New Drug (Furosemide) Could Cure Tinnitus, Say Scientists
- Thread starter Grace
- Start date
MemberI contacted the Professor who conducted this research recently.
It sounds like its too early to tell if this drug will be helpful and safe.
She said that they are still testing their hypothesis on animal models and sounds like they are a long way of human trials.
She did admit that the drug at HIGH DOSES can potentially cause/worsen t, but didn't further comment on safe doses etc (probably cause she doesn't know)
She also said this drug will probably be most helpful in the acute phase (though she failed to define the duration of this) whilst the t is potentially being generated by overexcited brain cells, during which input to the ear can still modulate the early stage.
It sounds like its too early to tell if this drug will be helpful and safe.
She said that they are still testing their hypothesis on animal models and sounds like they are a long way of human trials.
She did admit that the drug at HIGH DOSES can potentially cause/worsen t, but didn't further comment on safe doses etc (probably cause she doesn't know)
She also said this drug will probably be most helpful in the acute phase (though she failed to define the duration of this) whilst the t is potentially being generated by overexcited brain cells, during which input to the ear can still modulate the early stage.
This is an old drug, tradename Lasix. It is a loop diuretic. Two of the known side effects are tinnitus and hearing loss.
I like all the comments to this thread interesting reading and food for thought,Thanks everyone.
Just got this in my email, not sure if it has been posted before.
From Action on Hearing Loss
One step closer to a cure for tinnitus?
Posted on: Wednesday, August 20, 2014 by james robins
People with tinnitus experience sound in their ears, such as a ringing or buzzing, when there is no corresponding external sound. For some the condition can have a serious impact on day-to-day life, causing depression, anxiety, stress and sleep problems.
Helmy Mulders is working on tinnitus research which we're funding at the University of Western Australia. She tells us about the latest findings, which could help develop a future cure for tinnitus.
Ear damage is a trigger for tinnitus
Tinnitus is a common condition often described as a ringing or buzzing sound in the head or ears, in the absence of an actual physical sound. This phantom sensation affects 10 to 15% of the human population, mostly without a problem, but in about 1% of people tinnitus causes severe disruptions of daily life. It can cause problems sleeping, evoke stress and anxiety and result in depression. Unfortunately there is, as yet, no cure for tinnitus. There are several treatments available but they are generally aimed at masking the tinnitus or reducing the anxiety and stress associated with it.
Neuroscientists have shown that perception of a physical stimulus, e.g. sound, touch or light, is caused by activity in specific brain pathways, which are triggered by signals from a peripheral receptor (like the rod and cone cells in the eye or hair cells in the cochlea). Therefore, it is thought that tinnitus, which is a perception without a physical stimulus, is due to abnormal, spontaneous activity (not resulting from an actual stimulus) in the brain.
Tinnitus is also strongly associated with damage to the cochlea. Many scientists now believe that trauma to the cochlea leads to changed input from the ear to the brain which then causes altered patterns of activity in the brain itself. This suggests that damage to the inner ear is the trigger for the development of tinnitus. Exactly which brain changes are responsible for causing tinnitus is still under investigation.
Two phases of tinnitus development
In our laboratory we have been working on an animal model studying the effects of cochlear damage and hearing loss on nerve cell activity in the brain. Using this model we showed that the spontaneous nerve cell activity (not evoked by sound) in a part of the brain which processes sound, the auditory midbrain, increases after inner ear damage caused by a loud sound exposure. Similar observations have been made in other areas of the brain that are involved in the processing of sound as well.
We also found that this increase in spontaneous activity could be suppressed by cutting or silencing the auditory nerve. However, there are two issues with this finding that are important to point out. Firstly, we could only suppress the increased activity in the midbrain if we reduced the auditory nerve activity in the first few weeks after the cochlear trauma and not at any later point in time. Secondly, we do not believe that this means that the auditory nerve itself has increased activity.
