May 5 - 9, 2019 Niagara-on-the-Lake Ontario, Canada hearinglossconference.org - International Hearing Loss Conference
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May 5 - 9, 2019 Niagara-on-the-Lake Ontario, Canada hearinglossconference.org
PROGRAM AT A GLANCE
International Conference on Hearing Loss
Program-At-A-Glance
Sunday Monday Tuesday Wednesday Thursday
Time
5-May 6-May 7-May 8-May 9-May
7:00 AM
7:15 AM Breakfast Breakfast Breakfast
Tiara Restaurant Tiara Restaurant Tiara Restaurant
7:30 AM
(7:00am - 8:30am) (7:00am - 9:00am) (7:00am - 9:00am)
7:45 AM
8:00 AM
8:15 AM
8:30 AM Opening Barbara Shinn-
Larry Roberts Susan Shore
8:45 AM (8:30am - 9:00am) Cunningham
(8:30am - 9:15am) (8:30am - 9:15am) Departure
9:00 AM (8:30am - 9:15am)
Charlie Liberman
9:15 AM Matt Dye Sylvie Hébert Craig Formby
(9:00am - 9:45am)
9:30 AM (9:15am - 9:45am) (9:15am - 9:45am) (9:15am - 9:45am)
9:45 AM Jos Eggermont Magda Wojtczak Jian Wang Sharon Kujawa
10:00 AM (9:45am - 10:15am) (9:45am - 10:15am) (9:45am - 10:15am) (9:45am - 10:15am)
10:15 AM Lukas Rüettiger Xu-Friedman Phil Gander Alain Dabdoub
10:30 AM (10:15am - 10:45am) (10:15am - 10:45am) (10:15am - 10:45am) (10:15am - 10:45am)
Registration /Information Desk Open 7:30am-6:00pm
10:45 AM Coffee Break Coffee Break Coffee Break
Registration /Information Desk Open 8:00am-5:00pm
11:00 AM (10:45am-11:15am) (10:45am-11:15am) (10:45am-11:15am)
11:15 AM Anu Sharma Roland Schaette Brian Allman Dan Polley
Registration /Information Desk Open 8:00am-6:00pm
11:30 AM (11:15am - 11:45am) (11:15am - 11:45am) (11:15am - 11:45am) (11:15am - 11:45am)
11:45 AM Helmy Mulders Jaime Garcia-Anoveros Pascal Barone Thanos Tzounopoulos
12:00 PM (11:45am - 12:15pm) (11:45am - 12:15pm) (11:45am - 12:15pm) (11:45am - 12:15pm)
12:15 PM Chris Plack Ian Bruce Amir Amedi Rick Alstschuler
12:30 PM (12:15pm - 12:45pm) (12:15pm - 12:45pm) (12:15pm - 12:45pm) (12:15pm - 12:45pm)
12:45 PM
1:00 PM Lunch Lunch Lunch
1:15 PM Tiara Restaurant Tiara Restaurant Tiara Restaurant
1:30 PM (12:45pm - 2:00pm) (12:45pm - 2:00pm) (12:45pm - 2:00pm)
1:45 PM
2:00 PM Barbara Canlon Enrique Lopez-Poveda Karen Gordon Richard Salvi
2:15 PM (2:00pm - 2:30pm) (2:00pm - 2:30pm) (2:00pm - 2:30pm) (2:00pm - 2:30pm)
2:30 PM Early Investigator Early Investigator
Early Investigator Talks Early Investigator Talks
2:45 PM (2:30pm - 3:15pm)
Talks Talks (2:30pm - 3:15pm)
(2:30pm - 3:15pm) (2:30pm - 3:15pm)
3:00 PM
3:15 PM Coffee Break
3:30 PM (3:15pm - 3:45pm)
3:45 PM Mike Heinz Ben Auerbach
4:00 PM (3:45pm - 4:15pm) (3:45pm - 4:15pm)
4:15 PM Jean Luc Puel Andrew Dimitrijevic
4:30 PM Posters Session 1 (4:15pm - 4:45pm) (4:15pm - 4:45pm) Posters Session 2
(3:15pm - 6:00pm) (3:15pm - 6:00pm)
4:45 PM
5:00 PM
5:15 PM
5:30 PM
5:45 PM Registration
6:00 PM (5:00pm - 7:00pm) Group Photo
6:15 PM
6:30 PM
6:45 PM
7:00 PM
7:15 PM
7:30 PM
7:45 PM
Conference Banquet
8:00 PM Excursions
Château des Charmes
8:15 PM (6:00pm - 10:00pm)
Welcome Barbecue
8:30 PM
(7:00pm - 10:00pm)
8:45 PM
9:00 PM
9:15 PM
9:30 PM
9:45 PM
10:00 PM
TABLE OF CONTENTS
Welcome Letter . . . . . . . . . . . . . . . . . . . . . . 2
IHLC Program Committee . . . . . . . . . . . . . . . . . 2
General Congress Information . . . . . . . . . . . . . . . 3
Conference Venue Floor Plan . . . . . . . . . . . . . . . 4
IHLC Social Functions . . . . . . . . . . . . . . . . . . 5
Invited Speakers . . . . . . . . . . . . . . . . . . . . . 7
Detailed Daily Program . . . . . . . . . . . . . . . . . . 19
IHLC Delegates . . . . . . . . . . . . . . . . . . . . . . 24
IHLC Travel Award Winners . . . . . . . . . . . . . . . . 28
IHLC Congress Poster Author Index . . . . . . . . . . . . 29
IHLC Congress Poster Floor Plans . . . . . . . . . . . . . 31
IHLC Congress Posters, Titles, Authors and Affiliations . . . 32
IHLC Congress Sponsors . . . . . . . . . . . . . . . . . 37
Sponsor thank you (Back Cover) . . . . . . . . . . . . . . 40
Notes:
International Hearing Loss Conference | 1
WELCOME LETTER Welcome to the 4th International Hearing Loss Conference It is our distinct pleasure to welcome you to Niagara-on-the-Lake and the 4th International Hearing Loss Conference! This vibrant and exciting meeting has continued to grow since the first meeting in 2004 in Niagara Falls, NY. We have registrants from 13 countries from all corners of the globe. With a successful fundraising effort, we were pleased to offer 27 travel awards to trainees in addition to financial support of all the keynote and invited speakers. We are grateful to the Program Committee for all their hard work in organizing an exciting scientific program. The success of this meeting is, in large part, due to their tremendous efforts. The Program Committee was led by Richard Salvi and Larry Roberts, and included Blake Butler, Brain Allman, Anu Sharma, Prudence Allen, and Marshall Chasin. From their efforts, we have four keynote speakers, 32 invited speakers, and 16 early-investigator oral presentations selected from the abstract submissions. Please enjoy the beauty that is Niagara-on-the-Lake and the excellent facilities of the Queen’s Landing Hotel. First known as Butlersburg, Niagara-on-the-Lake was incorporated in 1781 as the Town of Newark by Loyalists who fled the U.S. during the American Revolution. In 1792 the newly renamed Niagara was the capital of Upper Canada, but lost that distinction to York (now Toronto) due to Niagara-on-theLake’s proximity to the U.S., which was deemed a vulnerable position at that time. During the War of 1812, Niagara-on-the-Lake was burnt to the ground. Rebuilt, it became a commercial centre, thanks to a vibrant shipping industry. In 1880, the present name was adopted. Today, Niagara-on-the-Lake attracts more than two million visitors annually. The picturesque main street is a testament to the beauty of 19th century architecture. A landmark on this street is the clock tower monument, erected as a memorial to 10 of the town’s men who lost their lives in World War I. Known by the locals as NOTL, this picturesque village is known for its wineries and the summer Shaw Festival, a series of theatre productions. Tuesday afternoon there are a number of excursions to choose from. If you have not already registered for an excursion, please visit the registration desk and decide among the opportunities. We are grateful for all the behind the scenes work by Pam Prewett and Podium Conference Specialists. They have been wonderful partners in putting the conference together and planning over the past few years. Cordially, Steve Lomber Conference Chair Program Committee IHLC Congress Management Steve Lomber, Chair University of Western Ontario Podium Conference Specialists Larry Roberts McMaster University Marischal De Armond Robert Harrison SickKids Pam Prewett Brian Allman University of Western Ontario Alaina Laflamme Blake Butler University of Western Ontario Richard Salvi University at Buffalo Anu Sharma University of Colorado Boulder Prudence Allen University of Western Ontario Marshall Chasin Marshall Chasin & Associates, Toronto 2 | International Hearing Loss Conference
GENERAL CONFERENCE INFORMATION
Meeting Venue Notes:
Queen’s Landing
155 Byron Street
Niagara-on-the-Lake, ON
Canada
Tel: +1-905-468-2195
All conference sessions and the Welcome Barbecue
will take place at this location, and the Conference
Banquet will take place at an offsite venue.
