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There is an interesting interaction between newborn hearing screening programs (which typically use OAE), and AN. Where we practice in Chicago, AN is not a common diagnosis, even though some authors report a prevalence as high as 27% of AN in hearing loss in 10-12 year olds.
Another problem with AN case finding is the vulnerability of the definition to diagnostic error.
A third problem with AN is that it is just implausible that there should be selective nerve damage to the hearing part of the 8th nerve, without damage to the vestibular part as well.
To summarize this section, there are significant questions about the definition, existence and prevalence of AN. Logically, the diagnostic process might not necessarily prove that the site of lesion is the auditory nerve. McMahon and others pointed out that a brainstem disorder could also cause similar testing pattern as that said to be diagnostic of an auditory neuropathy (2008).
In the authors opinion, in adult patients diagnosed with AN, a more generalized peripheral neuropathy should be considered including testing for the more common treatable types of neuropathy (i.e. One would expect that other heavy metals might also cause neurotoxicity (such as arsenic or lead).
One would expect that cochlear implants (CI)would be useless for AN caused by cochlear nerve damage (or absence), but potentially useful for AN caused by cochlear damage. Ji et al, reported that only a single one of their 8 implanted subjects attained speech capability (2015). Budenz et al (2013) reported that "Children with a diagnosis of AN without associated cognitive or developmental disorders have speech and language outcomes comparable to other children who received a CI. Can et al (2015) reported that 2% of late preterms with hyperbilirubinemia had AN (same as controls).
Gibson and Sanli (2007) studied 39 children with auditory neuropathy and concluded that the more likely mechanism was selective loss of inner hair cells. Zong et al (2015) reported a mutation in a family containing variation in a gene termed AIFM1. Lepcha et al (2015) reported that ANS occurred in 1.12% of patients in an Indian ENT clinic. Morelet et al (2014) reported a group of 9 Amish persons, who were interrelated, with a mutation in SLITRK6, who had a syndrome with some aspects of AN. As the stapes push back and forth against the cochlea, the fluid is compressed, producing waves in the fluid-filled compartments.
Cochlear implant —a surgically implanted device behind the ear on the temporal bone provides sound to a person with severe or profound sensorineural hearing loss.
Many cases of sensorineural hearing loss can be prevented by avoiding sustained incidences of loud noises.
Hearing loss in the presence of Hansen’s disease may or may not be the result of the disease itself. Evaluation of audiovestibular function was also carried out in 50 fresh cases of leprosy and after 3 months, 6 months and 1 year of multidrug therapy to ascertain any ototoxic side effects of antileprosy drugs. In the most complete study available of hearing loss in patients diagnosed with Hansen’s disease, Rawlani et al (2013) performed audiometry and tuning fork testing on test subjects and normal controls. The study found that the incidence of hearing loss was significantly higher in test subjects than controls. Until proven otherwise, it seems wise to assume that sensorineural hearing loss can be caused by the leprosy bacilli in some cases.


