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J.D. Gray: What is permanent hearing loss could be reversed?
This is ASHA Voices. I’m J.D. Gray.
Today on the podcast, we’re speaking with two researchers at the forefront of hearing research. Today’s guests help us rethink what’s possible in hearing treatment, from genetic therapy to laser-based optical tools.
Listen to ASHA Voices episode: What If Permanent Hearing Loss Could Be Reversed?
Jeff Holt investigates a genetic form of hearing loss. Jeff already found success reversing the hearing loss in mice. And, how did the researchers test the rodents’ hearing? By unexpectedly playing loud music and looking for a response in the subjects, nicknamed Beethoven mice:
Jeff Holt: “A deaf mouse doesn’t jump at all, no matter how loud a sound you play. But after introducing our gene therapy into the ears of Beethoven mice, we find they jump again.”
We’ll tell you what happens when this gene is working effectively, and what happens when it isn’t.
When researcher Tina Stankovich *(Stahn-co-vich)* told an optical engineer she wanted to see the cellular structures inside the inner ear, she added that she didn’t know of anyone else looking into it.
Tina Stankovic: “And then he said, “Well, it means one of two things. First, it’s either an unimportant problem, or two, it must be really difficult.” So I said, “I can definitely assure you it’s the latter. It is a super important problem.”
Gray: Coming up, the fruits of this collaboration, including what tools they are using to look at this important and really difficult problem.
Plus, we’ll have a conversation with an award-winning researcher who works with voice disorders. We talk about the twist in his path that changed everything.
I’m J.D. Gray, and this is ASHA Voices.
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Support for ASHA Voices comes from the ASHA Continuing Education Registry. You can earn ASHA Continuing Education Units by joining the ASHA C-E Registry. Learn more at asha-dot-org-slash-C-E.
Support for ASHA Voices comes from ASHA Professional Development. Call for posters for ASHA’s 2020 Connect Conferences is open now through February 12. Submit yours today!
We’re going to turn our attention now to the process of transduction. Transduction is the thing that allows sound to go from out there to in here, inside your head. Transduction occurs somewhere in between when a noise like the strum of a guitar is made, and when it’s converted to the electrical signal in your brain. It’s happening right now as you listen to this podcast.
Jeff Holt is a researcher at the Boston Children’s Hospital and his research is giving us insight into what happens during this process, especially during one very key part.
I spoke with Jeff -at the 2019 ASHA Convention, where he presented as a part of the Research Symposium on Hearing.
Jeff made a discovery about a genetic form of hearing loss. At the origin of the research was a family experiencing this genetic type of hearing loss, but as Jeff began to look at what was happening in the inner ear with respect to transduction, it led him to a protein. That protein has a technical-sounding name T-M-C-One. Where this discovery led Jeff, that was unexpected.
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Jeff Holt: So we discovered the function of TMC1. TMC1, we realized, functions as an ion channel and it converts sound information into electrical signals. It opens and closes to allow ions to flow into sensory hair cells. The ions we’re talking about are calcium, potassium, sodium. Things like that carry a positive charge, and when they flow into the cell, they generate an electrical signal.
J.D. Gray: Okay, so help me visualize. What would this protein look like inside the ear?
Jeff Holt: So it’s within the sensory hair cells. At the membrane of the sensory hair cells, and specifically at the very tips of the hair bundle. So when the hair bundles wiggle back and forth, they’re taking that mechanical information of sound and they’re physically pulling open this ion channel protein.
Jeff Holt: You can imagine something like a donut where the center of the donut, and you’ve got a donut hole and when it’s open the ions will flow through that donut hole into the cell.
J.D. Gray: When it’s closed, nothing can flow through.
Jeff Holt: Exactly.
J.D. Gray: And so what did you find with the family?
