A Temporary Relief For Tinnitus Sufferers

IRA FLATOW: This is Science Friday. I’m Ira Flatow. And now for more than 50 million Americans, there is no such thing as peace and quiet. Because every moment of silence is accompanied by a persistent ringing in the ears. Do you have it? I certainly have it.

Tinnitus. It’s a problem that affects people of all ages. I got mine when I was in my 30s when a firecracker experiment went off near my head, and my ear’s been ringing ever since. And there really is no generally accepted cure for the constant buzzing or ringing or humming going on between your ears. For people with severe cases, it can be a huge burden.

And most people have to learn to live with it. But now there’s a new treatment for tinnitus on the horizon that embraces a new way of thinking about hearing loss. And joining me to discuss it is my guest, Dr. Susan Shore. She’s professor of otolaryngology at the Kresge Hearing Research Institute, University of Michigan. Dr. Shore, welcome to Science Friday.

DR. SUSAN SHORE: Thank you very much, Ira.

IRA FLATOW: Can you remind our listener, how does the pathway of regular hearing work?

DR. SUSAN SHORE: Well, the sound enters the outer ear and the middle ear, and then eventually gets into the inner ear, where there’s a bunch of hair cells that transduce that mechanical energy into electrical energy in the neurons that go into the brain. And then we hear.

IRA FLATOW: And so what happens with tinnitus? What’s going on there? When a person has tinnitus, what do we suspect is going on between the nerve fibers and the hair cells in the cochlea?

DR. SUSAN SHORE: Well, it’s actually more complicated than just between the nerve cells and the hair cells in the cochlea. What happens initially for most people who have tinnitus is that the hair cells or the nerve fibers themselves become damaged. And that means that they can’t connect with the cells in the brain very well. This is called deafferentation.

So the cells in the brain, which are the ones that really are generating tinnitus, make up for that lack of auditory nerve input to their cell bodies. And they draw in inputs from other senses. One of those senses is the somatosensory or touch system. And so when these cells draw in the somatosensory input, they sort of go overboard, and they draw in too much input.

So the cells begin to fire very fast, and they begin to synchronize with each other, as if there were sound there. But there isn’t a sound there. And so that’s what we figured out over the past decade or so, that the cells that are actually responsible for the tinnitus and sending this phantom signal to the rest of the brain reside in the first part of the brain that gets input from the ear. It’s called the cochlear nucleus.

IRA FLATOW: And so what does your treatment do?

DR. SUSAN SHORE: Well, our treatment harnesses a process that these cells undergo that’s called spike time independent plasticity. And these cells can change their firing rates long term– like for hours– depending on how they’re stimulated. And they have to be stimulated by the ear and also by the somatosensory system. So when there is a certain interval and order between these two forms of stimulation, these cells can increase their firing rate or decrease their firing rate, depending on the interval and order between the two stimulations.

So we figured out by studying spike time independent plasticity in these fusiform cells that if we stimulated these cells with a particular order, an interval between somatosensory stimulation and auditory stimulation, we could depress the firing rate of these neurons. We could desynchronize the circuit, and we could get rid of tinnitus in the guinea pigs that we were recording from.

IRA FLATOW: And how do you do that stimulation?

DR. SUSAN SHORE: Well, to stimulate the auditory nerve, we use sound. But to stimulate the somatosensory nerve, in our initial studies we used deep brain stimulation by putting an electrode right into the brain stem stations of the somatosensory system. But later on for our studies that we wanted to become translational, we used an electrode that we just pasted on the skin of the animal, and then later on in the humans. So it’s just an electrical pad that sits on either the neck or the face.

IRA FLATOW: And how well does it work in people?

DR. SUSAN SHORE: Well, we had an initial trial with 20 people. And we had a very well-controlled double blinded study, where for four weeks people received either a bimodal stimulation, which was the therapy– so the auditory combined with the somatosensory stimulation. And after four weeks, most of these people said that their tinnitus loudness had been reduced. And we measured that.

And also the way they felt about their tinnitus had gotten better. So they were less bothered by it. They could sleep better. They had less psychological issues with it, et cetera. And then after the four weeks, they had a rest period of four weeks, and then they received the other treatment, which was a sham treatment. And the sham treatment was auditory stimulation alone without the somatosensory stimulation.