Registration
Congress registration fees include access to all
sessions including the welcome barbecue, breakfast,
speaker presentations, breakfast, grazing lunches,
coffee breaks, poster sessions, and conference
banquet.
Name Badges
Your name badge is your admission ticket to all
conference sessions, welcome barbecue, breakfast,
lunch, and coffee breaks. Please wear it at all times.
At the end of the conference we ask that you recycle
your name badge at one of the name badge recycling
stations, or leave it at the Registration Desk.
Registration and Information Desk Hours
The Registration and Information Desk, located in the
Pavilion/Atrium Foyer, will be open during the following
dates and times:
Sunday May 5 5:00 - 7:00pm
Monday May 6 7:30am - 6:00pm
Tuesday May 7 8:30am - 5:00pm
Wednesday May 8 8:30am - 6:00pm
If you need assistance during the meeting, please visit
the Registration Desk.
Staff
Congress staff from Podium Conference Specialists
can be identified by orange ribbons on their name
badges. For immediate assistance, please visit us
at the registration desk at the bottom of the stairs.
Complimentary WIFI Information:
Complimentary Wifi is available in the hotel lobby
on the ground floor and in your hotel guestroom.
Network: datavalet
International Hearing Loss Conference | 3
CONFERENCE VENUE FLOOR PLAN
CARLISLE WINDSOR
YORK
SOMERSET
WEDGE-
WOOD
MAIN LEVEL
BALMORAL LOYALIST
BACCHUS LOUNGE
WR
INTERNET
LIBRARY
WR
WR WR
BUSINESS
CENTRE
TIARA
GRAND GEORGIAN BALLROOM RESTAURANT
SCARLET
JADE
ELEVATORS (A) (B) (C)
SERVERY
WR
IMPERIAL ATRIUM
WR (A)
KITCHEN
WR
MAGNOLIA IMPERIAL
(B)
TRILLIUM
4 | International Hearing Loss Conference
IHLC SOCIAL FUNCTIONS
Opening Barbecue Notes:
Sunday, May 5
5:00 – 7:00pm
Baccus Lounge/Tiara Restaurant Patio
Join us to celebrate IHLC! Enjoy a delicious barbecue
on the patio while catching up with old friends and
making new ones. A cash bar will also be offered.
Conference Banquet
Wednesday, May 8
6:00 – 10:00pm
Château des Charmes Winery
The Conference Banquet offers a unique experience.
Picture rows upon rows of vines, the sun casting a
reddish hue over the vineyards as it gently sets and the
most challenging decision you have to make is whether
you would like Chardonnay or Cabernet-Merlot with
your hors d’oeuvre. Château des Charmes is unlike
any other setting in Canada. We’ll dine in the Vineyard
Courtyard, a unique and versatile outdoor hospitality
space. Surrounded by romantic rose gardens, the
award winning St. David’s Bench Vineyard and set
against the back-drop of the Niagara Escarpment, a
UNESCO World Biosphere Reserve, the IHLC banquet
dinner is set for an evening amongst the vines.
Transportation is included.
International Hearing Loss Conference | 5
IHLC EXCURSIONS
The IHLC organizing committee has created a conference program that provides an evening of exploration on
Tuesday, May 7. Join in one of the suggested tours below, or explore the numerous vineyards and beautiful town
of Niagara-on-the-Lake on your own.
Hornblower Niagara Cruises
Feel the breeze in your hair and refreshing mist on your skin as you experience the
thundering roar of the Mighty Falls. Join us on this most memorable experience of the
Falls aboard a private charter known as the ‘Niagara Guardian’. The 142-passenger jet
boat will cruise you around the Niagara Gorge, past the American and Bridal Veil Falls
and bring you up close and personal with the Canadian Horseshoe Falls. This private
charter offers an entirely seated experience featuring safety belts and a railing around
the edge of the boat for the safety and security of guests.
Tuesday, May 7 Tour departs at 5:30pm from Queen’s Landing Hotel
Meeting point: Queen’s Landing main entrance
Duration: 1½ to 2 hours
Cost: $60.00 per person Includes transportation
Niagara Wine Trolley Tour
Explore Wine Country on board a wine country trolley tour! Experience TWO
of Canada’s most celebrated wineries and taste many award-winning wines.
A knowledgeable winery tour director will share local history and information as
you travel along the scenic Niagara Parkway via popular wine routes, past vineyards,
orchards, and through historic Niagara-on-the-Lake.
Tuesday, May 7 Tour departs at 5:00pm SHARP
Meeting point: Queen’s Landing main entrance
Duration: 1½ hours
Cost: $70.00 per person Includes a wine tasting at each winery,
charcuterie platter at Konzelmann Estate Winery, transportation
with the Niagara-on-the-Lake Trolley Company.
DINING
The following restaurants have offered discounts to IHLC delegates. Simply show your name badge when you arrive
to receive your discount.
Backhouse Niagara’s Finest Thai
242 Mary Street | backhouse.xyz 88 Picton Street | niagarasfinestthai.com
15% discount on tasting menus and a complimentary glass 10% discount on all regularly priced food.
of bubble upon arrival on Monday, May 6. Closed Tuesdays.
Masaki Sushi
60 Picton Street | masakisushi.ca
10% discount on all regularly priced food.
Chili Jiao
271 Mary Street | chilijiao.com
10% discount on all regularly priced food.
