The relationship between the findings of vestibular evoked myogenic potentials and severity of obstructive sleep apnea syndrome

  • Bülent UlusoyEmail author
  • Osman Gül
  • Çağdaş Elsürer
  • Mete Kaan Bozkurt
  • Baykal Tülek
  • Muslu Kazım Körez
  • Hakan Ekmekçi
  • Bahar Çolpan



Our study aimed to evaluate the effects of chronic hypoxic state in Obstructive Sleep Apnea Syndrome (OSAS) on brainstem pathways using Vestibular Evoked Myogenic Potential (VEMP) test and to investigate the presence of new markers likely to be correlated with the severity of the disease.


The study was planned as prospective and double blind. A total of 60 patients (120 ears) diagnosed with mild, moderate and severe OSAS were included in the study and the patients are grouped as 20 patients in each group. Twenty volunteer healthy individuals (40 ears) shown to be without OSAS were included in the study. VEMP measurements were made in 60 study group patients (120 ears) and in 20 healthy controls (40 ears). The groups were compared in terms of variables such as the acquisition rate of oVEMP and cVEMP waves, interval between the waves, latency and amplitude of the waves. p < 0.05 values were considered as significant.


The results of cVEMP test showed that the rate of wave acquisition in the moderate and severe OSAS groups was significantly lower than the control group and mild OSAS groups (p = 0.008). There was no difference between the control group and the mild OSAS group in terms of the rate of obtaining the wave (p > 0.05). In the moderate and severe OSAS groups, P1N1 amplitude and N1P2 amplitude values were found to be significantly lower than the mild OSAS group (p = 0.007 and p = 0.017, respectively). In the oVEMP test, there was no significant difference between the mild OSAS group and the control group in terms of the wave yield (p > 0.05); however, it was found that the rate of wave acquisition in the moderate and severe OSAS groups was significantly lower than the mild OSAS group (p = 0.041). There was inverse correlation between the N1P2 interval and P1N1 amplitude value and AHI in simple regression analysis and multiple regression analysis (p = 0.012 and p = 0.021; p = 0.009 and p = 0.040, respectively).


The negative effects of chronic intermittent hypoxia related with OSAS on the brainstem and vestibular system can be demonstrated by VEMP tests. Especially, the inability to obtain the wave is the most important finding showing this situation. Also, we think that N1P2 interval and P1N1 amplitude markers can be used to detect the subclinical negative effect of chronic hypoxia on vestibular nuclei in the brainstem.


Obstructive sleep apnea syndrome Cervical vestibular evoked myogenic potentials Ocular vestibular evoked myogenic potentials Hypoxia Brainstem 



Financial support was received from Selçuk University (Project number; 18401106).

Compliance with ethical standards

Conflicts of Interest

There is no conflict of interest between all authors.

Ethics Committee

The approval of this study was obtained from the ethics committee of our hospital (2017/368).