We predicted that that wouldn’t work because in order to induce this long term plasticity, you have to have the combined auditory somatosensory stimulation. And indeed, it did not work. None of the patients benefited significantly from the auditory alone. Or actually, that’s not completely accurate. Four of the 20 benefited slightly from the auditory alone. But most of them benefited from the bimodal stimulation.

IRA FLATOW: You know, we have millions of listeners. And they’re all going to want to get in on your study.

DR. SUSAN SHORE: Yes, I know. We’ve already received 1,400 emails.

IRA FLATOW: So what can they do? Are we just waiting for some FDA approval on a technique that might be available to them?

DR. SUSAN SHORE: Well, we’re having another trial, where we want to do more people to verify the technique and also to tweak it a little bit because for this first trial, we used four weeks of treatment. And we saw a cumulative improvement over four weeks. So in the next trial, we want to go to six weeks, and hope that that cumulative increase will make the treatment last for longer. So that they don’t have to have a refresher every day, or every week, even. It could be that they have a refresher every month. We don’t know. These are details that we still have to work out.

IRA FLATOW: I would imagine that you would have to craft your treatment to suit every person’s individual frequency problems. Would that be correct?

DR. SUSAN SHORE: Yes, that’s what we’ve done in this first trial, is that the auditory part of the bimodal stimulus consists of the person’s actual tinnitus. So we first measure their tinnitus spectrum using an interactive computer program. And then we transpose that into the actual signal that’s presented as part of the bimodal stimulus.

IRA FLATOW: Quite interesting. Well, I know from the reaction you’ve gotten and the reaction you’re going to get from after today’s program that those of us– and I include myself with those. Luckily I don’t suffer from a terrible case of tinnitus. But I know there are people. I want to bring on another guest who’s researching ways these damaged nerve fibers are contributing to a different kind of hearing problem.

And that’s Dr. Charles Liberman, director of the Eaton-Peabody Laboratories at Mass Eye and Ear. Dr. Liberman, and welcome to Science Friday.

DR. CHARLES LIBERMAN: Hi, Ida– Ira. Really happy to be here.

IRA FLATOW: It’s quite all right. It’s good to have someone get my name wrong for once. I get everybody else’s name wrong. I know you were not involved in this treatment study of tinnitus, but you were part of a group that coined the phrase hidden hearing loss. What is that?

DR. CHARLES LIBERMAN: Well, it’s called hidden hearing loss because what we discovered is that there can be a lot of damage to the inner ear that Susan just talked about that can hide behind a normal audiogram. You said you were exposed to a firecracker, and that caused your tinnitus. I don’t know what your audiogram looks like. But many times after a firecracker incident like yours, the audiogram– the standard hearing test that an audiologist might apply to you– might look completely normal.

And so it would be mysterious in a way, as if my ear is normal, why am I having tinnitus? Why are strange things going on? And basically, what we’ve discovered recently is that even with a normal audiogram, there can actually be amazing amounts of damage to the nerve fibers that take the information from the sensory cells to the brain. So that’s why it’s called hidden hearing loss.

And so the idea is that with this kind of nerve damage, you might not have any trouble detecting a sound. That’s what the audiogram tests when the audiologist asks you if you can hear the tone. But you might very well have trouble understanding, especially complex signals like speech in a noisy environment. It’s like trying to understand conversations in a restaurant.

And I’m sure, as you know, the older many of us get, the more problems we have understanding in noisy environments. We can hear that somebody’s talking, but we have more and more trouble understanding it.

IRA FLATOW: Mm hmm. What about when you have temporary ringing in your ears? You get back from a concert, there’s some ringing, but it goes back to normal. Anything we should worry about there?

DR. CHARLES LIBERMAN: Well yeah, I think you really should worry about it. In fact, exactly what I tell people is that if you expose yourself to sound, and afterwards you hear a little ringing in your ears, or perhaps you feel like you have cotton in your ears, you probably have a temporary hearing loss that could be measured by an audiologist. It might recover, but what we’ve shown in animal models is that noise exposures that cause this kind of completely reversible hearing loss as measured by the audiogram can nonetheless cause permanent loss of nerve fibers.

And that’s the hidden hearing loss idea again. You think you dodged the bullet. Your thresholds went back to normal. But perhaps every time that happens, you’ve lost a few nerve fibers. And as time goes on, that may slowly cause the kinds of deafferentation problems that Susan was referring to that can ultimately trigger problems with tinnitus.

