Welcome, everyone, to the webinar on Cochlear Dead Regions and Implications for Fittings. We're so glad you could be here today to learn more about various audiogram configurations that could mean your patient has cochlear dead regions and how you'll need to fit that patient's hearing aids. Your moderators for today are me, Fran Vinson, IHS membership and marketing manager. And me, Ted Annitz, senior marketing specialist. Our expert presenter today is Ted Benema, PhD. In addition to Ted's many years as a practicing audiologist, he is also a seasoned professor, having taught at several colleges and universities throughout Canada. In fact, Ted created Canada's fourth hearing instrument practitioner program while at Conestoga College in Kitchener, Ontario. Ted is a passionate speaker, and he continues to give presentations on hearing loss and hearing aids across North America and beyond. Ted is also the author of the textbook, Compression for Clinicians, now in its second edition. We're very excited to have him as our presenter today. But before we get started, just a few housekeeping items to go over. Please note that we are recording today's presentation so that we may offer it on demand through the IHS website in the future. This webinar is available for one continuing education credit to the International Hearing Society. We've uploaded the CE quiz to the handout section of the webinar dashboard for you. You can also find out more about receiving continuing education credit at our website at ihsinfo.org. Click on the webinar banner on the homepage or choose webinars from the professional development menu on the left side of the page. You will find the CE quiz along with the information on how to submit it to IHS for credit there as well. If you'd like a copy of the slideshow from today's presentation, which I highly recommend you keep for future reference, you can find the download from the handout section of the webinar dashboard. Or you can get it from the webinar page at the IHS website. Feel free to download the slides from either area now. Tomorrow, you'll receive an email with a link to a survey on this webinar. It is free and your feedback will help us create valuable content for you moving forward. By the end of today's 60-minute presentation, you should be able to do the following. Describe cochlear dead regions in terms of cochlear hair cells and the cochlear traveling wave. Outline audiograms associated with cochlear dead regions. Explain the rationale for the threshold equalizing TEN test. State some examples and implications of cochlear dead regions for hearing aid fittings. At the end, we'll move on to a Q&A session. You can send us a question for Ted at any time by entering your question in the question box on your webinar dashboard, which is usually located to the right or the top of your webinar screen. We'll take as many as we can in the time we have available. Now I'm going to turn it over to Ted, who will guide you through today's presentation. Ted? Hello, hello. It's good to be here again. Another webinar with IHS. This one is on the cochlear dead regions and implications for fittings. As was just mentioned, the first section of this talk will be on cochlear hair cells, the traveling wave itself, and cochlear dead regions. The neat thing about cochlear dead regions, well, it's not a nice thing, but the amazing thing about cochlear dead regions is that to understand them and to understand why they give rise to the particular audiograms that they do, one is forced to understand better the cochlea and its unique physiology, its unique anatomy with hair cells and its physiology. Anatomy is what something is formed of. Physiology is always how it works. The hair cells are the anatomy and the traveling wave is how these hair cells are stimulated. It's really quite amazing how this works. One must have a good appreciation of this to understand the cochlear dead region concept and why, again, it gives rise to the particular audiograms that it does, because these audiograms are the ones that will red flag you or make you suspicious of cochlear dead regions. These regions do have implications for hearing aid fittings. Here's a picture I drew of the cochlea. No, it's not orange, but this whole picture here is about the size of your pinky fingernail. I mean, it's small. It's smaller than a sugar cube. The gray area is the temporal bone. It's also known as the pitreous bone, peter, the rock. It's about the hardest bone in your body. Inside that bone is carved or like an auger shape is the cochlea. So the cochlea isn't so much a presence as it is an absence. It's like me telling you, go across the street and pull out that telephone pole. Take it out of the ground. And so you do. And then I say, okay, now give me the hole. I want the hole, because you see the cochlea is like an auger shaped hole gouged into the hardest bone of the body. So it's very inaccessible, difficult to get at. And that's why you really can't operate on hair cells either the same way you can on an eyeball. I mean, the eyeball is right there in front of your face. Hearing with the end organ of hearing is not all that accessible. At any rate, looking at these orange areas, as we all know, the wide base of the cochlea, where I'm drawing my cursor here, represents the high frequencies. The middle is the mid frequencies. The apex, the narrow end, represents the low frequencies. And as we can all appreciate as clinicians, when you think of the cochlea, all sound activation, all traveling waves ripple, they're rippling in the cochlea. They enter the cochlea through the base. So the base of the cochlea is where the well-trodden carpet is. All sounds go through the base of the cochlea, the treble region, in order to get to anywhere else. And you can think of the carpet analogy. I mean, the carpet by the door is where it gets most dirtiest, because everybody walks through that area to get anywhere else in the room. And this is really why people suffer from treble high-frequency hearing loss more than they do from base hearing loss, because the base frequencies are cozy and comfortable way up here at the apex, and not all sounds go through them to get to anywhere else. So it's always the trouble with treble, is what I call it. At any rate, when you're looking at hair cells, they are going to be located in these triangular regions, the scala media, not anywhere else in the cochlea, and specifically in these triangular