Audiology - Science topic

As its not part of this paper, it may be in the master thesis (see references): Kılıç N. Speech, spatial and quality of hearing scale (SSQ) for Turkish language and evaluation of adults with normal hearing and sensorineural hearing loss by SSQ [in Turkish] Gazi University Institute of Health Sciences. Normalization and Adaptation of MSc Thesis; 2017.

But luckily, there is another paper: Kılıç N, Şahin Kamışlı Gİ, Gündüz B, Bayramoğlu İ, Kemaloğlu YK. Turkish Validity and Reliability Study of the Speech, Spatial and Qualities of Hearing Scale. Turk Arch Otorhinolaryngol 2021;59:172-187.

And in its appendix the complete Turkish SSQ is included. Therefore, you must pick out the twelve questions to make it Turkish SSQ12 ;)

CI would not be an ideal choice. for real binaural experience the inputs to both ears need to be synchronized and CI changes the frequency spectrum of input signal. so binaural benefit is still not proved in those cases.

BAHA and CROS would ideal do lot of good in those cases, i think

Definite MD

A. Two or more spontaneous episodes of vertigo(1,2), each lasting 20 minutes to 12 hours(3).

B. Audiometrically documented low- to mediumfrequency sensorineural hearing loss(4,5) in one ear, defining the affected ear on at least one occasion before, during or after one of the episodes of vertigo(6,7).

C. Fluctuating aural symptoms (hearing, tinnitus or fullness) in the affected ear(8). D. Not better accounted for by another vestibular diagnosis(9).

Do a google search of topics that interests you? Search for dissertations in those areas of study. And also talk to your supervisor if you have been assigned one

Hello Ms.Danielle Blasl,

In this case, we had better determine the type of hypothesis ( sample size based on proportion).

According to Louw, Christine, Robert H. Eikelboom, and Jannie Hugo. "Prevalence of hearing loss at primary health care clinics in South Africa." African health sciences 18.2 (2018): 313-320.

- The expected proportion is 17.5%.

- population size for South Africa is 57,725,600.

- Deviation from the expected proportion: we assume 5%.

- Confidence level = 95%

and calculate on R or STATCALC software.

Best Regards

Hallo Fr. Zimmermann,

ich habe Ihnen gerade auch per eMail geschrieben, da Sie sich an KIND Hörgeräte gewandt haben. Ihre Frage lässt sich so allgemein nicht beantworten, und es ist schade, dass Sie erst in einer relativ späten Phase Ihrer Bachelorarbeit damit anfangen. Erste Anlaufstellen sind natürlich die einschlägigen Fachpublikationen, angefangen von Sachbüchern (z.B. das Buch "Hearing Aids" von Harvey Dillon) bis hin zu den Fachzeitschriften. Die vielleicht wichtigsten in diesem Gebiet sind z.B. die "Hörakustik" und "Zeitschrift für Audiologie" auf deutsch, aber viel mehr gibt es natürlich auf englisch, z.B. in "Hearing Journal", "Hearing Review", dem "Journal of the Acoustical Society of America", dem "International Journal of Audiology" und vielen mehr. Dann kann man noch Online-Quellen durchsuchen, besonders die pubmed-Datenbank (https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&uact=8&ved=2ahUKEwirpIO1y8_fAhVMThoKHb-nDl4QFjAAegQIBRAC&url=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpubmed%2F&usg=AOvVaw3wSoQDpTQYyl4YdYW3Tzwi). Überall da wird man aber nur fündig, wenn man nach etwas konkreteren Themen suchen kann.

Ich hoffe, Ihnen hiermit dennoch ein wenig geholfen zu haben und verbleibe

mit schönen Grüßen,

Martin Kinkel

In Czech Republic there are general protocol for prevention of occupational NIHL. It is based on categories according to the level of risk for workers:

Category 1: Noise under the 75 dB LAeq, 8h.

Category 2 or 2R (some more risk workplaces or consequences): Noise between 75 and 85 dB LAeq, 8h and concurrently impulse noise below 140dB.

Category 3: Noise between 85 and 105dB LAeq, 8h and concurrently impulse noise below 150dB.

Category 4: Every worker on workplace with more than 105dB LAeq, 8h or more than 150dB of impulse noise. And workers with faster development of hearing loss.

Workers from these categories are examined in the regular intervals (First examination is before starting work and then in the intervals.):

Category 1: No regular examination.

Category 2R: Once per 3 years.

Category 3: Once per 2 years.

Category 4: Once per year.

Younger workers than 21 years: Once per year for cat. 2R, 3 and once per half a year for cat. 4.

