|Figure: cVEMP obtained in an individual with a profound right sensorineural hearing loss, using a Bio-Logic Navigator Pro. This shows that (sensorineural) hearing is not necessary to obtain a VEMP. This recording was obtained using binaural stimulation (see comments regarding this method).||Audiogram in person with the cVEMP shown to the right. There is a profound hearing loss, presumably sensorineural rather than mixed.|
Although it is common to assume that VEMPs are generated completely by the saccule (for cVEMPs) or utricle (for oVEMPs), this is a gross oversimplification. This assertion is based on the observation that in some patients, cVEMPs and oVEMPs can be obtained in people with complete hearing loss(Chihara et al, 2009). Logically, although hearing is not necessary for a VEMP, this does not prove that otolith input is sufficient for a VEMP. Nevertheless, as shown in the review of the literature below, the evidence is far from conclusive.
Furthemore, just because cVEMP's can be "obtained" it doesn't mean that they are uncorrelated with hearing loss, and in our experience, both hearing and vestibular function correlate with cVEMP amplitude. However, this conclusion is not (so far) well documented in the literature.
Wu and Young (2002) reported that after sudden deafness, there was no significant difference between the cVEMP amplitudes on the deaf side compared to the intact side. This would imply that the portion of the VEMP that can be attributed to auditory input is relatively small. On the other hand, Hong et al (2008) did find more abnormal VEMPs in patients with profound sudden hearing loss than less severe hearing loss. This suggests the opposite conclusion. Iwasaki et al (2005) compared acoustic to galvanic VEMPs in patients with SHL and vertigo. Galvanic responses were normal in patients with SHL, while acoustic were absent in 17/22. This finding conflicts with the others reviewed above. As galvanic VEMPs are difficult to obtain due to current spread, perhaps this was a technical problem. Korres et al (2011) found abnormal VEMPs in about 1/3 of patients with SHL. Again, results that conflict with other studies.
Fujimoto et al (2015) found abnormal oVEMPs in 43% of patients with SHL. We find this puzzling.
Overall, these papers are "all over the place", and a larger more definitive study would be welcome.
Figure: VEMP obtained in an individual with a modest left sided conductive hearing loss, using a Bio-Logic Navigator Pro. The VEMP on the right was normal, and the VEMP on the left, entirely absent. P1 designates the potential that occurs at 13 msec (often called P13)
Persons with conductive hearing loss, even just a small amount such as 10-15 dB, often do not have air conducted cVEMPs, presumably because the sound stimulus, conventionally delivered by earphones, does not get to the saccule. The saccule has a high threshold, and if you are stimulating the ear close to that threshold (i.e. 95 dB), it is easy to drop below it.
VEMPs are reduced in middle ear effusion (Wang and Lee, 2007)
Thus in otosclerosis, air conducted cVEMPs should be absent, but sometimes are found in early otosclerosis (Yang and Young, 2007) .This means that cVEMPs are less useful in older persons, who often have a component of conductive hearing loss due to otosclerosis and related disorders, and also should be interpreted with a recent audiogram, including bone and air conduction testing, in hand. A way around this may be to do bone-conduction cVEMPs when the air-conduction cVEMP is absent. While this substitutes for the bone conduction audiogram, it requires more testing and potentially may fatigue the patient. Also, bone-conduction stimuli are generally not very strong.
A person with a present air conducted VEMP and conductive hearing loss may have SCD. Here the "conductive hearing loss" is actually a conductive hyperacusis superimposed on a sensorineural hearing loss.
Noise induced hearing loss is easy to diagnose from the typical "Noise notch" at about 4K.
Several groups (Wang and Young, 2007; Akin et al, 2012) reported that cVEMP's are reduced in persons with noise induced hearing loss. They attributed this effect to saccule damage. While theoretically possible, we are dubious that a structure that requires 70db to elicit a minimal response would be very sensitive to noise. The saccule would more reasonably be damaged by excessive changes in linear acceleration as it is loaded by the otoconia.
VEMPs are reduced by acute acoustic trauma (Wang et al, 2006). One would conjecture that this might be due to hearing loss or saccule damage or both.
Instead our opinion is that there simply is reduction of air conducted VEMP's from hearing reduction. Similarly, Zhou, Kenna, Stevens and Licameli (2008) reported cVEMP's are reduced in children with sensorineural hearing loss, and attributed this effect to saccule damage. We think that these authors made the same logical error as Wang and Young.
It is well established (and logical) that VEMPs are reduced by conductive hearing loss.
More data is needed concerning how much auditory input contributes to VEMP responses.