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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. To evaluate the medicolegal relevance of middle latency responses for objectively approximating frequency-specific hearing levels in subjects with occupational hearing loss, we compared the middle latency response with the cortical response in 22 reliable subjects who had noise-induced hearing loss and were submitting claims for compensation and 21 subjects who had noise-induced hearing loss but were exaggerating the level of this loss and also were submitting claims for compensation. Suspicious audiometric findings seem fairly common in medicolegal patients; the prospect of material gain may promote either deliberate exaggeration of hearing loss or perhaps unconscious elevation of response criteria [1]. The sites of MLR generators have not been determined yet with certainty: For No, Po, and Na, the medial geniculate ganglion and the thalamus have been suggested, as has the inferior colliculus. To date, few published reports contain clinical results obtained with the MLR in patients with known and suspected hearing loss [10, 11]. The investigated subjects are separated into two groups: subjects with reliable behavioral hearing thresholds at conventional audiometric techniques and unreliable subjects suspected of exaggerating their occupational hearing loss. Two ears in which neither behavioral nor ERA potential could be identified (total deafness) were eliminated. For ERA, a Medelec (United Kingdom) Audiostar SM 27388.1 ERA system was used with Madsen ERA electrodes.
The positive electrode was placed at the mastoid, and the reference was placed at the vertex. No statistically significant difference in age was determined between the two groups (at the level of p = .05).
Near the electrophysiological threshold level, superimposition of four displayed ERA traces resulting from identical stimulations is a very appropriate method for improving pattern recognition and for decision making about the presence or absence of a response.
Our previous study [2] showed that, in subjects with noise-induced hearing loss (sloped audiogram), BERA thresholds correlate significantly better with CERA thresholds on 3 kHz than on 2 and 1 kHz.
The late components demonstrate variability associated with changes in subject wakefulness, attention, or state of consciousness [11]. In most cases, the difference in threshold (the mode) between SVR and ERP was 10 dB (one step in the stimulus intensity regulation).
Middle latency components of auditory evoked potentials, especially the time-saving 40-Hz response, seem efficient and reliable for evaluating the true pure-tone thresholds (l, 2, and 3 kHz) in medicolegal patients exaggerating their noise-induced hearing loss. As MLRA is not actually a time-saving procedure as compared with CERA, and because it seems less sensitive than the SVR for approximating the true threshold, the use of MLRA seems best limited to situations in which a control or a confirmation of the SVR is wanted. 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.
A Comparison Between Middle Latency Responses and Late Auditory Evoked Potentials for Approximating Frequency-Specific Hearing Levels in Medicolegal Patients with Occupational Hearing Loss. Middle latency components of auditory evoked potentials, especially the time-saving 40-Hz response, seem efficient and reliable for evaluating the true pure-tone thresholds (l, 2, and 3 kHz).
In a previous study [2] focused on brainstem (BERA) and cortical evoked response audiometry (CERA), we showed that when dealing with compensation claimants with professional noise-induced hearing loss, only electric response audiometry (ERA) techniques provide a reliable threshold approximation.
The MLR has neurogenic as well as myogenic components; however, most of what is typically viewed as an MLR is neurogenic in origin.
Middle latency response audiometry using the 40- stimuli-per-second paradigm (event-related potential).
In our study, we compare MLRs and SVRs versus behavioral hearing thresholds in subjects who have been exposed professionally to damage risk (intense noise) and are claiming financial compensation.
In addition, the study included 21 subjects (26 investigated ears) with noise-induced hearing loss who exaggerated the level of this loss and also claimed compensation. Rare discordance between cortical evoked response audiometry and middle latency response audiometry results. Test-retest reliability of a 40-Hz event-related potential (4,096 stimulations) at the electrophysiological threshold level (80 dB, 2 kHz). Figures 7 and 8 show plots of the mean ( ± 1 standard deviation) behavioral, CERA, and MLRA threshold values for the 22 reliable subjects and the 21 exaggerators, respectively, at 1,2, and 3 kHz.
Mean ( ± 1 standard deviation) behavioral, cortical evoked response audiometry (CERA), and middle latency response audiometry (MLR) threshold values for the 22 reliable subjects, respectively, at 1,2, and 3 kHz. Mean ( ± 1 standard deviation) behavioral, cortical evoked response audiometry (CERA), and middle latency response audiometry (MLR) threshold values for the 21 exaggerators, respectively, at 1,2, and 3 kHz. Mean decibel values (average, 1, 2, and 3 kHz) for perceptual, cortical evoked response audiometry (CERA), and middle latency response audiometry (MLR) thresholds in reliable and exaggerating subjects.
