This study aimed to characterise the ipsilateral, contralateral and bilateral masseter vestibular-evoked myogenic potential using clicks and 500 Hz tone burst stimuli in healthy adults.

Masseter vestibular-evoked myogenic potential was recorded from 20 healthy participants aged 19–28 years (11 males and 9 females). Masseter vestibular-evoked myogenic potential was recorded using 500 Hz tone burst and click stimuli in ipsilateral, contralateral and bilateral modes.

A statistically significant difference was observed between ipsilateral and contralateral stimulation for p11 latency, n21 latency and p11-n21 amplitude for both click and 500 Hz tone burst stimuli. The amplitude of the p11-n21 complex was higher for ipsilateral, contralateral and bilateral stimulations for 500 Hz tone burst than for click stimulus.

This study showed a significant difference for p11-n21 amplitude between click and 500 Hz tone burst evoked masseter vestibular-evoked myogenic potential. In addition, bilateral stimulation elicited a larger response than ipsilateral and contralateral stimulation.

To describe a case of asymptomatic superior semicircular canal dehiscence.

Clinical case report.

A 50-year-old man presenting with right-sided Ménière´s disease also showed an enhanced response on vestibular evoked myogenic potential testing for the left ear. Unilateral left-sided superior semicircular canal bone dehiscence was clearly visualised on a subsequent temporal bone computed tomography scan. These findings were consistent with superior canal dehiscence syndrome. However, the patient did not complain of any specific superior canal dehiscence syndrome symptoms. Given that vestibular evoked myogenic potential testing may detect asymptomatic forms of superior canal dehiscence, as noted in this case, such testing seems to exhibit reduced specificity for superior canal dehiscence syndrome.

An enhanced response on vestibular evoked myogenic potential testing in isolation appears to be a weaker indicator of superior canal dehiscence syndrome, and rather a marker of superior semicircular canal dehiscence.

Limited data are available on the effects of otosclerosis and otosclerosis surgery on the utricle and saccule. This study aimed to determine the effect of otosclerosis and stapedotomy on vestibular-evoked myogenic potentials.

This retrospective study included 16 otosclerosis patients and 18 controls. Thirty-two ears of 16 patients with otosclerosis were divided into 2 groups based on whether the ear had been operated on or not. All patients and subjects underwent 500 Hz air- and bone-conducted ocular and cervical vestibular-evoked myogenic potentials testing.

Overall comparison of response rates showed a significant difference among the groups. Further statistical tests showed that this difference arose from differences between both operated and unoperated groups and the control group, for air-conducted cervical and ocular vestibular-evoked myogenic potentials.

Otosclerosis and stapedotomy may affect the elicitability of vestibular-evoked myogenic potentials. Otosclerosis is associated with lower response rates for air-conducted ocular and cervical vestibular-evoked myogenic potentials, regardless of whether operated on. Having been operated on does not significantly increase the response rate of air-conducted vestibular-evoked myogenic potentials.

Individuals with superior semi-circular canal syndrome often describe vestibular symptoms elicited by loud sounds, as well as other pressure-induced symptoms. They also often report other symptoms, including autophony, hyperacusis, cognitive dysfunction, spatial disorientation, anxiety and migraine headaches. Symptoms occur due to the presence of a ‘third window’ created by the dehiscence of the superior semi-circular canal. This case report describes a minimally invasive technique to provide soft reinforcement of the round window.

Our patient underwent a permeatal procedure whereby the tympanic membrane was raised to allow inspection of the middle ear. The round window niche was identified and the round window membrane was reinforced with fat. The mucosa of the bony meatus leading to the round window was then disrupted before the application of a double layer of perichondrium to allow further reinforcement.

The case provides support for the use of ‘soft reinforcement’ as a simple and effective technique to treat the symptoms of superior canal dehiscence syndrome.

Several studies have reported that the audiovestibular system is affected in patients with chronic kidney disease.

This study aimed to investigate how the audiovestibular system is affected in patients with various stages of chronic kidney disease.

Sixty participants were divided into three groups: group 1 – controls; group 2 – chronic kidney disease patients receiving conservative treatment; and group 3 – chronic kidney disease patients undergoing regular haemodialysis. Assessments included: standard and high-frequency audiometry and otoacoustic emissions testing, oculomotor tests, and combined vestibular-evoked myogenic potentials testing.

