Video Head Impulse Test to Preoperatively Identify the Nerve of Origin of Vestibular Schwannomas

Video Head Impulse Test to Preoperatively Identify the Nerve of Origin of Vestibular Schwannomas Abstract BACKGROUND Identification of the nerve of origin in vestibular schwannoma (VS) is an important prognostic factor for hearing preservation surgery. Thus far, vestibular functional tests and magnetic resonance imaging have not yielded reliable results to preoperatively evaluate this information. The development of the video head impulse test (vHIT) has allowed a precise evaluation of each semicircular canal, and its localizing value has been tested for some peripheral vestibular diseases, but not for VS. OBJECTIVE To correlate patterns of semicircular canal alteration on vHIT to intraoperative identification of the nerve of origin of VSs. METHODS A total 31 patients with sporadic VSs were preoperatively evaluated with vHIT (gain of vestibule-ocular reflex, overt and covert saccades on each semicircular canal) and then the nerve of origin was surgically identified during surgical resection via retrosigmoid approach. vHIT results were classified as normal, isolated superior vestibular nerve (SVN) pattern, isolated inferior vestibular nerve (IVN) pattern, predominant SVN pattern, and predominant IVN pattern. Hannover classification, cystic component, and distance between the tumor and the end of the internal auditory canal were also considered for analysis. RESULTS Three patients had a normal vHIT, 12 had an isolated SVN pattern, 5 had an isolated IVN pattern, 7 had a predominant SVN pattern, and 4 had a predominant IVN pattern. vHIT was able to correctly identify the nerve of origin in 89.7% of cases (100% of altered exams). CONCLUSION The pattern of semicircular canal dysfunction on vHIT has a localizing value to identify the nerve of origin in VSs. Acoustic neuroma, Head impulse test, Vestibulo-ocular reflex, Saccades, Vestibular nerve, Vestibular function tests ABBREVIATIONS ABBREVIATIONS IAC internal auditory canal IVN inferior vestibular nerve LSC lateral semicircular canals MRI magnetic resonance imaging ms milliseconds PSC posterior semicircular canals SSC superior semicircular canals SVN superior vestibular nerve VEMP vestibular-evoked myogenic potential vHIT video head impulse test VS vestibular schwannoma VOR vestibule-ocular reflex Vestibular schwannoma (VS) is a benign tumor arising from Schwann cells of one of the branches of the vestibular nerve, representing around 90% of the tumors of the cerebellopontine angle.1 Theoretically, schwannomas of the cerebellopontine angle may arise from the common vestibular, superior vestibular, or inferior vestibular divisions of the 8 cranial nerve, or less frequently, from the cochlear or facial nerves, lateral, or at the level of the Obersteiner–Redlich zone, which is typically located near the internal acoustic meatus.2,3 The relevance of identifying the nerve of origin in VS lies in its prognostic factor for hearing preservation after surgery,4–7 with tumors arising from the superior vestibular nerve (SVN) having a 61% to 75% of hearing preservation, compared to 16% to 28% for an inferior vestibular nerve (IVN) origin,5,6 in cases when hearing preservation was attempted. Thus far, most studies trying to preoperatively predict the origin using magnetic resonance imaging (MRI)8 and functional tests5,8–11 have been unsuccessful, or limited to a rather specific subset of patients, so intraoperative identification remains the only reliable method, and in large tumors, adequately discerning its origin becomes challenging, and in some cases, not entirely possible. The video head impulse test (vHIT) was first described in 2005 as an improvement of the clinical head impulse using videonystagmoscopy.12 It is a noninvasive test that allows quantitative evaluation of the gain of vestibule-ocular reflex (VOR), as well as the identification of covert (occurring while the head is still moving) and overt (occurring once the head movement is finished) saccades on lateral semicircular canals (LSC), superior semicircular canals (SSC), and posterior semicircular canals (PSC) semicircular canals (Figure). vHIT in patients with VS has been reported by otologist groups describing its sensitivity, association with vestibular symptoms and vestibular recovery after surgery,13–18 but no attempts to correlate its alteration to a specific vestibular nerve dysfunction has been reported. FIGURE. View largeDownload slide A, Decreased gain of VOR on the right posterior semicircular canal (black arrow), with presence of covert (blue arrow) and overt (green arrow) saccades. B, Axial gadolinium-enhanced fat-suppressed T1-weighted MRI of the same patient demonstrating a right intracanalicular vestibular schwannoma (Hannover-T1). FIGURE. View largeDownload slide A, Decreased gain of VOR on the right posterior semicircular canal (black arrow), with presence of covert (blue arrow) and overt (green arrow) saccades. B, Axial gadolinium-enhanced fat-suppressed T1-weighted MRI of the same patient demonstrating a right intracanalicular vestibular schwannoma (Hannover-T1). Given that the SVN transmits information from the lateral and SSC, and the IVN from the posterior semicircular canal, we propose that in patients with no known peripheral vestibulopathy, vHIT alteration of a particular semicircular canal may indirectly translate an underlying nerve dysfunction of the corresponding nerve. Aware of the possible alteration of the other vestibular branch by the same factors that supposedly cause cochlear dysfunction,14 we propose that the affected vestibular branch will present a more prominent alteration than its counterpart, thus, allowing us to identify the nerve of origin. METHODS From March, 2016 to June, 2017, 31 patients with unilateral, sporadic VS underwent surgical treatment at the Neurological Institute of Curitiba (INC), Brazil. Patients with previous treatment, known vestibular disease, intraoperative or histological diagnosis other than VS, or intralabyrinthine extension of the tumor were excluded from the analysis. Surgery was performed via retrosigmoid approach by the senior author (R.R.), as previously described,19 identifying the nerve of origin in the internal auditory canal (IAC). The lead surgeon was not aware of the result of vHIT before the procedure. The study was approved by our Institutional Review Board, and the requirement to obtain signed consent was waived. All patients were preoperatively evaluated with MRI with an inner ear protocol, which was then analyzed by a single neuroradiologist (B.T.), and vHIT, performed and interpreted by an experienced neuro-otologist (P.S.). Morphologically, tumors were staged using the Hannover classification.20 The presence of a cystic component, and the distance between the tumor and the end of the IAC at the level of the cochlea was also considered for analysis. vHIT was performed using ICS Impulse video goggles (GN Otometrics, Taastrup, Denmark) and Vestlab 7.1 software for data analysis. The procedure consisted on the analysis of eye movement with a videooculography camera that recognizes movement up to 250 Hz and a sensor that measures head movement. The patient is asked to fix his gaze at a target 1 m