hearing loss as a consequence. Decompressing the cochlear nerve may result in improvement in tinnitus if the auditory nerve is not too damaged for recovery. The aim of the study is to find a cut-off point for this recovery based on clinical data.
MATERIALS AND METHODS: Twenty patients undergo a microvascular decompression of the vestibulocochlear nerve for unilateral intractable tinnitus. Pre- and postoperative visual analogue scale for tinnitus intensity and tinnitus questionnaires for tinnitus distress are analyzed before and after microvascular decompression.
RESULTS: Of the 20 patients studied, 10 had improvements on their tinnitus visual analogue score intensity postoperatively, 8 were unchanged, and 2 worsened. On the Tinnitus Questionnaire scores, 7 of 13 patients improved and 6 of the 13 patients worsened. If decompression is performed before the end of the 4th year of tinnitus duration, a significant tinnitus intensity improvement can be obtained (P < .05); after 4 years, improvement cannot be obtained (P = .55). However, the tinnitus distress does not seem to decrease significantly.
CONCLUSION: Microvascular decompression of the cochlear nerve can improve tinnitus intensity in selected patients if decompression