Jeff Holt: Right, so there are we estimate 5 to 8,000 patients in the US who carried mutations in TMC1. And some of the mutations are recessive, meaning you inherit one copy from each parent. And if you’ve got two mutations, one from each parent that carry this recessive mutation, you’re not going to have any auditory function at all. Profound deafness would result. Some of the mutations are dominantly inherited. Just one copy from one parent could carry a TMC1 mutation that leads to a progressive hearing loss, with an onset in the mid teen years progressing to about the mid twenties.
J.D. Gray: When you say mutation, what does that mutation look like? Is it not present or is it shaped differently?
Jeff Holt: Right. So within the amino acid sequence of the TMC1 protein, there’s a change in that amino acid sequence. So the amino acids are critical to the properties of this protein. And if you change it, sometimes it has no effect and those can be passed along, people can have normal hearing. But sometimes it has a profound effect and the protein doesn’t function at all. So it doesn’t open and close and prevents ions to permeate the cell.
J.D. Gray: It just remains closed.
Jeff Holt: It just remains closed.
J.D. Gray: Okay. So the protein assists in transduction. Can you give listeners a little background on what happens during transduction?
Jeff Holt: Sure. So at the tips of these hair cells, stereocilia, there’s a little apparatus. It’s sort of like a Rube Goldberg machine. There’s a filament that connects one psyllium to another, and when that filament—it’s called a tip link—gets stretched, it applies a force, a tension, to the ion channel protein.
J.D. Gray: Like a rubber band?
Jeff Holt: It’s kind of like a rubber band. Exactly. It’s got some stretchiness to it but when you pull on that rubber band, that tension gets transmitted to the ion channel TMC1, which opens and closes in response to this force.
J.D. Gray: Okay. And so if someone, strums a guitar, what happens to get that signal to your brain?
Jeff Holt: Right. So the first step is that sound wave entering the ear through the middle ear spaces into the inner ear, where the vibrations will oscillate the basilar membrane. Hair cells on the basilar membrane are moving up and down, wiggling their hair bundles. Tip links are being stretched, and TMC1 proteins are opening and closing. When they do that, that’s the key step, right? As those proteins open and close, allowing ions to flow into the cell. That electrical signal is eventually transmitted to the base of the hair cell, where there’s a synapse with the eighth cranial nerve, and the nerve then will transmit that information from the cochlea to the brain.
J.D. Gray: And you’ve identified where the mutations in TMC1 would occur that would create no sound to get to reach the brain.
Jeff Holt: Exactly. So you have a mutation in TMC1, you’re going to block that rate at the initiation point. That signal transmission pathway is blocked before it ever begins.
J.D. Gray: Tell me a little bit about the research you did to make this discovery.
Jeff Holt: Right. So we had some ideas that the TMC family of proteins might be involved. So we generated mice that lacked TMCs, and sure enough those mice had hearing loss. One of the steps that we did was then to put the correct DNA sequence back into the mice and found that we could recover their function. So they began to hear again. We’re thinking now that this may be a potential therapy someday in the future.
J.D. Gray: How did you know they could hear again? What was that test like?
Jeff Holt: Th e same sort of tests we use in humans. We can record an auditory brainstem response, and we can play different loudnesses and different pitches or different frequencies of sound and map out the audiogram for a mouse, just like you would for a human. Mice with TMC mutations have flat lines. They have no audiograms whatsoever, and so they’re profoundly deaf. But after we introduced the correct sequence back into the inner ears of these deaf mice, we found that they could hear again.
J.D. Gray: Set the scene for me. What music were you playing? Where were the mice? What did it look like?
Jeff Holt: Well, one of the mutations in TMC1 is known as Beethoven, named after the classical music composer, Ludwig Von Beethoven. The reason that name was selected was Beethoven, the musician, also had a progressive hearing loss.