Pure tone evaluation is used. Differences between the two examinations are evaluated at frequencies 0.5, 1, 2 and 4 kHz. We are using evaluation of hearing loss in percentage by Fowler. (First mentioned here: https://jamanetwork.com/journals/jamaotolaryngology/article-abstract/572444)

Acceptable hearing losses are 15% in 30 years of age, 25% in 40 years of age and newer more than 40% during working life. And losses shouldn’t be higher than 1% in one year on both ears. If the losses are higher examinations are in shorter intervals and special organizational measures and equipment during work are used or workplace is changed.

I hope this would be helpful.

Hi, search for the conferences in your field and you will get your choice conference.

With this population, we will look at using the CDP technology and the mismatch of surface versus visual dependency with these patients as often they become highly visually dependent. We then apply a sensory re-weighting load technique to balance out the visual versus surface dependency to allow the patient to maximize the use of each efficiently - it is amazing how well they do despite no vestibular function.

Interestingly, we have dabbled with the VOXX socks and orthotics group as their technology, albeit a little pseudo-science, has demonstrated increased somatosensory balance score on the SOT on the CDP with repeated testing suggesting the sock improve somatosensory cues and thus improve balance performance.

@Eduard;

I am wandering how to visualize “Qi (of Qigong)”, atmosphere or vibration of far fine level, sunbeam may be analyzed by your method, I think. With proper and enough training, as well as warming up, we can recognize and feel that we are in the field in which vibration between doctor and patient are coming and going.

My question is, if there is method with such fine detector system.

What is the evidence that testing with English word lists is not valid. Patients and testers are naturally reluctant for the use of English lists on foreign speakers, but in my experience meaningful results can be obtained.

My present research on PIL (pauciballary indeterminate leprosy indicates that F.D. may be one manifestation. Pl. get a detail investigation & needful before progress of deafness. Thanks.

Thank you for this link, the site is interesting.

I'll look for published research and data sources. Please forward anything else you know about.

Best regards.

Do a google scholar search with "bimodal" "cochlear implant" "hearing aids" and you'll get a more comprehensive list. But these should help you get started-

Ching, T. Y. C., Van Wanrooy, E., & Dillon, H. (2007). Binaural-bimodal fitting or bilateral implantation for managing severe to profound deafness: a review. Trends in amplification, 11(3), 161-192.

Ching, T. Y., Incerti, P., & Hill, M. (2004). Binaural benefits for adults who use hearing aids and cochlear implants in opposite ears. Ear and hearing, 25(1), 9-21.

Ching, T. Y., Incerti, P., Hill, M., & van Wanrooy, E. (2006). An overview of binaural advantages for children and adults who use binaural/bimodal hearing devices. Audiology and Neurotology, 11(Suppl. 1), 6-11.

Ching, T. Y., Hill, M., Brew, J., Incerti, P., Priolo, S., Rushbrook, E., & Forsythe, L. (2005). The effect of auditory experience on speech perception, localization, and functional performance of children who use a cochlear implant and a hearing aid in opposite ears: El efecto de la experiencia auditiva sobre la percepción del lenguaje, la localización y el desempeño funcional en niños que usan un implante coclear y un auxiliar auditivo en el oído opuesto. International Journal of Audiology, 44(12), 677-690.

Dear Prof. Pattanaik, Thank you very much for these clear definitions. While the survey centres on current educational practice, your extensive experience using materials in Indian institutions would be very valuable. Best regards, Tom.

"Cerebrobasilar insufficiency one of the causes of sensorineural hearing loss"...

  ...and is mediated more than likely by reduced perilymph pressure and resultant reversible hydrops, as mentioned previously.   There is no plausible central cause of this.

   I have neither seen nor read of any central cause of congenital deafness, ie due to a cortical lesion.  However, it is probable that a congenital cochlear loss will lead to faulty cortical development, even anatomical changes. 

   On line with Previc's work, I think in normals there is slight but significantly better hearing in right ears, sufficient to induce left hemisphere dominance for speech.  All the evidence suggests that the cortical hemispheres are equipotential at birth, or at least before any auditory input is received.  Hence lateralisation must be peripherally driven.

   Most of the studies I have read on the congenitally deaf have been uninterpretable, since the degree of residual hearing and the onset of the deafness is unstated. 

Sorry, I'm not an electrophysiologist, I'm an acoustician

Hi,

Actually, transfer function in middle ear is affected by three components:

1- Stiffness

2- Mass

3- Resistance 

In the first stage of most of the middle ear impairments, stifness component is affected and low frequencies are stiff controlled. So we can see low frequency hearing loss in most of the middle ear impairments. Of course, in some of the middle ear impairments gradually the high frequencies are affected that it shows the mass of the system has increased. 

