Monday, April 25, 2011

Brains Are Wired So We Can Better Hear Ourselves

Berkeley - Like the mute button on the TV remote control, our brains filter out unwanted noise so we can focus on what we're listening to. But when it comes to following our own speech, a new brain study from the University of California, Berkeley, shows that instead of one homogenous mute button, we have a network of volume settings that can selectively silence and amplify the sounds we make and hear.

Activity in the auditory cortex when we speak and listen is amplified in some regions of the brain and muted in others. In this image, the black line represents muting activity when we speak. (Courtesy of Adeen Flinker)

Neuroscientists from UC Berkeley, UCSF and Johns Hopkins University tracked the electrical signals emitted from the brains of hospitalized epilepsy patients. They discovered that neurons in one part of the patients' hearing mechanism were dimmed when they talked, while neurons in other parts lit up.

Their findings, published today (Dec. 8, 2010) in the Journal of Neuroscience, offer new clues about how we hear ourselves above the noise of our surroundings and monitor what we say. Previous studies have shown a selective auditory system in monkeys that can amplify their self-produced mating, food and danger alert calls, but until this latest study, it was not clear how the human auditory system is wired.

"We used to think that the human auditory system is mostly suppressed during speech, but we found closely knit patches of cortex with very different sensitivities to our own speech that paint a more complicated picture," said Adeen Flinker, a doctoral student in neuroscience at UC Berkeley and lead author of the study.

"We found evidence of millions of neurons firing together every time you hear a sound right next to millions of neurons ignoring external sounds but firing together every time you speak," Flinker added. "Such a mosaic of responses could play an important role in how we are able to distinguish our own speech from that of others."

While the study doesn't specifically address why humans need to track their own speech so closely, Flinker theorizes that, among other things, tracking our own speech is important for language development, monitoring what we say and adjusting to various noise environments.

"Whether it's learning a new language or talking to friends in a noisy bar, we need to hear what we say and change our speech dynamically according to our needs and environment," Flinker said.

He noted that people with schizophrenia have trouble distinguishing their own internal voices from the voices of others, suggesting that they may lack this selective auditory mechanism. The findings may be helpful in better understanding some aspects of auditory hallucinations, he said.

Moreover, with the finding of sub-regions of brain cells each tasked with a different volume control job – and located just a few millimeters apart – the results pave the way for a more detailed mapping of the auditory cortex to guide brain surgery.

In addition to Flinker, the study's authors are Robert Knight, director of the Helen Wills Neuroscience Institute at UC Berkeley; neurosurgeons Edward Chang, Nicholas Barbaro and neurologist Heidi Kirsch of the University of California, San Francisco; and Nathan Crone, a neurologist at Johns Hopkins University in Maryland.

The auditory cortex is a region of the brain's temporal lobe that deals with sound. In hearing, the human ear converts vibrations into electrical signals that are sent to relay stations in the brain's auditory cortex where they are refined and processed. Language is mostly processed in the left hemisphere of the brain.

In the study, researchers examined the electrical activity in the healthy brain tissue of patients who were being treated for seizures. The patients had volunteered to help out in the experiment during lulls in their treatment, as electrodes had already been implanted over their auditory cortices to track the focal points of their seizures.

Researchers instructed the patients to perform such tasks as repeating words and vowels they heard, and recorded the activity. In comparing the activity of electrical signals discharged during speaking and hearing, they found that some regions of the auditory cortex showed less activity during speech, while others showed the same or higher levels.

"This shows that our brain has a complex sensitivity to our own speech that helps us distinguish between our vocalizations and those of others, and makes sure that what we say is actually what we meant to say," Flinker said.

Taken from

Monday, April 18, 2011

Musicians Less Likely to Experience Age Related Changes in Auditory Cortex

ScienceDaily - The old adage "use it or lose it" applies to hearing, suggests a new study. Older musicians do not experience certain changes in the auditory cortex he part of the brain involved with hearing hat are associated with aging, according to research presented at Neuroscience 2010, the annual meeting of the Society for Neuroscience, held in San Diego.

"This finding is important because it suggests that age-related changes in the auditory cortex that contribute to decline in auditory perception may be mitigated by musical training," said Benjamin Zendel, a doctoral student who co- authored the study with Claude Alain, PhD, of the University of Toronto.