It’s fun we can use Beethoven’s music. We’ll play his Fifth Symphony. That’s one of my favorites or Fur Elise is another one that’s popular in the lab. But, sure enough, when we do that to mice that have been treated, we can get ABRs that recover. We can also use another behavioral trick, which is an acoustic startle response. Just like you might be startled if somebody snuck up behind you and played a sudden loud sound, the mice will as well, and they’ll jump and so we can measure their jump. A deaf mouse doesn’t jump at all, no matter how loud a sound you play. But after introducing our gene therapy into the ears of Beethoven mice, we find they jump again.
J.D. Gray: Wow.
J.D. Gray: Tell me a little bit more about how you’re able to restore this protein in these mice. What kind of therapy is that?
Jeff Holt: We’re using a gene therapy that takes advantage of a viral vector. It doesn’t cause disease in humans at all. It’s rather benign. It’s a nice vector because viruses bring eons of evolution and their job is to get into cells. They infect cells. And so we can take advantage of that. We removed the viral genes and we put in any DNA sequence we’re interested in. In the experiments we’re talking about, we put in the DNA sequence for TMC1 back into the virus, and then the virus we inject into the ear, which can do its job of infecting hair cells, carrying the TMC1 DNA into those cells. The cell then knows what to do with the DNA. It takes DNA, converts it into the TMC1 protein, which restores function.
J.D. Gray: When you begin researching TMC1 did you anticipate that you might find a way to reverse the deafness that this family had experienced genetically?
Jeff Holt: No, that was not our initial goal. Our initial idea was really just to understand how the cells were working. We wanted to understand this sensory transduction process. How they take a mechanical stimulus of sound and convert it into an electrical signal. When we discovered the TMC1 gene was doing that key job, we realized that the gene carries all these different mutations, at least 40, that lead to hearing loss. And so in the process of understanding the biology, we realized, “Hey, this is also an opportunity to help patients.”
J.D. Gray: Have you thought much about people who could use this?
Jeff Holt: Absolutely. We’ve been contacted by a number of patients, some who carry TMC1 mutations and are following our progress quite closely. We’ve also begun talking with various industry partners who might be able to help move this towards clinical trials.
J.D. Gray: I’m wondering if there’s anything else about this research that has surprised you
Jeff Holt: So the strategy that we developed to target the Beethoven mutation, it’s a CRISPR-Cas strategy using genome editing. We think that the strategy may be more broadly applicable. We’ve targeted just the TMC1 gene in this case, but the general strategy could be used to target at least 15 other hearing loss genes that we’ve analyzed.
Jeff Holt: And so we’re thinking now, how can we adapt this to target some of these other forms of genetic hearing loss. And it may also be useful for targeting other forms of inherited human disease. Maybe up to 20% of dominantly inherited human disease could be addressed with these sorts of strategies.
Gray: Jeff Holt is a researcher at the Boston Children’s Hospital. We spoke at the 2019 ASHA Convention, where Jeff presented as a part of the Research Symposium on Hearing.
Coming up… we’ll hear from a researcher looking at sensorineural hearing loss, and we’ll talk about the roadblocks she’s found that are standing in the way of reversing the most common form of hearing loss.
And we’ll hear from award-winning researcher Bob Hillman.
This is ASHA Voices.
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Support for ASHA Voices comes from the ASHA Continuing Education Registry. The ASHA C-E Registry serves more than 120,000 ASHA members, and offers access to opportunities to earn ASHA C-E-Us to keep your license up to date. Learn more about these and many other benefits at asha-dot-org-slash-C-E
Support for ASHA Voices comes from ASHA Professional Development. Want to showcase your work and contributions to the field of communication sciences and disorders during a poster session? Submit your poster proposal to ASHA’s 2020 Connect Conferences by February 12. Go to ASHA dot org slash events slash connect to find out more.
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Tina Stankovich *(Stahnk – oh – vich)* is a surgeon and an auditory neuroscientist working at the Massachusetts Eye and Ear and Harvard Medical School. Tina’s researching ways to reverse sensorineural hearing loss. Like Jeff Holt, Tina also presented at the Research Symposium on Hearing as a part of the 2019 ASHA Convention. She says this is the most common type of hearing loss and points to info from the World Health Organizations that says more than a billion young people are at risk for experiencing this type of hearing loss.