Acoustic reflexes would likely not be present even in the event of a sensory loss due to elevated thresholds. I would suggest testing otoacoustic reflexes, auditory  brainstem response, and try to elicit an acoustic startle. I would suspect that the OAEs would be absent and the ABR to click stimuli present with prolonged wave V latencies. You may get a startle reflex if you use a broadband stimulus of high enough intensity. If OAEs are present you should perform electrocochleography looking for coclear microphonic - suspect auditory neuropathy/dysynchrony.

Unfortunately we do not have information on hypersensitivity, but the possibility of a change in the growing stages is interesting. Expression of the origin of the trigeminal ganglion may be involved.

iwao

I definitely understand what you are saying. It is quite a common site. But what we have to look for here is if they are really P1 or not based on the morphology of the wave. If you are confident about it bot worry. Just use peak to peak amplitudes. That should solve your problems. But it would be great if you could post some pics of those waveforms.

What degree of unilateral hearing loss are you considering? I have seen losses such as that from above to total unilateral deafness. The trick is to make sure that you have used enough contralateral masking of the better ear to make sure that the responses you are seeing are indeed those of the better ear and not  responses to a cross-over  signal heard in the better ear. 

What do you mean by "reliable"? If by reliable you mean present  and easily detectable in all normal listeners, a main issue with the ABR BIC is that it is small in amplitude and sometimes hard to see in background noise (especially since the subtraction procedure results in the waveform noise increasing 1.4X noise). One must ensure sufficient trials are recorded to ensure waveform noise is 1/3rd to max 1/2 the amplitude of the BIC.

As already noted, BICs for MLRs and especially N1-P2 are much larger in amplitude. Numerous pubs have shown this, for example:

Picton, T. W., Rodriguez, R. T., Linden, R. D., & Maiste, A. C. (1985). The neurophysiology of human hearing. Human Communication Canada, 9, 127-136

McPherson, D. L., & Starr, A. (1993). Binaural interaction in auditory evoked potentials: brainstem, middle- and long-latency components. Hearing Research, 66, 91-98.

Fowler, C. G., & Mikami, C. M. (1996). Phase effects on the middle and late auditory evoked potentials. Journal of the American Academy of Audiology, 7, 23-30.

If by "reliable", however,  you refer to how well it determines normal vs impaired binaural processing. Well, there are few data concerning this and certainly far too few data for it to be used clinically.  See for example:

Levine, R. A., Gardner, J. C., Fullerton, B. C., et al. (1993). Effects of mulitple sclerosis brainstem lesions on sound lateralization and brainstem auditory evoked potentials. Hearing Research, 68, 73-88.

Pratt, H., Polyakov, A., Ahronson, V., et al. (1998). Effects of localized pontine lesions on auditory brain-stem evoked potential and binaural processing in humans. Electroencephalography and clinical neurophysiology, 108, 511-520.

Delb, W., Strauss, D. J., Hohenberg, G., & Plinkert, P. K. (2003). The binaural interaction component (BIC) in children with central auditory processing disorders (CAPD). [Comparative Study]. Int J Audiol, 42(7), 401-412.

He, S., Brown, C. J., & Abbas, P. J. (2012). Preliminary results of the relationship between the binaural interaction component of the electrically evoked auditory brainstem response and interaural pitch comparisons in bilateral cochlear implant recipients. Ear Hear, 33(1), 57-68. doi: 10.1097/AUD.0b013e31822519ef

Hope this helps.

I don't have more experience in clinical practice and i don't see it in my observations up to now, but according to the one of audiology field references(Handbook of clinical Audiology,JACK KATZ,SIXTH EDITION), in a study, Ciardo et al.(2005) administered a muscle relexant  to block stapedius  reflex activity during sergery.The mucle relaxant did not obliterate the RIARs of otosclerosis patients, but it did block the real ipsilateral reflexes of patients withe normal middle ear functioning.In a other study, Ciardo et al.(2003) found that RIARs occoured in normal ears, in ears with monaural deafness or otosclerosis with normal otoscopy and type A tympanograms, and in ears on the side of facial nerve palsy.Based on these observationThe RIAR is due to the subtractive (eardrum)artifact ratger than representing a clinical entity.

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Hai, I am agree with sir Jeffrey,

but, even if the damage is only at peripheral level, its effect can be seen at central level also. To best of my understanding, I want to explain in two theories:-

1-->According to Discordant damage of inner & outer hair cells. There is Intact IHC but damaged OHC stereocilia. The region where IHC cilia are still present but OHC cilia are missing, the tectorial membrane sags down on to the IHC cilia causing them to depolarize. Depolarization causes opening of calcium channels which increase calcium concentration in the hair cells which responsible for release of neuro transmitter. During hyper-polarization there will be release of calcium from the cell

 Abnormal neural activity can arise from both enhanced and strongly reduced extra cellular calcium concentration.