regions, the hair cells are located right where I'm drawing with my cursor there, and right where I'm drawing here, and right where I'm drawing here, in these little tiny areas. And notice that the hair cell region is actually narrower at the base of the cochlea, and it gets wider as you get to the narrow end of the cochlea. It's backwards from what one would normally think. At any rate, we'll move on to show this picture of healthy hair cells. We've got healthy inner hair cells here, and healthy outer hair cells here. And we can say, just in reference to what our previous slide was, this is probably at the wide base of the cochlea, at the treble region, because at the apex of the cochlea, the narrow region, you've actually got about five rows of these outer hair cells. At the base region where the treble frequencies are, you've got about three rows. At any rate, let's concentrate on the term afferent. Afferent means brain-going. The inner hair cells are afferent. That means they take sound information and send it to the brain. All senses are afferent. Touch, smell, vision, hearing, all sensory information goes from the outside to the brain. So sensory information is afferent. Motor information, your muscles, they take information from your brain. They're different. They're efferent. At any rate, talking about afferent, you've got the inner hair cells sending information to your brain. Why do you have the outers? Well, you have the outers to help these inner hair cells pick up soft sounds below conversational speech, sounds of 10, 20, 30, 40 dB. Those sounds need the help of the outer hair cells in order that the inner hair cells can pick them up and send them to the brain. Very interesting. If you're looking at outer hair cells, this is a picture of damaged outer hair cells. Outer hair cells, as we said, are efferent. They take info from the brain and help the inner hair cells pick that soft information, pick it up and send it to the brain. So they receive information from the brain. In any system, the moving part tends to die first. The outer hair cells are literally moving. They're mechanical. They stretch and shrink constantly. In any system, as I said, the moving part tends to go first. The speakers in your stereo system will die first before the amplifier does. The CD player, the DVD player, the moving part tends to go. Here's a picture of the outer hair cells in action. You can see three rows of outer hair cells here and notice their hairs. Their hairs are jammed into the underside of this big blue bleb here called the tectorial membrane. When soft sounds come into the cochlea or when soft sounds activate the cochlea, these outer hair cells somehow, and we don't know exactly how, they're given a message to shrink and pull this membrane down so that the hairs on the inner hair cells can be bent. Isn't that wild? I mean, you have to think about how fast all of this is taking place with every syllable of speech going on. It's one of the fastest reaction systems in the body. When sounds are loud, they create such a big traveling wave in the cochlea that the action of the outer hair cells isn't necessary. There's enough fluid motion going on in the cochlea to bend those hairs by themselves. But when sound is soft, the mechanical action of these outer hair cells is required in order to pull down this tectorial membrane so that it bends the hairs on the inner hair cells. You can really see that the cochlea is not a one-way street. It's a two-way street. It's got afferent information going from the inner hair cells, efferent information given to the outer hair cells, a whoppingly complex but amazingly beautiful organ we have called the cochlea. The cochlea, by the way, comes from the word cochleas, which is Greek for snail shell. Remember, always think about the cochlea as being about the size of an eardrum, and it's about the size of a fingernail, small. Cochlear dead regions are not due to outer hair cell damage. Outer hair cell damage, outer hair cells, as you can read on the slide here, they amplify and they sharpen the traveling wave peak. They amplify soft sound information so that the inner hair cells can pick it up. They also sharpen the peak, as we'll see in the next slide. But anyway, damage to the outer hair cells reduces the size of the basilar membrane vibration. In plain language, the basilar membrane is the floor upon which all the hair cells stand. That's the floor that ripples. That's the wave. That's the rippling action of the floor upon which the hair cells stand that activates the hair cells. Damage to outer hair cells reduces that traveling wave height or amplitude. And if you had no outer hair cells, you would have about a 50 to 60 dB sensorineural hearing loss. And that's the most common degree of hearing loss around, presbycusis. Anybody who knows me will now be able to predict what I'm going to say next. You ever heard of the word Presbyterian? Well, that's Church of the Elders. Presbycusis is hearing in the elders. Presbyopia, your arms aren't long enough to read the page. Presbyopia hits you when you're about 40, presbycusis hits you around 60, 65 years of age. And at any rate, if I, like a thief in the night, went and took out all of your outer hair cells and tested you in the next morning, you would have about a 50 to 60 dB sensorineural hearing loss. Presbycusis usually infers outer hair cell damage at the base of the cochlea, where the high frequency hair cells are. More severe sensorineural hearing loss, so hearing loss greater than 50 or 60 dB, is going to necessarily mean inner hair cell damage as well. Those cause about 50 to 60 dB hearing loss, greater than that's going to be a combination of damage then to outer and inner hair cells. So if you have damage to inner hair cells, you've really got a problem. Houston, you've got a problem, because that means a garbled message is being sent up to the brain. And that's why severe hearing loss often presents with worse speech discrimination than mild to moderate hearing loss does. It's because with severe hearing loss, inner hair cells as well as outers are damaged. At any rate, a loss of sharpening of the traveling wave results in increased difficulty hearing in noise, big complaint of most of our clients. A slight drop in speech discrimination, but not all that much. This is what happens with outer hair cell pathology. Let's look at this next slide. Outer hair cell contributions to the traveling wave. Now look at