  1. 1.
    Rosengren SM, Colebatch JG, Young AS, Govender S, Welgampola MS (2019) Vestibular evoked myogenic potentials in practice: methods, pitfalls and clinical applications. Clin Neurophysiol Pract 4:47–68. CrossRefPubMedPubMedCentralGoogle Scholar
  2. 2.
    Mutlu M, Bayir O, Yuceege MB, Karagoz T, Firat H, Ozdek A, Akin I, Korkmaz H (2015) Vestibular evoked myogenic potential responses in obstructive sleep apnea syndrome. Eur Arch Otorhinolaryngol 272(11):3137–3141. CrossRefPubMedGoogle Scholar
  3. 3.
    De Natale ER, Ginatempo F, Paulus KS, Pes GM, Manca A, Tolu E, Agnetti V, Deriu F (2015) Abnormalities of vestibular-evoked myogenic potentials in idiopathic Parkinson's disease are associated with clinical evidence of brainstem involvement. Neurol Sci 36(6):995–1001. CrossRefPubMedGoogle Scholar
  4. 4.
    Di Stadio A, Dipietro L, Ralli M, Greco A, Ricci G, Bernitsas E (2019) The role of vestibular evoked myogenic potentials in multiple sclerosis-related vertigo. A systematic review of the literature. Mult Scler Relat Disord 28:159–164. CrossRefPubMedGoogle Scholar
  5. 5.
    Jordan AS, White DP, Fogel RB (2003) Recent advances in understanding the pathogenesis of obstructive sleep apnea. Curr Opin Pulm Med 9(6):459–464CrossRefPubMedGoogle Scholar
  6. 6.
    Wong AM, Wang M, Garner DJ, Bowditch S, Paul E, Adams MJ, Hamilton GS, Mansfield DR (2019) Obstructive sleep apnoea predicted by the STOP-BANG questionnaire is not associated with higher rates of post-operative complications among a high-risk surgical cohort. Sleep Breath. CrossRefPubMedGoogle Scholar
  7. 7.
    Xia Y, Fu Y, Xu H, Guan J, Yi H, Yin S (2016) Changes in cerebral metabolites in obstructive sleep apnea: a systemic review and meta-analysis. Sci Rep 6:28712. CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Zhou J, Camacho M, Tang X, Kushida CA (2016) A review of neurocognitive function and obstructive sleep apnea with or without daytime sleepiness. Sleep Med 23:99–108. CrossRefPubMedGoogle Scholar
  9. 9.
    Guilleminault C, Ramar K (2009) Neurologic aspects of sleep apnea: is obstructive sleep apnea a neurologic disorder? Semin Neurol 29(4):368–371. CrossRefPubMedGoogle Scholar
  10. 10.
    Chen CH, Young YH (2003) Vestibular evoked myogenic potentials in brainstem stroke. Laryngoscope 113(6):990–993. CrossRefPubMedGoogle Scholar
  11. 11.
    Iber C A-IS, Chesson L. and Quan SF. (2007) The AASM manual for the scoring of sleep and associated events: rules, terminology, and technical Specifications. 1st edn., WestchesterGoogle Scholar
  12. 12.
    Cohen J (1988) Statistical power analysis for the behavioral sciences, 2nd edn. Lawrence Earlbaum Associates, HillsdaleGoogle Scholar
  13. 13.
    Heide G, Luft B, Franke J, Schmidt P, Witte OW, Axer H (2010) Brainstem representation of vestibular evoked myogenic potentials. Clin Neurophysiol 121(7):1102–1108. CrossRefPubMedGoogle Scholar
  14. 14.
    Casale M, Vesperini E, Potena M, Pappacena M, Bressi F, Baptista PJ, Salvinelli F (2012) Is obstructive sleep apnea syndrome a risk factor for auditory pathway? Sleep Breath 16(2):413–417. CrossRefPubMedGoogle Scholar
  15. 15.
    Zhang JH, Fung SJ, Xi M, Sampogna S, Chase MH (2010) Apnea produces neuronal degeneration in the pons and medulla of guinea pigs. Neurobiol Dis 40(1):251–264. CrossRefPubMedGoogle Scholar
  16. 16.
    Canessa N, Castronovo V, Cappa SF, Aloia MS, Marelli S, Falini A, Alemanno F, Ferini-Strambi L (2011) Obstructive sleep apnea: brain structural changes and neurocognitive function before and after treatment. Am J Respir Crit Care Med 183(10):1419–1426. CrossRefPubMedGoogle Scholar
  17. 17.
    O'Donoghue FJ, Wellard RM, Rochford PD, Dawson A, Barnes M, Ruehland WR, Jackson ML, Howard ME, Pierce RJ, Jackson GD (2012) Magnetic resonance spectroscopy and neurocognitive dysfunction in obstructive sleep apnea before and after CPAP treatment. Sleep 35(1):41–48. CrossRefPubMedPubMedCentralGoogle Scholar
  18. 18.
    Wang W, Su J, Kong D, Pang J, Kang J (2016) Gender, nocturnal hypoxia, and arousal influence brainstem auditory evoked potentials in patients with obstructive sleep apnea. Sleep Breath 20(4):1239–1244. CrossRefPubMedGoogle Scholar
  19. 19.
    Fu Q, Wang T, Liang Y, Lin Y, Zhao X, Wan J, Fan S (2019) Auditory deficits in patients with mild and moderate obstructive sleep apnea syndrome: a speech syllable evoked auditory brainstem response study. Clin Exp Otorhinolaryngol 12(1):58–65. CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of Otorhinolaryngology-Head and Neck Surgery, Faculty of MedicineSelçuk UniversityKonyaTurkey
  2. 2.Department of Chest Disease, Faculty of MedicineSelçuk UniversityKonyaTurkey
  3. 3.Department of Statistics, Faculty of ScinceSelçuk UniversityKonyaTurkey
  4. 4.Department of Neurology, Faculty of MedicineSelçuk UniversityKonyaTurkey

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