Butler’s Bar & Grill
284 Mary Street | butlersgrill.com
10% discount on all regularly priced food.
6 | International Hearing Loss Conference
INVITED SPEAKERS
Brian Allman shifts in auditory brain stem response (ABR) measures and can
University of Western Ontario, lead to changes in Gap Detection and/or behavioral responses
indicative of tinnitus in animal models. Losses in hair cell func-
Canada tion(s) or loss of hair cells is linked to ABR temporary or permanent
Over the past 10 years, my research has threshold shifts respectively. Loss of inner hair cell-auditory nerve
focused on basic questions investigating connections (synaptopathy) can be associated with changes in ABR
how the cortex integrates information from suprathesholds and loss of dynamic range. There are successful
more than one sense (e.g., vision and strategies for prevention of noise-induced hair cell dysfunction and/
hearing), as well as on clinically- or loss including anti-oxidant treatment. Post-noise treatments can
relevant questions as to how the cortex reduce further loss in hair cells that have not entered cell death
adapts to hearing loss and its perceptual implications. In address- cycles, however there are not yet any successful treatments to
ing these research themes, I have used numerous animal models replace lost hair cells. There are successful strategies to prevent
(mice, rats, ferrets and cats) and a combination of techniques, noise-induced cochlear synaptopathy such as use of anti-excitotox-
including electrophysiological recordings from cortical neurons, as icity agents as well as successful strategies to induce re-connection
well as a variety of behavioural paradigms, ranging from reflexive of lost synapses including use of neurotrophins. While noise-
tests of sensory-motor gating to perceptual judgment tasks requiring induced effects in the cochlea are considered inducing agents for
executive function. With respect to the neuroplasticity induced by the progression of events leading to tinnitus, the specific necessary
hearing loss, my lab has taken a multi-faceted approach that ranges or sufficient cochlear changes have yet to be firmly identified. Our
from in vitro investigations of the sensory cells in the inner ear, all studies are testing synaptopathy as an inducer for noise-induced
the way up to studying cortical processing at the level of single tinnitus in the rat model (using broad band and small arms fire like
neurons, local microcircuits and sensory perception. It remains a noises) and determining if prevention or repair will influence the
long-term goal of my research program to reveal the brain circuits progression and reduce the incidence of tinnitus.
and cellular mechanisms that contribute to the perceptual
consequences commonly associated with hearing loss-induced
brain plasticity. Amir Amedi
Hebrew University, Jerusalem
Crossmodal plasticity in auditory, visual and multisensory
cortical areas following noise-induced hearing loss Amir Amedi is the Director of The make
Following hearing loss, crossmodal plasticity occurs whereby there SENSE Center for Brain imaging, Rehab
is an increased responsiveness of neurons in the deprived auditory and Augmentation of the SENSES. He is
system to the remaining, intact senses (e.g., vision). Using a Professor at the Department of Medical
electrophysiological recordings in noise-exposed rats, our recent Neurobiology at the Hebrew University,
studies have revealed that crossmodal plasticity is not restricted to PhD in Computational Neuroscience
the core auditory cortex; higher-order auditory regions as well as (ICNC, Hebrew University) and Post-
visual and audiovisual cortices show differential effects following doctoral and Instructor of Neurology (Harvard Medical School). He
noise-induced hearing loss. Unexpectedly, the cortical area showing is recipient of The Krill Prize for Excellence in Scientific Research,
the greatest relative degree of multisensory convergence post-noise the Wolf Foundation (2011), the international Human Frontiers
exposure transitioned away from the normal audiovisual area toward Science Program Organization Career Development award
a neighboring, predominantly auditory area. Thus, our collective (2009), the JSMF Scholar Award in Understanding Human
results suggest that crossmodal plasticity induced by adult-onset Cognition (2011). He received 2 consecutive ERC grants
hearing impairment manifests in higher-order cortical areas as a (www.BrainVisionRehab.com 2013-2018; ExperieSENSE 2018-
transition in the functional border of the audiovisual cortex. Our 2023). He is an internationally acclaimed brain scientist with 15
ongoing studies have begun to reveal the implications of this cross- years of experience in the field of brain neuroplasticity and
modal plasticity on the rats’ ability to perceive the precise timing of multisensory integration. In 2017 he founded www.ReNewSenses.
audiovisual stimuli using novel behavioral tasks that are consistent com where he is engaged in developing novel Sensory substitution
with studies of perceptual judgement in humans. Device and AI algorithms to help the visually and hearing impaired.
How technology, life experiences and imagination shapes brain
Rick Altschuler specialization
(“The best technologies make the invisible visible.” -Beau Lotto).
University of Michigan, USA My lab studies the principles driving specializations in the human
Rick Altschuler received his Ph.D. in brain and their dependence on specific experiences during
Anatomy at the University of Minnesota development (i.e. critical/sensitive periods) versus learning in
in 1978 and then moved to the Lab of the adult brain. I will cover the work done under our
Neuro-Otolaryngology at NINCDS at the www.BrainVisionRehab ERC project which focuses on studying
National Institutes of Health where he Nature vs. Nurture factors in shaping up category selectivity in
studied neurotransmitters and receptors the human brain. A key part of the project involves the use of
of the cochlea and cochlear nucleus. Sensory-Substitution-Devices (SSD). I will focus on work with the
He joined Kresge Hearing Research Institute at the University of EyeMusic algorithm developed in my lab which convert invisible
Michigan in 1985 where he is now a Professor in the Departments visual input to blind using music and sound. In the second part of
of Otolaryngology and Cell and Development Biology. He also has the talk I will cover speech to touch sensory substitution approach
an appointment at the VA Ann Arbor Healthcare System. He is which improve performace of hearing impaired in noisy
currently studying noise induced and age-related hearing loss and environments. From basic science perspective the most intriguing
vestibular dysfunction, tinnitus and mechanism based therapeutic results came from studying blind without any visual experience
interventions for prevention and treatment. using SSDs to understand online visual feed arriving from a video
camera. Specifically, I will discuss work aiming at unraveling the
Noise induced cochlear hair cell loss, synaptopathy and properties driving the sensory brain organization and at uncovering
tinnitus: Mechanisms and strategies for prevention and repair the extent to which specific unisensory experiences during critical
Noise overstimulation can lead to temporary and/or permanent periods are essential for the development of the natural sensory
specializations. Our work focused on two fundamental discoveries:
International Hearing Loss Conference | 7
INVITED SPEAKERS
1- Using the congenitally blind adult brain as a working model of a Pascal Barone
brain developing without any visual experience, we documented
that essentially most if not all higher-order ‘visual’ cortices can CNRS/University of Toulouse,
maintain their anatomically consistent category-selectivity (e.g., for France
body shapes, letters, numbers and even faces) even if the input is Pascal Barone is the team leader of C3P
provided by an atypical sensory modality learned in adulthood. (Crossmodal Compensation and Cortical
We also found that such task-specific sensory-independent Plasticity) a team dedicated to under-
specializations can emerge as fast as after a few hours of training. standing mechanisms of cortical plasticity
Our work strongly encourages a paradigm shift in the in normal subjects and deaf patients.
