The use of stereotactic radiosurgery (SRS) expanded to include the treatment of vestibular schwannomas (VSs) in 1969; since then, efforts to increase tumour control and to reduce cranial neuropathy have continued. Using the currently recommended marginal dose of 12-13 Gy, long-term reported outcomes after SRS include not only excellent tumour control rates of 92-100 % but also outstanding functional preservation of the trigeminal and facial nerves, with values of 92-100 % and 94-100 %, respectively. Nonetheless, hearing preservation remains in the range of 32-81 %. Previous studies have suggested possible prognostic factors of hearing preservation such as the Gardner-Robertson grade, radiation dose to the cochlea, transient volume expansion (TVE) after SRS, length of irradiated cochlear nerve, marginal dose to the tumour, and age. However, we still do not clearly understand why patients lose their hearing after SRS for VS.Relevant to these considerations, one study recently reported that the auditory brainstem response (ABR) wave V latency and waves I and V interval (IL_I-V) correlated well with intracanalicular pressure values and even with hearing level. The demonstration that ABR values, especially wave V latency and IL_I-V, correlate well with intracanalicular pressure suggests that patients with previously elevated intracanalicular pressure might have an increased chance of hearing loss on development of TVE, which has been recognised as a common phenomenon after SRS or stereotactic radiotherapy (SRT) for intracranial schwannomas.In our experience, the ABR IL_I-V increased during the first 12 months after SRS for VSs in patients who lost their serviceable hearing. The effect of increased ABR IL_I-V on hearing outcome also became significant over time, especially at 12 months after SRS, and was more prominent in patients with poor initial pure-tone average (PTA) and/or ABR values. We hypothesise that patients with considerable intracanalicular pressure at the time of SRS are prone to lose their serviceable hearing due to the added intracanalicular pressure induced by TVE, which usually occurs within the first 12 months after SRS for VSs. Using these findings, we suggested a classification system for the prediction of hearing outcomes after SRS for VSs. This classification system could be useful in the proper selection of management modalities for hearing preservation, especially in patients with only hearing ear schwannoma or neurofibromatosis type 2.Advances in diagnostic tools, treatment modalities, and optimisation of radiosurgical dose have improved clinical outcomes, including tumour control and cranial neuropathies, in patients with VSs. However, the preservation of hearing function still falls short of our expectation. A prediction model for hearing preservation after each treatment modality will guide the proper selection of treatment modalities and permit the appropriate timing of active treatment, which will lead to the preservation of hearing function in patients with VSs.