this horizontal yellow line. That is the basilar membrane. Think of that as high frequencies here on the right, mid frequencies in the middle, and low frequencies here on the left. So in this case, you've got a traveling wave, this black ripple here, the floor upon which the hair cells are standing, has been rippled. And in this case, we've got a low-frequency traveling wave because its main peak is in the low-frequency region of the cochlea. This orangish line around here, it kind of looks like a kite. And I call that, well, that's the envelope of the traveling wave. You can see where all the ripples are connected. Now the envelope of the traveling wave is shaped, as I said, like a kite. You can see how it's asymmetrical. Notice how it's sharper in the front, that the wave front is steeper than the long, shallow tail. The tail is very long and shallow. The front is more steep. It's an asymmetrical shape, and this is important regarding cochlear dead regions. We'll get to that in just a second here. But notice in light blue here, this traveling wave is sharpened and amplified, both. Outer hair cells amplify the wave, as you can see here by the dotted line, and also, as you can see by the dotted line, outer hair cells sharpen that wave. Now think about the significance of sharpening the wave. This wave by itself has kind of a dull, rounded peak. And notice how many hair cells are stimulated at once. It's like a comb without that many teeth. I mean, if you've got no outer hair cells, a frequency of stimulation causes many hair cells to react at once. Outer hair cells actually serve to sharpen the peak of the traveling wave so that you can discriminate between frequencies that are right next to each other. If you haven't got the outer hair cells, you haven't got that fine frequency resolution. And that's why people with outer hair cell damage have difficulty hearing speech in background noise. They have difficulty separating frequencies that are close together. They have that difficulty as it is. So in a noisy environment, they have increased difficulty separating speech from background noise. It's all about the anatomy of the cochlea. This is why I think understanding the anatomy of the cochlea is so important for clinicians. The implications of having a traveling wave with damage to outer hair cells is illustrated here. The top shows a traveling wave with two tones. This person is given two tones of stimulation at the same time. He's got two sharp peaks, easily distinguishable from each other. This person has normal, healthy hair cells. The middle panel shows damage to the outer hair cells. It's the traveling wave caused by the two sounds. The peaks are both smaller and they are more dull and rounded. The third or bottom panel shows what happens when this person is aided with hearing aids. Sure, we've made this middle traveling wave bigger, but we haven't restored its sharpness. And we can't. Humpty Dumpty fell off the wall. Humpty Dumpty had a great fall. We can't put them back together again. This is why hearing aids have a two-fold task. They not only need to amplify, but secondly, they need to increase the signal to noise ratio. Because the person with hair cell damage cannot separate frequencies close together anymore. This person needs the help of directional microphones and digital noise reduction to help increase the signal to noise ratio. So hearing aids, one, amplify, and two, have to increase the signal to noise ratio. Because the loss of hair cells means the traveling wave is no longer amplified and it's no longer sharpened. But that's most mild to moderate sensorineural hearing loss. Cochlear dead regions actually are due to inner hair cell damage. So outers tend to die before inner hair cells. Again, they are the moving part. They're more susceptible to aging and noise damage. And by the way, noise-induced hearing loss is the second most common cause of hearing loss. The sad thing about NIHL is that it's preventable. We can't do all that much about aging, however. If someone can figure that out, I'm all ears. At any rate, the second point here, if outer hair cell damage causes about 50 to 60 dB hearing loss, more severe sensorineural loss means inner hair cell damage as well. Inner hair cell damage, as we said, really deteriorates speech discrimination. Because now a garbled message is sent afferently on to the brain. The question now goes, what audiograms suggest cochlear dead spots? And to understand that, let's look at the next few slides. The asymmetrical traveling wave talks to us all about the resultant audiogram. Here are two traveling waves you can see, two envelopes. An intense low-frequency traveling wave moves the entire basilar membrane. Look at this big orange kite. It's the same traveling wave envelope we saw earlier. But a high-intensity, high-frequency sound has a short traveling wave, and it's always light blue in color. No, I'm just kidding. But notice how it still has that asymmetrical shape. It's just shorter. It's confined to the base of the cochlea, but it still has that asymmetrical shape. Now, when we move over to this next slide, we can discuss what's called the upward spread of masking. Think of this orange wave, this low-frequency wave, made by a low-frequency sound. Think of like the rumbling of a truck. And here is a soft, high-frequency sound. Think of a canary in your kitchen. Well, the rumbling of a truck. Notice how the envelope easily masks the soft, high- frequency sound. You can think of, look at how background noise easily masks the soft, high-frequency consonants of speech. The consonants, all the high pitches of sound, those are softer and higher in frequency. Background noise is like a truck that drives right over them. Lows mask highs quite easily due to the shape of the wave. But it doesn't work the other way around. Look at this slide. Here's a soft rumbling of a truck. And now here's a fanatically angry canary. Beep, beep, beep, beep, beep, beep, beep. Well, she can peep all she wants. That traveling wave can be made larger and larger, but by gum, it's stuck at the base of the cochlea. It's not going out here. Do you see? And that's why lows mask highs better than highs mask lows. It's called the upward spread of masking. And that's just the way the cochlea works. It's the nature of the anatomy of the cochlea. So audiograms associated with cochlear dead regions hinge on this anatomy. We'll see. Look at this slide. Low-frequency dead