Part II: A Call for Implementing the Comprehensive Neurodiagnostic Audiology Evaluation: Effects of Concussion on Central Auditory and Vestibular Function

Dr. Frank Musiek
April 8, 2020

Jennifer Gonzalez, Au.D., Ph.D., CCC-A

Speech and Hearing Sciences, College of Health Solutions, Arizona State University


As mentioned in Part I of this two-part series, corpus callosum strain has been documented in the literature to be the most reliable indicator for concussion cases in football (Laksari et al., 2018; Kleiven, 2006; Hernandez et al., 2015). Such damage to the corpus callosum significantly impacts central auditory and vestibular function, especially for tasks that require interhemispheric transfer of information. Due to the high likelihood of central auditory and vestibular dysfunction following concussion, including measures of both central auditory and vestibular function in the post-concussion workup is strongly recommended.

Hernandez and colleagues (2015) reported that callosal damage disturbs perceptual abilities; results in the traditional post-concussion symptoms of visual impairment, disorientation, and memory loss; and leads to decreases in performance on cognitive tasks and increases in reaction time. As visual impairments, disorientation, and disrupted perception are commonly experienced post-mTBI, it follows that the most common vestibular problems experienced post sport-related concussion are benign paroxysmal positional vertigo (BPPV), vestibulo-ocular reflex (VOR) impairment, visual motion sensitivity, and balance impairment, with visual motion sensitivity being the most common of the four problems (Mucha, Fedor, & Demarco, 2018).

Visual motion sensitivity, also known as visually induced dizziness, visual vertigo, visual-vestibular mismatch, or space-motion discomfort, is commonly experienced by individuals with chronic vestibular dysfunction and is rooted in an overreliance on visual inputs to maintain postural stability (Bronstein, 2004; Guerraz et al., 2001; Pavlou et al., 2006, 2011, 2013). It is provoked in full-field visual environments in which the visual stimuli are repetitive or in motion. Supermarket aisles, crowds, movie theaters, traffic, and riding in cars moving at constant speeds are commonly noted as particularly bothersome by patients with visual motion sensitivity (Bronstein, 2004; Bronstein et al., 2013).  Individuals who experience visual motion sensitivity report increased disorientation and sensations of being pulled in the direction of visual motion stimulation (e.g., full-field optokinetic stimulation) despite sitting or standing completely still (Becker-Bense et al., 2012; Bronstein et al., 2013; Dichgans & Brandt, 1978; Fushiki et al., 2005; Querner et al., 2002; Vitte et al., 1994).  Increased postural instability during and shortly after optokinetic visual motion stimulation has also been objectively documented in patients with visual motion sensitivity, with patients experiencing the sensitivityexhibiting longer sway path lengths than age-matched controls (Van Ombergen et al., 2016).

Studies utilizing positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and magnetoencephalography (MEG) have investigated cortical activation patterns during visually-induced self-motion perception (i.e., full-field optokinetic stimulation) in normal individuals, and results reveal significant activations of bilateral medial parieto-occipital visual areas, the intraparietal sulcus, and the striate and extrastriate visual cortex, including the visual motion sensitive area MT/V5 and the MST (Brodmann Areas19 and 37) in the temporo-occipital junction (Becker-Bense et al., 2012; Brandt et al., 1998; Deutschländer et al., 2008). Deactivations have also been reported in the posterior insula and parieto-insular multisensory vestibular cortices (PIVC) as well as in the posterior region of the superior temporal gyrus, inferior parietal lobule, anterior cingulate gyrus, hippocampus, and the corpus callosum (Becker-Bense et al., 2012; Brandt et al., 1998; Dieterich et al., 2003; Kikuchi et al., 2009; Kleinschmidt et al., 2002; Rommer et al., 2015).  Brandt and colleagues (1998) and Becker-Bense and colleagues (2012) reported that these excitatory visual and inhibitory vestibular activation patterns in normal individuals occur simultaneously, which is suggestive of a reciprocal interaction between the processing of visual and vestibular inputs. This reciprocal interaction, if functioning normally, would keep individuals from experiencing visual-vestibular mismatch and resulting inaccurate perceptions of self-motion with visual stimulation alone and with head motion. Damage resulting from concussion to any of these cortical areas just mentioned, including the corpus callosum, may contribute to the development of an imbalance in the simultaneous and reciprocal firing of excitatory and inhibitory neurons in this network, leading to the onset of visual motion sensitivity.