Of course, hearing aids and hearing devices can assist with this type of hearing loss, but I asked Tina what other techniques and ideas were on the horizon.
Tina Stankovich: Well, there are several. One of the issues is that the inner ear cannot be biopsied today, and we cannot see cells inside it to establish very precise diagnosis for a given patient. And that is because the inner ear is a very small and delicate organ. And if you take a coin, a penny, and you’ll see that Lincoln is on the penny, and if you look at Lincoln’s upper face on a penny, the human cochlea, which is the organ of hearing, in cross section is the size of Lincoln’s upper face on a penny.
So you have this very small delicate structure that’s coiling. It’s embedded in the densest bone in the body, and it’s located deep in the base of the skull. So for these reasons, we have been unable to routinely biopsy this organ because even just in attempting to biopsy you would destroy it. And we have not been able to see cells inside it because the current modern imaging techniques that are clinically used, such as computed tomography scans, known as CAT scans or MRIs, which stands for magnetic resonance imaging, do not have the resolution required to see what is really happening at a cellular level in the human inner ear.
So these are the big bottlenecks diagnostically, which really leads to the bottlenecks therapeutically. And what I mean by that is that right now there are no drugs that are FDA-approved to treat hearing loss, which is really astounding if this is the most common sensory deficit across the globe. We are working on enabling better diagnosis and better therapy for hearing loss that would be personalized for a given patient.
J.D. Gray: Tell me a little bit about that.
Tina Stankovich: On the diagnostic side, we are developing an imaging probe that we could place inside a living human inner ear to, for the first time, see what is happening at a cellular level in a given patient. Today all we know about the cellular basis of human hearing loss is based on studying autopsy specimens. So that means that in any given patient, we really don’t know what’s happening in their inner ear at any given point in time.
And that’s one approach that we are taking diagnostically—better imaging. And for that we are using optical tools, basically laser light that allows us to excite the tissue and collect the reflected light. And we are also working on a liquid biopsy of the inner ear. So it’s not a tissue biopsy, but we actually taking a tiny amount of fluid from the inner ear. I have told you that this organ is really small, so the total volume of fluid in the inner ear is about three drops of water. It’s salt water. We even give it a special name. It’s called perilymph. And it’s very similar to the fluid that bathes all of our cells.
So there is very little to begin with. And what we have recently shown the feasibility of is taking a fraction, actually a fiftieth part of a drop of fluid to establish diagnosis. We did this after noise trauma in an animal model, in a mouse model. And here we can detect molecular changes in as little as a half a microliter of fluid.
J.D. Gray: Wow. And what kind of changes are these?
Tina Stankovich: There are changes in what we call inflammatory cytokines. These are signaling molecules that allow recruitment of other cells into the inner ear, and they can also cause localized damage. But they also play important roles in normal cell to cell communication. But once stressed, such as after acoustic trauma, then there is a lot more of these inflammatory cytokines produced.
J.D. Gray: What I want to know is, do you see anything on the horizon that might allow for a drug to treat sensorineural hearing loss?
Tina Stankovich: I think a lot is happening in the field. I think this is a very exciting era to be in. For the longest time, we have been unable to do much aside from devices. But now, because our knowledge of what’s happening at a molecular level has allowed us to start thinking about what is on the horizon, I think there is a promise in gene therapy.
And I think the inner ear has lots of advantages when it comes to delivering gene therapy because there are many genes—by now about 200 genes—that have been identified to cause hearing loss. So hearing loss is one of the most heterogeneous disorders, and these gene therapies can be delivered directly into the inner ear by via localized delivery. So that’s one promising area of research.
J.D. Gray: When you say gene therapy, help me picture kind of with that might be? Is that something that would be injected?