Fifty per cent of group 2 and 60 per cent of group 3 had bilateral sensorineural hearing loss. High-frequency pure tone audiometry showed reduced detectability and higher thresholds at 12 kHz and 16 kHz in patients than in controls. Otoacoustic emissions, tracking, optokinetic and combined vestibular-evoked myogenic potential tests showed abnormal results in chronic kidney disease cases.

Both the auditory and vestibular pathways are affected in different stages of chronic kidney disease. High-frequency pure tone audiometry, otoacoustic emissions and combined vestibular-evoked myogenic potentials could be performed routinely in patients with chronic kidney disease, regardless of the disease stage.

This paper discusses our technique of carrying out cervical and ocular vestibular-evoked myogenic potential testing in a single position. The described technique allows for a symmetrical, natural flexion of the neck muscles, which is helpful as many of our patients have suffered traumatic deceleration injures.

Patients with suspected vestibular pathology referred by specialists were sequentially assessed in a tertiary referral neuro-otology unit within a teaching hospital using our technique and our previously established normative database. All patients underwent standardised vestibular assessment in addition to cervical and ocular vestibular-evoked myogenic potential assessment. Our normative data are in keeping with that reported by other centres.

Many of the patients had abnormal vestibular-evoked myogenic potentials, which is in line with a history suggesting otolithic disease.

Both cervical and ocular vestibular-evoked myogenic potentials offer several parameters for detecting abnormalities. The technique reported enables us to assess patients in an accurate fashion whether or not they have suffered traumatic neck injuries.

Otolithic function is poorly understood, but vestibular-evoked myogenic potential testing has allowed the documentation of pathology in patients who complain of imbalance.

Seventy-four patients with traumatic and non-traumatic vestibular disease were sequentially assessed at a tertiary referral neuro-otology unit in a teaching hospital. A detailed history of all patients was taken and standard vestibular assessment was conducted using the technique described in the companion paper. The results of both groups of patients were analysed and the rate of abnormalities was assessed.

There was a high rate of abnormalities, including bilateral pathology, in a significant number of patients. Many patients in both groups inexplicably failed to recover.

Vestibular-evoked myogenic potentials are helpful in documenting pathology, including bilateral pathology, which is outlined in the literature as being exceedingly difficult to compensate for.

This study aimed to evaluate the presence of the N3 potential (acoustically evoked short latency negative response) in profound sensorineural hearing loss, its association with the cervical vestibular evoked myogenic potential and the relationship between both potentials and loss of auditory function.

Otological examinations of 66 ears from 50 patients aged from 4 to 36 years were performed, and the vestibular evoked myogenic potential and auditory brainstem response were measured.

The N3 potential was recorded in 36 out of 66 ears (55 per cent) and a vestibular evoked myogenic potential was recorded in 34 (52 per cent). The N3 potential was recorded in 23 out of 34 ears (68 per cent) with a vestibular evoked myogenic potential response and absent in 19 out of 32 ears (59 per cent) without a vestibular evoked myogenic potential response. The presence of an N3 potential was significantly associated with a vestibular evoked myogenic potential response (p = 0.028), but there was no significant difference in the latency or amplitude of the N3 potential in either the presence or absence of a vestibular evoked myogenic potential.

The presence of an N3 potential in profound sensorineural hearing loss with good or poor vestibular function can be explained by the contribution of the efferent cochlear pathway through olivocochlear fibres that join the inferior vestibular nerve. This theory is supported by its early latency and reversed polarity, which is masked in normal hearing by auditory brainstem response waves.

This study aimed to define the characteristics and use of ocular and cervical vestibular evoked myogenic potentials for evaluating paediatric cochlear implant candidates.

Ocular and cervical vestibular evoked myogenic potentials of 34 paediatric cochlear implant candidates were analysed. All patients also underwent a routine audiological examination, including computed tomography.

In all, 27 patients with normal inner-ear structures had absent or impaired vestibular evoked myogenic potential responses. In paediatric candidates with inner-ear malformations, ocular and cervical vestibular evoked myogenic potentials had lower thresholds and higher amplitudes. Vestibular evoked myogenic potential responses in this cohort were classified into three groups. There was significant concordance between vestibular evoked myogenic potentials and temporal bone computed tomography findings.