2-->AGAIN IF WE TALK ABOUT REORGANIZATION OF THE AUDITORY CORTEX.

Restricted HF cochlear damage results in profound reorganization of the auditory cortex.Cortical neuron that had characteristic frequency corresponding to those in the damaged parts of the cochlea show a CF equal to the edge frequency of the damaged area (Harrison et al. 1991, Royan, 1993).

There is excess of cortical cells representing a very restricted area of cochlea.

Spontaneous and stimulated activity of those cells is likely to be more synchronized than it was before damage.

 Increased incidence of tinnitus with age may also be result of changes in neural organization.

 SOMETIMES NOISE TRAUMA INCREASES SPONTANEOUS ACTIVITY IN COCHLEAR NUCLEUS. ACCORDING TO MOLLER TINNITUS MIGHT BE BECOZ OF SPECIAL MANIFESTATION INCREASED SPONTANEOUS ACTIVITY IN EXTRA LEMINSCAL PATHWAY. ACCORDING TO EGGERMONT ,1997, CAN BE PRESENT IN SECONDARY AUDITORY CORTEX. 

I hope, the information is useful. 

 

I agree with Dr. Vijaya Kumar Narne because of limitations its not used in present hearing aids. The concept of extending low frequencies in hearing aids started in 1970s (Martin & Pickett, 1970; Sweetow, 1977 etc). They suggested that in presence of noise this concept doesn't work. However, the hearing aids studied had narrow range of frequency response. Thus, Sung and Sung (1982) suggested that extending both low and high frequencies significantly improves speech perception even in presence of noise. Beck (1986) suggested that scores improve and there is no upward spread of masking. There are many studies in 70's and 80's which supported extended low-frequency amplification. However, there are criticisms to the conclusions drawn and presently its not used extensively.

Please find below the review articles on the topic which I could find: 

An extensive review of Extended Low-frequency information can be found in the pdf file attached with the answer. 

The important articles related to extended low-frequency amplification are: 

Sung RJ, Sung GS: Low frequency amplification and speech intelligibility in noise. Hear lnstr 1982. 33(1): 20,47

In addition, the only recent study (2000) which I found was a review article explaining the possible advantages of low-frequency amplification supporting extended low frequency amplification. Please find the link. 

Wish this is useful.

Regards,

Prashanth

Hi, 

 I suggest the TEAch. The Persan version of it is available in IUMS.

My answer will be relevant to young children who have shown ANSD from birth. Hearing aid(s) should not be fitted until behavioral thresholds of audibility can be obtained. One would most likely not fit a hearing aid for a child with ANSD whose thresholds are nearly normal or severe-profound. Those with mild to moderately severe loss who benefit from hearing aids tend to be the same ones who have cortical auditory evoked potentials. Assuming CAEPs are not clinically readily available in the situation you describe, a quick and dirty way to guess whether a hearing aid might help is to measure even rudimentary speech recognition in each ear separately at (for example) 50dBHL and again at 70-80dBHL. If the child's speech recognition clearly improves at a higher intensity, a hearing aid should be fitted, appropriate to the thresholds of audibility, while visual supports for communication are maintained. Gary Rance's research has suggested that roughly half of children with ANSD can benefit from hearing aids. 

Attention - Their air conduction was not blocked completely! Each hearing protection has its limits and block sound from only a certain level. The manufactorer providing HML Values for the Hearing Protector - often found on the box. See: http://www.howardleight.com/earplugs/neutron

You can use the HML value to calculate the intensity of the sound that is still heard through ear protection. See: https://www.noisemeters.com/apps/occ/prot-hml.asp

For example: earbuds HML is 21 18 14 and sound have intensity 50 dB - >> Estimated level at the ear is 30.5 dB.

We have some longitudinal threshold data that we've collected on a large group of children who are hard of hearing.  When we look at changes in threshold over time within children, we did not find that age was a significant predictor of either mean changes in threshold or variability in thresholds over time using linear mixed models.  The paper describing this work is currently under review, but I can share that as soon as it's accepted for publication.

Diane Sabo has written about minimum response levels in some of her previous research, but that term is typically used to describe non-threshold responses obtained through Behavioral Observation or other unconditioned test methods.  Minimum response levels tend to be higher than behavioral thresholds obtained using VRA or another conditioned test procedure. 

Not pure tones, but very interesting!