regions can masquerade as moderate reverse sensorineural loss. Here's a reverse hearing loss, a rising audiogram. Not all that common, but we've encountered them. We've all encountered them. And now look what's happening here. What I've done is I've laid a line across the top of the cochlea. Think of that as the basilar membrane. I've unrolled the cochlea. By the way, if you've unrolled the cochlea, how long would it be? Well, in the United States, it would be about an inch. In Canada, it would be about two and a half centimeters. A centimeter is a good thing to know. It's about the width of your index fingernail. At any rate, here's a traveling wave caused by a low-frequency sound. Now pretend again like a thief in the night. I went into your ear and I pulled out all, not only the outer hair cells, but now I took out all the inner hair cells below 1,000 hertz, left all the hair cells that represent above 1,000 hertz, but just removed all the low-frequency inner hair cells. Well, if I tested you the following morning, yep, your high frequencies would be normal. But do you think your low frequencies would be at the bottom here? Not a chance. Your low frequencies would look like this. And you know why? Because when I stimulated the low frequencies with enough intensity, the tail of the wave sloped into the mid-frequencies and you'd raise your hand. Yep, I heard something. You'd be hearing, in quotes, low frequencies with mid-frequency hair cells. Isn't that weird? I mean, that's called off-frequency hearing. It's got to sound weird. And we'll tackle that topic at the end. Low-frequency traveling wave in a totally dead inner hair cell region will stimulate healthy hair cells in mid- to high-frequency regions. Once you've made that, once you've presented it louder than about 50 or 60, the traveling wave size is big enough to cause its tail to stimulate healthy mid-frequency hair cells. So an asymmetrical traveling wave with a steep front, longer, shallower tail, total deafness in the lows will look like a moderate low-frequency sensory neural loss. It's called audiological checkmate. You can't do anything about it. It's just the way it is. That's why it's important to take a case history because this could be due to Meniere's and then it's not due to cochlear dead regions. But we're all clinicians. We know. But we're going to tackle some of these topics as we move through. This slide is showing high-frequency dead regions. But high-frequency dead regions have to be a severe and they have to be a precipitous sensory neural hearing loss. Has to be. And the reason why, again, is because of the shape of the traveling wave. Notice if I stimulate at 2,000 hertz, pretend like a thief in the night. I had come into your cochlea and I damaged all inner hair cells above 1,000 hertz and left all the hair cells representing frequencies below 1,000 hertz, left them alone. Well, if I tested you the next morning, this is the audiogram you'd see. And how come? Well, think of 2,000 hertz. I'd have to make it fairly loud in order for the front of that wave to just stick into the mid-frequency regions and stimulate mid-frequency hair cells. So a high-frequency traveling wave in a totally dead inner hair cell region will stimulate healthy hair cells in the mid to low regions, but it's got to be quite intense in order to do this. The steep wave front has to be intense for this to happen. Due to the asymmetrical traveling wave shape, severe precipitous sensory neural hearing loss actually looks like a mirror image of the traveling wave front. Weird. For example, look at this. Here's a hearing loss, the same one we showed you over here. I'm just moving now to show you what happens if I stimulate at 1,000 hertz. I'd have to make the sound fairly, a little bit loud, and then this would stick into the high-frequency region and you'd hear it. If I go to 1,500 hertz, I'm going to have to make it quite a bit more intense for the front of that wave to just barely stimulate mid-healthy, mid-frequency hair cells. And if I go deeper into the heart of a Texas Saturday night and stimulate at 2,000 hertz, I have to really increase the intensity so that the front of that wave still stimulates healthy mid-frequency hair cells. So from here to here to here, this explains the reason why dead spots in the high frequencies will result in, A, a severe high-frequency loss, and B, a precipitous high-frequency loss. Again, the reason is because of the shape of the traveling wave envelope. Cookie-bite audiograms are kind of like a combination of the above. Cookie-bite audiograms, as we know, are generally genetic in cause, and usually the deepest area in the center is actually a cochlear dead region. It's best to amplify the sides and don't concentrate so terribly much in the dead center. We'll discuss now how cochlear dead regions rose to public consciousness in our field. The man who came up with the concept really is Brian Moore, PhD, a world-renowned psychoacoustician from Cambridge University in the UK. Bloody well, eh? Testing for cochlear dead regions. He came up with the threshold equalizing noise test, the TEN test. I'm not advocating here that everybody goes out and buys the TEN test because I don't think it's necessary. But Moore gave us a gift in this test because understanding this test forces us to understand cochlear physiology. We'll just describe it. He came up with this test around 2001, and it's rather heavy slog reading, but it's interesting. The TEN test noise, it's a broadband noise and it's delivered ipsilaterally to the tones. In the headphone, the tones are delivered to the ear. You raise your hand when you hear them. And when you're doing the TEN test, you're delivering that broadband noise into the same ear and seeing what intensity masks the tone. So unlike regular masking, you're not putting noise into the good ear to find out how bad the bad ear is. You're masking the same ear as is getting the tone. The TEN test has a unique spectral shape. The noise has a very unique spectral shape. For normal hearing loss, it gives equal masked thresholds. For example, if you had zero dBHL thresholds and I dumped in 50 dB of that TEN noise to your ear, you would have a 50 dB flat hearing loss across all frequencies on the audiogram. That's what we mean by it's having a unique spectral shape. So no, you can't just use your speech masking noise on your audiometers. Many people ask me that. And the reason why you can't is because