“Nearly Dead Zones” Take Trivia Bowl XIV

 The "Nearly Dead Zones" took top honors at Trivia Bowl XIV held at the conclusion of the AAA convention in San Antonio. The team consisted of front row (l to r): Catherine Palmer, Mary Kay Chisholm, Gail Gudmundsen, Chuck Berlin, Robert Sweetow, Brenda Ryals,; (back row, l to r) Liz Fabry, David Fabry, Dennis Van Vliet, and David Hawkins. The “Up Chuck Berlin’s” took second place honors, while the perennial “Trapezoid Bodies” came in third place.

San Antonio — More than 600 attendees from the 2003 American Academy of Audiology Convention in San Antonio gathered for friendly competition at the XIVth Annual Trivia Bowl. Sixty teams compared their collective knowledge during the event, sponsored by Siemens Hearing Instruments, Inc, and co-sponsored by Knowles Electronics and Rayovac Corp.

The competition gives audiologists a chance to test their technical and loosely-related trivia knowledge and share professional camaraderie with their peers. In addition, Siemens Hearing Instruments President and CEO William Lankenau presented a donation to the Advancement of Audiology and Hearing Science Foundation to further support the education of audiology.

Questions prepared by program Masters of Ceremonies Gus Mueller, PhD, and Jerry Northern, PhD, challenged the participants on trivial events drawn from audiology history, clinical applications, items from the news media of the past year, and trade journals. The competition resulted in three winning teams, one winning student team, and one winning team for the best name competition.

The "Nearly Dead Zones" took first place, while the "Up Chuck Berlin’s" took second place, and the "Trapezoid Bodies" placed third. "Simply Ear-Resistible," this year’s winning student team, included members from Utah State University. The award for the team with the best name went to "Viva Las Tragus!" The members of the "Nearly Dead Zones" team and the winning student team will have their names engraved on Trivia Bowl XIV trophies on display at the American Academy of Audiology headquarters.


Med-El to purchase Symphonix Assets
Durham, NC — Med-El announced that it would be acquiring the assets of Symphonix Inc, the developer of the FDA- and CE-approved Vibrant® Soundbridge® middle ear implant. Symphonix closed its operations in mid-November of 2002 due to the slow adoption of its middle ear implant technology (see HR Dec. 2002, page 12). Previous to the closing, the company had been seeking strategic alternatives like a partnership agreement with another company or the outright sale of the company. In essence, the purchase by Med-El would revive the Soundbridge product, which is said to have great potential but has battled difficult financial circumstances and what Symphonix company officials generally characterized as slow market adoption due to the relative newness of the technology.

 The Vibrant Soundbridge consists of an external audioprocessor and a surgically implanted FMT and VORP.

In addition to procuring the Soundbridge, Med-El has appointed the device’s inventor, Geoffrey Ball, as its chief technical officer.

The Soundbridge consists of two components, one implanted in the middle ear and the other worn like a BTE hearing aid. The surgically implanted portion is designed to leave the ear canal open and unobstructed, and has been recommended for mild-to-severe sensorineural hearing loss. There are two main internal components to the device: the Vibrating Ossicular Prosthesis (VORP) which consists of a receiving coil, internal magnet, demodulator, conductor link; and the Floating Mass Transducer (FMT). Both are encased in silicone elastomer. The FMT, which is the size of a grain of rice, is an electromagnetic transducer that is attached to the long process of the incus via a titanium attachment clip. This technology mechanically vibrates the ossicular chain by mimicking the natural frequency response of the human ear to sound. The external component, or Audio Processor, is about the size of five quarters, stacked on top of each other, and is worn behind the pinna, covered by hair. It is held in place by magnetic attraction to the implanted magnet in the receiver portion of the VORP. The device is designed to vibrate the small bones in the middle ear, enhancing the natural hearing process.

Med-El, which has its headquarters in Innsbruck, Austria, is a manufacturer of cochlear implants with 14 subsidiaries. It distributes its product in 70 countries. The company says it plans to distribute the product on a global basis.


CMS Set to Issue Ruling on Audiologist Definition Change
Washington, DC — The Centers for Medicare & Medicaid Services (CMS) are on track to approve a new definition of a “qualified audiologist” relative to the Medicaid regulation that would make state licensure the only criterion for treating Medicaid patients. As one of the focuses of activity and discussion at the recent American Academy of Audiology (AAA) convention, approval of the regulation would represent a major victory for the organization. Private insurance companies often inappropriately use the Medicaid definition of an audiologist that lead to insurance denials. Approval of the proposed change would create a new definition of a “qualified audiologist” in the Medicaid program that would be consistent with current Medicare law, according to the organization. Invited guest-speaker at the AAA convention, former Kansas Senator and presidential candidate Bob Dole, spoke out in favor of the regulation change.

Specifically, the proposed regulation, if finalized, would change the Medicaid definition of who is a “qualified audiologist.” According to AAA and Craig Johnson, AuD, chair of the AAA and Academy of Dispensing Audiologists’ Political Action Committees, the new definition would: 1) Make state license or regulation the sole credential necessary to be reimbursed for serving Medicaid patients (Medicare has provided for state licensure since 1994), just as in other professions, such as medicine; 2) Expand the number of audiologists eligible to be reimbursed for services, thereby enhancing access for those enrolled in the Medicaid program; 3) Provide a more consistent definition of an audiologist that private insurance carriers can follow; 4) Make the Medicaid definition consistent with the Medicare definition; and 5) Eliminate the connection between Medicaid and the private organization designation.