away, then the examiner rotates the patient's head randomly 15° to 20° on the horizontal plane, with a duration of 150 to 200 milliseconds (ms), producing a peak acceleration of 2000° to 6000° per second squared. The window of analysis from 0 to 150 ms allows the evaluation of both LSC. The vertical semicircular canals are evaluated with a 45° head rotation to the right (left superior and right PSC) and then to the left (right superior and left PSC), producing an anterior and then posterior impulse. Twenty stimuli for every semicircular canal are performed to assure a sustained response. The evaluated parameters were: gain of VOR (relationship between the velocity of head and eye movements) of every canal, expressed as percentage to evaluate the functional deficit of the affected ear, and the presence of overt and covert saccades. Gain of VOR classified as normal or abnormal according to age-dependent normative values.21 vHIT results were then classified as normal, when no alteration was observed; isolated SVN dysfunction pattern, when there was any alteration on the LSC and/or SSC without abnormalities on the PSC; isolated IVN dysfunction pattern, when only alterations on the PSC were found; and predominant SVN/IVN dysfunction pattern, when there was alteration of the PSC associated with alteration of the LSC and/or SSC. The predominant alteration of one canal over the others was established by the presence of VOR alteration over the presence of saccades. When VOR of 2 semicircular canals were abnormal, the percentage of VOR gain was used to determine which canal was altered the most (lower VOR gain was considered as more altered). vHIT data were then compared with intraoperative identification of the nerve of origin. RESULTS A total of 31 patients were evaluated, 13 were women, with a mean age of 46.9 yr old (range 19-67). Thirteen tumors originated from the left vestibular nerves. There were 4 Hannover-T1, 5 Hannover-T2, 5 Hannover-T3, and 17 Hannover-T4 tumors. There was no significant difference in vHIT results according to Hannover classification, cystic component, or IAC filling. Surgical Results Surgical identification of the nerve of origin was achieved in 29 of the 31 patients. Both cases on which the origin could not be recognized were Hannover-T4b lesions, on which intracanalicular anatomy was highly distorted, even difficulting recognition of the facial nerve. Of the remaining, 19 (61.3%) arose from the SVN, and 10 (32.3%) from the IVN. vHIT Results Three cases had a normal exam, 12 had a semicircular canal dysfunction compatible with a SVN alteration, 5 were compatible with an IVN alteration, and 11 cases had an exam compatible with alteration of both vestibular nerves, 7 with predominance of SVN dysfunction, and 4 of IVN dysfunction. Semicircular canal alterations and its association with tumor size are shown in Table 1. TABLE 1. vHIT Pattern and Hannover Classification   Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31    Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Patterns of semicircular canal dysfunction and subsequent classification in superior or IVN patterns, according to tumor size. View Large TABLE 1. vHIT Pattern and Hannover Classification   Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31    Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Patterns of semicircular canal dysfunction and subsequent classification in superior or IVN patterns, according to tumor size. View Large Table 2 summarizes individual findings of the 31 cases. In 9 cases, isolated alteration of the LSC was found, 1 with only VOR alteration, 3 with VOR + overt saccades, 1 with only covert saccades, and 4 with VOR alteration + covert and overt saccades. TABLE 2. Age, Tumor Size, vHIT Results, and Intraoperative Identification of the Nerve of Origin of Individual Cases     Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN      Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Abnormal gain of VOR was highlighted in shaded cells. View Large TABLE 2. Age, Tumor Size, vHIT Results, and Intraoperative Identification of the Nerve of Origin of Individual Cases     Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN      Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Abnormal gain of VOR was highlighted in shaded cells. View Large In 5 cases, isolated alteration of the PSC was found, 1 with only VOR alteration, 2 with covert saccades, and 2 with VOR alteration + covert and overt saccades. In 3 cases, alteration of both LSC and SSC were found, all had alteration of VOR + covert and overt saccades on the LSC, 2 had only VOR alteration on the SSC, and 1 had only covert and overt saccades on the SSC. In 6 cases, alteration of both LSC and PSC was found, all of them had VOR alteration on the PSC, and 2 also had covert saccades, 1 had overt saccades, and 3 had covert and overt saccades on the same semicircular canal. LSC abnormalities were: 1 case with overt saccades, 2 with covert saccades, 1 with covert and overt saccades, 1 with VOR alteration + overt saccades, and 1 with VOR alteration + covert and overt saccades. In 5 cases, alteration of LSC, SSC and PSC was found. Three patients had VOR alteration + covert and overt saccades in all semicircular canals; 1 had VOR alteration + overt and covert saccades on the LSC and VOR alteration and overt saccades on the SSC and PSC; and 1 had VOR alteration + overt and covert saccades on LSC and PSC, and only overt saccades on the SSC. In the 11 cases where vHIT showed a semicircular canal alteration compatible with dysfunction of both nerves, the predominant of dysfunction of one nerve over the other was established by the presence of VOR alteration in 4 cases, and on the other 7 by the degree of VOR gain on each canal. vHIT to Identify the Nerve of Origin of VS Of the 19 surgically identified SVN schwannomas, vHIT showed an isolated SVN dysfunction pattern in 10 cases, a predominant SVN dysfunction pattern in 7 cases, and a normal exam in 2 cases, giving a correct preoperative diagnosis in 89.5% of cases. Of the 10 IVN lesions, vHIT showed an isolated IVN dysfunction pattern in 5 cases, a predominant IVN dysfunction pattern in 4 cases, and a normal test in 1 case, giving a correct preoperative diagnosis in 81.8% of cases. Overall, vHIT lead to a correct identification of the nerve of origin in 100% of altered exams, and in 26 of the 29 surgically identified cases (89.7%), without a false-localizing test in our series. The 2 patients on which intraoperative identification of the origin could not be achieved showed an isolated SVN dysfunction pattern. DISCUSION The nerve of origin of VS has been a topic of interest since the first descriptions of the tumor. Early reports found the origin on the SVN in 80% to 90% of cases,22,23 with more recent reports showing a wide variation, but with a tendency of IVN predominance.2,6,24–26 Our series found 65.5% of tumors arising from the SVN, with 2 cases on which the origin could not be assessed intraoperatively, but its functional pattern on vHIT suggested an SVN origin, as well. The reason for such variations has yet to been elucidated, but may be related to a geographical or ethnic factor, or to the method for establishing the origin (retrosigmoid, middle fossa, or