Tina Stankovich: Yeah. It would be injected into the inner ear directly. So you don’t need to inject it via blood stream. And in that case, it wouldn’t go anywhere else. It would just stay within the inner ear. But of course, it’s not for everyone because not everything can be cured by gene therapy. And it also depends on when a patient comes to see a physician. If they come at the time when the ear is missing most of its architecture, then gene therapy will not work. Cells have to be there to be helped by gene therapy.
And in terms of drugs, we are very interested in drug repositioning, which is a fancy name for drug repurposing. And what it means is looking at the drugs that are already out there and FDA approved for other indications and trying to understand whether they would be relevant for hearing restoration. And that is extremely interesting because when you look at the traditional drug development, it’s a process that’s unfortunately not very successful, because 80 to 90% of clinical trials fail. And most of them fail for safety reasons.
And it’s really astounding because these drugs were taken to clinical trials because they showed incredible promise in animal models. And it usually takes about 10 years for a clinical trial to be completed. And this is a super costly enterprise that costs in excess of two and a half billion dollars. Well, that’s inefficient. And what we are looking at is to expedite that whole process by, first of all, focusing on drugs that are already known to be safe. So we avoid that first bottleneck of drugs failing because they’re not safe.
Secondly, that allows us to cut down the time needed to complete a study from 10 years to five years. And thirdly, this is much less expensive. It’s still expensive. It’s estimated to cost about $300 million because you still have to pay for regulatory studies and phase two clinical trials.
J.D. Gray: Tell me a little bit about other researchers in this field. And is this a growing field?
Tina Stankovich: Oh, yeah. This is definitely a growing field. Now that technology is advancing in many ways, we can start addressing these issues. So the advances in science are typically paralleled by advances in technology.
J.D. Gray: You’ve mentioned the breakthroughs in science has made some of this research possible, but I’m wondering, were there other attempts to try to solve this big question of why before that?
Tina Stankovich: It’s a really interesting question. I started looking at this imaging of the inner ear some 10 years ago, and it was at a symposium where we were encouraged to think out of the box and say, what are the bottlenecks and what should we be working on?
And I approached an optical engineer from Switzerland, Demetri Psaltis, and we started talking. And then he asked, “Well, who else is working on this?” And I said, “Nobody really that I know of, in terms of a dedicated effort to see cellular structures in the inner ear.” And then he said, “Well, it means one of two things. First, it’s either an unimportant problem, or two, it must be really difficult.” So I said, “I can definitely assure you it’s the latter. It is a super important problem.” And we started collaborating, and over the years, we have developed new tools to look inside the inner ear.
And now I have … I’m also working with Gary Tierney at Massachusetts General Hospital, who has developed very innovative tools to interrogate other structures in the body, including in the cardiovascular system and gastrointestinal system, basically using micro optical coherence tomography. That’s a big word. But all it means is that you can use laser light to start to see structures that you couldn’t see otherwise. So now, working with him, we are developing this tiny imaging probe that we hope to insert into the inner ear of living people to really see what’s going on.
So basically there wasn’t that much happening 10 years ago, but now that there is a proof of feasibility, lots of people are becoming very interested in this, which is great because that’s needed for progress to happen in the field. There has to be a critical mass of investigators working on the same problem. And we never know where major breakthroughs will come from. All that we can do is keep working really hard on what we hope will make a difference.
Gray: Tina Stankovich *(Stahnk – oh – vich)* is a surgeon and an auditory neuroscientist working at Massachusetts Eye and Ear and Harvard Medical School.
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At the 2019 ASHA Convention, ASHA Journals awarded Bob Hillman the 2019 Kawana Award. Named after ASHA’s former publications director, Alfred Kawana, this award is an honor given to someone for a lifetime achievement in scholarly publications.
Bob Hillman is an SLP specializing in voice and voice disorders. He currently holds posts at the Massachusetts General Hospital at the Voice Center, Harvard Medical School, the MGH Institute of Health Professions, Boston University, and Harvard University.