speech masking noise is usually pink noise, which has more energy in the lows and less in the mid and the highs. Well, here's the TEN noise spectrum. It too has more energy in the lows, but it has a very unique shape unlike pink noise. It has a specific shape like this. At any rate, that's why you've got to use the TEN noise if you're using the TEN test. So here's an example of a person that I tested some years ago in Canada. And she had, okay, hearing levels were, you know, fair to middling, you know, not great, but not bad. I dumped in 30 dB of that TEN noise and it elevated her thresholds to 30. Didn't do much to this one because that threshold couldn't hear the noise. Okay, got 50, you know, 5 dB, but what's 5 dB among friends? Now, the main assumption behind the TEN test is low, let's look at this slide here in red, white, and blue. Such an American slide. What do you say? Look at the red area first. Pretend that's the dead area. Low frequency cochlear dead region resulting in 50 dB thresholds. Remember that reverse rising audiogram we showed you earlier? That's why I say 50 and not 120. Now, look at the blue here where I'm pointing to the right. Soft, ipsilateral TEN noise, for example, 30, will elevate the thresholds for the low frequency sounds. And you'll say, how? Well, laying this broadband noise across the whole cochlea, it's a broadband noise. If these thresholds here come from this region here, well, then masking this region here will have an effect on these thresholds. And again, in black, it says because the thresholds in the dead region come from the higher frequencies, they don't truly arise from low frequency air cells. So just a wee bit of masking noise will have an effect. Now, if the hearing loss in the low frequencies is a true moderate low frequency sensory neural loss, and it's not due to a dead region, then the soft ipsilateral TEN noise will have very little effect. It'll mask the healthy high frequency thresholds, as it should, and elevate them as a result. But the low frequency thresholds wouldn't even be able to hear the TEN. See these low thresholds here? If they were real, they wouldn't be able to hear the soft sound. So they wouldn't be affected at all. And so the thresholds in the lows would be unchanged. Again, for high frequency dead regions, look at the main assumptions again. High frequency cochlear dead regions in red here, resulting in 80 dB HL thresholds. Go to the left. Soft ipsilateral TEN noise, e.g. 30 dB, will elevate the thresholds for these high frequency tones. And again, why? Because the thresholds in the dead region come from low frequency hair cells. These thresholds here are coming from these hair cells here. These thresholds don't truly arise from the high frequency hair cells. And so a wee bit, 30 dB of broadband noise will have an effect, and it will increase these high frequency thresholds. Again, appreciating the anatomy of the cochlea, the unique asymmetrical shape of the traveling wave, all helps to understand why reverse audiograms result from low frequency dead spots and high frequency severe precipitous loss results from high frequency dead regions. If the hearing loss in the highs is a true severe high frequency sensory neural loss and not due to a dead region, well, then that soft ipsilateral TEN noise will again have little effect. It'll mask the healthy low frequency thresholds and elevate them as a result, but the high frequency thresholds here won't even be able to hear this noise. And as a result, they'll be unchanged. So now let's look at some examples, some examples and implications for fittings. When you're looking here, this is actually, again, from a real live subject, and it's great to have students when you're teaching at a university because you get slave work done for you there. It's just great. I was just able to assign the project and get the results and use them. Here you go, a person with mild to moderate high frequency hearing loss, right ear, mild to moderate or normal in the lows and dropping to a moderate loss in the highs for the left ear. Okay, we put in 30 decibels of TEN noise. Look what it did. It moved her good hearing down to 30, as it should, and it didn't have much effect here. It had a wee bit of an effect here, could be that her worst high frequency hearing was actually dead, could be. And again, the same general scene is noted in the left ear. It moves the good low frequency thresholds down to the level of the TEN noise that we put in the ear, and it didn't have much effect on the highs, except way at 8,000. Look at this person now with profound high frequency sensorineural loss. Cochlear dead spots just by looking at the audiogram are suspected because just the shape of the audiogram kind of raises or rings a bell, kind of, you never know. Okay, we put 30 decibels of TEN noise ipsilaterally in her right ear. It shifted her good low frequency threshold to 30, 35, so here you go. But lookie, lookie, what happened over here in the highs? It also affected these, and it shouldn't have. They shouldn't have even been able to hear the tone, the noise. The same situation was noted in her left ear. Well, let's put in more TEN noise. Let's dump in more. Let's put in 50. Well, when we put in 50, it shifts her good thresholds to 50, and it did similar in the left ear. Why this one went to 40, I don't know. Blame the student who did the test. At any rate, notice here in the highs. The high frequency thresholds are affected by as much as 20 dB. Shouldn't be because they wouldn't even hear the noise. Remember, the noise is draped across like this, and if the noise is draped across causing a 50 dB hearing loss in someone with normal hearing or shifting any threshold better than 50 to 50, if these thresholds in the highs are like in the 90 to 100, 80 to 100, they shouldn't even be able to hear that 50, and yet they're shifted. So it means that these high frequencies are masquerades, masqueraders. They came to the party uninvited. They aren't real. Implications for fittings. Moderate reverse sensorineural loss. Severe precipitous high frequency sensorineural loss on the right. Fit the transitions. You can help the dying. You can't help the dead. If you're fitting someone on the left ear with a rising hearing loss, first of all, as clinicians, how much success do we enjoy fitting reverse hearing losses? Not all that much, do we? For one thing, we're amplifying a lot of low-frequency background noise. But for another