translabyrinthine approaches, autopsy, etc). Several attempts to preoperatively diagnose the nerve of origin of VS have been published, with rather limited usefulness. Inoue et al8 reported that caloric tests were not helpful in obtaining information regarding nerve of origin, but using MRI, they were able to predict the origin in 75% of mostly intracanalicular VS (67% from IVN and 86% from SVN). Chen et al27 described vestibular-evoked myogenic potential (VEMP) alterations in cerebellopontine tumors as a sign of involvement of the IVN, and Murofushi et al28 described it particularly for VS, but no attempt to correlate this data to the nerve of origin was attempted. He et al,5 using VEMP and caloric tests in 68 patients, were able to correctly identify 21.4% schwannomas arising from the IVN and 50% arising from the SVN. However, other authors have demonstrated that the percentage of abnormal responses in caloric tests, VEMP and auditory brainstem response tests are not significantly different between patients with SVN and IVN schwannomas,9–11 with a lack of VEMP response found exclusively in IVN schwannomas as the only apparently specific finding.11 Regarding vHIT, previous reports have shown alteration of the exam in 23% to 90% of patients with VS, without any particular alteration specific for VS.15,16,29–32 Walther and Blödow33 proposed a possible functional localizing role of vHIT and VEMP in vestibular neuritis, which Taylor et al29 tested it on VS, finding 10.4% of abnormalities referable to the IVN, 12.5% to the SVN, 53% to both vestibular nerves, and further 18.8% had no abnormality. The alterations that suggested a single-nerve dysfunction could be considered as belonging to the nerve of origin, but a surgical correlation was not sought. Rahne et al34 recently published a series of 5 patients on which vHIT and VEMP alterations were giving as score in order to assess the nerve of origin of VS, with promising results. In 4 cases, they were able to correctly predict the origin, and interestingly, on those cases, vHIT results alone were sufficient to identify the nerve. In our series, we proposed a simple hypothesis considering the anatomophysiological correlation between semicircular canals and vestibular nerves, mainly determined on vHIT by the VOR, a reflex arc that exclusively involves those structures, without cortical interference, therefore, considered in our evaluation as the most important parameter of vestibular dysfunction. Refixation saccades (both covert and overt) are a physiologically phenomenon used by the central vestibular pathways to compensate for the low gain of VOR, and even though its occurrence is not fully understood, they are known to also involve the pontine reticular formation, interpositus nuclei and nodule of vermis, with possible cortical influence.17 The presence of saccades without VOR alteration has not been physiologically explained, but its localizing value has been validated in some peripheral vestibular disorders.16,35 In our series, 3 patients had covert saccades without VOR abnormalities, 1 in LSC and 2 in PSC, on which its localizing value was demonstrated, as the surgically identified nerve of origin was correlated with the altered semicircular canal on the 3 cases. In 17 patients, vHIT showed an alteration compatible with a single-vestibular nerve abnormality, on which a correlation was directly made. On the other 11 cases, where vHIT suggested dysfunction both vestibular nerves, a clear predominance of one vestibular nerve dysfunction was evidenced following our protocol, which allowed us to correctly identify the origin on all cases on which vHIT was altered. Interestingly, tumor size and IAC filling did not significantly altered the pattern of nerve dysfunction on vHIT, which would be expected as a bigger lesion would produce a more significant alteration on the vestibular nerve not originating the tumor. The presence of 3 normal tests in our series shows that vestibular function in patients with VS is not merely influenced by the presence of the tumor, but involves a much more complex system, on which central compensation plays a pivotal role. Since there are many factors in the pathogenesis of both vestibular and cochlear dysfunction in VSs, which have yet to be elucidated, our results must be interpreted with caution. Given our relatively small sample, we can’t grant that our correlation will hold true for all VS, even though our series consisted mainly of large tumors, which are usually more difficult to functionally evaluate. The use of the retrosigmoid approach, which allows direct visualization of both vestibular nerves on the IAC, and a single surgeon to identify the nerve of origin, as well as a single otolaryngologist to interpret the vHIT, increases the confidence on our results, minimizing differences that may arise from an inadequate evaluation of this variables. CONCLUSION There is a correlation between patterns of dysfunction on semicircular canals and vestibular nerves on vHIT, which can be used to preoperatively identify the nerve of origin in VSs. Disclosure The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article. REFERENCES 1. Kohan D, Downey LL, Lim J, Cohen NL, Elowitz E. Uncommon lesions presenting as tumors of the internal auditory canal and cerebellopontine angle. Am J Otol . 1997; 18( 3): 386– 392. Google Scholar PubMed  2. Roosli C, Linthicum FHJr, Cureoglu S, Merchant SN. What is the site of origin of cochleovestibular schwannomas?. Audiol Neurotol . 2012; 17( 2): 121– 125. Google Scholar CrossRef Search ADS   3. Bridger MWM, Farkashidy J. The distribution of neuroglia and schwann cells in the 8th nerve of man. J Laryngol Otol . 1980; 94( 12): 1353– 1362. Google Scholar CrossRef Search ADS PubMed  4. Brackmann DE, Owens RM, Friedman RA et al.   Prognostic factors for hearing preservation in vestibular schwannoma surgery. Am J Otolaryngol . 2000; 21( 3): 417– 424. Google Scholar CrossRef Search ADS   5. He YB, Yu CJ, Ji HM, Qu YM, Chen N. Significance of vestibular testing on distinguishing the nerve of origin for vestibular schwannoma and predicting the preservation of hearing. Chin Med J . 2016; 129( 7): 799– 803. Google Scholar CrossRef Search ADS PubMed  6. Jacob A, Robinson LLJr, Bortman JS, Yu L, Dodson EE, Welling DB. Nerve of origin, tumor size, hearing preservation, and facial nerve outcomes in 359 vestibular schwannoma resections at a tertiary care academic center. Laryngoscope . 2007; 117( 12): 2087– 2092. Google Scholar CrossRef Search ADS PubMed  7. Cohen NL, Lewis WS, Ransohoff J. Hearing preservation in cerebellopontine angle tumor surgery: the NYU experience 1974-1991. Am J Otol . 1993; 14 (5): 423– 433. Google Scholar PubMed  8. Inoue Y, Ogawa K, Momoshima S, Kanzaki J. The diagnostic significance of the 3D-reconstructed MRI in vestibular schwannoma surgery: prediction of tumor origin. Eur Arch Otorhinolaryngol . 2002; 259( 2): 73– 76. Google Scholar CrossRef Search ADS PubMed  9. Suzuki M, Yamada C, Inoue R, Kashio A, Saito Y, Nakanishi W. Analysis of vestibular testing in patients with vestibular schwannoma based on the nerve of origin, the localization, and the size of the tumor. Otol Neurotol . 2008; 29( 7): 1029– 1033. Google Scholar CrossRef Search ADS PubMed  10. Ushio M, Iwasaki S, Chihara Y et al.   