conceptualization of our sensory brain by suggesting that visual My early works exploring the neuronal
experience during critical periods is not necessary to develop mechanisms of prenatal axogenesis have clearly demonstrated the
anatomically consistent specializations in higher-order ‘visual’ or high specificity of the cortical connectivity during early development,
‘auditory’ regions. This also have implications to rehabilitation by a result that have a strong theoretical influence in understanding the
suggesting that multisensory rather than unisensory training might development of sensory functions and the impact of early sensory
be more effective. I will also discuss initial results from our new deprivation on brain reorganization. Based on a tied collaboration
ERC ExperieSense project which focuses on studying Nature vs. with the ETN department at the Purpan hospital in Toulouse, I
Nurture factors in shaping topographical maps in the brain. In this presently conduct a multidisciplinary approach to better understand
project we focus on transmitting invisible topographical information the neuronal mechanisms of brain plasticity in deafness in animal
to individuals with sensory deprivation but also augmented models and in humans. Our work is based on a multidisciplinary
topographical information to normally sighted by using similar approach at both a fundamental and a clinical level, it encompasses
training and SSD protocols to couple it with input from ‘invisible’ behavioral and brain imaging (PET) studies in patients as well as
sensors (like infrared or ultrasound images) and testing whether in normal hearing subjects. Because the success of rehabilitations
novel topographical representations can emerge in the adult brain relies on the functional plasticity in the auditory system, our work is
to input that was never experienced during development (or aimed at understanding the reorganization of the cortical network
evolution). involved in auditory processing that occurs during deafness and
following the progressive recovery through a cochlear implantation
(See also Amedi et al. Task Selectivity as a Comprehensive or with hearing aids. Our complementary projects aim to a better
Principle for Brain Organization. Trends in Cognitive Sciences understanding of hearing restoration coupled to the evaluation of
2017). rehabilitation strategies.
Functional segregation in the auditory cortex: evidence from
Ben Auerbach brain reorganization in unilateral deaf patients
University at Buffalo, USA In patients with unilateral hearing loss (UHLp), binaural processing
is obviously disrupted and spatial localization of the sound source
Dr. Benjamin D. Auerbach graduated is impaired as well as the ability in understanding speech in noisy
from Cornell University with a Bachelor’s environments. At the brain level, a limited number of studies have
in Biological Sciences and received his explored the functional reorganisation that occurs in the adult after
Ph.D. in Neuroscience from the a unilateral deafness. We conducted an original study aimed at
Massachusetts Institute of Technology. investigating in UHLp the relationships between the severity of
He is currently a Research Assistant unilateral hearing loss, the resulting deficit in binaural processing
Professor at the Center for Hearing and and the extent of cortical reorganisation across the auditory areas.
Deafness at the University at Buffalo. Dr.
Auerbach’s research We have recruited 14 UHL patients (hearing loss 37-120 dB HL)
interests include auditory plasticity, hyperacusis, and autism and aged-matched hearing controls. All subjects were evaluated
spectrum disorders. for free-field sound localization abilities and speech in noise
comprehension (French Matrix test). All subjects went through a
Comparing auditory circuit disruptions across diverse models fMRI protocol to evaluate the activation pattern across auditory
of hyperacusis areas during a natural sounds discrimination task. First, brain
Hyperacusis is a complex hearing disorder that encompasses a imaging analysis clearly demonstrated that in non-primary areas
wide-range of reactions to sound, including excessive loudness, (NPAC), UHL induces a shift toward an ipsilateral aural dominance.
increased aversion/fear of sound, or even pain. While often Such reorganization, absent in the PAC, is correlated to the hearing
associated with hearing loss and tinnitus, sound tolerance loss severity and to lower spatial localization ability performances.
disturbances are actually observed across a broad spectrum of Second, a regression analysis between brain activity and patient’s
neurological disorders. Thus, hyperacusis is diverse in both its performances, clearly demonstrated a link between the sound
etiology and phenotypic expression, and it is imperative to consider localisation deficit and a functional alteration that impacts
this diversity when attempting to elucidate its physiological specifically the posterior auditory areas known to process spatial
mechanisms. Here we will describe a series of recent studies hearing. On the contrary, the core of the auditory cortex appeared
utilizing novel behavioral paradigms aimed at distinguishing between relatively preserved and maintains its normal implication in
the diverse ways in which sound perception may be altered in processing non-spatial acoustical information.
hyperacusis. We have combined these novel assays with acute
and chronic in vivo electrophysiological recordings to examine the Altogether our study adds further evidences of a functional
neurophysiological correlates of hyperacusis using three distinct dissociation in the auditory system and shows that binaural deficits
models: salicylate-induced ototoxicity; noise-induced hearing loss; induced by UHL affect predominantly the dorsal auditory stream.
and an Fmr1 KO rat model of Fragile X syndrome, a leading
inherited form of autism that consistently presents with auditory
hypersensitivity. This multifaceted approach allows us to determine
if different forms of hyperacusis are mechanistically distinct
disorders with overlapping presentation, or if they share a common/
convergent pathophysiological mechanism.
8 | International Hearing Loss ConferenceINVITED SPEAKERS
Ian Bruce and the reciprocal feedback of metabolism on circadian oscillators
McMaster University, Canada in the inner ear. We anticipate that a better understanding of clock
processes will lead to innovative therapeutics for a spectrum of
Ian C. Bruce, Ph.D. is a Professor and auditory disorders.
Associate Chair of Graduate Studies in
Electrical & Computer Engineering at Dr. Canlon has been head of the Experimental Audiology Section at
McMaster University in Hamilton, the Karolinska Institute for the past 25 years and has had numerous
Ontario, Canada. He is engaged in major administrative duties at the Karolinska Institute. She is
interdisciplinary research and academic currently Editor-in-Chief for Hearing Research. She received her
activities in electrical & biomedical bachelor degree from Brooklyn College, City University of New
engineering, neuroscience, psychology, and music cognition. His York and then her Master´s at the University of Michigan. She
research is focused on applying cutting-edge experimental and then moved to Stockholm and obtained her Ph.D. at the Karolinska
computational methods to better understand, diagnosis and treat Insitute. After a post-doc at Institute Pasteur, Paris and CNRS-IN-
hearing disorders. Research applications pursued by his lab include SERM, Montpellier she established her laboratory at the Karolinska
hearing aids, cochlear implants, diagnosis & treatment of tinnitus, Institute and became professor in 2001.