Ocular and cervical vestibular evoked myogenic potential waveforms were different in paediatric candidates with normal and abnormal inner-ear structures. Therefore, vestibular evoked myogenic potential responses can indicate temporal bone structure.

To study the possible damage to the vestibular system in patients with post-mumps sensorineural hearing loss.

Nineteen patients with recent mumps infection participated in the study. All patients had unilateral profound sensorineural hearing loss or total hearing loss. Patients were subjected to video-nystagmography and vestibular-evoked myogenic potential testing.

Eight patients (42.1 per cent) had normal video-nystagmography results and intact vestibular-evoked myogenic potentials on both sides, whereas the other 11 patients (57.9 per cent) had vestibular lesions in the form of marked canal weakness and absent vestibular-evoked myogenic potential responses on the same side as hearing loss. The overall findings indicated a peripheral site for the lesions.

The majority of patients with post-mumps sensorineural hearing loss had peripheral vestibular pathology in the same ear as hearing loss. Further research should be directed to saving the inner ear following mumps infection.

This study aimed to review the current advances in superior semicircular canal dehiscence syndrome and to ascertain its aetiology, whether dehiscence size correlates with symptoms, signs and investigation results, the best investigations, and its surgical management.

A literature search using the key words ‘superior semicircular canal dehiscence’ was performed using the Allied and Complementary Medicine Database and the Embase, Health Management Information Consortium, Medline, PsycINFO, British Nursing Index, Cinahl and Health Business Elite databases for the period January 2009 to May 2014. Systematic reviews, meta-analyses, randomised controlled trials, prospective and retrospective case series, case reports, and observational studies were included.

Of the 205 papers identified, 35 were considered relevant.

The aetiology of superior semicircular canal dehiscence syndrome is unclear. Dehiscence size significantly affects the air–bone gap and ocular vestibular evoked myogenic potential thresholds. Computed tomography evaluation has a high false positive rate. The middle cranial fossa approach is the surgical standard for treating this syndrome; however, the transmastoid approach is gaining popularity.

This study compared vestibulocollic reflex and vestibulo-ocular reflex functioning in subjects with and without human immunodeficiency virus. It also described test results throughout progression of the disease and compared the results of human immunodeficiency virus positive subjects who were receiving antiretroviral therapies with those not receiving this treatment.

Subjects comprised 53 adults with human immunodeficiency virus (mean age 38.5 ± 4.4 years) and 38 without human immunodeficiency virus (mean age 36.9 ± 8.2 years). Clinical examinations included cervical vestibular-evoked myogenic potential and bithermal caloric testing.

Abnormal cervical vestibular-evoked myogenic potential and caloric results were significantly higher in the human immunodeficiency virus positive group (p = 0.001), with an odds ratio of 10.2. Vestibulocollic reflex and vestibulo-ocular reflex involvement increased with progression of the disease. There were more abnormal test results in subjects receiving antiretroviral therapies (66.7 per cent) than in those not receiving antiretroviral therapies (63.6 per cent), but this difference was insignificant.

Human immunodeficiency virus seems to influence vestibulocollic reflex pathways. Combining cervical vestibular-evoked myogenic potential and caloric testing may be useful to detect early neurological involvement in human immunodeficiency virus positive subjects.

To describe a case of bilateral superior and posterior semicircular canal dehiscences, and the use of a unilateral transmastoid approach to address both right-sided defects simultaneously.

In a patient with right-sided hyperacusis, bilateral dehiscence of both the superior and the posterior semicircular canals was identified, located adjacent to the common crus, together with a right-sided, anterosuperiorly positioned sigmoid sinus and a high-riding jugular bulb. Results for audiography and cervical vestibular evoked myogenic potential testing were consistent with right-sided semicircular canal dehiscence. At surgery, a right-sided transmastoid approach provided access to plug both defects simultaneously, following posterior mobilisation of the sigmoid sinus. The patient's hyperacusis was completely resolved, with a 10–30 dB improvement in his right ear air conduction hearing, without decrement in bone conduction.