AAA and ADA have been strong advocates for the regulation change. More recently, the American Speech-Language-Hearing Association has also come out in favor of change after initially opposing it on the grounds that an earlier version failed to recognize the value of the CCC-A designation, which the organization views as critical to maintaining professional standards. CMS closed commentary on the issue earlier this month and is expected to issue a ruling on the regulation soon.


Researchers Find Genetic Links to Progressive Hearing Loss
Memphis, Tenn — Researchers may have found a link between progressive hearing loss and a gene called p19Ink4d (Ink4d), according to Neil Segil, PhD, and colleagues from the House Ear Institute (HEI) in Los Angeles and St. Jude’s Childrens Hospital in Memphis, Tenn, who have published their findings in the May 2003 issue of Nature Cell Biology (for background information, see the article by Segil and Andrew Groves, PhD, “The Challenge of Hair Cell Regeneration,” in the March 2001 HR, p. 23). The lead author of the paper is Ping Chen, PhD, a senior research associate at HEI. Other authors included Frederique Zindy (St. Jude), Caroline Abdala, and Xiankui Li (House Ear Institute), and Feng Liu (USC).

Normally, the Ink4d gene keeps healthy cells from inappropriately dividing. Mice lacking the Ink4d gene become progressively hearing impaired because the absence of Ink4d causes certain cells in their inner ears to attempt to divide. However, this inappropriate attempt to divide causes sensory hair cells to instead enter into programmed cell death, a process known as apoptosis.

This finding in mice represents a potentially unrecognized form of progressive hearing loss, a problem that also occurs in humans, according to the investigators. If problems in Ink4d also occur in humans, this finding could explain the slow development of deafness in some people. In the absence of the braking effect of normally functioning Ink4d genes, sensory hair cells in people’s ears might attempt to divide, setting off apoptosis.

This observation in mice suggests that a person who lacks one or both copies of Ink4d—or who has Ink4d genes that are not very active—might suffer progressive hair cell death and experience hearing loss just as mice do, according to Segil. He speculates that the lack of one or both Ink4d genes makes the person more susceptible to hair cell loss from a variety of different traumas, such as loud noise or certain medicines. According to this theory, trauma could stimulate hair cells to attempt to divide, and in turn, lead to apoptosis. This suggests that a person with a full set of Ink4d genes might be less susceptible to loud noise than a person with only half the set.

This leads to great promise relative to screening for hearing loss. “It might be possible one day to screen a person for susceptibility to hearing loss by measuring the level of Ink4d they have,” says Segil. “We could use that information to warn people they are at increased risk for hearing loss due to trauma.”

Unfortunately, the requirement that these cells need to remain dormant (ie, not divide) may mean that gene therapy—which is aimed at replacing lost sensory hair cells through cell division to restore hearing— might only stimulate these cells to try undergo apoptosis and die, thus worsening the condition, reports Martine Roussel, PhD, a co-author of the paper and a member of the St. Jude Department of Genetics and Tumor Cell Biology, and a professor in the Department of Molecular Sciences at the University of Tennessee in Memphis.

Sensory hair cells respond to sound waves by setting off electric impulses in nerves that help generate the sense of hearing. Rows of these cells form during development of the embryo. Together with supporting cells, they make up the organ of Corti in the inner ear. These cells normally do not multiply after they are formed in the embryo; therefore, they can’t multiply to replace lost or damaged sensory hair cells later in life. However, in the absence of Ink4d, they may attempt to divide.

“In fact, in the mice that lacked Ink4d, hair cells sometimes tried to divide,” says Roussel. “This led to apoptosis and hearing loss in these mice.” The dominant role of Ink4d in sensory hair cells is unique. In other parts of the brain, nerve cell division is controlled in part by either Ink4d or by another gene, Kip1. In these cells, the loss of either gene does not completely take the brakes off of cell division. However, the researchers found this was not the case hair cells, where the loss of Ink4d alone in mice led to failed attempts at cell division and, ultimately, apoptosis.

The researchers studied mice that lacked both copies of Ink4d (known as “Ink4d -/-” mice—normally, one copy of each gene is inherited from each parent). Using biochemical techniques that highlighted hair cells under the microscope, they observed hair cell loss in mice that were 2.5 weeks old. When the Ink4d -/- mice were 7 weeks old, hair cell loss had progressed even further. Specifically, the innermost of four rows of sensory hair cells suffered a 43.3% loss of cells, and the three outer rows suffered losses of 27.8%, 8.1%, and 8.5%, respectively. Mice that had both copies of the Ink4d gene (Ink4d + did not suffer loss of sensory hair cells).

The researchers also used DPOAE tests performed at weeks 7 and 15 in both Ink4d +/+ and Ink4d -/- mice. The ears of normal mice produced normal responses to sound waves entering the ear, but the ears of mice lacking Ink4d did not respond to this stimulation. ABRs were used to compare the nerve response to sound in mice with and without Ink4d. At 7 weeks of age the Ink4d -/- mice had responses similar to Ink4d+ mice. However, by 15 weeks, the sound level had to be increased significantly before the hair cells of the Ink4d -/- mice responded.

“The fact that mice lacking Ink4d lost so much of their sense of hearing by week 15 was a result of the loss of many of their sensory hair cells,” says Roussel. The study’s findings suggest that progressive deafness due to the absence or mutation of Ink4d might respond to gene therapy. However, Roussel cautions that such therapy could also be dangerous. “Some cells, like the sensory hair cells of the inner ear, are not designed to reproduce once they are formed in the embryo,” Roussel said. “It’s a delicate balance between stimulating cells to reproduce to replace lost cells, and setting off unintended apoptosis, which could make things much worse.”

The work was supported by the National Institutes of Health, ALSAC, and the Oberkotter Foundation.