speech & music perception, digital speech processing, and genetic
hearing loss. The clockwork of the cochlea
This lecture is based on our discovery showing that the peripheral
Dr. Bruce received the B.E. (electrical and electronic) degree from auditory system, the cochlea, is regulated by a molecular circadian
The University of Melbourne, Australia, in 1991, and the Ph.D. clock, which opened an exceptional opportunity for understanding
degree from the Department of Otolaryngology, The University of unique features of the auditory system that were previously
Melbourne in 1998. From 1993 to 1994, he was a Research and unknown. We have found, in the mouse, that the same noise
Teaching Assistant at the Department of Bioelectricity and exposure causes greater physiological and morphological conse-
Magnetism, Vienna University of Technology, Vienna, Austria. quences during nighttime compared to daytime exposures. Conse-
He was a Postdoctoral Research Fellow in the Department of quently, a robust molecular circadian clock machinery including the
Biomedical Engineering at Johns Hopkins University, Baltimore, circadian genes Per1, Per2, Bmal1, and Rev-Erb, was identified in
MD, USA, from 1998 to 2001, before moving to McMaster in 2002. the cochlea and was found to regulate this differential sensitivity to
Dr. Bruce is an Associate Editor of the Journal of the Acoustical day or night noise exposure. Using RNAseq we recently identified
Society of America, a Fellow of the Acoustical Society of America, 7211 genes in the cochlea that have circadian expression and a
a Member of the Association for Research in Otolaryngology, and a large proportion of them regulate cell signaling, hormone secretion,
Registered Professional Engineering in Ontario. and inflammation. Nearly ¾ of these genes show maximal
expression at nighttime, a finding which can only be captured when
Computational modeling of diverse forms of cochlear pathology performing analyses around the clock. Why is this important?
Computational models of auditory processing can be useful tools A “broken” clock may enhance the risk for developing hearing loss,
in understanding the normal function of the ear and the auditory as it has been shown for a wide variety of diseases including
pathways of the brain. In addition, computational models that can metabolic, cardiovascular, neoplastic and inflammatory disorders.
incorporate pathology may be helpful in understanding the effects of However, before investigating the consequences of clock disruption
hearing impairment and in the development of improved devices for on auditory functions, a better understanding of the circadian
those with hearing loss, such as hearing aids and cochlear implants. components that characterize the auditory system are needed.
However, incorporating pathology into physiological models of
auditory processing faces some difficulties including: i) incomplete
accuracy in even explaining normal function, ii) limited physiological Alain Dabdoub
detail regarding the site of the pathology, and/or iii) uncertainty Sunnybrook Research Institute,
in explaining a human subject’s experimental data due to a lack of Canada
definite knowledge about the pathology that they have.
Dr. Dabdoub is the research director of
In this talk, I will review efforts by a number of research groups, the Hearing Regeneration Initiative at
including my own, to develop, validate and apply models of a Sunnybrook Research Institute and an
diverse range of cochlear pathologies. Methodologies for modelling associate professor in the Department of
outer hair cell impairment, inner hair cell impairment, cochlear Otolaryngology Head & Neck Surgery and
synaptopathy, and pathologies caused by genetic mutations will Department of Laboratory Medicine at the
be explored. Approaches to overcoming uncertainties about patterns University of Toronto, Canada.
of pathologies in human subjects will also be discussed.
Dr. Dabdoub’s research program focuses on discovering and
elucidating the molecular signaling pathways involved in the
Barbara Canlon development of the mammalian inner ear. The goal of his
Karolinska Institute, Sweden laboratory is to connect developmental biology to inner ear
diseases and ultimately to regenerative medicine for the
Dr. Canlon’s laboratory is working to amelioration of hearing loss through cellular regeneration of
understand the normal hearing process sensory hair cells and primary auditory neurons.
and causes of hearing deterioration as
a step toward the prevention of hearing Connecting the cochlea to the brain: Development and
loss. In an effort to learn how hair cells regeneration of the primary auditory neurons
and nerve fibers become damaged, Dr. Primary auditory neurons, also known as spiral ganglion neurons,
Canlon’s group is conducting molecular are responsible for transmitting sound information from cochlear
experiments to identify key players in this process. Dr. Canlon sensory hair cells in the inner ear to cochlear nucleus neurons in
has recently discovered that the cochlea contains a self-sustained the brainstem. Auditory neurons develop from neuroblasts
circadian clock, which continues to tick in culture. The current delaminated from the proneurosensory domain of the otocyst and
research focus is to understand the molecular mechanisms through keep maturing until the onset of hearing. These neurons degenerate
which the circadian clock regulates cell and organismal metabolism due to noise exposure and aging resulting in permanent hearing
International Hearing Loss Conference | 9INVITED SPEAKERS
impairment. Thus, auditory neurons are a primary target for Jos Eggermont
regeneration for the amelioration of hearing loss. Glial cells
surrounding auditory neurons originate from neural crest cells and University of Calgary, Canada
migrate to the spiral ganglion during development. These glial cells Born 1942. M.Sc in physics (1967), Ph.D.
survive after neuron degeneration and loss making glial cells ideal in biophysics (1972). Research Associate
for gene therapy and cellular reprogramming. Department of Otorhinolaryngology at
Leiden University in the Netherlands
Using combinatorial coding, we have successfully converted glial (1972-1978) interrupted from 1976-1977
cells into induced neurons in vitro and assessed the induced as research fellow at the House Ear
neurons using morphology, immunohistochemistry, their ability to Institute in Los Angeles, California. !978-
innervate peripheral and central targets, as well as transcriptomic 1986 professor in Biophysics, Nijmegen University Netherlands.
analyses comparing their properties to endogenous auditory 1986-2013 Professor in Psychology, Physiology and Pharmacology
neurons and control cells. Furthermore, we have developed a at the University of Calgary, Alberta, Canada. Alberta Heritage
preclinical mouse model of neuropathy with the aim of converting Foundation for Medical Research Scholar and Scientist (1986-
glial cells in vivo. Neuron replacement therapy would have a 2013). 1997-2013 Campbell McLaurin chair for Hearing
significant impact on research and advancements in cochlear Deficiencies. 2013-present Emeritus Professor at the University
implants as the generation of even a small number of auditory of Calgary.
neurons would result in improvements in hearing.
Published >220 peer reviewed articles; ~ 100 book chapters and
6 single authored books and 4 edited books. Received >20,000
Andrew Dimitrijevic citations (Google Scholar), h-factor = 81.
Sunnybrook Research Institutes,
Canada Selected Honors:
• Elected corresponding member of the Royal Netherlands
Andrew Dimitrijevic is a scientist at the Academy of Arts and Sciences (1989)
Sunnybrook Health Sciences Centre,
Department of Otolarygology, Head and • Elected Fellow of the Acoustical Society of America (1998)
Neck Surgery, Sunnybrook Research • Elected Fellow of the Royal Society of Canada (2014)
Institute. He is also faculty at the • Editor-in-Chief of “Hearing Research” (2005-2010)
University of Toronto, Departments of
Otolarygology, Head and Neck Surgery, Institute of Medical Hearing loss and the brain
Sciences, Program in Neuroscience. Hearing loss is in in the ear, but hearing problems originate in the
brain. This suggests that the loss of auditory neural activity that
Dr. Dimitrijevic completed his PhD at the University of Toronto enters the central auditory system thereby alters it functioning.