Instead, we think that development of increased activity in the brain has two phases. In the first phase, cells in the brain become hyper-excitable i.e. they respond more vigorously to the reduced input from the auditory nerve following damage to the cochlea. In the second phase, the cells in the brain stop needing signals from the auditory nerve to be active and their increased activity is now caused by another mechanism.
If the increased spontaneous activity in the brain after cochlear damage is involved in the generation of tinnitus, our results may well have therapeutic implications. They suggest that early onset tinnitus could be altered by changing the spontaneous activity of the auditory nerve. This might explain why cutting the auditory nerve can have a beneficial effect in some tinnitus sufferers but not in others. The former are still in the first phase of tinnitus development whilst the latter group are in phase 2. However, cutting the auditory nerve leads to complete deafness and therefore is not a desirable therapy.
Could drug treatments supress tinnitus?
A drug that lowers the spontaneous activity of the auditory nerve would be of more use, clinically. One such drug is furosemide, a common diuretic drug used to treat, among other things, high blood pressure. Interestingly, there are already reports that furosemide can suppress tinnitus in some people. Does furosemide perhaps suppress tinnitus of recent onset (phase 1 tinnitus)?
To try to answer this, we used our animal model to investigate whether a single dose of furosemide could block the early behavioural signs of tinnitus. We found that furosemide could indeed block the tinnitus that emerged in the first weeks after cochlear damage. This supports our hypothesis that early onset tinnitus can be reduced by a drug that affects auditory nerve activity. The next step, therefore, is to find out if the same is true in people. We also have no idea about how long the early stage of tinnitus lasts in humans (and it may vary considerably depending on the cause of the tinnitus and other factors) - this needs to be determined.
Whether long-term suppression of tinnitus can be achieved using furosemide is also a question that needs to be answered. And finally, furosemide cannot be administered to all people with tinnitus; it has some potentially serious side effects and needs to be administered under close medical supervision. If it is shown to be effective in treating people with tinnitus, more research would be required to investigate other possible drugs that can affect auditory nerve spontaneous activity without having other side-effects.
Sticky
From Action on Hearing Loss
One step closer to a cure for tinnitus?
Posted on: Wednesday, August 20, 2014 by james robins
People with tinnitus experience sound in their ears, such as a ringing or buzzing, when there is no corresponding external sound. For some the condition can have a serious impact on day-to-day life, causing depression, anxiety, stress and sleep problems.
Helmy Mulders is working on tinnitus research which we're funding at the University of Western Australia. She tells us about the latest findings, which could help develop a future cure for tinnitus.
Ear damage is a trigger for tinnitus
Tinnitus is a common condition often described as a ringing or buzzing sound in the head or ears, in the absence of an actual physical sound. This phantom sensation affects 10 to 15% of the human population, mostly without a problem, but in about 1% of people tinnitus causes severe disruptions of daily life. It can cause problems sleeping, evoke stress and anxiety and result in depression. Unfortunately there is, as yet, no cure for tinnitus. There are several treatments available but they are generally aimed at masking the tinnitus or reducing the anxiety and stress associated with it.
Neuroscientists have shown that perception of a physical stimulus, e.g. sound, touch or light, is caused by activity in specific brain pathways, which are triggered by signals from a peripheral receptor (like the rod and cone cells in the eye or hair cells in the cochlea). Therefore, it is thought that tinnitus, which is a perception without a physical stimulus, is due to abnormal, spontaneous activity (not resulting from an actual stimulus) in the brain.
Tinnitus is also strongly associated with damage to the cochlea. Many scientists now believe that trauma to the cochlea leads to changed input from the ear to the brain which then causes altered patterns of activity in the brain itself. This suggests that damage to the inner ear is the trigger for the development of tinnitus. Exactly which brain changes are responsible for causing tinnitus is still under investigation.
Two phases of tinnitus development
In our laboratory we have been working on an animal model studying the effects of cochlear damage and hearing loss on nerve cell activity in the brain. Using this model we showed that the spontaneous nerve cell activity (not evoked by sound) in a part of the brain which processes sound, the auditory midbrain, increases after inner ear damage caused by a loud sound exposure. Similar observations have been made in other areas of the brain that are involved in the processing of sound as well.