Zendel and Alain presented participants with complex sounds under two conditions: active, in which they focused on the sounds, and passive, while they were doing another activity. During these tests, the researchers used electroencephalography to measure the participants' brain waves lectrical activity caused by the firing of brain cells.

During periods of attentive listening, the auditory cortices of older musicians responded the same as those of younger adults, whereas older non-musicians showed typical age-related changes. The researchers note that the musicians spend much of their time paying attention to the details of sound, and this experience may be important for sparing auditory cortex responses.

"Our findings suggest that musical training, which is widely available, may enhance neural connections in the auditory cortex and thus might be useful in preventing age-related changes that contribute to hearing difficulties," Zendel said.

Research supported by the Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council of Canada.

Taken from


Wednesday, April 13, 2011

Discover Sound Check Hearing Screener App, Now Available on iTunes from Starkey

Sound Check is a hearing screener app designed to quickly evaluate an individual's hearing to determine if it is within a normal range, or if there is potential hearing loss.

Sound Check:
  • Displays results in an easy-to-understand format
  • Includes learning materials and links to websites with detailed information on hearing loss and how to get help
  • Has a hearing professional locator feature
  • Automatically saves screening results to track changes over time or for further discussion with a qualified hearing professional
Download the FREE Sound Check app today or call your Starkey Representative at 800.328.8602 to learn more.

Click here to download via a computer:
  • Make sure that iTunes is installed
  • Follow the prompts to download and then sync with your iPhone, iPad or iPod Touch

To download directly to your iPhone, iPad or iPod Touch:
  • Turn on your device
  • Launch App Store (you will be required to have an iTunes account)
  • Search for Starkey
  • Select the Sound Check app to download
  • Follow the prompts to download and install

Monday, April 11, 2011

GUMC Researcher Says Tinnitus Is Much More Than a 'Hearing Problem'

The irritating phantom noises that tinnitus patients hear are a result of the brain trying, but failing, to repair itself

Washington, DC – Tinnitus appears to be produced by an unfortunate confluence of structural and functional changes in the brain, say neuroscientists at Georgetown University Medical Center (GUMC).

The phantom ringing sounds heard by about 40 million people in the U.S. today are caused by brains that try, but fail to protect their human hosts against overwhelming auditory stimuli, the researchers say in the January 13th issue of Neuron. They add that the same process may be responsible for chronic pain and other perceptual disorders.

The researchers say that the absence of sound caused by hearing loss in certain frequencies, due to normal aging, loud-noise exposure, or to an accident, forces the brain to produce sounds to replace what is now missing. But when the brain's limbic system, which is involved in processing emotions and other functions, fails to stop these sounds from reaching conscious auditory processing, tinnitus results.

"We believe that a dysregulation of the limbic and auditory networks may be at the heart of chronic tinnitus," says the study's lead investigator, Josef P. Rauschecker, PhD, a neuroscientist. "A complete understanding and ultimate cure of tinnitus may depend on a detailed understanding of the nature and basis of this dysregulation."

Tinnitus isn't curable, although antidepressants appear to help some patients, as does the use of masking noise to diminish focus on the ringing sensations.

Using functional Magnetic Resonance Imaging (fMRI), the Georgetown researchers tested 22 volunteers, half of whom had been diagnosed with chronic tinnitus. They found that moderate hyperactivity was present in the primary and posterior auditory cortices of tinnitus patients, but that the nucleus accumbens exhibited the greatest degree of hyperactivity, specifically to sounds that were matched to frequencies lost in patients.

The nucleus accumbens is part of the corticostriatal circuit, which is involved in evaluation of reward, emotion, and aversiveness, says Rauschecker. "This suggests that the corticostriatal circuit is part of a general 'appraisal network' determining which sensations are important, and ultimately affecting how or whether those sensations are experienced," he says. "In this study, we provide evidence that these limbic structures, specifically the nucleus accumbens and the ventromedial prefrontal cortex, do indeed differ in the brains of individuals with tinnitus."

Functional lapses in these same areas have also been implicated to altered mood states and to chronic pain. "Both of these conditions may also involve the inability to suppress unwanted sensory signals," Rauschecker says.

