The vibration stimuli as well as sound stimuli that are used to elicit oVEMPs excite many structures — the cochlea, the otoliths, the semicircular canals, proprioceptive input, so there are many choices for input.
There is some evidence that these are utricular in origin. Curthoys et al (2016) reported in guinea pigs that both bone and air conducted inputs causes “phase locking” of afferents in both the utricle and saccule, and furthermore that this produces a limit on neural firing. Phase locking occurs up to 1500 for bone and 3000 for air, implying that guinea pig afferents can fire as high as 3000 spikes/second (thats very high !). On the other hand, phase locking at low frequencies (i.e. 100 hz) limits responses, presumably because afferents cannot fire less than about 100 spikes/sec. Fife et al (2017) stated that “it is not known whether oVEMP/cVEMP responses accurately identify vestibular function specifically related to the saccule/utricle”. We think this is fair, as of 2017. We have unproven claims.
Sound can excite the semicircular canals as well as the utricle, and does this especially so in SCD (superior canal dehiscence). The corallary is that sound (in disease states), could excite the superior canal, and cause a VOR in the vertical eye muscles — including the inferior rectus and inferior oblique. This means that the input AND output might be different in disease than in normal subjects.
If oVEMPS are indeed utricular, they should enter the brain through the superior vestibular nerve. If oVEMPS also have some saccule component, there could also be some input through the inferior vestibular nerve. Of course, if one considers the multiple other structures that can be activated by sound (i.e. the cochlea, the semicircular canals), or vibration (i.e. all of the above plus proprioceptors), there are a large number of potential generators for oVEMPS, that might vary according to whether one is working with a normal individual or a patient with pathology.
the ocular VEMPs (oVEMPs) reflect the function of the vestibular nuclei and the crossed vestibulo-ocular reflex (VOR) pathways, mostly contained in the medial longitudinal fasciculus (MLF). Therefore, lesions involving the vestibular nuclei can present abnormalities of both cVEMPs and oVEMPs. The medullary lesions involving the descending MLF or the spinal accessory nucleus impair cVEMPs. In contrast, the lesions involving the MLF, the crossed ventral tegmental tract, oculomotor nuclei and the interstitial nucleus of Cajal can impair oVEMPs.
he output system for oVEMPs is the surface EMG under the eyes. It is generally assumed that the output is the extraocular muscles. For the central signal to activate the extraocular muscles, it must traverse one or more of the oculomotor nerves (3,4,6), and the neuromuscular junction of the eye muscle (s). Logic would suggest that the inferior oblique muscle is the one that is being picked up by the usual electrode placement.
If sound were exciting other structures than the utricle, such as the superior semicircular canal (which happens), then one would expect that there would be vestibular ocular reflexes in all of the muscles measured by the oVEMP (i.e. inferior oblique, inferior rectus), and laterality would be gone as well. In other words, one could not depend on the left eye reflecting the output of the right utricle.
Other factors. The oVEMP is a tiny response and the person interpreting the test has a strong influence on oVEMP latency and amplitude . This is not the case for cVEMPs. This suggests that oVEMP studies could easily be affected by bias, and that ideally they should use blinded interpreters.