Bloomington, Minn — Just in time for the International Hearing Society (IHS) conference in Boston, ReSound has introduced the Alera TS™, which combines an advanced hearing aid with a tinnitus sound generator (TSG).
TSGs are a common approach in tinnitus sound therapy. They work by administering sounds that are designed to make the disturbing tinnitus noise less noticeable, drawing the patient’s attention away from the tinnitus tones.
Michael Piskosz, MS, ReSound, commented in the press announcement, “This kind of sound therapy, when combined with informed counseling, is recognized as a highly effective way of managing tinnitus.”
Alera TS also provides flexibility for individualized sound therapy. Hearing professionals can customize the device to address the personalized needs of each tinnitus sufferer.
The Alera TS is being introduced at a time when tinnitus is the most prevalent physical disability reported by military service members and veterans.
ReSound stated in its press release that 83% of Veterans Administration audiologists reported a significant or satisfactory improvement in their patients’ tinnitus symptoms after activating the TSG feature.
Research continues into the causes of tinnitus. The latest research is not focused on the ear, but in the brain where it’s now thought the condition really originates.
A study by a team of UC Berkeley neuroscientists has uncovered new cerebral mechanisms behind tinnitus, a currently incurable condition that produces a constant ringing or buzzing sound in the ear in the absence of other noise.
The study, published Sept. 6 in the journal Proceedings of the National Academy of Sciences, provides an alternative hypothesis to the prevailing view that tinnitus is associated with neurons in the region of the cortex that is affected by hearing loss. The research, which was conducted by the UC Berkeley Helen Wills Neuroscience Institute, shows that the higher-frequency neurons in the area of the cortex affected by hearing loss are responsible for the high-pitched noise characteristic of tinnitus.
According to Shaowen Bao, co-author of the study and adjunct assistant professor of neuroscience at UC Berkeley, this study is the first to attribute tinnitus to the sensory-deprived region — which is affected by hearing loss — of the cortex.
“Researchers have come up with the prevailing theory based on numerous studies and findings,” he said. “However, these findings are somewhat inconsistent. We hope we can get a more coherent idea of what’s happening.”
According to the American Tinnitus Association, tinnitus affects more than 50 million Americans with varying degrees of severity ranging from barely noticeable to debilitating. Although scientists have yet to identify a cure for the condition, popular treatment options include masking the tinnitus noise with music, which provides temporary relief, and training the neurons in the auditory cortex to enhance their response to lost frequencies, which helps to gradually reconnect the ear to the sensory-deprived neurons.
Bao and his team treated hearing-impaired rats with two drugs in order to increase their brain’s production of the GABA neurotransmitter, which inhibits the spontaneous firing of the sensory-deprived neurons — the cause of the ringing associated with tinnitus. But although these drugs were effective in treating the symptoms of tinnitus in rats, they cannot be used on humans because of the long-term side effects associated with them.
Although this is his first study on tinnitus, Bao said he hopes to build off this research to provide further insight into the field.
“We are very interested in using these molecular and cellular tools to pinpoint the mechanisms behind tinnitus and hearing loss more precisely,” he said.
Michael DeWeese, UC Berkeley assistant professor of physics and member of the institute, who researches the inability to focus attention on important sounds in the presence of distractors, said that researchers are focusing on this condition.
“Tinnitus is actually a very serious problem, and I think that many people are very surprised to hear that,” he said. “In the very worst cases, sufferers are suicidal.”
One day there could be a growth hormone that would regrow damaged hair cells in the inner ear. Not only could this lead to restoring hearing for those with age-related hearing loss, this would also help those with corresponding tinnitus symptoms.
Louisville, Ky— Researchers from Western Kentucky University and the University of Louisville have identified a growth hormone that repairs hair cell damage in the ear of a zebrafish. The findings may one day lead to a therapy for repairing cochlea hair cells in humans.
As hearing professionals are well aware, loud noise, especially repeated loud noise, can cause irreversible damage to the hair cells inside the cochlea and eventually lead to deafness. In mammals, this is irreversible; however both birds and fish are able to regrow the damaged hair cells and restore hearing. But how?
Researchers from Western Kentucky University and the University of Louisville experimented with zebrafish and examined their internal repair process.
They first looked for the zebrafish genes that were switched on or off after acoustic trauma and found distinct patterns of gene expression. Two days after noise injury in the zebrafish, inner ear cells were busy dividing to repair and replace the damaged hair cells.
The researchers traced the repair to an alteration in the regulation of 839 genes. Many of the cellular pathways involved were the same as those involved in cancer. This included a massive 64 fold increase in the transcription of growth hormone.
They then investigated the effect of injecting growth hormone (GH) on cell proliferation in control zebrafish utricles and saccules, since GH was significantly increased in the zebrafish following acoustic trauma.
The GH injection increased cell proliferation in the inner ear of non-sound-exposed zebrafish, suggesting that GH could play an important role in sensory hair cell regeneration in the teleost ear.
The research, published in BioMed Central’s open access journal BMC Neuroscience, may one day lead to a growth hormone therapy for repairing damaged hair cells in humans.
Like my grandfather said to me once, “Don’t shit in a flushing toilet.” But he was dying of Alzheimer’s at the time, and wasn’t exactly shitting in toilets any more anyway. He also yelled, “FISH! FISH!” And if that doesn’t sum everything up, I don’t know what does.
September 11, 2001, Glendale California. Shortly before 6 a.m. A ringing phone wakes me up. I hear my girlfriend groggily answer it, and I can hear, all the way over on my side, the voice of her mother, upset about something. Lots of “What? What? What?” coming from that side of the bed.
“What’s she on about?” I manage to mumble.
“My mom says a plane hit the World Trade Center in New York.”
“She says to turn on the TV!” There’s an urgency in her voice, and annoyed at what I think is her mom being confused and upset over nothing, I find the remote and turn on CNN.
There it is. A gaping hole. Smoke billowing out. We can see flames.
Now I’m awake.
It must have been some massive failure of the air traffic control system, some huge computer foulup. I tell her that somehow, some pilot wasn’t looking out his window, was looking at some instruments that were obviously completely screwed up, and flew right into the building.
But then I start thinking about how many systems would have to break down for that to happen. And what would a plane be doing flying that low anyway?
Still believing it was some small commuter plane, the CNN anchor breaks in and says they’re getting reports it was a jet. An airliner.
And as confirmations come in that it was a jet that hit the WTC, that’s when we see the second plane. Not sure of what we just saw, the news network (I can’t remember if we stayed with CNN or if we started flipping around) helpfully replayed the footage.
Our mouths are hanging open. I start to say, “How the hell can a computer mix up explain a f—ing SECOND plane—” but as we both look at each other we have the same sudden, sickening thought forming in our heads, and the news anchor says at the same time, crystallizing the realization and finishing the thought for us, “This can’t be an accident. This is a terrorist attack.”
Cecil the cat jumped into bed with us, wondering why we were awake so damn early and decided to capitalize on the opportunity and meowed for food.
I don’t think our eyes left the television the whole day.