under the supervision of Terry Picton. He went on to postdoctoral Specifically, hearing loss causes tonotopic map changes in
positions at the University of British Columbia under the thalamus and cortex, not at more peripheral subcortical structures,
supervision of David Stapells and University of California, Irvine likely as a result of changes in the balance between excitation and
under the supervision of Arnie Starr. Dr. Dimitrijevic was faculty inhibition, which may also cause central gain changes. Hearing loss
at Cincinnati Children’s Hospital Medical Center before coming is also known to increase spontaneous firing rates and neural
to Sunnybrook. synchrony in cochlear nucleus, midbrain, thalamus and auditory
cortex, but also in non-classical auditory sensitive areas. Sever
Dr. Dimitrijevic uses high density EEG recordings to understand hearing loss, for instance at > 8 kHz, results in atrophy of part of
sensory and cognitive aspects of hearing in both normal hearing auditory cortex, and also in prefrontal cortical areas related to
and hearing impaired populations. Web site: executive functions. In addition to these changes, the ‘auditory
http://www.cibrainlab.com connectome’ may be changed either directly through deafferentation,
Cortical oscillations in hearing loss: An emerging field with but also through increasing demands on cognitive processes such
emerging concepts as attention and memory to make sense of the deteriorated acoustic
Performing even a simple audiogram requires a number of cognitive signals resulting from hearing loss. These plastic changes can also
tasks such as selective attention, motivation and working memory. result in tinnitus and hyperacusis, and potentially in advancing the
The neural mechanisms of these cognitive processes are slowly onset of mild cognitive impairment.
emerging. In recent years there has been an explosion in the
interest in brain oscillations in auditory cognition research. Coupled
with an increased awareness that cognition plays a crucial role Phil Gander
everyday communication, such as listening to speech in noise or University of Iowa, USA
tackling the cocktail party problem has made the field of brain Phillip Gander is an assistant research
oscillations and audition ripe for investigation. While classic early scientist in the Department of
evoked potentials provide excellent indices of sensory encoding, Neurosurgery and the Department of
induced brain oscillations appear to index higher order cognitive Otolaryngology at The University of Iowa.
tasks such as attention and working memory. With hearing loss, He conducts research using electrocor-
the compensatory role of cognition as indexed with brain oscillations ticography (ECoG) in the Human Brain
as a result of reduced sensory fidelity has begun to be examined. Research Laboratory of Matt Howard, MD,
Brain rhythms spanning delta, theta, alpha, beta and gamma and using neuroimaging (PET, EEG) in the Iowa Cochlear Implant
frequencies appear to play specific roles in hearing cognition. Clinical Research Center. With the unique opportunities afforded
This talk will provide an overview of these brain rhythms in normal by both research environments he investigates questions related to
audition and compensatory roles with hearing loss. auditory object processing in collaboration with Tim Griffiths, MD,
Newcastle University. He previously worked as a research fellow at
the National Biomedical Research Unit in Hearing, Nottingham,
UK with Deb Hall. Phillip received his PhD in Psychology,
Neuroscience, and Behaviour in 2009 from McMaster University,
10 | International Hearing Loss ConferenceINVITED SPEAKERS
Hamilton, ON, where he worked with Larry Roberts and Laurel Auditory nociception
Trainor. Loud and/or persistent noise damages the cells of the organ
of Corti within the cochlea, among which the outer hair cells
Phillip’s research focus is auditory cognition from the perspective of (OHCs) are particularly vulnerable. Throughout most of the body,
cognitive neuroscience. Using psychophysics and neuroimaging he nociceptive neurons of the dorsal root and trigeminal ganglia detect
studies how the auditory system forms perceptual representations this kind of tissue damage. However, while a few somatosensory
and the factors that contribute to their formation including learning, nociceptors from trigeminal ganglia innervate cochlear vessels,
memory, and attention, under normal conditions and when they are they do not innervate the organ of Corti. This brings the question
disordered (e.g., hearing loss, cochlear implants, and tinnitus). In of whether noise-induced damage is undetected or whether the
addition to investigating the brain bases of sound processing he ear has its own nociceptive neurons. The organ of Corti receives
places a strong emphasis on translating basic scientific findings into innervations by only two types of afferent neurons, both of which
benefits for patients. are in the cochlear spiral ganglia. Most (~95%) of these are type
Human intracranial recordings during tinnitus perceptual change I afferents, which contact inner hair cells and get stimulated when
these release glutamate. This represents the canonical auditory
Advances are being made regarding putative neural mechanisms for
pathway by which sound information is thought to be transmitted
tinnitus within animal models, however difficulty remains regarding
from the cochlea to the brain. The other afferents, type II, send
the extent these models relate to factors that are relevant to the
processes that extend and branch under the OHCs. Recordings of
human experience of tinnitus. These limitations include neuro-
type II afferents revealed no activation by sound, so their function
physiological correlates, changes in perceptual strength, degree of
is unclear. We found that, blocking the canonical auditory pathway
distress, and amount of impact on cognition and quality of life. An
with a mutant in which IHCs do not release glutamate, sound
important step in the utility of animal models is to find similarities
stimulation could still activate neurons in the cochlear nucleus,
among these characteristics to the human experience of tinnitus.
but only if of an intensity that damages the organ of Corti and kills
The most tractable among them is the category of neuro-
OHCs. This reveals a form of communication from cochlea to brain
physiological correlates, unfortunately, clear patterns in measures
different from that provided by the canonical auditory pathway.
of human brain activity related to tinnitus remain elusive. The work
This communication is most likely carried by type II afferents, which
outlined in this presentation covers recent investigations of
in many other respects reassemble somatosensory nociceptors.
intracranial EEG in medically refractory epilepsy patients. Results
This represents a novel form of sensation, a hybrid of pain and
from two patients are described measured during a perceptual
hearing that we termed auditory nociception. We further propose
manipulation of tinnitus using a 30s white noise residual inhibition
that type II afferents may act as auditory nociceptors. Sensitization
paradigm. Wide spread activity throughout the brain was found
of such a pain-like system in in the inner ear might account for the
during a change in tinnitus intensity, along with focal cross-
pathological sensation of pain hyperacusis often reported by
frequency activity changes, which are proposed as hubs for
individuals with a history of noise trauma.
oscillatory coupling of activity related to distinct functions of a
broader tinnitus network. The results align with models of tinnitus
activity generated from human non-invasive recordings. In one Karen Gordon
patient, stimulation of Heschl’s gyrus was possible to explore the
potential for perceptual modulation of tinnitus. After stimulation, SickKids/University of Toronto,
effects similar to residual inhibition were described by the patient. Canada
Importantly the patient reported no change in hearing function Karen Gordon, PhD, is a Professor in
during stimulation, which challenges the idea that tinnitus has the Department of Otolaryngology and a
functional equivalence to normal auditory perception. Graduate Faculty Member in the Institute
of Medical Science at the University
of Toronto. She works at the Hospital
Jaime Garcia-Anoveros for Sick Children in Toronto, Ontario,
Northwestern University, USA Canada, as a Senior Scientist in the Research Institute and an
Jaime García-Añoveros, PhD, is a Audiologist in the Department of Communication Disorders. She is
professor of Anesthesiology, Physiology Director of Research in Archie’s Cochlear Implant Laboratory and
and neurology at Northwestern University holds the Bastable-Potts Health Clinician Scientist Award in Hearing
and a fellow at the Hugh Knowles Center Impairment and Cochlear Americas Chair of Auditory Development.