Loudness Scaling test !

Monaural and binaural possible !

Audiosensitivity ("hyperacusis") is due to a state of cochlear hyperactivity.  There is no known psychiatric or neurological cause.  It can be demonstrated by abnormalities of acoustic reflexes -- reversed stapedial reflexes and/or lowered stapedial reflex thresholds.  PTA thresholds often fluctuate noticeably within and between ears yet still remain within normal limits.   The usual (?only) cause of inner ear hyperactivity is endolymphatic hydrops, a very common but underrecognised result of anything that causes perilymph pressure to fall. 

Thanks for your reply. I know Laurie, and have been working with her for a while now :-). 

The question is in regard to tinnitus matching and not hearing loss

As discussed above, the client may have (C) APD with specific problems in difficulty understanding speech. Initially The Institute of Hearing Research coined the term ‘Obscure Auditory Dysfunction’ (OAD) (Saunders and Haggard, 1989) for such condition. In addition, Hinchcliffe (1992) coined the term ‘King-Kopetzky Syndrome’ (KKS) to explain the condition seen in adults which is usually hereditary. 

Assessment strategies:

1. Detailed case history regarding the complaints and possible symptoms of (C) APD

2. Screening checklist for auditory processing in adults (SCAP-A) developed by Vaidya and Yathiraj (2014) can be tried to screen for (C) APD.

3. Speech in Noise test and other APD test battery, if required as suggested earlier.

4. BIOMARK is an objective test for assessing auditory processing problems which can also  be tried if the facility is available.

5. As suggested earlier, P300, MMN and other cognitive potentials may be tried for further evaluations.

Treatment strategy would depend on the nature of auditory processing problem detected.  IF the problem is only listening in presence of noise - the options could be:

1. Personal FM devices which can enhance SNR and improve speech perception in presence of noise.

2. Noise Desensitization Therapy is found to be effective.

3. Therapy activities to improve speech perception in noise

4. Appropriate counselling on communication strategies to improve speech perception in noise. 

The management is individualistic based on the client's difficulties, needs and preferences in the management approach. 

While the causes of Tullio phenomenon are diverse, I believe the commonest we encounter here in sub-saharan Africa is due to Superior canal dehiscience. I agree with Eduardo Martin-Sqnz that surgical options is only beneficial with large dehiscience.

When electromagnetic and mechanical systems interact there must be a transducer, somewhere.  Sound reception necessarily involves (typically vibratory) motion , so it is easy to imagine that electric and magnetic fields could be result according to Faraday's and Maxwell's laws.  Since the body also has electromagnetic properties (galvanic skin response, nerve impulses, etc.), these fields could easily induce small currents.  Who can say (yet) if some small current might affect your opinion about something?  Unfortunately, absence of evidence is also not evidence.

Finding a reliably reproducible effect of this kind would be very interesting, but it would need to be carefully verified.  Do you know of one?

This is an interesting question. I have been "involved" with this topic since the 1908s, thus my answer is somewhat long, and certainly reflects my personal opinion.  However, any answer to this question is not without controversy.

As noted above, the primary reason for using "dBnHL" is to account for the differences between behavioural thresholds at each frequency, so that "0 dBnHL" represents the median or mean threshold for normal adults. This is the same concept as "dB HL", which uses (nearly) continuous tones. As also noted above, however, in contrast with behavioural HL, even with the "nHL" correction, one still has to apply "eHL" correction factors reflecting  differences between AEP (usually ABR) thresholds and behavioural thresholds; correction factors which are different for infants compared to adults.

Unfortunately, it is not so simple as dBHL, because "dBnHL" has had to be calculated for so many different stimuli (e.g., clicks for ABR, 5-cycle brief tones for ABR, chirp stimuli for ABR or ASSR, 40-60-ms tones for corticals). Complicating this issue further is that different presentation rates are used -- behavioural thresholds change with rate (even though AEP, especially ABR, thresholds do not show such changes with rate). Finally, and very importantly, the physical calibration of non-continuous tones is a little more complicated; most clinicians and many researchers, and, indeed, many audiometric calibration technicians, do not know how to calibrate these stimuli.

My colleagues and I have been pretty adamant that individual clinics should not typically determine their own "nHL" values, as this requires large numbers of normal subjects, careful threshold procedures, and quiet test rooms. Rather, assuming they are using stimuli essentially identical to others' studies which investigated nHLs (or a "standard" such as the ISO standard), they should have their stimuli carefully calibrated acoustically to the previously published nHL calibration standard.