Is the nerve origin of the vestibular schwannoma correlated with vestibular evoked myogenic potential, caloric test, and auditory brainstem response? Acta Otolaryngol . 2009; 129( 10): 1095– 1100. Google Scholar CrossRef Search ADS PubMed  11. Tsutsumi T, Tsunoda A, Noguchi Y, Komatsuzaki A. Prediction of the nerves of origin of vestibular schwannomas with vestibular evoked myogenic potentials. Am J Otol . 2000; 21 (5): 712– 715. Google Scholar PubMed  12. Ulmer E, Chays A. Head impulse test de curthoys and halmagyi. Ann Otolaryngol Chir Cervicofac . 2005; 122( 2): 84– 90 Google Scholar CrossRef Search ADS PubMed  13. Kim HJ, Park SH, Kim JS et al.   Bilaterally abnormal head impulse tests indicate a large cerebellopontine angle tumor. J Clin Neurol . 2016; 12( 1): 65– 74. Google Scholar CrossRef Search ADS PubMed  14. von Kirschbaum C, Gürkov R. Audiovestibular function deficits in vestibular schwannoma. Biomed Res Int.  2016; 2016 p. 9. doi: https://doi.org/10.1155/2016/4980562. Google Scholar CrossRef Search ADS   15. Blödow A, Blödow J, Bloching MB, Helbig R, Walther LE. Horizontal VOR function shows frequency dynamics in vestibular schwannoma. Eur Arch Otorhinolaryngol . 2015; 272( 9): 2143– 2148. Google Scholar CrossRef Search ADS PubMed  16. Blödow A, Pannasch S, Walther LE. Detection of isolated covert saccades with the video head impulse test in peripheral vestibular disorders. Auris Nasus Larynx . 2013; 40( 4): 348– 351. Google Scholar CrossRef Search ADS PubMed  17. Batuecas-Caletrio A, Rey-Martinez J, Trinidad-Ruiz G et al.   Vestibulo-ocular reflex stabilization after vestibular schwannoma surgery: a story told by saccades. Front Neurol.  2017; 8 p. 15. doi: https://doi.org/10.3389/fneur.2017.00015. Google Scholar CrossRef Search ADS PubMed  18. Batuecas-Caletrio A, Santacruz-Ruiz S, Muñoz-Herrera A, Perez-Fernandez N. The vestibulo-ocular reflex and subjective balance after vestibular schwannoma surgery. Laryngoscope . 2014; 124( 6): 1431– 1435. Google Scholar CrossRef Search ADS PubMed  19. Leal AG, Silva EBJr, Ramina R. Surgical exposure of the internal auditory canal through the retrosigmoid approach with semicircular canals anatomical preservation. Arq Neuropsiquiatr . 2015; 73( 5): 425– 430. Google Scholar CrossRef Search ADS PubMed  20. Tatagiba M, Acioly MA. Vestibular schwannoma: current state of the art. In: Ramina R, de Aguilar PR, Tatagiba M, eds. Samii's Essentials in Neurosurgery . 2nd ed. Berlin Heidelberg: Springer-Verlag; 2014: 265– 283. 21. McGarvie LA, MacDougall HG, Halmagyi GM, Burgess AM, Weber KP, Curthoys IS. The video head impulse test (vHIT) of semicircular canal function - age-dependent normative values of VOR gain in healthy subjects. Front Neurol.  2015; 6. doi: https://doi.org/10.3389/fneur.2015.00154. 22. Ylikoski J, Palva T, Collan Y. Eighth nerve in acoustic neuromas: Special reference to superior vestibular nerve function and histopathology. Arch Otolaryngol . 1978; 104( 9): 532– 537. Google Scholar CrossRef Search ADS PubMed  23. Ramsden R. Acoustic tumors. In: Kerr A, Booth J, eds. Scott Brown's Otolaryngology: Otology . London: Butterworths; 1987: 500– 533. 24. Khrais T, Romano G, Sanna M. Nerve origin of vestibular schwannoma: a prospective study. J Laryngol Otol . 2008; 122( 02): 128– 131. Google Scholar CrossRef Search ADS PubMed  25. Komatsuzaki A, Tsunoda A. Nerve origin of the acoustic neuroma. J Laryngol Otol . 2001; 115( 05): 376– 379. Google Scholar CrossRef Search ADS PubMed  26. Clemis JD, Ballad WJ, Baggot PJ, Lyon ST. Relative frequency of inferior vestibular schwannoma. Arch Otolaryngol Head Neck Surg . 1986; 112( 2): 190– 194. Google Scholar CrossRef Search ADS PubMed  27. Chen CW, Young YH, Tseng HM. Preoperative versus postoperative role of Vestibular-Evoked myogenic potentials in cerebellopontine angle tumor. Laryngoscope . 2002; 112( 2): 267– 271. Google Scholar CrossRef Search ADS PubMed  28. Murofushi T, Matsuzaki M, Mizuno M. Vestibular evoked myogenic potentials in patients with acoustic neuromas. Arch Otolaryngol Head Neck Surg . 1998; 124( 5): 509– 512. Google Scholar CrossRef Search ADS PubMed  29. Taylor RL, Kong J, Flanagan S et al.   Prevalence of vestibular dysfunction in patients with vestibular schwannoma using video head-impulses and vestibular-evoked potentials. J Neurol . 2015; 262( 5): 1228– 1237. Google Scholar CrossRef Search ADS PubMed  30. Batuecas-Caletrio A, Santa Cruz-Ruiz S, Muñoz-Herrera A, Perez Fernandez N. The map of dizziness in vestibular schwannoma. Laryngoscope . 2015; 125( 12): 2784– 2789. Google Scholar CrossRef Search ADS PubMed  31. Blödow A, Helbig R, Wichmann N, Wenzel A, Walther LE, Bloching MB. Video-Kopfimpulstest oder thermische Prüfung?. HNO . 2013; 61( 9): 781– 785. Google Scholar CrossRef Search ADS PubMed  32. Weber KP, MacDougall HG, Halmagyi GM, Curthoys IS. Impulsive testing of semicircular-canal function using video-oculography. Ann N Y Acad Sci . 2009; 1164( 1): 486– 491. Google Scholar CrossRef Search ADS PubMed  33. Walther LE, Blödow A. Ocular vestibular evoked myogenic potential to air conducted sound stimulation and video head impulse test in acute vestibular neuritis. Otol Neurotol.  2013; 34( 6): 1084– 1089. Google Scholar CrossRef Search ADS PubMed  34. Rahne T, Plößl S, Plontke SK, Strauss C. Preoperative determination of nerve of origin in patients with vestibular schwannoma. HNO . 2018; 66( S1); 16– 21. Google Scholar CrossRef Search ADS PubMed  35. Perez-Fernandez N, Eza-Nuñez P. Normal gain of VOR with refixation saccades in patients with unilateral vestibulopathy. Int Adv Otol . 2015; 11 (2): 133– 137. Google Scholar CrossRef Search ADS   Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Operative Neurosurgery Oxford University Press

Video Head Impulse Test to Preoperatively Identify the Nerve of Origin of Vestibular Schwannomas

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Congress of Neurological Surgeons
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Copyright © 2018 by the Congress of Neurological Surgeons
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2332-4252
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2332-4260
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10.1093/ons/opy103
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Abstract