Due to the highly vestibular nature of the traditional post-concussion symptoms, the audiologist’s role in the evaluation of the concussed individual often involves obtaining an audiogram and the administration and interpretation of comprehensive diagnostic vestibular and balance assessments. However, given the significance of corpus callosum strain resulting from concussion, consideration should be given to the involvement of the corpus callosum in central auditory skills such as binaural integration, binaural separation, and temporal patterning/sequencing in addition to vestibular and balance function. Turgeon and colleagues’ (2011) investigation of central auditory processing function in participants with concussion using auditory closure, temporal patterning/sequencing, and dichotic listening tasks found that more than 50% of their participants demonstrated abnormal performance for at least one measure. Additionally, Bergemalm and Lyxell’s (2005) findings indicated that nearly 60% of participants who experienced a head injury seven to 11 years prior to participating in their study demonstrated central auditory processing deficits at the time of the study. Regarding vestibular and balance function, damage to the genu of the corpus callosum has been significantly associated with gait difficulty; damage to the rostrum, genu, and rostral body result in decreased bilateral motor coordination and transfer of visuomotor tasks; damage to the rostrum, posterior midbody, isthmus, and splenium has been associated with the classic presentation of a right ear advantage (REA) on verbal dichotic listening tasks; and damage to the splenium has been reported to lead to confusion, ataxia, dysarthria, seizure, headache, hemiparesis, increased muscle tone, and “verbal-visual disconnection” (Benavidez et al., 1999; Goldstein et al., 2019; Matsukawa et al., 2011; Park et al., 2017).

Due to the likelihood of callosal damage resulting in both central auditory and vestibular dysfunction, it is this author’s position that strong consideration should be given to pursuing a comprehensive neurodiagnostic audiology evaluation, including measures assessing both vestibular and central auditory processing function – beyond basic videonystagmography (VNG) and audiometric evaluations – for every individual encountered in the audiology clinic with a recent and previous history of concussion. Due to the risk of corpus callosum involvement with concussive events with and without loss of consciousness, every effort should be made to include measures targeting interhemispheric transfer of information and visual-vestibular mismatch in the assessment battery. As function may improve or degrade over time, monitoring of central auditory processing and vestibular and balance task performance over time is recommended.




