OBJECTIVES: Traumatic brain injury occurs frequently worldwide. Half of traumatic brain injuries are related to falls or motor vehicle accidents. The term “concussion” is often used to describe a minor form of traumatic brain injury. These often involve decelerative events to the head (e.g., flexion/extension injury) and can also cause damage to the vestibular system of the inner ear. MATERIALS AND METHODS: The European Society for Clinical Evaluation of Balance Disorders meets yearly and has proposed an investigation and analysis of the vestibular consequences of traumatic brain injury. This review paper outlines these discussions. RESULTS: The Society discussed all aspects of trauma-induced vestibular disorders along with diagnosis and management. They also assessed the diagnostic tests available to investigate these disorders. CONCLUSION: Trauma-induced vestibular disorders are difficult to manage, as our level of understanding of the pathology can be poor and anatomical localization can also be difficult. Accordingly, a definitive diagnosis cannot be pinpointed in many patients, but an extensive history taking is crucial to determine the nature and extent of vestibular involvement. Trauma can not only result in microtrauma to the central nervous system but can also significantly affect peripheral vestibular structures, particularly the otolith organs. The committee hopes that better understanding of trauma to the vestibular system, along with improvements in the field of radiology and vestibular assessments, will aid in more precise techniques of pinpointing pathology in order to develop an adapted treatment plan. Cite this article as: Mallinson A, Maire R, Beyaert C, et al. Understanding and managing trauma induced vestibular deficits. J Int Adv Otol. 2021;17(6):559-565.

Nystagmus produced in response to air-conducted sound (ACS) stimulation—the Tullio phenomenon—is well known in patients with a semicircular canal (SCC) dehiscence (SCD). Here we consider the evidence that bone-conducted vibration (BCV) is also an effective stimulus for generating the Tullio phenomenon. We relate the clinical evidence based on clinical data extracted from literature to the recent evidence about the physical mechanism by which BCV may cause this nystagmus and the neural evidence confirming the likely mechanism. The hypothetical physical mechanism by which BCV activates SCC afferent neurons in SCD patients is that traveling waves are generated in the endolymph, initiated at the site of the dehiscence. We contend that the nystagmus and symptoms observed after cranial BCV in SCD patients is a variant of Skull Vibration Induced Nystagmus (SVIN) used to identify unilateral vestibular loss (uVL) with the major difference being that in uVL the nystagmus beats away from the affected ear whereas in Tullio to BCV the nystagmus beats usually toward the affected ear with the SCD. We suggest that the cause of this difference is a cycle-by-cycle activation of SCC afferents from the remaining ear, which are not canceled centrally by simultaneous afferent input from the opposite ear, because of its reduced or absent function in uVL. In the Tullio phenomenon, this cycle-by-cycle neural activation is complemented by fluid streaming and thus cupula deflection caused by the repeated compression of each cycle of the stimuli. In this way, the Tullio phenomenon to BCV is a version of skull vibration-induced nystagmus.

The third window syndrome, often associated with the Tullio phenomenon, is currently most often observed in patients with a superior semicircular-canal dehiscence (SCD) but is not specific to this pathology. Clinical and vestibular tests suggestive of this pathology are not always concomitantly observed and have been recently complemented by the skull-vibration-induced nystagmus test, which constitutes a bone-conducted Tullio phenomenon (BCTP). The aim of this work was to collect from the literature the insights given by this bedside test performed with bone-conducted stimulations in SCD. The PRISMA guidelines were used, and 10 publications were included and analyzed. Skull vibration-induced nystagmus (SVIN), as observed in 55 to 100% of SCD patients, usually signals SCD with greater sensitivity than the air-conducted Tullio phenomenon (ACTP) or the Hennebert sign. The SVIN direction when the test is performed on the vertex location at 100 Hz is most often ipsilaterally beating in 82% of cases for the horizontal and torsional components and down-beating for the vertical component. Vertex stimulations are more efficient than mastoid stimulations at 100 Hz but are equivalent at higher frequencies. SVIN efficiency may depend on stimulus location, order, and duration. In SCD, SVIN frequency sensitivity is extended toward high frequencies, with around 400 Hz being optimal. SVIN direction may depend in 25% on stimulus frequency and in 50% on stimulus location. Mastoid stimulations show frequently diverging results following the side of stimulation. An after-nystagmus observed in 25% of cases can be interpreted in light of recent physiological data showing two modes of activation: (1) cycle-by-cycle phase-locked activation of action potentials in SCC afferents with irregular resting discharge; (2) cupula deflection by fluid streaming caused by the travelling waves of fluid displacement initiated by sound or vibration at the point of the dehiscence. The SVIN direction and intensity may result from these two mechanisms’ competition. This instability explains the SVIN variability following stimulus location and frequency observed in some patients but also discrepancies between investigators. SVIN is a recent useful insight among other bedside examination tests for the diagnosis of SCD in clinical practice.