IRA FLATOW: Well, you say that though that standard ear test that we take for hearing loss does not detect the nerve damage. Is there a machine or a way to detect if we have nerve damage?

DR. CHARLES LIBERMAN: Well, we and a bunch of other people are working on it. I think the simple answer is yes, probably. Certainly in one person, we could sort of track it longitudinally. There are electrophysiological tests, which audiologists do, that are kind of like electrocardiograms that measure the summed electrical activity of your nerve fibers in your auditory pathway that are responding to sounds. And we and others have shown that the amplitude of these potentials can go down in people after noise exposure in a way that is consistent with perhaps there being noise damage.

IRA FLATOW: So it’s not that simple little test then that we’re talking about.

DR. CHARLES LIBERMAN: It’s more complicated.

IRA FLATOW: Yes, complicated. Dr. Shore, are hidden hearing loss and tinnitus possibly connected, do you think?

DR. SUSAN SHORE: Well, yes, they’re connected in the sense that whatever causes a decrease in the input into the central nervous system from the cochlea has the potential to cause tinnitus. And in fact, in the study that’s reported in the first half of this paper that we were talking about is an animal study in which we induced the tinnitus using noise damage. And we used very carefully controlled noise damage so we could really control the amount of temporary threshold shift that we induced in animals.

So in this case, we designed the noise exposure to give us a temporary threshold shift that is like hidden hearing loss. And this was enough to induce tinnitus in about half of the animals. The other half of the animals didn’t get tinnitus, and that in itself is a very interesting phenomenon and should be studied in both animal models and in humans. Why is it that the animals that got the exact same noise exposure and have the exact same synapse loss, none the less, half of them got tinnitus and half of them did not get tinnitus? The difference lies in the brain.

IRA FLATOW: I’m Ira Flatow. This is Science Friday from PRI, Public Radio International. Let me ask both of you about nerve damage in hearing loss. There has been recent research about possibly using stem cells to repair the hair cells, and could they be used also, not just for hair cells, but possibly the nerve cells?

DR. CHARLES LIBERMAN: Well, yeah, absolutely. And there are other therapies that I think are well beyond the science fiction phase. One of the really interesting things about hidden hearing loss is initially the damage is just the loss of the connections, the so-called synapses between the hair cells and the nerve fibers. And at that point in time, if you sort of catch it early, we and others have already shown in animal models that we know what molecules to deliver to the inner ear to cause the nerve fibers to send out new connections and to make new functional connections. So we in a number of people are working on possible therapies that might be on the horizon to reconnect these disconnected nerve fibers to their hair cell targets.

IRA FLATOW: And Dr. Shore, do you think there is a cure possibly for tinnitus? Is it a curable problem?

DR. SUSAN SHORE: I think it’s probably a preventable problem. So if you take care of your hearing like you do your other senses, then I think the best therapy would be to avoid getting it in the first place. But I think that there are some promising therapies coming up by trying to understand the mechanisms that are underlying the disorder. I don’t know that we can say we can cure it. But we can certainly– at least with this treatment that we’ve developed– in some groups of people, we can make it not as bothersome.

IRA FLATOW: And remind us what the best way would be to try to prevent getting tinnitus.

DR. SUSAN SHORE: Well, prevent getting hearing loss. So the same way that you would do hearing loss prevention by protecting your ears. Not going to rock concerts or protecting your ears when you go to them.

IRA FLATOW: Yeah.

DR. CHARLES LIBERMAN: Yeah, it’s pretty clear that the most reliable way in humans to bring tinnitus on is with noise over exposure. There are probably a number of other ways, but as in your case, it’s a remarkably reliable way it’s the biggest problem for disability and returning vets. And so noise damage is key, and avoiding noise damage in many cases is doable.

IRA FLATOW: You know, it’s the old story about you can’t convince anybody until you have it yourself. Once it’s gone, it’s gone. And all your teenagers and kids are going to rock concerts or whatever. Thank you very much for taking time today. This is fascinating. Thank you both, Dr. Susan Shore, Professor of otolaryngology at Kresge Hearing Research Institute, University of Michigan, and Dr. Charles Liberman, director of the Eaton-Peabody Laboratories at Mass Eye and Ear.

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