Pathophysiological mechanisms of intraoperative and postoperative hearing deficits in cerebellopontine angle surgery: An experimental study

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Abstract
Pathophysiological mechanisms responsible for intraoperative and postoperative hearing deficits associated with cerebellopontine (CP) angle operations were explored experimentally in dogs. The CP angle operative manipulations performed were the same as those experienced by human patients, and auditory evoked potentials were monitored intraoperatively. As a result of the operative manipulations, petechial or confluent hemorrhages occurred at the compressed portions of the cochlear nerve, and intravascular clots were often observed. Disintegration of the nerve fibers was verified by ultrastructural examination. Moreover, rupture of the microvasculature within the cochlear nerve occurred at locations remote from the operative site, due to stretching of the nerve trunk. The Obersteiner-Redlich zone, the Schwann-glial junction of the cochlear nerve, was a locus minoris resistentiae in CP angle surgery; the vasa nervorum easily bled at this zone and the peripheral and central myelins easily separated at their junctional zones (“central” avulsion injury). Intracochlear hemorrhages were identified as the most probable cause of the sudden loss of all components of the auditory evoked potentials, a frequent predictor of postoperative hearing loss, although rupture, occlusion, or vasospasm of the main trunk of the internal auditory artery have also been implicated as possible causes of such hearing losses. The results of this study show that hearing preservation is highly dependent on preserving not only the nerve at the operative site but also the remote O-R zone and intracochlear structures.