We also found that this increase in spontaneous activity could be suppressed by cutting or silencing the auditory nerve. However, there are two issues with this finding that are important to point out. Firstly, we could only suppress the increased activity in the midbrain if we reduced the auditory nerve activity in the first few weeks after the cochlear trauma and not at any later point in time. Secondly, we do not believe that this means that the auditory nerve itself has increased activity.
Instead, we think that development of increased activity in the brain has two phases. In the first phase, cells in the brain become hyper-excitable i.e. they respond more vigorously to the reduced input from the auditory nerve following damage to the cochlea. In the second phase, the cells in the brain stop needing signals from the auditory nerve to be active and their increased activity is now caused by another mechanism.
If the increased spontaneous activity in the brain after cochlear damage is involved in the generation of tinnitus, our results may well have therapeutic implications. They suggest that early onset tinnitus could be altered by changing the spontaneous activity of the auditory nerve. This might explain why cutting the auditory nerve can have a beneficial effect in some tinnitus sufferers but not in others. The former are still in the first phase of tinnitus development whilst the latter group are in phase 2. However, cutting the auditory nerve leads to complete deafness and therefore is not a desirable therapy.
Could drug treatments supress tinnitus?
A drug that lowers the spontaneous activity of the auditory nerve would be of more use, clinically. One such drug is furosemide, a common diuretic drug used to treat, among other things, high blood pressure. Interestingly, there are already reports that furosemide can suppress tinnitus in some people. Does furosemide perhaps suppress tinnitus of recent onset (phase 1 tinnitus)?
To try to answer this, we used our animal model to investigate whether a single dose of furosemide could block the early behavioural signs of tinnitus. We found that furosemide could indeed block the tinnitus that emerged in the first weeks after cochlear damage. This supports our hypothesis that early onset tinnitus can be reduced by a drug that affects auditory nerve activity. The next step, therefore, is to find out if the same is true in people. We also have no idea about how long the early stage of tinnitus lasts in humans (and it may vary considerably depending on the cause of the tinnitus and other factors) - this needs to be determined.
Whether long-term suppression of tinnitus can be achieved using furosemide is also a question that needs to be answered. And finally, furosemide cannot be administered to all people with tinnitus; it has some potentially serious side effects and needs to be administered under close medical supervision. If it is shown to be effective in treating people with tinnitus, more research would be required to investigate other possible drugs that can affect auditory nerve spontaneous activity without having other side-effects.
Sticky
Furosemide is discussed on pages 15–16 of this 2009 survey paper by Salvi et al. : http://www.ncbi.nlm.nih.gov/pubmed/21765586. The authors write,
Furosemide (Lasix®) is a loop-inhibiting diuretic used to treat congestive heart failure and
edema. It inhibits the Na-K-2Cl cotransporter that transports sodium, potassium and
chloride ions into and out of cells. The Na-K-2Cl cotransporter is expressed in the
inner ear, as well as in the brain. Furosemide also blocks GABAA receptors. The drug has been proposed as a treatment for tinnitus of cochlear origin because it strongly suppresses the endolymphatic potential and other cochlear responses. It has been reported that ~50% of patients note a reduction in tinnitus symptoms following
intravenous furosemide treatment; these positive responders were hypothesized to have
cochlear tinnitus, whereas those who did not respond were assumed to have central tinnitus.
In contrast, patients with presumably central tinnitus (i.e., tinnitus emanating from a
surgically ablated ear) did not show a reduction in their tinnitus. Furosemide has also
been found to suppress tinnitus in ~40% of patients with Meniere's disease. However,
high doses of furosemide can also induce temporary hearing loss and tinnitus.
Thus, the data on the use of furosemide to treat tinnitus and conclusions regarding its central
versus cochlear mode of action are difficult to interpret, especially when considering that
Na-K-2Cl transporters are present in both the ear and brain.
