September 18, 2012 Audiology

Audiology in Brief: September 18, 2012

New Recommendations Cite Lack of Evidence

In newly released recommendations, the U.S. Preventive Services Task Force (USPSTF) cites a lack of sufficient evidence for or against hearing loss screenings for older adults who don't display hearing loss symptoms. USPSTF is an independent, congressionally authorized task force supported by the federal government that makes evidence-based recommendations about clinical preventive services.

"I think the recommendation is nothing more than a call to action for researchers," said Jaynee A. Handelsman, ASHA vice president of audiology practice. "The gist of the recommendation is that there is not sufficient evidence to say whether we are or we're not supposed to be screening adults 50 years old and older."

ASHA recommends hearing screenings for adults at least every decade through age 50, and at three-year intervals thereafter. The USPSTF states that future studies should focus on adults 70 years and older to determine the effects of treatment on outcomes at different ages. To read the USPSTF recommendation, visit the USPSTF website.

New Stroke, Tinnitus Treatments?

Researchers at the University of Texas at Dallas recently demonstrated how nerve stimulation paired with specific experiences, such as movements or sounds, can reorganize the brain. This technology could lead to new treatments for stroke, tinnitus, autism, and other disorders.
The research team looked at whether repeatedly pairing vagus nerve stimulation with a specific movement would change neural activity in laboratory rats' primary motor cortex. To test the hypothesis, they paired the vagus nerve stimulation with movements of the forelimb in two groups of rats.

After five days of stimulation and movement pairing, the researchers examined the brain activity in response to the stimulation. The results, published in Cerebral Cortex, showed that rats who received the training along with the stimulation displayed large changes in the organization of the brain's movement control system. The animals receiving identical motor training without stimulation pairing did not exhibit any brain changes, or plasticity.

Because of the belief that repeated use of an affected limb causes reorganization of the brain essential to recovery, people who suffer strokes or brain trauma often undergo rehabilitation that includes repeated movement of the limb to regain motor skills. This study suggests that pairing vagus nerve stimulation with standard therapy may result in more rapid and extensive reorganization of the brain, offering the potential for speeding and improving recovery following stroke. Read more at PubMed.

Gene Therapy for Hearing Loss

A new gene therapy approach can reverse hearing loss caused by a genetic defect in a mouse model of congenital deafness, according to a preclinical study published in Neuron. The findings present a promising therapeutic avenue for treating people who are born deaf.

About half the cases of congenital hearing loss are caused by genetic defects. However, the current treatment options—hearing amplification devices and cochlear implants—do not restore hearing to normal levels. Correcting the underlying genetic defects has the potential to restore hearing, but previous attempts to reverse hearing loss caused by genetic mutations have not been successful.

Researchers injected vesicular glutamate transporter-3 (VGLUT3)—a protein crucial for inner hair cells to send signals that enable hearing—into the inner ears of mice with hereditary deafness caused by a mutation in a gene coding for this protein. Two weeks after the injection, all the mice's hearing was restored. This improvement lasted from seven weeks to 1.5 years in adult mice, and at least nine months in newborn mice.

The therapy did not damage the inner ear, and it corrected some structural defects in the inner hair cells. Because the specific gene delivery method used is safe and effective in animals, the findings hold promise for future human studies. Search doi: 10.1016/j.neuron.2012.05.019.


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