thing, maybe we're chasing after something that isn't there. We need to take a good case history. Maybe it's Meniere's. Maybe it's just an honest-to-goodness low-frequency loss, genetic, and these thresholds here are real. Then again, maybe it's an honest-to-goodness profound hearing loss, and this person is deaf in the low frequencies. Again, could be genetic. Maybe. You need to take a good case history to understand, to help in your assessment here. But also, look at the light blue area I shaded here. This is where I'd concentrate if I were fitting this person. I'd work on the damaged areas and not so much the worst areas. Again, you can help the dying. You can't help the dead. And it's the same with the right ear. Look at the severe or the right ear, they're both right ear, but look at the high-frequency severe precipitous loss. Again, over here, I would focus on the red area, this red triangle, the transition where the hair cells are dying. They're not necessarily dead. If I were trying to fit in vain these areas in the very high frequencies, I mean, you'd be asking for screaming, whistling feedback anyway. Well, this is kind of weird what happened to this little O here. It kind of moved over from 8,000 and squeezed over. Now, what things we'll do in the middle of the night. At any rate, again, the idea here, implications for fitting, you can fit the transitions, not the worst thresholds. Left corner audiograms are interesting. And many companies, manufacturers, beginning with Phonak and then Widex, and now other manufacturers as well, are working on various forms of frequency transposition or frequency compression is what Phonak does. You know, when you're looking at audiograms like this, this person belongs in a unique clinical camp. This person's speech is going to likely be different. They might very well have pitched, but like I'm speaking to you now, and I'm not trying to imitate with ridicule. What I am trying to indicate is that the person has never heard the high-frequency consonants, and so he or she doesn't pronounce them. He or she speaks with the frequencies that he or she hears, mainly the lows. Well, hearing aids today are offering some types of frequency transposition, thereby moving frequencies from the highs and positioning them in low-frequency areas so that highs can be made use of, so that the low-frequency hair cells can sense high-frequency sounds. I look at frequency transposition as like a bridge between a hearing aid and a cochlear implant. We've all heard a compression. Well, compression deals with intensity, okay? Compression doesn't normally deal with frequency. This is frequency compression. You're taking highs, and you're moving them over. Phonak literally squeezes them over. Widex lifts them and takes them over. Different strokes for different folks, but the idea is generally the same, transposing the highs and moving them over to the left so that the low frequencies can make use of high-frequency information. Do you ever wonder why... You ever hear how I sound like Andy Rooney, the late Andy Rooney from 60 Minutes? Do you ever wonder why, ever wonder what sounds are like for people with dead regions? I recall testing people with reverse sensory neural hearing loss when I first started out in audiology. I suspect dead low-frequency regions, when the reliability is poorer for the lows. Let's say you've got a reverse loss, and it's 50 dB threshold at 125 Hz or 250 Hz. When I retest, the threshold will be 40. If I retest, the threshold will be 55 or 60. I'll get these kind of floating thresholds that aren't reliable, whereas thresholds above 1,000 Hz will be, ding, quite right on. But the lows won't be as much. But I've never asked the client what the pure tone sounded like when I'm looking at the slide here. And I should have. I do recall testing people with pronounced high-frequency sensory neural loss. I remember a guy in Bellingham, Washington, where I went to school at Western Washington. And this guy, he was sitting across from me at a table, and I had a Beltone portable audiometer. And when I tested him at 1,000, he was normal. At 2,000, he was down at about 50. At 4,000, he was off the board. I could hear the sound coming from the headphone at 90 dB. I could hear it from across the table. And I asked him, Don't you hear that? He goes, No, but I feel something. It feels like a tickle, kind of a scratch. Other clients have reports as well. They say that the tones in the dead region sound like noise. However, these observations are quite inconsistent. And so the ratings of clarity alone shouldn't be used as reliable indicators of cochlear dead regions. Keep it simple. You don't need the TEN test, really. As Bob Dylan says, you don't need a weatherman to tell you where the wind blows. Just wet your finger and stick it up in the air. I mean, look with common sense. First at the shape of the audiogram. That's a dead giveaway. And then play a tone for the person in that dead region and ask the person what the quality of that tone is like. If the quality is poor, don't go there. So if you see suspicious audiograms, then suspect dead regions. Present a tone so client can hear it in that dead area, here being with quotes, and ask as to its quality. If it's poor, don't amplify in those frequencies. I'll stop here by giving you some references. Most of them are from Brian Moore. Brian Moore, the psychoacoustician out of Cambridge University. World-renowned. He publishes like mad. He's got articles and articles and articles. The last one's by a little old me in my old textbook. Chapter 2 covers cochlear dead regions. And I try to write it in plain language that's readable. But have a read there as well. I'll stop here, but thanks. It's been a slice. Again, thanks to IHS for letting me do this webinar for you. Cheers, and have a good one. Ciao for now. If we want, we can have some questions. Yes, don't go anywhere yet. So thanks, Ted. We're really excited to tell everyone that more than 250 of you have joined today on the webinar. We do have time for questions. So if you have a question, please enter it in the question box on your webinar dashboard. So our first question is from Mary. She's curious, how many people have cochlear dead regions? Oh, that's a good question. As we know, I mean, the reverse sensory neural hearing loss isn't all that common. And I just showed that one because, well, we just start with the lows and move to the highs. So with reverse