Abstract BACKGROUND Identification of the nerve of origin in vestibular schwannoma (VS) is an important prognostic factor for hearing preservation surgery. Thus far, vestibular functional tests and magnetic resonance imaging have not yielded reliable results to preoperatively evaluate this information. The development of the video head impulse test (vHIT) has allowed a precise evaluation of each semicircular canal, and its localizing value has been tested for some peripheral vestibular diseases, but not for VS. OBJECTIVE To correlate patterns of semicircular canal alteration on vHIT to intraoperative identification of the nerve of origin of VSs. METHODS A total 31 patients with sporadic VSs were preoperatively evaluated with vHIT (gain of vestibule-ocular reflex, overt and covert saccades on each semicircular canal) and then the nerve of origin was surgically identified during surgical resection via retrosigmoid approach. vHIT results were classified as normal, isolated superior vestibular nerve (SVN) pattern, isolated inferior vestibular nerve (IVN) pattern, predominant SVN pattern, and predominant IVN pattern. Hannover classification, cystic component, and distance between the tumor and the end of the internal auditory canal were also considered for analysis. RESULTS Three patients had a normal vHIT, 12 had an isolated SVN pattern, 5 had an isolated IVN pattern, 7 had a predominant SVN pattern, and 4 had a predominant IVN pattern. vHIT was able to correctly identify the nerve of origin in 89.7% of cases (100% of altered exams). CONCLUSION The pattern of semicircular canal dysfunction on vHIT has a localizing value to identify the nerve of origin in VSs. Acoustic neuroma, Head impulse test, Vestibulo-ocular reflex, Saccades, Vestibular nerve, Vestibular function tests ABBREVIATIONS ABBREVIATIONS IAC internal auditory canal IVN inferior vestibular nerve LSC lateral semicircular canals MRI magnetic resonance imaging ms milliseconds PSC posterior semicircular canals SSC superior semicircular canals SVN superior vestibular nerve VEMP vestibular-evoked myogenic potential vHIT video head impulse test VS vestibular schwannoma VOR vestibule-ocular reflex Vestibular schwannoma (VS) is a benign tumor arising from Schwann cells of one of the branches of the vestibular nerve, representing around 90% of the tumors of the cerebellopontine angle.1 Theoretically, schwannomas of the cerebellopontine angle may arise from the common vestibular, superior vestibular, or inferior vestibular divisions of the 8 cranial nerve, or less frequently, from the cochlear or facial nerves, lateral, or at the level of the Obersteiner–Redlich zone, which is typically located near the internal acoustic meatus.2,3 The relevance of identifying the nerve of origin in VS lies in its prognostic factor for hearing preservation after surgery,4–7 with tumors arising from the superior vestibular nerve (SVN) having a 61% to 75% of hearing preservation, compared to 16% to 28% for an inferior vestibular nerve (IVN) origin,5,6 in cases when hearing preservation was attempted. Thus far, most studies trying to preoperatively predict the origin using magnetic resonance imaging (MRI)8 and functional tests5,8–11 have been unsuccessful, or limited to a rather specific subset of patients, so intraoperative identification remains the only reliable method, and in large tumors, adequately discerning its origin becomes challenging, and in some cases, not entirely possible. The video head impulse test (vHIT) was first described in 2005 as an improvement of the clinical head impulse using videonystagmoscopy.12 It is a noninvasive test that allows quantitative evaluation of the gain of vestibule-ocular reflex (VOR), as well as the identification of covert (occurring while the head is still moving) and overt (occurring once the head movement is finished) saccades on lateral semicircular canals (LSC), superior semicircular canals (SSC), and posterior semicircular canals (PSC) semicircular canals (Figure). vHIT in patients with VS has been reported by otologist groups describing its sensitivity, association with vestibular symptoms and vestibular recovery after surgery,13–18 but no attempts to correlate its alteration to a specific vestibular nerve dysfunction has been reported. FIGURE. View largeDownload slide A, Decreased gain of VOR on the right posterior semicircular canal (black arrow), with presence of covert (blue arrow) and overt (green arrow) saccades. B, Axial gadolinium-enhanced fat-suppressed T1-weighted MRI of the same patient demonstrating a right intracanalicular vestibular schwannoma (Hannover-T1). FIGURE. View largeDownload slide A, Decreased gain of VOR on the right posterior semicircular canal (black arrow), with presence of covert (blue arrow) and overt (green arrow) saccades. B, Axial gadolinium-enhanced fat-suppressed T1-weighted MRI of the same patient demonstrating a right intracanalicular vestibular schwannoma (Hannover-T1). Given that the SVN transmits information from the lateral and SSC, and the IVN from the posterior semicircular canal, we propose that in patients with no known peripheral vestibulopathy, vHIT alteration of a particular semicircular canal may indirectly translate an underlying nerve dysfunction of the corresponding nerve. Aware of the possible alteration of the other vestibular branch by the same factors that supposedly cause cochlear dysfunction,14 we propose that the affected vestibular branch will present a more prominent alteration than its counterpart, thus, allowing us to identify the nerve of origin. METHODS From March, 2016 to June, 2017, 31 patients with unilateral, sporadic VS underwent surgical treatment at the Neurological Institute of Curitiba (INC), Brazil. Patients with previous treatment, known vestibular disease, intraoperative or histological diagnosis other than VS, or intralabyrinthine extension of the tumor were excluded from the analysis. Surgery was performed via retrosigmoid approach by the senior author (R.R.), as previously described,19 identifying the nerve of origin in the internal auditory canal (IAC). The lead surgeon was not aware of the result of vHIT before the procedure. The study was approved by our Institutional Review Board, and the requirement to obtain signed consent was waived. All patients were preoperatively evaluated with MRI with an inner ear protocol, which was then analyzed by a single neuroradiologist (B.T.), and vHIT, performed and interpreted by an experienced neuro-otologist (P.S.). Morphologically, tumors were staged using the Hannover classification.20 The presence of a cystic component, and the distance between the tumor and the end of the IAC at the level of the cochlea was also considered for analysis. vHIT was performed using ICS Impulse video goggles (GN Otometrics, Taastrup, Denmark) and Vestlab 7.1 software for data analysis. The procedure consisted on the analysis of eye movement with a videooculography camera that recognizes movement up to 250 Hz and a sensor that measures head movement. The patient is asked to fix his gaze at a target 1 m away, then the examiner rotates the patient's head randomly 15° to 20° on the horizontal plane, with a duration of 150 to 200 milliseconds (ms), producing a peak acceleration of 2000° to 6000° per second squared. The window of analysis from 0 to 150 ms allows the evaluation of both LSC. The vertical semicircular canals are evaluated with a 45° head rotation to the right (left superior and right PSC) and then to the left (right superior and left PSC), producing an anterior and then posterior impulse. Twenty stimuli for every semicircular canal are performed to assure a sustained response. The evaluated parameters were: gain of VOR (relationship between the velocity of head and eye movements) of every canal, expressed as percentage to evaluate the functional deficit of the affected ear, and the presence of overt and covert saccades. Gain of VOR classified as normal or abnormal according to age-dependent normative values.21 vHIT results were then classified as normal, when no alteration was observed; isolated SVN dysfunction pattern, when there was any alteration on the LSC and/or SSC without abnormalities on the PSC; isolated IVN dysfunction