for Clinical and Basic Science in Hearing Karen’s research focuses on auditory development in children who
and Its Disorders. He obtained his BS are deaf and use auditory prostheses including cochlear implants.
from UC Berkeley and his PhD from Her work is supported by research funding from the Canadian
Columbia University, followed by a postdoctoral appointment at Institutes of Health Research along with the Cochlear Americas
Harvard Medical School and the Massachusetts General Hospital, Chair in Auditory Development and generous donations.
prior to joining the faculty at Northwestern. His research has largely Should children with single sided deafness receive a cochlear
consisted in the identification and characterization of genes, ion implant?
channels and transcription factors involved in sensory organ We are studying whether children with profound deafness in one
function, formation and degeneration, with an emphasis on pain and ear and normal hearing in the other ear (ie. single sided deafness
hearing. This resulted in a macromolecular model for touch mecha- (SSD)) can benefit from cochlear implantation. Leaving these
notransduction, the identification and characterization of transduction children’s hearing loss untreated puts them at risk for social,
channels for touch and pain, of degeneration-causing mutations in educational and emotional deficits and, over time, allows an aural
somatosensory neurons and hair cells (the latter explaining various preference to develop, weakening the potential for bilateral/spatial
forms of deafness), of specialized lysosomes in cochlear hair cells hearing development. Concurrent vestibular and balance
and presbycusis, and of transcription factors in developing olfactory impairments further compromise these children’s access to spatial
and auditory neurons and hair cells. The developmental studies information. Consequences to academic skills and working memory
revealed a molecular mechanism by which separate cochlear outer will be discussed. Of the available treatment options, cochlear
and inner hair cells are formed. The combined study of pain and implantation provides the best method for providing auditory input to
hearing led to the emerging field of auditory nociception. a deaf ear but is not presently considered to be the clinical standard
International Hearing Loss Conference | 11INVITED SPEAKERS
of care in children with SSD and is not suitable in all cases. On the challenge to population neural coding may be required. These
other hand, cochlear implantation could have a particular role in anatomical, physiological, and behavioral data illustrate a valuable
children whose SSD is associated with congenital cytomegalovirus animal model for linking physiological and perceptual effects
and, when provided with limited delay, is well tolerated as measured of hearing loss. Funding: R01DC009838 (Heinz) and NIH
by consistent device use. Early outcomes also indicate a reversal R01DC015989 (Bharadwaj).
of aural preference as input from the cochlear implant restores
representation of the previously deprived ear to the auditory brain.
We continue to monitor children with SSD who receive cochlear Sharon Kujawa
implants to define longer term effects of this intervention on Mass Eye & Ear, USA
developing auditory and vestibular/balance function. Sharon G. Kujawa, Ph.D. is an Associate
Professor of Otolaryngology, Harvard
Medical School. She is the Director of
Mike Heinz Audiology Research and a Senior
Purdue University, USA Scientist in the Eaton-Peabody
Michael G. Heinz is a Professor at Purdue Laboratories, Massachusetts Eye and
University, with a joint appointment in Ear Infirmary, Boston, MA. Work in the
Speech, Language and Hearing Sciences Kujawa laboratory seeks to clarify mechanisms and manifestations
and Biomedical Engineering. He received of common forms of acquired sensorineural hearing loss in humans,
an Sc.B. degree in Electrical Engineering particularly those due to aging and exposure to noise and ototoxic
from Brown University in 1992. He then drugs. A major focus of current work is in understanding how these
completed a Masters in Electrical and etiologies cause loss of cochlear synapses, determining the
Computer Engineering at Johns Hopkins University in 1994. In functional consequences of that loss, and how the degeneration
2000, he received a Ph.D. from the MIT Division of Health can be manipulated pharmacologically to reveal mechanisms and
Sciences and Technology in the area of Speech and Hearing provide treatments.
Sciences. His post-doctoral work was in Biomedical Engineering
at the Johns Hopkins University School of Medicine. In 2005, he Noise-induced cochlear synaptopathy with and without sensory
joined the faculty at Purdue as an Assistant Professor, where his cell loss
NIH-funded lab has been investigating the relation between neuro- Noise exposure is a primary cause of acquired sensorineural
physiological and perceptual responses to sound with normal and hearing loss affecting many millions, worldwide. After decades of
impaired hearing through the coordinated use of neurophysiology, focus on the sensory hair cell component of noise-induced hearing
computational modeling, and psychoacoustics. In 2010, he was loss, animal studies have more recently begun to address peripheral
elected a Fellow of the Acoustical Society of America (ASA), and neural consequences of such exposure. This work has identified the
served as Chair of the ASA Technical Committee on Psychological loss of inner hair cell synapses with cochlear afferent neurons as
and Physiological Acoustics from 2011-2014. He currently serves a common and early manifestation of noise damage, across all
as the Co-Director of an NIH-funded (T32) Interdisciplinary mammalian species evaluated thus far. Our early studies of
Training Program in Auditory Neuroscience. He also serves as an noise-induced cochlear synaptopathy concentrated on exposures
Associate Editor for the Journal of the Association for Research in producing large but reversible threshold shifts without hair cell loss.
Otolaryngology (JARO). This model provided a powerful approach to initial studies because
it allowed a separation of the functional deficits due to synaptopathy
Physiological and behavioral assays of cochlear synaptopathy in from those due to hair cell loss, and because clues present in
chinchillas suprathreshold responses could be interpreted without an audibility
Moderate-level noise exposure can eliminate cochlear synapses confound. However, noise can produce temporary and/or
without permanently damaging hair cells or elevating auditory permanent threshold elevations, with and without hair cell loss,
thresholds in animals. Cochlear synaptopathy has been hypothe- depending on characteristics of the exposure and susceptibilities
sized to contribute to human perceptual difficulties in noise that of the individual. Thus, although the synaptopathy can be hidden
can be observed even with normal audiograms. However, it is in a normal audiogram, the real challenge to diagnosis may be in
difficult to test this hypothesis because of 1) ethical limits in mixed – neural plus sensory—pathology. Here, we consider
measuring human synaptopathy directly, and 2) synaptopathy has cochlear structure and function after noise exposure with and
been most completely characterized in rodent models for which without sensory cell loss.
behavioral measures at speech frequencies are challenging. We
recently established a relevant mammalian behavioral model by
showing that chinchillas have corresponding neural and behavioral Charlie Liberman
amplitude-modulation (AM) detection thresholds in line with human Mass Eye & Ear, USA
thresholds. Furthermore, immunofluorescence histology confirmed
synaptopathy occurs in chinchillas across a broad frequency range, M. Charles Liberman, Ph.D. is the
including speech frequencies, following a lower-frequency noise Schuknecht Professor of Otology and
exposure that avoids permanent changes in ABR thresholds and Laryngology at the Harvard Medical
DPOAE amplitudes. Auditory-nerve fiber responses showed that School and the Director of the Eaton-
low-SR fibers were reduced in percentage (but not eliminated) Peabody Laboratories at the
following noise exposure, as in guinea pigs. Non-invasive wideband Massachusetts Eye and Ear Infirmary.