-Golly
Furosemide (Lasix®) is a loop-inhibiting diuretic used to treat congestive heart failure and
edema. It inhibits the Na-K-2Cl cotransporter that transports sodium, potassium and
chloride ions into and out of cells. The Na-K-2Cl cotransporter is expressed in the
inner ear, as well as in the brain. Furosemide also blocks GABAA receptors. The drug has been proposed as a treatment for tinnitus of cochlear origin because it strongly suppresses the endolymphatic potential and other cochlear responses. It has been reported that ~50% of patients note a reduction in tinnitus symptoms following
intravenous furosemide treatment; these positive responders were hypothesized to have
cochlear tinnitus, whereas those who did not respond were assumed to have central tinnitus.
In contrast, patients with presumably central tinnitus (i.e., tinnitus emanating from a
surgically ablated ear) did not show a reduction in their tinnitus. Furosemide has also
been found to suppress tinnitus in ~40% of patients with Meniere's disease. However,
high doses of furosemide can also induce temporary hearing loss and tinnitus.
Thus, the data on the use of furosemide to treat tinnitus and conclusions regarding its central
versus cochlear mode of action are difficult to interpret, especially when considering that
Na-K-2Cl transporters are present in both the ear and brain.
-Golly
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
Seat of the pants response here...
Sounds to me like this Furosemide stuff is another quasi probable for potentially affecting the very early stages of T (only) and would dovetail into AM101 territory, and the whole: Trauma c/o noise or ototoxic drug, etc. -> "bouton goes BOOM" -> Glutamate overload -> which hypes stuff up so much it screws up restructuring & repair of fried bouton -> Kv channel (Kv3.1 in particular) gets caught up in the carnage and locks into T state -> brain plasticity (being soooo accommodating) adapts to new state as "acceptable" -> humanoid (or rat???) now has T.
Once we get past the acute phase, this 'window of early opportunity' shuts as the Glutamate aspect chills out and goes to cause excitement elsewhere.
Without going into all the mechanics and neurological details, it seem to me that this research is rather far behind the curve v. the K channels stuff and Autifony, and they are not even sure exactly how their drug is working. Thus I am not going to spend any time on trying to figure it out. However, any added insights or observations from researchers are always good to have as if the central model is correct, the equations coming in from different points of the compass should fit in to the model. If they don't the model has holes in it.
So far the Kv channels looks like the top dog approach and explanation by far.
Also note the "side effects profile" http://www.drugs.com/sfx/furosemide-side-effects.html ...and as always I check the Nervous System section for Professionals:
Nervous system
The doses of furosemide in cases of tinnitus, vertigo, or deafness ranged from 0.24 grams IV given over 40 minutes to 3 grams IV in divided doses over 9 hours and 2 grams IV in a single dose. It is recommended that infusion rates not exceed 4 mg/min to minimize the risk of ototoxicity.
Ototoxicity may be more likely and more severe due in patients with renal insufficiency.
Nervous system side effects have included headaches and dizziness. Cases of tinnitus and reversible or irreversible hearing impairment and deafness have been reported.
Mmmmmm.....Makes Retigabine seem rather appealing in comparison if wanting to be a guinea pig.
Best, Zimichael
Sounds to me like this Furosemide stuff is another quasi probable for potentially affecting the very early stages of T (only) and would dovetail into AM101 territory, and the whole: Trauma c/o noise or ototoxic drug, etc. -> "bouton goes BOOM" -> Glutamate overload -> which hypes stuff up so much it screws up restructuring & repair of fried bouton -> Kv channel (Kv3.1 in particular) gets caught up in the carnage and locks into T state -> brain plasticity (being soooo accommodating) adapts to new state as "acceptable" -> humanoid (or rat???) now has T.
Once we get past the acute phase, this 'window of early opportunity' shuts as the Glutamate aspect chills out and goes to cause excitement elsewhere.
