Vibration-induced nystagmus in patients with vestibular schwannoma: Characteristics and clinical implications. Issue 7 (July 2017)

• Record Type: Journal Article
• Authors: Lee, Jeon Mi; Kim, Mi Joo; Kim, Jin Won; Shim, Dae Bo; Kim, Jinna; Kim, Sung Huhn
• Is Part Of: Clinical neurophysiology. Volume 128:Issue 7(2017:Jul.)
• Page Start: 1372
• Page End: 1379
• Publication Date: 2017-07
• Subjects: CP canal paresis -- MRI magnetic resonance imaging -- MSPV maximum slow-phase velocity -- SCM sternocleidomastoid muscle -- VIN vibration-induced nystagmus; Vibration -- Nystagmus -- Vestibular schwannoma -- Vestibular loss; Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2017.02.023
• Languages: English
• ISSNs: 1388-2457

Abstract

Highlights: Evoking vibration-induced nystagmus (VIN) is useful for detecting vestibular asymmetry in vestibular schwannoma patients. VIN of the sternocleidomastoid muscle provides the most accurate information on vestibular asymmetry and tumor volume. VIN after total vestibular loss persists for at least 6 months even after vestibular compensation. Abstract: Objective: To investigate the clinical significance of vibration-induced nystagmus (VIN) in unilateral vestibular asymmetry and vestibular schwannoma. Methods: Thirteen patients with vestibular schwannoma underwent the VIN test, in which stimulation was applied to the mastoid processes and sternocleidomastoid (SCM) muscles on the ipsilateral and contralateral sides of lesions. Preoperative VIN was measured, and changes in VIN were followed up for 6 months after tumor removal. Significance of VIN was determined by evaluation of its sensitivity, correlation with vestibular function tests and tumor volume, and postoperative changes. Results: The overall pre and postoperative sensitivities of VIN were 92.3% and 100%, respectively, considering stimulation at all four sites. Maximum slow-phase velocity (MSPV) of VIN was linearly correlated with caloric weakness and tumor volume, especially when stimulation was applied to the SCM muscle. Postoperative MSPV of VIN exhibited stronger linear correlation with postoperative changes in canal paresis value and inverse correlation with tumor size upon stimulation of the ipsilateral SCM muscle than upon stimulation of other sites. During the 6-month follow-up period, persistence of VIN without changes in MSPV was observed even after vestibular compensation. Conclusions: Evoking VIN by stimulation of the mastoid processes and SCM muscles is effective for detecting vestibular asymmetry. It could also help determine the degree of vestibular asymmetry and volume of vestibular schwannoma if stimulation is applied to the SCM muscle. Significance: The results of this study could provide clues for the basic application of VIN in patients with vestibular loss and vestibular schwannoma.