It is essential, for our purpose, that the evoked potential is associated with actIvIty from very restricted regions of the cochlear partition. Sedatives modify SVR and impose limitations on its reliability for threshold assessment [10].
Mean values of ERP threshold in each group and for each frequency are higher than mean values of SVR threshold.
Most common relationship between cortical evoked response audiometry (CERA) and middle latency response audiometry (MLR) thresholds. A good correlation is found between the 40-Hz response threshold and the SVR threshold (long latency). Further information about sensitivity of MLR to drug effects and to subject wakefulness is expected. Dejonckere PH, Van Dessel F, de Granges de Surgeres G, Coryn CPo Definition of frequency-specific hearing thresholds in subjects exaggerating their noise-induced hearing loss. 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. A good correlation exists between the 40-Hz response threshold and the slow vertex response (SVR) threshold (long latency).
The myogenic component constitutes, for the most part, only the postauricular muscle response, which occurs between 12 and 20 msec after stimulus onset.
This technique is based on the fact that the MLR is a multipeaked response with interpeak intervals (Na-Nb-Nc) of approximately 25 msec (see Fig.
The middle latency response peaks to successive stimuli overlap and augment each other ("in-phase" addition).
However, whether MLR components arise in the primary cortex in humans is somewhat uncertain [10]. The latter is calculated by averaging the hearing loss in decibels at 1,2, and 3 kHz in the best ear with a weighting by the loss in the poorer ear. The average test period necessary to determine the thresholds at three frequencies in each ear with one technique is approximately 3 hours.


With respect to the spectrum of used stimuli (90-msec tone bursts), CERA has the best frequency specificity.
The 40-Hz ERP also is reduced during sleep [10] but, unlike the later cortical responses, the MLRs have been shown to be fairly stable during changes in subject state or attention [11]. Both also show a fairly close correlation with behavioral thresholds in cooperating subjects. Auditory evoked potentials in audiometric assessment of compensation and medicolegal patients.
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. With CERA (slow vertex responses [SVR]), it was possible to define frequency-specific thresholds at 1, 2, and 3 kHz in all 23 subjects exaggerating their occupational hearing loss and in all 13 control patients with comparable noise-induced hearing loss.
The middle latency response is a multipeaked response with interpeak intervals (Na-Nb-Nc) of approximately 25 msec.
1); note that Na, Nb, and Nc are the first, second, and third negative peaks, respectively.
The low filter used was 1 Hz and the high filter 30 Hz, and the analysis time was 500 msec.
In our working conditions, the time necessary to define a threshold with CERA was practically the same as that with ERP.
In this case, a potential still can be identified at 80 dB, but at 10 dB lower, only noise is seen. In Figure 9, an overview of both groups is presented, with the mean values for the three frequencies obtained with each of the three audiometric techniques. MLR can be evoked by tone pips, which have a relatively gradual onset and a duration of a few cycles. In this study, the typical audiometric frequency slope of occupational hearing loss is recognized also in most MLR audiograms. However, in most cases, the 40-Hz response is less sensitive than is the SVR (mode of difference, 10 dB). However, in most cases, the 40-Hz response is less sensitive (mode of difference, 10 dB) than is the SVR.
Figure 1 illustrates a typical waveform obtained by means of middle latency response audiometry (MLRA). Thus, at approximately 40 stimuli per second, the peaks to successive stimuli overlap and augment each other (Fig. In these stimuli, the energy concentrates at a nominal frequency of the brief tone, and the spread of energy is reasonably narrow.
Jeong et al (2013) reported patients with radiologic abnormalities of their cochlear nerve did much worse concerning CI response.
As middle latency response audiometry is not actually a time-saving procedure in comparison with cortical evoked response audiometry and as it seems less sensitive than the SVR for approximating the true threshold, the use of middle latency response audiometry seems best limited to situations in which a control or a confirmation of the SVR is wanted. However, long-time averaging (l00-500 stimuli and more), which enhances the signal-to-noise ratio, was necessary, and this renders CERA a time-consuming procedure. Pa (the first positive peak) occurs at between 25 and 35 milliseconds, and Pb (the second positive peak) appears approximately 25 msec after Pa. 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. Further information about the sensitivity of middle latency response to drug effects and to subject wakefulness (specifically, whether the patient is more or less sleepy) is expected. Middle latency responses (MLRs) also were found to be a sensitive measure near threshold [3-5] and can be evoked with frequency-specific stimuli [6,7]. This potential has been called the 40-Hz eventrelated potential (40-Hz ERP) and can be evoked with frequency-specific stimuli [7,9].
If AN is truly a neuropathy, one would think that AN should increase with age as do neuropathies in general.
Of course, the logical defense to the assertion that AN is an artifact of uncooperative patients is that everybody else is doing bad testing.



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