Without going into all the mechanics and neurological details, it seem to me that this research is rather far behind the curve v. the K channels stuff and Autifony, and they are not even sure exactly how their drug is working. Thus I am not going to spend any time on trying to figure it out. However, any added insights or observations from researchers are always good to have as if the central model is correct, the equations coming in from different points of the compass should fit in to the model. If they don't the model has holes in it.
So far the Kv channels looks like the top dog approach and explanation by far.
Also note the "side effects profile" http://www.drugs.com/sfx/furosemide-side-effects.html ...and as always I check the Nervous System section for Professionals:
Nervous system
The doses of furosemide in cases of tinnitus, vertigo, or deafness ranged from 0.24 grams IV given over 40 minutes to 3 grams IV in divided doses over 9 hours and 2 grams IV in a single dose. It is recommended that infusion rates not exceed 4 mg/min to minimize the risk of ototoxicity.
Ototoxicity may be more likely and more severe due in patients with renal insufficiency.
Nervous system side effects have included headaches and dizziness. Cases of tinnitus and reversible or irreversible hearing impairment and deafness have been reported.
Mmmmmm.....Makes Retigabine seem rather appealing in comparison if wanting to be a guinea pig.
Best, Zimichael
What I can say about furosemide is that, all my problem started with furosemide . The cause of my tinnitus. I don't want to smell it, touch it or even see it. I stay far away from it.
DutchGuy
Member
http://www.hear-it.org/step-closer-silencing-tinnitus#.VIWbmXpQOtA.twitter
December 08, 2014
A step closer to silencing tinnitus
Tinnitus may be eliminated by blocking the signals between the ear and the brain, an Australian study suggests.
For people suffering from tinnitus, the condition often affects their quality of life, such as causing trouble sleeping. Even though no cure for tinnitus currently exists, a study conducted by Australian researchers brings hope that a cure may be within reach.
After injecting a drug to reduce the signals from the ear to the brain in guinea pigs with tinnitus, the guinea pigs no longer showed signs of tinnitus. According to the researchers, the findings are promising. However, studies on humans suffering from tinnitus are still needed to confirm the method and results.
No tinnitus displayed
In the study, the guinea pigs were exposed to loud noise to trigger tinnitus. After confirming that the guinea pigs had tinnitus, the researchers treated the animals with a drug called furosemide. Furosemide lowers the activity in the auditory system, reducing neural hyperactivity in the part of the brain responsible for sound. In other words, furosemide blocks the signals.
After the treatment, the guinea pigs displayed no signs of tinnitus.
Silencing the noise
Today, people suffering from tinnitus can use practical steps to manage their condition e.g. listening to comforting sounds to get their attention away from the constant ringing.
According to Dr. Ralph Holme, Head of Biomedical Research at Action on Hearing Loss in the UK, the practical steps are not enough. "What people who suffer from tinnitus want the most is a cure to silence the noise. The research we have funded takes us a step closer to this goal," he says.
To reduce the risk of contracting tinnitus, the researchers advise people to wear ear protection when at concerts and avoid high volumes on music players.
About the study
The study was conducted by researchers at the University of Western Australia and was published by PLOS ONE, an international online publisher with focus on scientific research.
Source:www.plosone.org
December 08, 2014
A step closer to silencing tinnitus
Tinnitus may be eliminated by blocking the signals between the ear and the brain, an Australian study suggests.
For people suffering from tinnitus, the condition often affects their quality of life, such as causing trouble sleeping. Even though no cure for tinnitus currently exists, a study conducted by Australian researchers brings hope that a cure may be within reach.
After injecting a drug to reduce the signals from the ear to the brain in guinea pigs with tinnitus, the guinea pigs no longer showed signs of tinnitus. According to the researchers, the findings are promising. However, studies on humans suffering from tinnitus are still needed to confirm the method and results.