In our previous studies, we determined nHL calibrations for all stimuli using a 10/s stimulus rate, regardless of the actual rate used to record the AEP in the study (we did this because the ABR and MLR do not show better thresholds with increasing rates, whereas behavioural thresholds do). The ISO standard mentioned above by Stig Arlinger states that a 20/s rate should be used when determining nHL calibrations -- I am not sure why they selected 20/s, but the difference in threshold would be very small (only 1-2 dB) (Stapells et al., JASA, 1982).

The above confusing situation is made worse by the fact that there is not yet agreement as to formal RETSPLs/RETFLs (i.e., "standards")  even for the most commonly used stimuli for ABR testing. As Stig Arlinger has noted above, there is an ISO standard for brief stimuli, specifically clicks and brief-tone stimuli. However, these "standards" are not fully accepted, especially for tonal stimuli (e.g., they are not commonly used in North America). They tended to ignore or discredit substantial preceding research into nHL thresholds and, in the case of tonal nHLs, they have some significant differences. (Oddly, the reference force levels for bone conduction in these "standards" were estimated from pure-tone standards, rather than directly determined.) 

The move towards  "standard" reference thresholds is important, but it must also take into account previous research and consider differences. My greatest concern is that the large majority of research into adult and, importantly,  infant tone-ABR thresholds has been carried-out using nHL values that are different from the ISO standard -- any possible move to a different standard must consider how this relates to the results (and interpretation) of the past and future studies.

Problems will still remain even if a standard becomes widely accepted worldwide. Every time a new or different stimulus comes out (e.g., chirp stimuli), no standard will exist, and some sort of nHL needed.

Lately, I have wondered if we should never have moved to developing "nHL". Rather, perhaps we should have just used well-established pure-tone "HL" calibrations, and then determined what are the normal ABR (or MLR or ASSR) offsets/corrections. (This would eliminate problems with calibration, but would still entail questions with determining the offsets/corrections.) This is essentially what most researchers carrying out threshold assessments using the ASSR or CAEP (cortical auditory evoked potential) have resorted to.

Given the current situation, although not all would agree with me, I recommend one use the nHL calibrations from the study(ies) one is trying to emulate. For example, if you are testing infant ABR thresholds using the stimuli and parameters I have recommended, then you would use the nHL calibrations I have published. On the other had, if you are using Michael Gorga's stimuli and parameters, then use his published calibrations. I expect, with time, there will be more movement towards use of standard reference thresholds as we understand/explain current differences.

An added point: Not sure why you are interested in the ipsi/contra ABR, but note that in an adult in response to air-conducted stimuli, the "contralateral" ABR (i.e., recorded with electrode on mastoid/earlobe contralateral to the stimulated ear) does NOT represent different pathways than that recorded in the ipsilateral channel. Rather, it is a view of the same generators from a different angle.

There two schools on measuring Acoustic Reflex in Contra-lateral ear.  One is contra with reference to Probe ear (Right Contra : Probe in Left ear and Stimulus in Right Ear). Some Other consider contra with reference to stimulus ear (i.e Right Contra: Stimulus Presented in Left ear). Usually what specified in books is contra with reference to Probe Ear. 

Vijay

Yes, personal choice, but the difference in cost to society between the two choices is massive (swings in the neighborhood of negative $2,000,000-3,000,000 to positive the same). I think as a profession our duty is to empower the deaf--I am the deafest of the deaf, but have taken advantage of the progress in empowerment through technology and rehabilitation so that I've been fortunate in being a net contributor in society. If we could focus on helping the upcoming generations of deaf to know of these empowerments (we actually have many deaf educators fighting it tooth and nail, much to my dismay), we would find that more and more will choose NOT to live as a dependent on society, and will go on and exceed the current dismal economic/education level of the deaf today.

But somehow the pseudo glorification in remaining deaf perpetuated by many deaf educators and deaf interpreters strikes too much terror in the hearts of many younger deaf people. Amazingy, when I speak to deaf groups and often to the chagrin of their normal hearing interpreters the young deaf swarm around me wanting to know how they can break out of their silent incarceration and advance their education. The ultra limited world of signing doesn't get them very far in a hurry, certainly nothing like being oral/aural. Given the choice on a level playing field of presentation, they want to know how to achieve academically, in a field of their choosing, and how to take advantage of the technology and resources available for the asking. They tell me they've been made to feel like a traitor if they wear hearing aids; most of them, like you, Nathan, can actually wear hearing aids and do very well with some training) OR, in the case of cochlear implantation they have been made to be terrified of getting one with horror stories of days of yore that have not existed for decades

Anyway, I think it a worthy project that Caitlin is pursuing. But the PRIMARY role of an audiologist is to empower in the oral/aural framework, and to be a support and mentor for those who want to bust out of the straight jacket of deafness.  