In properly selected patients, a transmastoid approach can be used to effectively manage superior semicircular canal dehiscence and posterior semicircular canal dehiscence simultaneously. Pre-operative computed tomography is recommended to evaluate the dehiscence sites and to identify complicating vascular anatomy.

To analyse cervical vestibular evoked myogenic potential response parameters in normal volunteers and vertiginous patients.

A prospective study of 50 normal subjects and 50 patients with vertigo was conducted at Chiang Mai University Hospital, Thailand. Cervical vestibular evoked myogenic potential responses were measured using air-conducted, 500-Hz, tone-burst stimuli with subjects in a sitting position with their head turned toward the contralateral shoulder.

The mean ± standard deviation age and male:female ratio in the normal (44.0 ± 9.3 years; 12:38) and vertigo groups (44.7 ± 9.8 years; 17:33) were not significantly different. The prevalence of absent responses in the normal (14 per cent) and vertigo ears (46 per cent) differed significantly (p < 0.0001). Other cervical vestibular evoked myogenic potential parameters (i.e. response threshold, P1 and N1 latency, P1–N1 interlatency and interamplitude, inter-ear difference in P1 threshold, and asymmetry ratio) showed no inter-group differences.

The absence of a cervical vestibular evoked myogenic potential response is useful in the identification of vestibular dysfunction. However, patients should undergo a comprehensive battery of other vestibular tests to supplement their cervical vestibular evoked myogenic potential response findings.

The vestibulocochlear nerve is a sensory nerve that serves the organs of hearing and equilibrium. Neuropathies of the nerve, particularly auditory neuropathy, may be caused by primary demyelination or axonal disease. Cochlear amplification function is normal in cases of auditory neuropathy, but afferent neural conduction in the auditory pathway is disordered. It is highly probable that the vestibular nerve has some involvement in disorders affecting the cochlear nerve.

To provide an overview of vestibular test findings in individuals with auditory neuropathy.

A structured literature search was carried out, with no restrictions to the dates searched.

Auditory neuropathy implicated the vestibular branch of the VIIIth cranial nerve as well as the cochlear nerve. However, there was variability in terms of vestibular test findings.

Previous evidence shows that the n10 component of the ocular vestibular evoked myogenic potential indicates utricular function, while the p13 component of the cervical vestibular evoked myogenic potential indicates saccular function. This study aimed to assess the possibility of differential utricular and saccular function testing in the clinic, and whether loss of saccular function affects utricular response.

Following vibration conduction from the mid-forehead at the hairline, the ocular n10 component was recorded by surface electromyograph electrodes beneath both eyes, while the cervical p13–n23 component was recorded by surface electrodes over the tensed sternocleidomastoid muscles.

Fifty-nine patients were diagnosed with probable inferior vestibular neuritis, as their cervical p13–n23 component was asymmetrical (i.e. reduced or absent on the ipsilesional side), while their ocular n10 component was symmetrical (i.e. normal beneath the contralesional eye).

The sense organ responsible for the cervical and the ocular vestibular evoked myogenic potentials cannot be the same, as one response was normal while the other was not. Reduced or absent saccular function has no detectable effect on the ocular n10 component. On vibration stimulation, the ocular n10 component indicates utricular function and the cervical p13–n23 component indicates saccular function.

Vestibular evoked myogenic potentials are short latency electrical impulses that are produced in response to higher level acoustic stimuli. They are used clinically to diagnose sacculocollic pathway dysfunction.

This study aimed to compare the vestibular evoked myogenic potential responses elicited by click stimuli and short duration tone burst stimuli, in normal hearing individuals.

Seventeen subjects participated. In all subjects, we assessed vestibular evoked myogenic potentials elicited by click and short duration tone burst stimuli.

The latency of the vestibular evoked myogenic potential responses (i.e. the p13 and n23 peaks) was longer for tone burst stimuli compared with click stimuli. The amplitude of the p13–n23 waveform was greater for tone burst stimuli than click stimuli. Thus, the click stimulus may be preferable for clinical assessment and identification of abnormalities as this stimulus has less variability, while a low frequency tone burst stimulus may be preferable when assessing the presence or absence of vestibular evoked myogenic potential responses.