No tinnitus displayed
In the study, the guinea pigs were exposed to loud noise to trigger tinnitus. After confirming that the guinea pigs had tinnitus, the researchers treated the animals with a drug called furosemide. Furosemide lowers the activity in the auditory system, reducing neural hyperactivity in the part of the brain responsible for sound. In other words, furosemide blocks the signals.
After the treatment, the guinea pigs displayed no signs of tinnitus.
Silencing the noise
Today, people suffering from tinnitus can use practical steps to manage their condition e.g. listening to comforting sounds to get their attention away from the constant ringing.
According to Dr. Ralph Holme, Head of Biomedical Research at Action on Hearing Loss in the UK, the practical steps are not enough. "What people who suffer from tinnitus want the most is a cure to silence the noise. The research we have funded takes us a step closer to this goal," he says.
To reduce the risk of contracting tinnitus, the researchers advise people to wear ear protection when at concerts and avoid high volumes on music players.
About the study
The study was conducted by researchers at the University of Western Australia and was published by PLOS ONE, an international online publisher with focus on scientific research.
Source:www.plosone.org
Don't get your hopes up too much. I don't know the details but there are articles testing the effect of furosemide on tinnitus dating back to the 90s. If it was a promising cure it would probably be in use already. I wouldn't be surprised if some members on here had already tested it at some point so they may be able to discuss further.
1MW
Member
- Nov 25, 2014
- 614
- Tinnitus Since
- 2008 but cured and relapsed from benzos
- Cause of Tinnitus
- ssnhl/benzos/unknown
Furosemide is very old drug and have tested many times for T.
It has proven that is ototoxic and can worsen T and hearing.
No hope here only more T and hearing loss.
Scientist that say will cure T with furosemide are fraudulent and need some more papers
to get a good position in a university don't believe them furosemide is a scam.
It has proven that is ototoxic and can worsen T and hearing.
No hope here only more T and hearing loss.
Scientist that say will cure T with furosemide are fraudulent and need some more papers
to get a good position in a university don't believe them furosemide is a scam.
- Aug 24, 2014
- 179
- Tinnitus Since
- 07/2009
- Cause of Tinnitus
- Loud Music and being dumb
http://app.laboratoryequipment.com/news/2014/11/research-finds-narrow-window-treat-tinnitus
Neuroscientists from the Univ. of Western Australia have discovered that tinnitus caused by abnormal auditory pathway activity may be treatable with furosemide, a drug that reduces cross-talk between the cochlea and the brain.
Tinnitus patients "hear" distinct tones in the absence of real sounds, a perceptual phenomenon that detrimentally affects their concentration, sleep and mental wellbeing.
The experience of tinnitus has been linked to spontaneous firing of the auditory nerve cells a hyperactivity in the brain observed after hearing loss.
Prof. Helmy Mulders of UWA's Auditory Laboratory investigated the efficacy of treating tinnitus in animals using furosemide, a diuretic drug usually prescribed to reduce swelling and water retention.
She found that single as well as repetitive use of furosemide reduced hyperactivity in the auditory nerve and midbrain, interfering with neurotransmitter release from the ear's inner hair cells to the auditory nerves.
"It strengthens our argument that the hyperactivity is somehow involved in the generation of tinnitus."
Six-week treatment window
Mulders' research suggests furosemide is only therapeutically effective in the first six weeks after hearing loss, when auditory neurons appear hyper-excitable.
"There is possibly a therapeutic window for people with early onset tinnitus who might respond to treatment that affects the spontaneous firing rate of the auditory nerve," Mulders said.
Mulders conducted the research using her well-established experimental animal model for tinnitus research, which involved guinea pigs deafened on one side.
To identify animals demonstrating tinnitus after the acoustic injury, Mulders studied the sensitivity of their natural alarm reaction to a sudden loud noise, the startle pulse in the gap pre-pulse inhibition (GPPI) test.
Silence in the time before the startle pulse reduced the startle reaction evoked by the loud noise in control animals. Yet, some animals with hearing loss did not seem to behave in this way.