The reason for this lies in the later maturation of the cochlear amplifier mechanism that is responsible for the so-called "tip" of the higher-frequency tuning curves of auditory nerve fibers in mammals. You will find an excellent study of this phenomenon in:

Echteler SM, Arjmand E and Dallos P (1989) Developmental alteration in the frequency map of the mammalian cochlea. Science 341, 147-149.

I reviewed such developmental phenomena in the following paper:

Manley, GA. (1996) Ontogeny of frequency mapping in the peripheral auditory system of birds and mammals: a critical review. Auditory Neurosci 3: 199-214.

Unfortunately, this journal went out of publication, but I have attached the file.

Best regards,

Geoff Manley

I recomend you the Jacobson and Shepard Experience.

They have a fanstatic ENG manual.

"Balance Function Assessment and Management.Gary Jacobson, PhD, Neil Shepard, PhD"

In our clinical practise , we use Fowler and Sisi test for recruitment analysis.

They are valuable and very common test and can differentiate easily both recruitment and hyperacusis symptoms.

I have never seen such nor can I find it at Pubmed under "gestational tympanic membrane perforation" nor "tympanic membrane perforation pregnancy." All I have done now for 35 years is ears and I have done over 8000 ear surgeries, about 40% of that for chronic ear diisease. If you are seeing such, I encourage you to photo-document it and publish it with the audiologic findings. 

This is an important fact to know as all of us are aware of the speech banana but most of us are unaware of how much is the absolute average values of speech sounds. The best way to understand that is using LTASS measures and understanding the amplitude and frequency of speech sounds used in the Speech spectrum. 

An excellent review article which explains about the origin and also provides us with the values regarding the speech spectrum is published in Ear and Hearing by Olsen, Hawkins and Van Tassel (1987). Please find the link.

Hope this information is useful

Regards,

Prashanth

There is a recent research work on this topic published in Ear and Hearing. You may be able to find more clear answers in that article. Its a very good study with good literature review.  Please find the link.

Warm Regard and Wishes,

Prashanth

Dear Kaylah;

I'm not familiar with any past McGurk study that was exhaustive in exactly that way. But I  wanted to pass on that, given your interests you might like to check out Norm Erber's work - maybe it can satisfy some of your needs;

Erber, N. (1972). Auditory, visual, and auditory-visual recognition of consonants by children with normal and impaired hearing, JSHR, 15, 413-422. 

Erber presented the consonants /p,t,k,b,d,g,m,n/ under A, V, and AV conditions, to children with varying degrees of hearing loss. The paper includes confusion matrices for all of the stimulus - response pairs.

Hack, Z., and Erber, N. (1982). Auditory, visual, and auditory-visual perception of vowels by hearing-impaired children. JSHR, 25, 100-107. 

Hack & Erber presented 10 AE vowels under A, V, and AV conditions, to children with varying degrees of word recognition skills. The paper also includes confusion matrices for all of the stimulus-response pairs. 

I realize that these were not McGurk studies, per se, but thought that they might be interesting to you given the question you posted. Along the same lines, I wonder if you would like Lynne Bernstein's work. If you find a paper that is a McGurk study of all AE consonant pairs please let me know!

Best regards,

Carrie

I would consider the most important topic: vestibular neuritis or central pseudoneuritis. Use the HINTS algorytm! In case of peripheral neuritis: Head Impulse positive on the affected side,  horizontal-torsional spontaneous Nystagmus (slow phases toward the affected ear), Test of Skew:ocular Hypotropia on the affected side. I would add: a simultaneous ice test which inhibits or inverts the spontaneous nystagmus.

I think the cause of Meniere's disease is a pressure change in the inner ear, but not the increase in endolymphatic pressure as is universally assumed, rather a decrease in perilymph pressure, allowing the endolymph compartment to expand, ie hydrops. So anything that reduces perilymphatic, CSF or blood pressure will trigger hydrops. Hence I do not think there are any specific immunological, toxicological or biochemical causes of Meniere's disease. If anyone doubts this, can they please supply a name/reference for any autoimmune disorder that causes MD but does not also predispose to perilymphatic hypotension?

To answer such question some points need more details such as age, how was the hearing loss (sudden or progressive), the job of patient (is there noise exposure?), past medical history and family history.

A good review of information about speech banana and how the speech banana is derived. How the consonants and vowels placed is given in speech banana is given in review articles.

Olsen WO, Hawkins DB, Van Tasell DJ. (1987). Representations

of the long-term spectra of speech. Ear Hear,8:1008-108S .