pattern, when only alterations on the PSC were found; and predominant SVN/IVN dysfunction pattern, when there was alteration of the PSC associated with alteration of the LSC and/or SSC. The predominant alteration of one canal over the others was established by the presence of VOR alteration over the presence of saccades. When VOR of 2 semicircular canals were abnormal, the percentage of VOR gain was used to determine which canal was altered the most (lower VOR gain was considered as more altered). vHIT data were then compared with intraoperative identification of the nerve of origin. RESULTS A total of 31 patients were evaluated, 13 were women, with a mean age of 46.9 yr old (range 19-67). Thirteen tumors originated from the left vestibular nerves. There were 4 Hannover-T1, 5 Hannover-T2, 5 Hannover-T3, and 17 Hannover-T4 tumors. There was no significant difference in vHIT results according to Hannover classification, cystic component, or IAC filling. Surgical Results Surgical identification of the nerve of origin was achieved in 29 of the 31 patients. Both cases on which the origin could not be recognized were Hannover-T4b lesions, on which intracanalicular anatomy was highly distorted, even difficulting recognition of the facial nerve. Of the remaining, 19 (61.3%) arose from the SVN, and 10 (32.3%) from the IVN. vHIT Results Three cases had a normal exam, 12 had a semicircular canal dysfunction compatible with a SVN alteration, 5 were compatible with an IVN alteration, and 11 cases had an exam compatible with alteration of both vestibular nerves, 7 with predominance of SVN dysfunction, and 4 of IVN dysfunction. Semicircular canal alterations and its association with tumor size are shown in Table 1. TABLE 1. vHIT Pattern and Hannover Classification   Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31    Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Patterns of semicircular canal dysfunction and subsequent classification in superior or IVN patterns, according to tumor size. View Large TABLE 1. vHIT Pattern and Hannover Classification   Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31    Hannover  vHIT  T1  T2  T3  T4  n  Normal  1  1  1  –  3  Isolated SVN pattern     LSC  1  1  2  5  9   LSC + SSC  1  –  1  1  3  Isolated IVN pattern     PSC  –  1  –  4  5  Predominant SVN pattern     LSC + PSC  –  1  –  1  2   LSC + SSC + PSC  –  –  1  4  5  Predominant IVN pattern     PSC + LSC  1  1  –  2  4  Total  3  5  4  17  31  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Patterns of semicircular canal dysfunction and subsequent classification in superior or IVN patterns, according to tumor size. View Large Table 2 summarizes individual findings of the 31 cases. In 9 cases, isolated alteration of the LSC was found, 1 with only VOR alteration, 3 with VOR + overt saccades, 1 with only covert saccades, and 4 with VOR alteration + covert and overt saccades. TABLE 2. Age, Tumor Size, vHIT Results, and Intraoperative Identification of the Nerve of Origin of Individual Cases     Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN      Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Abnormal gain of VOR was highlighted in shaded cells. View Large TABLE 2. Age, Tumor Size, vHIT Results, and Intraoperative Identification of the Nerve of Origin of Individual Cases     Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN      Tumor characteristics  LSC  SSC  PSC  Surgery  Pattern of vHIT dysfunction  Age  Hannover  Side  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  VOR  Covert saccades  Overt saccades  Nerve of origin  Normal pattern  56  T1  Right  0.95      0.91      0.72      IVN    65  T2  Right  1.16      1.04      0.81      SVN    53  T3a  Left  0.92      0.88      1.01      SVN  Isolated SVN pattern  37  T4a  Left  0.66  +  +  0.93      0.9      SVN    67  T4a  Left  0.57    +  0.61      0.81      SVN    65  T3a  Left  0.53    +  0.88      1.1      SVN    24  T4b  Left  0.71  +  +  0.73      0.93      Not identifiable    41  T4b  Right  0.48  +  +  0.48      0.67      Not identifiable    48  T1  Right  0.59  +  +  0.86  +  +  0.89      SVN    67  T3a  Left  0.53  +  +  0.57      1.28      SVN    33  T4a  Left  0.52    +  0.72      0.97      SVN    19  T1  Left  0.78      0.82      1.1      SVN    60  T2  Right  0.81  +    1.18      0.87      SVN    59  T3b  Right  0.68  +  +  –      –      SVN    31  T4a  Right  0.66  +  +  0.7      0.68      SVN  Isolated IVN pattern  51  T2  Left  0.87      0.84      0.47      IVN    41  T4a  Right  0.88      0.75      0.89  +    IVN    48  T4a  Right  0.9      1      0.74  +    IVN    44  T4b  Right  0.96      0.8      0.39  +  +  IVN    41  T4a  Right  0.88      1.2      0.5  +  +  IVN  Predominant SVN pattern  35  T4b  Left  0.56  +  +  0.65      0.62  +  +  SVN    50  T4a  Right  0.51  +  +  0.78    +  0.54  +  +  SVN    48  T4b  Left  0.29  +  +  0.46  +  +  0.63  +  +  SVN    57  T2  Left  0.62    +  0.77      0.67  +    SVN    58  T3a  Right  0.27  +  +  0.6  +  +  0.44  +  +  SVN    54  T4a  Right  0.33  +  +  0.64  +  +  0.66  +  +  SVN    49  T4b  Right  0.25  +  +  0.34    +  0.6    +  SVN  Predominant IVN pattern  50  T2  Left  0.69  +    0.74      0.6  +    IVN    36  T4b  Right  0.9  +  +  0.75      0.66    +  Not identifiable    34  T1  Right  0.94    +  0.93      0.51  +  +  IVN    45  T4b  Right  0.86  +    0.95      0.5  +  +  IVN  SVN, superior vestibular nerve; IVN, inferior vestibular nerve; LSC, lateral semicircular canal; SSC, superior semicircular canal; PSC, posterior semicircular canal Abnormal gain of VOR was highlighted in shaded cells. View Large In 5 cases, isolated alteration of the PSC was found, 1 with only VOR alteration, 2 with covert saccades, and 2 with VOR alteration + covert and overt saccades. In 3 cases, alteration of both LSC and SSC were found, all had alteration of VOR + covert and overt saccades on the LSC, 2 had only VOR alteration on the SSC, and 1 had only covert and overt saccades on the SSC. In 6 cases, alteration of both LSC and PSC was found, all of them had VOR alteration on the PSC, and 2 also had covert saccades, 1 had overt saccades, and 3 had covert and overt saccades on the same semicircular canal. LSC abnormalities were: 1 case with overt saccades, 2 with covert saccades, 1 with covert and overt saccades, 1 with VOR alteration + overt saccades, and 1 with VOR alteration + covert and overt saccades. In 5 cases, alteration of LSC, SSC and PSC was found. Three patients had VOR alteration + covert and overt saccades in all semicircular canals; 1 had VOR alteration + overt and covert saccades on the LSC and VOR alteration and overt saccades on the SSC and PSC; and 1 had VOR alteration + overt and covert saccades on LSC and PSC, and only overt saccades on the SSC. In the 11 cases where vHIT showed a semicircular canal alteration compatible with dysfunction of both nerves, the predominant of dysfunction of one nerve over the other was established by the presence of VOR alteration in 4 cases, and on the other 7 by the degree of VOR gain on each canal. vHIT to Identify the Nerve of Origin of VS Of the 19 surgically identified SVN schwannomas, vHIT showed an isolated SVN dysfunction pattern in 10 cases, a predominant SVN dysfunction pattern in 7 cases, and