According to Mulders, those animals with unaffected startle behavior in the GPPI reacted this way because they perceived sound even in its absence — the defining characteristic of tinnitus.
"Furosemide suppressed the behavioral side of tinnitus in our animal model," she says.
Electrophysiological measures of enhanced spontaneous firing of auditory neurons in the absence of sound further linked hyperactivity in the auditory pathways to the experience of tinnitus in these animals.
Mulders will soon start a proof-of-principle trial with Prof. Peter Friedland from UWA's Ear Sciences Centre to test the furosemide effect in volunteer patients with tinnitus.
Neuroscientists from the Univ. of Western Australia have discovered that tinnitus caused by abnormal auditory pathway activity may be treatable with furosemide, a drug that reduces cross-talk between the cochlea and the brain.
Tinnitus patients "hear" distinct tones in the absence of real sounds, a perceptual phenomenon that detrimentally affects their concentration, sleep and mental wellbeing.
The experience of tinnitus has been linked to spontaneous firing of the auditory nerve cells a hyperactivity in the brain observed after hearing loss.
Prof. Helmy Mulders of UWA's Auditory Laboratory investigated the efficacy of treating tinnitus in animals using furosemide, a diuretic drug usually prescribed to reduce swelling and water retention.
She found that single as well as repetitive use of furosemide reduced hyperactivity in the auditory nerve and midbrain, interfering with neurotransmitter release from the ear's inner hair cells to the auditory nerves.
"It strengthens our argument that the hyperactivity is somehow involved in the generation of tinnitus."
Six-week treatment window
Mulders' research suggests furosemide is only therapeutically effective in the first six weeks after hearing loss, when auditory neurons appear hyper-excitable.
"There is possibly a therapeutic window for people with early onset tinnitus who might respond to treatment that affects the spontaneous firing rate of the auditory nerve," Mulders said.
Mulders conducted the research using her well-established experimental animal model for tinnitus research, which involved guinea pigs deafened on one side.
To identify animals demonstrating tinnitus after the acoustic injury, Mulders studied the sensitivity of their natural alarm reaction to a sudden loud noise, the startle pulse in the gap pre-pulse inhibition (GPPI) test.
Silence in the time before the startle pulse reduced the startle reaction evoked by the loud noise in control animals. Yet, some animals with hearing loss did not seem to behave in this way.
According to Mulders, those animals with unaffected startle behavior in the GPPI reacted this way because they perceived sound even in its absence — the defining characteristic of tinnitus.
"Furosemide suppressed the behavioral side of tinnitus in our animal model," she says.
Electrophysiological measures of enhanced spontaneous firing of auditory neurons in the absence of sound further linked hyperactivity in the auditory pathways to the experience of tinnitus in these animals.
Mulders will soon start a proof-of-principle trial with Prof. Peter Friedland from UWA's Ear Sciences Centre to test the furosemide effect in volunteer patients with tinnitus.
- Jul 21, 2013
- 842
- Tinnitus Since
- 01/2013
- Cause of Tinnitus
- Acoustic trauma from headphones
Not good enough. It's apparently ototoxic and doesn't work on most people with tinnitus since most tinnitus patients with it still have had it for longer than a month and a half.
As well, many people can't get to a doctor in that period of time. Might as well start looking at another avenue than continuing research down this path, but I've seen enough researchers waste their time with mediocre ideas that this team inevitably will as well...
dont quote me on this but i think there may be a connection between frusemide and t as it depletes potassium...
I have a strong feeling , there will be a cure soon, I Havnt realized how common this thing is untill I got it 2 weeks ago !! Companies need to make a drug cause they will be making real lot of money out of it
Old news. There's already a thread in the research news section:
https://www.tinnitustalk.com/threads/new-drug-furosemide-could-cure-tinnitus-say-scientists.5132/
http://www.google.com/patents/US4954486
found this it from 1989 very old and now seems abandoned for some reason. (probably does not work).
found this it from 1989 very old and now seems abandoned for some reason. (probably does not work).
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