To say Bob is prolific in his publications doesn’t begin to capture what’s significant about his career. With over four decades of publishing on the voice and voice disorders, his name is attached to more than 35 journal articles at ASHA alone.
Bob’s career involves a forked road, and the path he took surprised me. He joined me at the 2019 ASHA Convention to discuss his career and his publications.
We spoke the day after Bob received his award.
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J.D. Gray: First off, congratulations.
Bob Hillman: Thanks very much.
J.D. Gray: How have you celebrated so far?
Bob Hillman: It was nice. At the ceremony last night I had a table of people join me who were former colleagues and some students, so it was terrific just to be with that group and to have them there and acknowledge… And, you know, actually a bunch of folks in that group were colleagues on some of these publications that you just mentioned, so I felt like we were sharing the honor, so it was very nice.
J.D. Gray: That’s a generous sentiment. I’m wondering if being with them, reflecting on some of these publications, if it gave you any reflections on your career?
Bob Hillman: Well certainly some of those folks I go back pretty far with, all the way back to when I started my career at Boston University. Then you mentioned a fork in the road. I had become a tenured faculty member at BU and then made the, at the time, seemingly insane decision to give up tenure and go back into more of a clinical setting to start a new combined research and clinical program at one of the hospitals in Boston.
J.D. Gray: If you don’t mind me asking, could you just set this up for me a little bit? How long had you waited to have this tenured position? Where were you at in your career? What year was it?
Bob Hillman: Yeah. So I had gone to BU in 1980 and had gotten tenure there after six years. That was my first academic job after getting a PhD. Then in 1992, after being there 12 years, I decided to make this move. So I walked away from tenure and started an academic position, so since… Started a clinical and research position, and since that time have lived in that environment.
J.D. Gray: I can imagine some people would see that as a risk, to step away from a tenured position.
Bob Hillman: Yeah. I mean, when… And I think it’s still the case.
J.D. Gray: How did you know that you could trust where you were going?
Bob Hillman: It really opened up other avenues. I ended up working more directly with surgeons and the disciplinary team in our center, and through that was exposed to kind of working more closely with the surgeons, managing patients together, kind of an initial interdisciplinary sort of approach to patient care that’s now become very much the thing.
You know, voice centers are now much more prevalent and follow in our disciplinary model, and that wasn’t necessarily the case back when we started doing this.
J.D. Gray: For folks listening not familiar with voice centers, could you kind of give a quick overview?
Bob Hillman: Yeah. Yeah. Again, they didn’t really exist back when we started this. We were one of the few. But it’s an attempt to bring together the professions, particularly the medical professions, that manage patients with voice disorders and not have them need to go to different places to get the services they need.
So it’s primarily a combination of otolaryngology, and, more specifically laryngology, which is a sub-specialty, and speech-language pathology, and more specifically speech-language pathologists who specialize in voice disorders. Then there are other ancillary services that are sometimes brought in, like psychology, respiratory and so forth, other disciplines.
J.D. Gray: You’re saying at this time the center that you were working at, a little bit ahead of the curve?
Bob Hillman: Yeah, it was. This was something… I left BU and went to the Massachusetts Eye and Ear Infirmary and it was the first voice center of its type in the New England area. There were a few other centers around the country, so yeah, we felt like we were at the sort of cutting edge of setting up this kind of facility.
Bob Hillman: The other part of it is that it wasn’t just a clinical facility. It was a clinical facility that integrated research into the whole operation, so we were seeing patients, at the same time running clinical studies, so the two really worked well together.
J.D. Gray: Tell me how it influenced your publishing career
Bob Hillman: As I said, we began working more closely with our laryngology colleagues, and so we would be involved in their studies, they were involved in ours. We were doing a lot of collaborative work, and it really I’d say accelerated the rate at which I had been publishing, which… You know, the fear was I was actually going to be less productive, and I ended up being more productive, surprisingly actually, both in terms of grant funding and in terms of publications. So it was kind of an interesting and somewhat unexpected outcome of what happened.