As said by people already: the medium only has influence on the propagation SPEED, not on the frequency of the source. The number of periods per second is defined by the source. The wavelength is dependent of the medium which follows from the constant frequency: wavelength = propagation speed / f. The sound waves in water activate the eardrums and we hear exact the same frequency as the source produces. An other story is the reverberation in water. Because the prop. speed in water is about 4 times as high as in air, the spatial impression is much smaller than the same space in air. Some people know that if you fill your lungs with helium, your speech will sound as Donald Duck then. That is caused by the fact that the sound SOURCE is altered by the higher prop. speed of helium in your throat and mouth cavities (the vocal tract). In this case the production of the sound is dependent of the gas in the vocal tract: the resonations (formants) depend on the gas present.

It is a very useful tool but very slow for hearing screening. In our daily practice we use it as a tool when is necessary to have a precise audiological assessment in a small infant with fail otoacustic emissions and ABRs. We have development a tool for ABR based on linear regression.

The answer to that depends on what hearing aids are being used. A good overview of some options can be located in this article. http://www.audiologyonline.com/articles/amplified-stethoscope-options-for-professionals-860. Additionally there is a new stethoscope coming into production, http://www.freedomscope.com/physicians_wireless_stethoscope.htm that should allow for streaming auscultation directly to hearing aids that have wireless capabilities. The hearing aids could then be configured not to filter any of the sounds and provide the best possible amplification and aesthetics. Although the article suggests the t-coil coupling is not always the best, I have found it preferable for the profound population, which poses more challenges.

I agree with Steven Marcrum. There is many articles published on it (look at JASA). Must of the studies uses different apparatus to test the MAA.

The LACE program can be bought at http://www.neurotone.com/lace-interactive-listening-program. It can assist with aural rehab, but not substitute it.

Acceleration (change in head velocity) is detected by the vestibular organs in the inner ear. Hence any sudden change in velocity, as with closed - and not open - head injuries is liable to overstimulate or damage the vestibular system (concussion). A widely overlooked cause of damage is a leak from cochlea to middle ear (perilymph fistula), which may occur on either side, and cause Menieriform symptoms. The clinical syndromes of perilymph fistula and post-concussion "neurosis" are identical (Grimm).

$70 per person with hearing loss per annum,nationally. Http://www.audiology.asn.au/pdf/listenhearfinal.pdf

I think we need more information to answer this... first off, when you use the term IREM, you're referring to a hearing aid integrated real ear measure (like that of Starkey's products), right? If so, I'm not sure what you're doing in a test box, as these are both on-ear measures. Or, are you asking about what types of stimuli would be best used for examining the differences?

For a comparison of IREM to a calibrated REM system, see this paper:

Musa,

As a university professor, I teach MFT in-depth and requests students to test each others using MFT before applying it for their actual case presentation if their subject has a middle ear problem. This means that they get the theoretical knowledge, indications, interpretation and clinical training for the use of standards Tymp and MFT as well as WBT in my Diagnostic I class. Since I have the equipment that does all these procedures, they are well trained in knowing normal vs. abnormal and differential diagnosis for a diagnosis based on the overall test findings. However, I agree with you that students in other programs may not have the same opportunity and thus won't get the same training in middle ear measures.

The presence of acoustic refelxes depends upon synchronisation of nerve fibers. In cases with AN/ANSD the pathology is mostly restricted to the auditory nerve and basically the portion of the nerve which is innervated by the schwann cells. The pathology at the brainstem will be rare.

Research suggests that the prevalence of hearing loss in diabetes patients is higher than in non-diabetic controls. Prior to the emergence of clinical hearing loss there do also appear to be sub-clinical changes in audiometric tests such as ABR and TOAEs that suggest central as well as peripheral neuropathy.

My reading of the evidence is that hearing loss is more prevalent in the diabetic population as a whole. I'm not sure whether anyone has compared type 1 and type 2 directly. There is a link with glycaemic control but this does not account for the whole variance in thresholds. For example length since onset of diabetes seems to be a factor regardless of glycaemic control.

In children there are some good recent papers on type 1 diabetes and I suspect type 2 will be becoming more of an issue as the incidence rises in the paediatric population. There is evidence for audiometric consequences of type 1 diabetes in children.

I know that there ia quite a bit of work going on in Saudi looking at diabetes in general and this might be a good place to look for audiology related papers.

Absent acoustic reflex in ANSD may not be due to reduced sensitivity to loudness perception. Because perceptual studies on loudness demonstrate no significant impairment loudness perception. Absent acoustic reflex in ANSD due to dys-synchronous firing.

I would look into other causes of conductive loss with intact reflexes, such as superior semicircular canal dehiscence.