a normal exam in 2 cases, giving a correct preoperative diagnosis in 89.5% of cases. Of the 10 IVN lesions, vHIT showed an isolated IVN dysfunction pattern in 5 cases, a predominant IVN dysfunction pattern in 4 cases, and a normal test in 1 case, giving a correct preoperative diagnosis in 81.8% of cases. Overall, vHIT lead to a correct identification of the nerve of origin in 100% of altered exams, and in 26 of the 29 surgically identified cases (89.7%), without a false-localizing test in our series. The 2 patients on which intraoperative identification of the origin could not be achieved showed an isolated SVN dysfunction pattern. DISCUSION The nerve of origin of VS has been a topic of interest since the first descriptions of the tumor. Early reports found the origin on the SVN in 80% to 90% of cases,22,23 with more recent reports showing a wide variation, but with a tendency of IVN predominance.2,6,24–26 Our series found 65.5% of tumors arising from the SVN, with 2 cases on which the origin could not be assessed intraoperatively, but its functional pattern on vHIT suggested an SVN origin, as well. The reason for such variations has yet to been elucidated, but may be related to a geographical or ethnic factor, or to the method for establishing the origin (retrosigmoid, middle fossa, or translabyrinthine approaches, autopsy, etc). Several attempts to preoperatively diagnose the nerve of origin of VS have been published, with rather limited usefulness. Inoue et al8 reported that caloric tests were not helpful in obtaining information regarding nerve of origin, but using MRI, they were able to predict the origin in 75% of mostly intracanalicular VS (67% from IVN and 86% from SVN). Chen et al27 described vestibular-evoked myogenic potential (VEMP) alterations in cerebellopontine tumors as a sign of involvement of the IVN, and Murofushi et al28 described it particularly for VS, but no attempt to correlate this data to the nerve of origin was attempted. He et al,5 using VEMP and caloric tests in 68 patients, were able to correctly identify 21.4% schwannomas arising from the IVN and 50% arising from the SVN. However, other authors have demonstrated that the percentage of abnormal responses in caloric tests, VEMP and auditory brainstem response tests are not significantly different between patients with SVN and IVN schwannomas,9–11 with a lack of VEMP response found exclusively in IVN schwannomas as the only apparently specific finding.11 Regarding vHIT, previous reports have shown alteration of the exam in 23% to 90% of patients with VS, without any particular alteration specific for VS.15,16,29–32 Walther and Blödow33 proposed a possible functional localizing role of vHIT and VEMP in vestibular neuritis, which Taylor et al29 tested it on VS, finding 10.4% of abnormalities referable to the IVN, 12.5% to the SVN, 53% to both vestibular nerves, and further 18.8% had no abnormality. The alterations that suggested a single-nerve dysfunction could be considered as belonging to the nerve of origin, but a surgical correlation was not sought. Rahne et al34 recently published a series of 5 patients on which vHIT and VEMP alterations were giving as score in order to assess the nerve of origin of VS, with promising results. In 4 cases, they were able to correctly predict the origin, and interestingly, on those cases, vHIT results alone were sufficient to identify the nerve. In our series, we proposed a simple hypothesis considering the anatomophysiological correlation between semicircular canals and vestibular nerves, mainly determined on vHIT by the VOR, a reflex arc that exclusively involves those structures, without cortical interference, therefore, considered in our evaluation as the most important parameter of vestibular dysfunction. Refixation saccades (both covert and overt) are a physiologically phenomenon used by the central vestibular pathways to compensate for the low gain of VOR, and even though its occurrence is not fully understood, they are known to also involve the pontine reticular formation, interpositus nuclei and nodule of vermis, with possible cortical influence.17 The presence of saccades without VOR alteration has not been physiologically explained, but its localizing value has been validated in some peripheral vestibular disorders.16,35 In our series, 3 patients had covert saccades without VOR abnormalities, 1 in LSC and 2 in PSC, on which its localizing value was demonstrated, as the surgically identified nerve of origin was correlated with the altered semicircular canal on the 3 cases. In 17 patients, vHIT showed an alteration compatible with a single-vestibular nerve abnormality, on which a correlation was directly made. On the other 11 cases, where vHIT suggested dysfunction both vestibular nerves, a clear predominance of one vestibular nerve dysfunction was evidenced following our protocol, which allowed us to correctly identify the origin on all cases on which vHIT was altered. Interestingly, tumor size and IAC filling did not significantly altered the pattern of nerve dysfunction on vHIT, which would be expected as a bigger lesion would produce a more significant alteration on the vestibular nerve not originating the tumor. The presence of 3 normal tests in our series shows that vestibular function in patients with VS is not merely influenced by the presence of the tumor, but involves a much more complex system, on which central compensation plays a pivotal role. Since there are many factors in the pathogenesis of both vestibular and cochlear dysfunction in VSs, which have yet to be elucidated, our results must be interpreted with caution. Given our relatively small sample, we can’t grant that our correlation will hold true for all VS, even though our series consisted mainly of large tumors, which are usually more difficult to functionally evaluate. The use of the retrosigmoid approach, which allows direct visualization of both vestibular nerves on the IAC, and a single surgeon to identify the nerve of origin, as well as a single otolaryngologist to interpret the vHIT, increases the confidence on our results, minimizing differences that may arise from an inadequate evaluation of this variables. CONCLUSION There is a correlation between patterns of dysfunction on semicircular canals and vestibular nerves on vHIT, which can be used to preoperatively identify the nerve of origin in VSs. Disclosure The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article. REFERENCES 1. Kohan D, Downey LL, Lim J, Cohen NL, Elowitz E. Uncommon lesions presenting as tumors of the internal auditory canal and cerebellopontine angle. Am J Otol . 1997; 18( 3): 386– 392. Google Scholar PubMed  2. Roosli C, Linthicum FHJr, Cureoglu S, Merchant SN. What is the site of origin of cochleovestibular schwannomas?. Audiol Neurotol . 2012; 17( 2): 121– 125. Google Scholar CrossRef Search ADS   3. Bridger MWM, Farkashidy J. The distribution of neuroglia and schwann cells in the 8th nerve of man. J Laryngol Otol . 1980; 94( 12): 1353– 1362. Google Scholar CrossRef Search ADS PubMed  4. Brackmann DE, Owens RM, Friedman RA et al.   Prognostic factors for hearing preservation in vestibular schwannoma surgery. Am J Otolaryngol . 