Background: Our primary objective was to monitor nonprogressive unilateral vestibular schwannomas (VSs) to assess the efficiency of rapid bedside examinations, such as the video head impulse test (vHIT) and skull vibration-induced nystagmus test (SVINT), in identifying vestibular damage. Methods: An observational study was conducted from March 2021 to March 2022 on all adult patients (>18 years old) with a confirmed nonprogressive VS (no active treatment). The SVINT (using a 100 Hz vibrator with two (SVINT2) or three (SVINT3) stimulation locations) and vHIT (for the six semicircular canals (SCCs)) were performed on all patients. The asymmetry of function between the vestibules was considered significant when the gain asymmetry was greater than 0.1. Rapid and repeatable assessment of VSs using two- and three-stimulation SVINT plus vHIT was performed to quantify intervestibular asymmetry. Results: SVINT3 and SVINT2 triggered VIN in 40% (24/60) and 65% (39/60) of patients, respectively. There was significant asymmetry in the vestibulo-ocular reflex (VOR), as shown by a VS-side gain < healthy-side gain in 58% (35/60) of the patients. Among the patients with significant gain asymmetry between the two vestibules according to the vHIT (VS-side gain < healthy-side gain), the proportion of patients expressing vestibular symptomatology was significantly greater than that of patients without any symptoms [67% (29/43) vs. 35% (6/17), respectively; p = 0.047]. Conclusions: The SVINT2 can be combined with the vHIT to form an interesting screening tool for revealing vestibular asymmetry. This work revealed the superiority of mastoid stimulation over vertex stimulation for SVINT in patients with unilateral vestibular loss.

Background: To establish in patients with peripheral vestibular disorders relations between skull vibration-induced nystagmus (SVIN) different components (horizontal, vertical, torsional) and the results of different structurally related vestibular tests. Methods: SVIN test, canal vestibular test (CVT: caloric test + video head impulse test: VHIT), otolithic vestibular test (OVT: ocular vestibular evoked myogenic potential oVEMP + cervical vestibular evoked myogenic potential cVEMP) performed on the same day in 52 patients with peripheral vestibular diseases (age < 65 years), and 11 control patients were analyzed. Mixed effects logistic regression analysis was performed to assert whether the presence of nystagmus in SVIN (3D analysis) have an association with the presence of peripheral vestibular dysfunction measured by vestibular explorations (CVT or OVT). Results: We obtained different groups: Group-Co (control group), Group-VNT (dizzy patients with no vestibular tests alterations), Group-O (OVT alterations only), Group-C (CVT alterations only), Group-M (mixed alterations). SVIN-SPV horizontal component was significantly higher in Group-M than in the other groups (p = 0.005) and correlated with alterations of lateral-VHIT (p < 0.001), caloric test (p = 0.002) and oVEMP (p = 0.006). SVIN-SPV vertical component was correlated with the anterior-VHIT and oVEMP alterations (p = 0.007; p = 0.017, respectively). SVIN-SPV torsional component was correlated with the anterior-VHIT positivity (p = 0.017). SVIN was the only positive test for 10% of patients (83% of Group-VNT). Conclusion: SVIN-SPV analysis in dizzy patients shows significant correlation to both CVT and OVT. SVIN horizontal component is mainly relevant to both vestibular tests exploring lateral canal and utricle responses. SVIN-SPV is significantly higher in patients with combined canal and otolith lesions. In some patients with dizziness, SVIN may be the only positive test.