And to the bulk of Audiologists, all hearing losses without air-bone gaps are sensorineural. No surprise, then, that assessments of auditory effects of Hansen’s disease are confusing when it comes to establishing site of lesion.
Next post examines the scant and conflicting literature on putative origins of leprosy-caused sensorineural hearing losses:  cochlear, peripheral and central. A related acronym, ANSD -- auditory neuropathy spectrum disorder -- is a less well defined version of AN.
On the other hand, it may be that the AN syndrome is just so imprecise that there is little clinical attention devoted to it and it deserves to remain obscure.
One would expect that AN would be always missed in these programs, because AN is defined by present OAEs.
Of course, the logical defense to this is that diagnostic methods for vestibular function are missing vestibular nerve damage.
Gibson and Sanli recently pointed out that a selective loss of inner hair cells might create a similar testing configuration (2007). This seems possible to us, but unlikely in the absence of imaging or clinical findings supporting a brainstem disorder.
Somewhat contrary to this idea that nerve disease can be detected with a VEMP is the observation that VEMPs are generally normal in vestibular neuritis.
This is not a common observation however, and of course, steroids are not a practical long term treatment.
If a child grows up with no hearing, they may not develop the central circuitry to hear (or it may die off). On the other hand, Fernandez et al (2015), from Brazil, reported that An patients had similar response to CI as children with CI. Our comment -- is the huge cost of CI justified by "at least partial measurable auditory benefit" ?
Tang et al (2015) reported no coherent genetic anomaly in 71 patients including some with AN. They had progressive hearing gloss, were nearsighted, had no DPOAE's (of course AN should have present OAE's), and had poor ABR's.
Frequency-Specific Electrocochleography Indicates that Presynaptic and Postsynaptic Mechanisms of Auditory Neuropathy Exist.
The inner ear, or labyrinth, is comprised of hearing (auditory) and balance (vestibular) areas of the auditory system. The waves create electrical impulses that travel through the cochlear nerve to the brain, then are translated into sound. When working in a factory where loud machines are used, wearing hearing protection devices can prevent hearing loss. No audiovestibular dysfunction was detected in these patients at any time during follow-up. Purely neural, non-congenital hearing loss in the absence of eighth nerve tumor is a rare and therefore unexpected entity in clinic. In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page. Some reports find cochlear aplasia -- a small cochlear nerve or bony aperture for the cochlear nerve (Jeong et al, 2013).
Ascertainment of hearing thresholds is intrinsically subjective -- if you don't admit to hearing the tones -- you fail the test.


Of course, in neonates with brain damage associated with a premature or rough delivery, this might be more likely. As AN patients are almost all children, perhaps there should be an aggressive attempt to implant very young children. This is easy to understand -- if there is no nerve to transmit hearing signals to the brain, a CI is wasted money and effort. The cochlea (auditory) converts vibrations into electrical signals by the use of specialized hair cells. This process, known as transduction, is performed by specialized sensory cells within the cochlea. This group, lacking the wiring for hearing, would be expected to do very poorly concerning acquisition of hearing. Otherwise, it would be very puzzling how a disorder of the 8th nerve could selectively damage the auditory portion or vestibular portion as the two parts of the nerve are extremely close and one would think that the same process that damages one would also damage the other. With different investigators setting their criteria for AN differently -- perhaps this is why we have such wide variation.
So in other words, a combination of normal OAE, very abnormal ABR (only a wave 1 or a present cochlear potential on ECOG, and very impaired conventional hearing testing given that it can be performed at all, given that one can believe the results, would seem somewhat (not definitely) likely to identify an auditory nerve disorder. This is a thorny issue, made worse by the fuzziness if the definition of AN or ANSD as you prefer. If one has a vaguely defined ANSD, that could include inner hair cell damage, one could argue that there might be a reason to give it a try. Degree of hearing loss varied from mild (43%) to moderate (43%) to moderately-severe (9%)  or severe(4%).
The Auditory Nerve:Sensorineural hearing loss, or nerve deafness, is a dysfunction of the cochlea, as opposed to the auditory nerve itself. Jeong et al (2013) reported patients with radiologic abnormalities of their cochlear nerve did much worse concerning CI response. It would be very easy to combine a normal OAE (which doesn't require any cooperation),with several tests that are greatly impaired by lack of cooperation (such as ABR), and diagnose AN.
This use of words is similar to saying that ALS (motor neuron disease) was a subtype of peripheral neuropathy. The auditory and vestibular nerves carry balance information from the semicircular canals to the brain. If AN is truly a neuropathy, one would think that AN should increase with age as do neuropathies in general.
Background noise poses the greatest difficulty that people who are hard of hearing have to contend with.
It does not eradicate background noise the way a normal working auditory system can, however, background noise can be suppressed. Of course, the logical defense to the assertion that AN is an artifact of uncooperative patients is that everybody else is doing bad testing. When sound waves enter the ear canal, a chemical is released, called a neurotransmitter, in the inner ear, which in turn sends this message to the brain. Sudden loud sounds, such as the deployment of an airbag in cars, results in too much this neurotransmitter to be released causing damage to the auditory nerve cells, causing a reduced ability to hear.



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