2000; 21( 3): 417– 424. Google Scholar CrossRef Search ADS   5. He YB, Yu CJ, Ji HM, Qu YM, Chen N. Significance of vestibular testing on distinguishing the nerve of origin for vestibular schwannoma and predicting the preservation of hearing. Chin Med J . 2016; 129( 7): 799– 803. Google Scholar CrossRef Search ADS PubMed  6. Jacob A, Robinson LLJr, Bortman JS, Yu L, Dodson EE, Welling DB. Nerve of origin, tumor size, hearing preservation, and facial nerve outcomes in 359 vestibular schwannoma resections at a tertiary care academic center. Laryngoscope . 2007; 117( 12): 2087– 2092. Google Scholar CrossRef Search ADS PubMed  7. Cohen NL, Lewis WS, Ransohoff J. Hearing preservation in cerebellopontine angle tumor surgery: the NYU experience 1974-1991. Am J Otol . 1993; 14 (5): 423– 433. Google Scholar PubMed  8. Inoue Y, Ogawa K, Momoshima S, Kanzaki J. The diagnostic significance of the 3D-reconstructed MRI in vestibular schwannoma surgery: prediction of tumor origin. Eur Arch Otorhinolaryngol . 2002; 259( 2): 73– 76. Google Scholar CrossRef Search ADS PubMed  9. Suzuki M, Yamada C, Inoue R, Kashio A, Saito Y, Nakanishi W. Analysis of vestibular testing in patients with vestibular schwannoma based on the nerve of origin, the localization, and the size of the tumor. Otol Neurotol . 2008; 29( 7): 1029– 1033. Google Scholar CrossRef Search ADS PubMed  10. Ushio M, Iwasaki S, Chihara Y et al.   Is the nerve origin of the vestibular schwannoma correlated with vestibular evoked myogenic potential, caloric test, and auditory brainstem response? Acta Otolaryngol . 2009; 129( 10): 1095– 1100. Google Scholar CrossRef Search ADS PubMed  11. Tsutsumi T, Tsunoda A, Noguchi Y, Komatsuzaki A. Prediction of the nerves of origin of vestibular schwannomas with vestibular evoked myogenic potentials. Am J Otol . 2000; 21 (5): 712– 715. Google Scholar PubMed  12. Ulmer E, Chays A. Head impulse test de curthoys and halmagyi. Ann Otolaryngol Chir Cervicofac . 2005; 122( 2): 84– 90 Google Scholar CrossRef Search ADS PubMed  13. Kim HJ, Park SH, Kim JS et al.   Bilaterally abnormal head impulse tests indicate a large cerebellopontine angle tumor. J Clin Neurol . 2016; 12( 1): 65– 74. Google Scholar CrossRef Search ADS PubMed  14. von Kirschbaum C, Gürkov R. Audiovestibular function deficits in vestibular schwannoma. Biomed Res Int.  2016; 2016 p. 9. doi: https://doi.org/10.1155/2016/4980562. Google Scholar CrossRef Search ADS   15. Blödow A, Blödow J, Bloching MB, Helbig R, Walther LE. Horizontal VOR function shows frequency dynamics in vestibular schwannoma. Eur Arch Otorhinolaryngol . 2015; 272( 9): 2143– 2148. Google Scholar CrossRef Search ADS PubMed  16. Blödow A, Pannasch S, Walther LE. Detection of isolated covert saccades with the video head impulse test in peripheral vestibular disorders. Auris Nasus Larynx . 2013; 40( 4): 348– 351. Google Scholar CrossRef Search ADS PubMed  17. Batuecas-Caletrio A, Rey-Martinez J, Trinidad-Ruiz G et al.   Vestibulo-ocular reflex stabilization after vestibular schwannoma surgery: a story told by saccades. Front Neurol.  2017; 8 p. 15. doi: https://doi.org/10.3389/fneur.2017.00015. Google Scholar CrossRef Search ADS PubMed  18. Batuecas-Caletrio A, Santacruz-Ruiz S, Muñoz-Herrera A, Perez-Fernandez N. The vestibulo-ocular reflex and subjective balance after vestibular schwannoma surgery. Laryngoscope . 2014; 124( 6): 1431– 1435. Google Scholar CrossRef Search ADS PubMed  19. Leal AG, Silva EBJr, Ramina R. Surgical exposure of the internal auditory canal through the retrosigmoid approach with semicircular canals anatomical preservation. Arq Neuropsiquiatr . 2015; 73( 5): 425– 430. Google Scholar CrossRef Search ADS PubMed  20. Tatagiba M, Acioly MA. Vestibular schwannoma: current state of the art. In: Ramina R, de Aguilar PR, Tatagiba M, eds. Samii's Essentials in Neurosurgery . 2nd ed. Berlin Heidelberg: Springer-Verlag; 2014: 265– 283. 21. McGarvie LA, MacDougall HG, Halmagyi GM, Burgess AM, Weber KP, Curthoys IS. The video head impulse test (vHIT) of semicircular canal function - age-dependent normative values of VOR gain in healthy subjects. Front Neurol.  2015; 6. doi: https://doi.org/10.3389/fneur.2015.00154. 22. Ylikoski J, Palva T, Collan Y. Eighth nerve in acoustic neuromas: Special reference to superior vestibular nerve function and histopathology. Arch Otolaryngol . 1978; 104( 9): 532– 537. Google Scholar CrossRef Search ADS PubMed  23. Ramsden R. Acoustic tumors. In: Kerr A, Booth J, eds. Scott Brown's Otolaryngology: Otology . London: Butterworths; 1987: 500– 533. 24. Khrais T, Romano G, Sanna M. Nerve origin of vestibular schwannoma: a prospective study. J Laryngol Otol . 2008; 122( 02): 128– 131. Google Scholar CrossRef Search ADS PubMed  25. Komatsuzaki A, Tsunoda A. Nerve origin of the acoustic neuroma. J Laryngol Otol . 2001; 115( 05): 376– 379. Google Scholar CrossRef Search ADS PubMed  26. Clemis JD, Ballad WJ, Baggot PJ, Lyon ST. Relative frequency of inferior vestibular schwannoma. Arch Otolaryngol Head Neck Surg . 1986; 112( 2): 190– 194. Google Scholar CrossRef Search ADS PubMed  27. Chen CW, Young YH, Tseng HM. Preoperative versus postoperative role of Vestibular-Evoked myogenic potentials in cerebellopontine angle tumor. Laryngoscope . 2002; 112( 2): 267– 271. Google Scholar CrossRef Search ADS PubMed  28. Murofushi T, Matsuzaki M, Mizuno M. Vestibular evoked myogenic potentials in patients with acoustic neuromas. Arch Otolaryngol Head Neck Surg . 1998; 124( 5): 509– 512. Google Scholar CrossRef Search ADS PubMed  29. Taylor RL, Kong J, Flanagan S et al.   Prevalence of vestibular dysfunction in patients with vestibular schwannoma using video head-impulses and vestibular-evoked potentials. J Neurol . 2015; 262( 5): 1228– 1237. Google Scholar CrossRef Search ADS PubMed  30. Batuecas-Caletrio A, Santa Cruz-Ruiz S, Muñoz-Herrera A, Perez Fernandez N. The map of dizziness in vestibular schwannoma. Laryngoscope . 2015; 125( 12): 2784– 2789. Google Scholar CrossRef Search ADS PubMed  31. Blödow A, Helbig R, Wichmann N, Wenzel A, Walther LE, Bloching MB. Video-Kopfimpulstest oder thermische Prüfung?. HNO . 2013; 61( 9): 781– 785. Google Scholar CrossRef Search ADS PubMed  32. Weber KP, MacDougall HG, Halmagyi GM, Curthoys IS. Impulsive testing of semicircular-canal function using video-oculography. Ann N Y Acad Sci . 2009; 1164( 1): 486– 491. Google Scholar CrossRef Search ADS PubMed  33. Walther LE, Blödow A. Ocular vestibular evoked myogenic potential to air conducted sound stimulation and video head impulse test in acute vestibular neuritis. Otol Neurotol.  2013; 34( 6): 1084– 1089. Google Scholar CrossRef Search ADS PubMed  34. Rahne T, Plößl S, Plontke SK, Strauss C. Preoperative determination of nerve of origin in patients with vestibular schwannoma. HNO . 2018; 66( S1); 16– 21. Google Scholar CrossRef Search ADS PubMed  35. Perez-Fernandez N, Eza-Nuñez P. Normal gain of VOR with refixation saccades in patients with unilateral vestibulopathy. Int Adv Otol . 2015; 11 (2): 133– 137. Google Scholar CrossRef Search ADS   Copyright © 2018 by the Congress of Neurological Surgeons This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

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Operative NeurosurgeryOxford University Press

Published: May 10, 2018

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