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. 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. 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. Microvascular decompression of the cochlear nerve can improve tinnitus intensity in selected patients if decompression is performed early, before the end of the 4th year. Tinnitus distress does not seem to change.