Based on their findings, the researchers argue that the key to understanding tinnitus lies in understanding how the auditory and limbic systems interact to influence perception – be it sound, emotions, pain, etc.

Monday, April 4, 2011

Scientists ID Key Protein that Links Diet with Healthy Hearing

Gainsville, Fla. - Restricting calories extends life and slows a range of age-related disorders in mice, rats and other organisms. But even after eight decades of research on the subject, scientists are still unclear just how caloric restriction exerts its age-battling influence.

Now, for the first time in mammals, researchers at the University of Florida and colleagues at the University of Wisconsin have sleuthed out the role of a key player in the process, using age-related hearing loss as an example. The protein in question, called Sirt3, could provide a new target for anti-aging drug therapies. The findings are reported in the Nov. 24 issue of the journal Cell.

The researchers found that when Sirt3 is absent, caloric restriction loses its anti-aging powers. They uncovered details of how the protein, an enzyme found primarily in mitochondria — the energy-producing centers of cells — wards off cell death by maintaining an environment that combats destructive chemicals.

“Knocking it out seems to be very negative for mitochondrial function and allows the accumulation of oxidative stress and damage to neurons and other cells,” said Christiaan Leeuwenburgh, one of the study’s senior authors who is chief of the biology of aging division in the UF College of Medicine department of aging and geriatric research and a member of the UF Institute on Aging. “That’s an important clue about the role that Sirt3 plays in protecting cells from age-related damage.”

Age-related hearing loss is the most common sensory disorder among the elderly, affecting more than 40 percent of people older than 65 and projected to affect 28 million Americans by 2030, according to the Department of Health and Human Services.

The disorder is marked by the death of sensory hair and nerve cells in the inner ear. While those cells are long-lived, they do not regenerate, so their demise means permanent loss of hearing. But all is not lost, since the environment in which those cells reside can be remodeled over time as damaged organelles such as mitochondria get replaced. Caloric restriction helps to rescue those damaged cells by reducing oxidative damage.

Having previously shown that restricting the diet induces expression of the protein Sirt3 in the inner ear, the researchers now show that Sirt3 aids caloric restriction by combating some of the chemical changes that play a major role in the process of aging.

The enzyme belongs to a class of compounds called sirtuins that are known to have anti-aging effects in lower organisms including yeast and flies. Until now, however, there wasn’t clear evidence that the effect extends to mammals.

“This is a major step in terms of understanding aging retardation by dietary restriction — it doesn’t work without Sirt3,” said Shinichi Someya, first author of the paper and an assistant scientist in genetics and medical genetics at the University of Wisconsin-Madison.

In normal mice, lowering calorie intake to 75 percent of a regular diet reduced hearing loss, but in Sirt3-deficient mice, dietary restriction had no such effect. Further, after caloric restriction, mice lacking Sirt3 lost more cellular structures vital for hearing — sensory hair and nerve cells in the ear — than did normal mice on a similarly restricted diet.

Corresponding with that observation, the researchers found that while caloric restriction reduced oxidative damage to DNA in inner ear cells in normal mice, it did not have that effect in mice that lacked Sirt3.

Closer examination revealed that Sirt3 regulates a mitochondria-based defense mechanism called the glutathione antioxidant system, via which caloric restriction works to help maintain the appropriate chemical balance needed to keep sopping up damaging oxygen-containing chemicals as they appear.

Effects seen in the ear were also observed in brain and liver tissue, suggesting that Sirt3 might have a role well beyond age-related hearing loss, and a potential benefit in cardiovascular and neurological diseases.

“They’ve taken it all the way from the physiological level down to the molecular level,” said S. Michal Jazwinski, a professor of medicine and biochemistry at Tulane University and director of the Tulane Center for Aging, who was not involved in the study. “This may be something that is generally operable in other tissues as well, and may explain the overall caloric restriction effect.”

The new findings identify Sirt3 as a target around which to focus anti-aging therapeutic efforts, including investigating ways to activate its production in the body.

“We’re now finally identifying the major genes involved in the action of caloric restriction, and this provides new opportunities for the development of therapies that may be able to provide the benefits of caloric restriction,” said Tomas Prolla, a professor of genetics and medical genetics at the University of Wisconsin-Madison, who led the research team.

Taken from