The anatomy of the membranous labyrinth within the vestibule has direct implications for surgical intervention. The anatomy of the otoliths has been studied, but there is limited information regarding their supporting connective tissue structures such as the membrana limitans in humans.

One guinea pig and 17 cadaveric human temporal bones were scanned using micro computed tomography, after staining with 2 per cent osmium tetroxide and preservation with Karnovsky's solution, with a resolution from 1 µm to 55 µm. The data were analysed using VGStudio Max software, rendered in three-dimensions and published in augmented reality.

In 50 per cent of ears, the membrana limitans attached directly to the postero-superior part of the stapes footplate. If attachments were present in one ear, they were present bilaterally in 100 per cent of cases.

Micro computed tomography imaging allowed three-dimensional assessment of the inner ear. Such assessments are important as they influence the surgical intervention and the evolution of future innovations.

Using American bullfrog models under normal conditions and under vestibular dysfunction, we investigated whether mechanical vibration applied to the ear could induce otoconial dislodgement.

Vibration was applied to the labyrinth of the bullfrog using a surgical drill. The time required for the otoconia to dislodge from the utricular macula was measured. Vestibular dysfunction models were created and the dislodgement time was compared with the normal models. The morphology of the utricular macula was also investigated.

In the normal models, the average time for otoconial dislodgement to occur was 7 min and 36 s; in the vestibular dysfunction models, it was 2 min and 11 s. Pathological investigation revealed that the sensory hairs of the utricle were reduced in number and that the sensory cells became atrophic in the vestibular dysfunction models.

The otoconia of the utricle were dislodged into the semicircular canal after applying vibration. The time to dislodgement was significantly shorter in the vestibular dysfunction models than in the normal models; the utricular macula sustained significant morphological damage.

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.