J.D. Gray: Didn’t your work there allow you to publish things that you wouldn’t have been able to if you….?
Bob Hillman: Yeah. It was the close connection with the medical side, with my colleagues, my surgeon colleagues. One of them I ended up beginning to work with there, and we’ve been working together for 30 years now, Steve Zeitesl, and we’ve now, about 15 years ago, moved the whole group and created a new even larger center at an even larger hospital in Boston, at Massachusetts General Hospital, where we are now.
So he is very much an innovator in the surgical world, and I would be involved in assessing his surgical outcomes, so that created a whole bunch of papers that we wrote together.
J.D. Gray: It doesn’t take a lot of Googling to find photos of you with someone like Steven Tyler. You had treatment on some vocalists, or you were working with vocalists who maybe some of our listeners would recognize.
Bob Hillman: Yeah. It doesn’t represent a majority of what we do, but because we’ve been doing this a while we have gotten to a point… Particularly Steve has gotten to a point where he attracts some pretty high-level performers, and the stakes are obviously pretty high when you’re operating on people like that.
We can mention the names of people that have been public. Some of those are public and some of those aren’t. So you mentioned Steven Tyler. Julie Andrews, more recently Adele, folks like that we have seen and taken care of.
J.D. Gray: Is there anyone that you’ve worked with that has come in to the Voice Center and needed your assistance that’s really stuck in your memory?
Bob Hillman: I think anybody who works in a voice center experiences this. We frequently have the experience that a patient comes in and either doesn’t have a voice because of a disease process and is really becoming isolated, is no longer able to communicate with family and friends, do their job effectively. And we’re able to through a variety of, or combination of, surgical approach potentially, medical treatment and voice therapy, get them back… Essentially give them their voice back.
That’s always a very rewarding experience. That happens literally on a weekly basis in our center. Patients come in in pretty bad shape, and we’re almost always able to improve their situation.
J.D. Gray: That’s incredible though. I just think of the fear they must feel if they have a voice and then do not have that same voice.
Bob Hillman: Yeah, and everybody pretty much says the same thing, and this is true of just human communication in general. It’s so taken for granted. We just talk. We don’t think about it unless you have a problem, and losing the voice is a huge deal when it happens.
People are so grateful and become emotional. I mean it becomes a big deal when you’re able to give someone that… It’s one of the most defining things about what makes us human, right? Giving them the ability to communicate again is huge.
Gray: Bob Hillman specializes in voice and voice disorders. He is the 2019 recipient of the Kawana Award for Lifetime Achievement in Publishing.
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ASHA Voices is produced by the American Speech-Language-Hearing Association and comes from the team behind the ASHA Leader magazine.
Support for ASHA Voices comes from the ASHA Continuing Education Registry. Learn how to earn and track ASHA C-E-Us at asha-dot-org-slash-C-E
Support for ASHA Voices also comes from ASHA Professional Development. There is still time to submit your poster proposal to ASHA’s 2020 Connect conference. Get yours in by February 12. Go to ASHA dot org slash events slash connect to find out more.
A special thanks goes to Lauren Calandruccio *(Cal – ann – drew- cio)*, who organized the 2019 Research Symposium on Hearing as a part of the ASHA Convention.
For more on the Research Symposium on Hearing, including recordings of Jeff and Tina’s presentations, go to asha dot org and search “research symposium on hearing.”
Production assistance comes from Pamela Lorence. I’m J.D. Gray, and this is ASHA Voices.
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Next time on ASHA Voices …
We’ll be talking about strategies for getting the results you want in dysphagia treatment. Among our guests, we’ll meet an SLP who uses her background in exercise science to promote an interdisciplinary approach to this important subject.
How to plan for success with dysphagia treatment.
That’s next time on ASHA Voices.