  1. Becker-Bense, S., Buchholz, H., Eulenburg, P., Best, C., Bartenstein, P., Schreckenberger, M., & Dieterich, M. (2012). Ventral and dorsal streams processing visual motion perception (FDG-PET study). BMC Neurosci, 13(81), 1-13.
  2. Benavidez et al. (1999). Corpus callosum damage and interhemispheric transfer of information following closed head injury in children. Cortex, 35, 315-336.
  3. Bergemalm, P.O. & Lyxell, B. (2005). Appearances are deceptive? Long-term cognitive and central auditory sequelae from closed head injury. International Journal of Audiology, 44, 39-49.
  4. Brandt, T., Bartenstein, P., Janek, A., & Dieterich, M. (1998). Reciprocal inhibitory visual-vestibular interation: Visual motion stimulation deactivates the parieto-insular vestibular cortex. Brain, 268(11), 1569-1574.
  5. Bronstein, A.M. (2004) Vision and vertigo. J Neurol251(4), 381-387.
  6. Bronstein, A.M., Golding, J.F., & Gresty, M.A. (2013). Vertigo and dizziness from environmental motion: Visual vertigo, motion sickness, and drivers’ disorientation. Semin Neurol, 33(03), 219-230.
  7. Deutschländer, A., Hüfner, K., Kalla, R., Stephan, T., Dera, T., Glasauer, S., Wiesmann, M., Strupp, M., & Brandt, T.  (2008). Unilateral vestibular failure suppresses cortical visual motion processing. Brain, 131, 1025-1034.
  8. Dichgans, J., & Brandt, T. (1978). Visual-vestibular interaction: Effects on self-motion perception and postural control. In Perception (pp. 755-804). Springer Berlin Heidelberg
  9. Dieterich, M., Bense, S., Stephan, T., Yousry, T.A., & Brandt, T. (2003). fMRI signal increases in cortical areas during small-field optokinetic stimulation and central fixation. Exp Brain Res, 148(1), 117-127.
  10. Fushiki, H., Kobayashi, K., Asai, M., & Watanabe, Y. (2005). Influence of visually induced self-motion on postural stability. Acta Oto-laryngol, 125(1), 60-64.
  11. Goldstein, A., Covington, B.P., Mahabadi, N., & Mesfin, F.B. (2019). Neuroanatomy, corpus callosum. NCBI Bookshelf. Retrived from:
  12. Guerraz, M., Yardley, L., Bertholon, P., Pollak, L., Rudge, P., Gresty, M.A., & Bronstein, A.M. (2001). Visual vertigo: Symptom assessment, spatial orientation and postural control, Brain, 124(8), 1646-1656.
  13. Hernandez, F., Wu, L.C., Yip, M.C., Laksari, K., Hoffman, A.R., Lopez, J.R., Grant, G.A., Kleiven, S., & Camarillo, D.B. (2015). Six degree-of-freedom measurements of human traumatic brain injury. Annals of Biomedical Engineering, 43(8), 1918-1934.
  14. Kikuchi, M., Naito, Y., Senda, M., Okada, T., Shinohara, S., Fujiwara, K., Hori, S.Y., Tona, Y., & Yamazaki, H.  (2009). Cortical activation during optokinetic stimulation – an fMRI study. Acta Oto-Laryngol, 129(4), 440-443.
  15. Kleinschmidt, A., Thilo, K.V., Büchel, C., Gresty, M.A., Bronstein, A.M., & Frackowiak, R.S.J.  (2002). Neural correlates of visual-motion perception as object-or self-motion. Neuroimage, 16(4), 873-882.
  16. Kleiven, S. (2006). Evaluation of head injury criteria using a finite element model validated against experiments on localized brain motion, intracerebralacceleration, and intracranial pressure. International Journal of Crashworthiness, 11(1), 65-79.
  17. Laksari, K., Kurt, M., Babaee, H., Kleiven, S., Camarillo, D. (2018). Mechanistic insights into human brain impact dynamics through modal analysis. Physical Review Letters, 120(13), 1-7.
  18. Matsukawa, H. et al. (2011). Genu of corpus callosum in diffuse axonal injury induces a worse 1-year outcome in patients with traumatic brain injury. Acta Neurochir, 153, 1687-1694.
  19. Mucha, A., Fedor, S, & DeMarco, D. Vestibular dysfunction and concussion. Handbook of Clinical Neurology, 158(3), 135-144.
  20. Park et al. (2017). Splenial lesions of the corpus callosum: Disease spectrum and MRI findings. Korean J Radiol, 18(4), 710-721.
  21. Pavlou, M., Bronstein, A.M., & Davies, R.A. (2013). Randomized trial of supervised versus unsupervised optokinetic exercise in persons with peripheral vestibular disorders. Neurorehabilitation & Neural Repair, 27(3), 208-218.
  22. Pavlou, M., Davies, R.A., & Bronstein, A.M. (2006). The assessment of increased sensitivity to visual stimuli in patients with chronic dizziness. J Vestib Res, 16(4, 5), 223-231.
  23. Pavlou, M., Quinn, C., Murray, K., Spyridakou, C., Faldon, M., & Bronstein, A.M. (2011). The effect of repeated visual motion stimuli on visual dependence and postural control in normal subjects. Gait & Posture, 33(1), 113-118.
  24. Querner, V., Krafczyk, S., Dieterich, M., & Brandt, T. (2002). Phobic postural vertigo. Exp Brain Res, 143(3), 269-275.
  25. Rommer, P.S., Beisteiner, R., Elwischger, K., Auff, E., & Wiest, G. (2015). Neuromagnetic cortical activation during initiation of optokinetic nystagmus: An MEG pilot study. Audiol & Neurotol, 20(3), 189-194.
  26. Turgeon, C., Champoux, F., Lepore, F., Leclerc, S., & Ellemberg, D. (2011). Auditory processing after sport-related concussions. Ear & Hearing, 32, 667-670.
  27. Van Ombergen, A., Lubeck, A.J., Van Rompaey, V., Maes, K., Stins, J.F., Van de Heyning, P.H., Wuyts, F.L., & Bos, J.E. (2016). The effect of optokinetic stimulation on perceptual and postural symptoms in visual vestibular mismatch patients. PLoS ONE, 11(4), 1-18.
  28. Vitte, E., Sémont, A., & Berthoz, A. (1994). Repeated optokinetic stimulation in conditions of active standing facilitates recovery from vestibular deficits. Experimental Brain Research, 102, 141-148.

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