middle‐ear muscle-reflex (MEMR) assays in awake chinchillas Dr. Liberman received his B.A. in Biology
showed large and consistent reductions in suprathreshold from Harvard College in 1972 and his Ph.D. in Physiology from
amplitudes following noise exposure, whereas suprathreshold ABR Harvard Medical School in 1976. He has been on the faculty at
wave-1 amplitude reductions were less consistent. The relative Harvard since 1979, has published over 180 papers on a variety
diagnostic strengths of MEMR and ABR assays were consistent of topics in auditory neuroscience and is the recipient of the Award
with parallel studies of noise-exposed and middle-aged humans. of Merit from the Association for Research in Otolaryngology, the
Behavioral assays of tonal-carrier AM detection in chinchillas Carhart Award from the American Auditory Society and Bekesy
before and after noise exposure found no significant performance Silver Medal from the Acoustical Society of America. His research
degradation, suggesting more complex stimuli that provide a greater interests include 1) coding of acoustic stimuli as neural responses
12 | International Hearing Loss ConferenceINVITED SPEAKERS
in the auditory periphery, 2) efferent feedback control of the elucidating this potential role of the MOCR by using cochlear
auditory periphery, 3) mechanisms underlying noise-induced and implants. We found that the sensitivity to amplitude modulation and
age-related hearing loss, 4) the signaling pathways mediating nerve the recognition of speech in noise improve over time similarly for
survival in the inner ear and 5) application of cell- and drug-based CI users and for normal-hearing listeners. Because the electrical
therapies to the repair of a damaged inner ear. stimulation delivered by cochlear implants is independent from the
MOCR, this demonstrates that noise adaptation does not require
Cochlear nerve degeneration in human presbycusis: the MOCR. On the other hand, we also found that cochlear implant
evidence for hidden hearing loss in the aging ear users show better speech-in-noise intelligibility with a binaural
The noise-induced and age-related loss of synaptic connections cochlear-implant sound coding strategy inspired by the contralateral
between cochlear-nerve fibers and hair cells is well-established MOCR than without it. Combined, the evidence suggests that
from histopathology in several mammalian species; however, its the MOCR can produce noise adaptation but compensatory
prevalence in humans, as inferred from electrophysiology, remains mechanisms can produce as much noise adaptation as the MOCR
controversial. Here we look for cochlear neuropathy in a temporal- when the MOCR is absent.
bone study of “normal-aging” humans, using autopsy material from
subjects aged 0 to 89 yrs, with no history of otologic disease.
Cochleas were immunostained to allow quantification of surviving Helmy Mulders
hair cells and peripheral axons of cochlear-nerve fibers. Mean inner University of Western Australia,
hair cell loss across audiometric frequencies was rarely > 15%, at Australia
any age. In contrast, neural loss greatly exceeded inner hair cell Helmy Mulders is an auditory neuro-
loss, with 7/11 subjects over 60 yrs showing > 60% loss of scientist with a particular interest in
peripheral axons re the youngest subjects, and with the age- centrifugal control and plasticity.
related slope of axonal loss outstripping the age-related loss of The last 9 years her focus has been the
inner hair cells by almost 3:1. The results suggest that a large study of the neural substrate of tinnitus
number of cochlear sensory neurons in the aging ear are in an animal model, using a variety of
disconnected from their hair cell targets. This primary neural techniques such as single neuron electrophysiology, behavioural
degeneration would not affect the audiogram, but likely contributes studies, immunocytochemistry and RT-PCR. She works in the
to age-related hearing impairment, especially in noisy environments. Auditory Laboratory at the University of Western Australia (UWA)
Thus, therapies designed to regrow peripheral axons could provide and has published >55 peer reviewed journal articles and book
clinically meaningful improvement in the aged ear. chapters. She is a full-time academic, coordinating and teaching
into the undergraduate and postgraduate Neuroscience programs
Enrique Lopez-Poveda and the Master of Clinical Audiology at UWA.
University of Salamanca, Spain Central plasticity after hearing loss - therapeutic implications
Enrique A. Lopez-Poveda, Ph.D. for tinnitus
(born 1970) is Associate Professor of Tinnitus is a common phantom auditory perception that can
Otorhinolaryngology at the University of severely affect quality of life. The precise neural mechanisms
Salamanca, and the Director of the remain as yet unknown which is likely to be a contributing factor
Auditory Computation and Psycho- to the fact that there is no cure. Tinnitus is strongly associated
acoustics Laboratory of the Neuroscience with cochlear trauma and hearing loss, which evokes plasticity in
Institute of Castilla y León (since 2003), the central auditory system, resulting in altered levels and patterns
and the Director of the Audiology Diploma of the University of of spontaneous activity. It has been suggested that tinnitus is
Salamanca (since 2006). He received a B.Sc. in physics from the generated from these alterations in neural activity in combination
University of Salamanca in 1993 and a Ph.D. in hearing sciences with changes in non-auditory regions such as frontostriatal circuitry.
from Loughborough University in 1996. His current research This latter circuitry may be involved in sensory gating of non-salient
interests include (1) understanding and modeling cochlear information at the level of the thalamus. Therefore, a breakdown of
compression; (2) understanding the roles of olivocochlear efferents this mechanism could potentially cause altered neural signals in the
in hearing; (3) reinstating the effects and benefits of olivocochlear auditory system to reach the cortex, leading to perception. In our
efferents to the users of hearing aids and cochlear implants; laboratory, we use rat and guinea pig models of cochlear trauma
and (4) understanding the factors behind the wide variability in and tinnitus to investigate the relationship between frontostriatal
outcomes across hearing-aid and cochlear-implant users. He has circuitry and the auditory system and the mechanisms of sensory
authored over 75 papers, one book and three patents on a variety gating. Electrophysiological recordings in auditory thalamus in
of topics in hearing science. He is (or has been) editor of two animals with and without cochlear trauma and/or tinnitus are
books, a member of the editorial board of Trends in Hearing (since combined with stimulation of elements of the frontostriatal circuitry.
2014), and an associate editor of Journal of the Acoustical Society Stimulation is achieved invasively by focal electrodes or non-
of America (2012-2015). He was elected Fellow of the Acoustical invasively by repetitive transcranial magnetic stimulation. Our results
Society of America in 2009, and of the International Collegium of demonstrate that activation of frontostriatal circuitry has a functional
Rehabilitative Audiology in 2015. effect on activity in auditory thalamus and that this effect changes
URL: http://audiolab.usal.es after cochlear trauma. Our data support the notion that sensory
gating is involved in tinnitus generation which has implications for
E-mail: ealopezpoveda@usal.es
potential therapeutic targets.
Tel.: (+34) 690 844 625
On the role of the medial olivocochlear reflex in adaptation
to noise
Sensory systems constantly adapt their responses to the current
environment. In hearing, adaptation may facilitate communication
in noisy settings, a benefit frequently (but controversially) attributed
to the medial olivocochlear reflex (MOCR) enhancing the neural
representation of speech. Here, I will review our efforts towards
International Hearing Loss Conference | 13You can also read