loss, I wouldn't say it's all that common. I mean, it's just when you get a reverse sensory neural loss, by all means do a good case history to help you as a clinician figure out what might be the cause of it. Because as I say, if a person's talking about dizzy spells and things like that, it's Meniere's. So it's not a cochlear dead region at all. The high-frequency dead regions are more common. And guess what the most common cause of high-frequency cochlear dead spots is? Noise, prolonged exposure to noise. So when you've got someone with a pronounced high-frequency loss and take a case history again, any noise exposure, well, probably he or she will say yes. So I would say high-frequency dead regions are much more common than low-frequency dead regions. Cochlear dead spots resulting in cookie-bite audiograms are rather rare as well. But I'd say of the three types, high-frequency cochlear dead regions are the most common. Thanks, Ted. Joanne wants to know if genetics play any role in cochlear dead regions. Yes, they do. That's a good question. Some people generally do have, they're born with it. You can think of many genetic anomalies that someone has, you know. Oh, gosh, let's just think some people have a, I knew someone with one brown eye and one blue eye. Interesting, isn't that wild? But anyway, back to her question. You can be born with dead regions in the cochlea. It's not an anomaly. It could be purely genetic that you have no low-frequency dead region, no hair cells or no high-frequency hair cells or no mid-frequency hair cells, as in the cookie-bite audiogram. But you see, with the cookie-bite audiogram, guess what? It's the frequencies in the middle that are likely the worst, as you can see by the thresholds, and they may very well be resulting from completely dead areas of the cochlea, and yet the loss just looks like it's moderate in the middle. For that person, the beauty of having digital hearing aids is we can control the amplification and the gain so well across the channels that we can manipulate exquisitely exactly where we want the gain to be. And with a cookie-bite loss, I wouldn't put the gain, I wouldn't concentrate it in the dead center. I wouldn't. I would fit the side transitions more. And with a precipitous high-frequency hearing loss, again, I would confine my amplification to about 2,000 hertz. I wouldn't go out much beyond that. But it's a good question. Yes, genetics can be a definite cause of cochlear dead regions as well. Awesome. Thanks, Chad. We have a question from Melissa. She asks, what do you do in the event that there is no transition? We have a client that goes from 15 decibel thresholds to 120 immediately. Wow. Wow. Interesting. Well, you can't fit that person as far as with traditional fitting. You could try frequency transposition. It is unique to me that you would find nothing like that steep of a drop. In her case, I would use frequency transposition. I would be looking at the best of the manufacturers for that and ask them very carefully what they might want to try in fitting this person. But definitely frequency transposition. Ha-Sheng has a question, Ted. He wants to know, what is the best hearing aid technology for patients with a dead region? Is it not frequency transposition or compression, or what are your thoughts on that? Well, you know, I'm going to say Phonak was the first one that really came out with what they call frequency compression. And they really involved Richard Seawald, who was a pediatric audiologist. He's now retired. But they involved him in studies. And he was able to note that children with completely dead high-frequency regions, their speech was very hyponasal at first. Their speech was much like this at first. And then with prolonged usage of Phonak's frequency compression, gradually in the speech of these children, the hyponasalness started to, in that you started to hear the letter S. You started to hear sh-sh-t. And the consonantal pronunciation began to improve because high-frequency information was being delivered to this child so that he or she could distinguish the difference between sh-sh-t and sh-sh-t. So which is the best at the risk of getting manufacturers upset? I really hesitate to say. But I will say Phonak pioneered the study with Richard Seawald, Ph.D. audiologist there. And then Widex soon emerged with a slightly different technology. They don't use frequency compression, but they literally move high-frequency regions over to the left. So instead of squeezing highs over to the left, they literally transpose them to the left. Six of one, half a dozen of the other. The end result, I would imagine, is going to be quite similar. But I will be honest with you. I don't know which one is the best. I will imagine Widex will say it's the best and Phonak will say it's the best. Thanks, Ted. Ronald wants to know, if the tonal quality is still intact in the high frequencies, would you still amplify or would you continue to sit the slope? I think I would try amplifying. But again, remember, even with common sense, or I should say use common sense, with that steep sloping high-frequency loss, you know when the 4,000 Hz is down at 100. Think of 1,000 Hz as going to be at 10 or 20. 2,000 Hz is down at 60 or 70. 4,000 Hz is down at around 90 to 100. Even if that person said he or she heard 4,000 Hz quite clearly as a tone, would you be delivering tons of gain to 4,000 Hz? Your hearing aid would be fighting feedback so hard. So that's a dicey question, that one. Because even if the person didn't have the classic cochlear dead regions, I'd still be amplifying the 4,000 Hz in that case with caution. Do you see what I mean? Thanks, Ted. Allie has a question. She has sort of a statement and a question. She says, we cannot use speech noise in this test due to the spectrum shape of this kind of noise. What if we use narrow band noise for each frequency? We can do an effective masking at first and then start the test based on that. What do you think? No, because I get your question. But what you're trying to address, if you use narrow bands of noise, no, it's not very effective because you're just masking the frequency in question. When you're doing a testing for dead spots, you want to lay a broad band across the whole audiogram and then just see where it makes common sense that it would mask. Let's say if you have a mild to moderate sensory neural loss. Well, if you lay 30 dB across the whole board, the thresholds below 30 dB should be unaffected by that 30 dB broad band noise because they couldn't hear it. But if the high frequency thresholds that are worse than 30 dB are affected, well, then you know that those high frequency thresholds are really coming from the other thresholds. And so the question isn't going to be answered as directly by using narrow bands of noise. And also, I'll say this common sense back. I'll say, why not make the test short? The narrow bands of noise, you'd be sitting there testing for a long time, and I'm not sure if your question would be answered. I would work with a test that's been calibrated and done with past research that has been shown to reveal cochlear dead regions and then stick with that. That's what I would do because the research is backing it up rather than cobbling together something from my own audiometer. Do you know what I mean? I guess that's where I come from. Keeps the testing shorter as well. Thank you, Ted. We have a question from Ellen. Ellen asks, how can you tell if you have reached the upward spread of masking? What will the patient report? How can you tell? Oh, I'd say that's a good question. Basically, let me answer it in twofold. The upward spread of masking occurs for all of us. It occurs for people with hearing loss. It occurs for people with normal hearing. It's the way the cochlea works. So if you and I with completely normal hearing hear a soft canary in our living room and the rumble of a truck coming down the street, the rumble of the truck will cover the peeping of the canary. It's going to do that just because of the upward spread of masking. It's just going to happen. So it's going to happen at any level, at soft levels, at medium levels, at louder levels, because of the shape of the traveling wave envelope. So the upward spread of masking isn't so much when it's going to occur, it's just a phenomenon that occurs, and it occurs at lots of intensity levels. If the canary was really soft and the truck was moderate, the upward spread of masking would occur. If the canary was moderate and the truck was loud, the upward spread of masking would occur. And what's the ratio of loud to soft? I can't really say. But let's look at the person who had the cochlear dead region in the low frequencies, the very first case that I gave you with the low frequency rising hearing loss. Upward spread of masking took place in that person. He had totally dead regions in the lows. And when I got the intensity to around 50 or 60, the mid frequencies began to hear it. So in that case, that particular case where a person was deaf below 1,000 hertz and totally normal above 1,000 hertz, the upward spread of masking enabled him to hear in quotes low frequency tones at around 50 or 60 dB. But back to my first point. Think of upward spread of masking not so much as when it happens in dB. Think of it as a phenomenon that happens, and that's why background noise wreaks havoc with people wearing hearing aids in general. That's why. It's why the noise masks the high frequency consonants. It's why we use directional mics, and it's why we try with digital noise reduction anything to improve the signal-to-noise ratio because of the phenomenon of the upward spread of masking. I hope that helps. Thanks, Ted. We had a ton of questions, everyone, and we have very little time left. So Ted, I'm going to ask you one more question, and then we're going to go on to the end of the webinar. We have a question from Bisla, and he wants to know, if you move pure tone to a different frequency, it becomes a different pure tone, and speech is even more complex than tones, right? So won't it confuse the brain? Are you talking about frequency transposition? You know, I don't know, Ted. Here's what I'll do. I think that this is what the person is asking. If you move a frequency of a tone over to a different frequency, it's going to sound different. Yes, it will. So high frequencies, and I have actually listened to some of these frequency transpositions, and yes, they will kind of sound weird. In other words, the earliest generations ones, they made people sound like Darth Vader. So then you were talking a lot like this. And a person, an adult wearing one of those hearing aids found it hard to get used to. They're better now than they used to be, but yes, they do make the sounds different. They do. But here's the bottom line. If a person with the high frequency dead regions was standing 10 feet away from me with his back turned to me, and I said to the person, let me know if you hear the difference, and the person's back is to me, he's not going to be able to tell. But if he wears the frequency transposition hearing aid, he'll be able to say, yep, they're different. They're not the same. If I said, with the transposition hearing aid, he would say, yep, I hear two different sounds. Without the frequency transposition hearing aid, he wouldn't be able to tell the difference. Okay, thank you, Ted. Well, everyone, sorry we weren't able to get to everyone's questions, but Ted, I want to thank you for an excellent presentation once again. And thank you, everyone, for joining us today on the IHS webinar, Cochlear Dead Regions and Implications for Fittings. If you'd like to get in contact with Ted, you can e-mail him. And actually, I need to make an adjustment to the e-mail that you see on the screen. That is not the correct e-mail. It is tvenema at sha.ca. That's t-v-e-n-e-m-a at s-h-a-w.ca. For all of you who are attending, we are going to send an e-mail out with his e-mail address and some other information. So no worries, you will have it. If you'd like more information about receiving a continuing education credit for this webinar, you can visit the IHS website at ihsinfo.org, click on the webinar banner, or find more info on the webinar tab under professional development. IHS members do receive a substantial discount on CE credit. So if you're not already an IHS member, you will find more info at ihsinfo.org. Please keep an eye out for the feedback survey you will receive tomorrow via e-mail. We ask that you take a moment to answer a few brief questions about the quality of today's presentation. So thank you again, everyone, for being with us today, and we will see you at the next IHS webinar.

cochlear dead regions

fitting hearing aids

hair cells

cochlea

specific frequencies

threshold equalizing TEN test

amplifying frequencies

transition areas

frequency compression technology

patient evaluation