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Phenotyping Noise Induced
Hearing Loss with Audiometry and
DPOAEs
Ishan Bhatt, Ph.D., NAU
Susan L. Phillips, Ph.D., UNCG
Mohsin Ahmed Shaikh, Ph.D. candidate, UNCG
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Disclosure
• Dr. Susan Phillips, Mr. Mohsin Ahmed Shaikh
and I have no relevant financial or nonfinancial
relationships to disclose.
• The material presented today is based on
audiometric and otoacoustic emissions (OAEs)
data collected from the School of Music,
University of North Carolina at Greensboro. The
study was approved by the Institutional Review
Board, UNCG (11-0335).
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Key Factors in Noise-induced
Hearing Loss
• Globally growing
hearing health
concern
Gene
Environment
• NIHL is a complex
disorder
• Some individuals are
more susceptible than
others
Gene-environment
interaction
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Importance of Phenotyping NIHL
• Success of gene
mapping lies on the
ability to define the
target phenotype (i.e.
trait of a disease) with
accuracy and precision
(Schulze & McMahon, 2004)
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Early Efforts: Phenotyping NIHL
• Definition: Absolute
audiometric thresholds
at high frequencies (3
to 8 kHz)
• Industrial population
• Confounding variables
(Sliwinska-Kowalska & Pawelczyk, 2013; Van Laer et al., 2006)
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Recent Efforts: Phenotyping NIHL
• Definition: Bilateral
audiometric notch
within 4 to 6 kHz
Potential NIHL Phenotypes
• Collage-aged student
musicians
• Better control over
confounding variables
(Phillips et al., 2012)
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Purpose of the Study
• To evaluate the 4-6 kHz audiometric notch using
a test battery of Distortion-Product Otoacoustic
Emissions (DPOAEs)
• Hypothesis: Musicians with 4-6 kHz audiometric
notch will exhibit reduced DPOAEs compared to
musicians without the notch
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Method
• Sample
77 musicians
18-31 years
Normal otoscopic examination and
tympanometric findings
• DPOAE measured in the left ear
• Online Survey
Primary instruments
Participation in ensembles
Exposure to music
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DPOAE Test Battery
• DPOAE I/O function (ILO 292-II V6):
2 f1 - f2 DP frequency at 2, 3, 4 and 6 kHz
L2 ranging from 75 to 30 dB SPL in 5 dB
steps
Formula-based approach: L1 = (0.4)L2+39
• 2f1 - f2 DPgram was measured from 2 to 8 kHz
in 9 data points/octave with L1 and L2 were 60
and 40 dB SPL respectively
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Statistical Analysis
• Repeated measure ANOVA
Within subject factors: 10 DP data points,
Between subject factors: Audiometric groups
and music exposure
Covariate: Gender
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Results
• 55/77(23 females and
32 males) participants
completed survey
• 18/55 showed 4-6 kHz
audiometric notch
• 5/55 showed high
frequency drop
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Results
continue…
• DPOAE I/O function:
 Main effect of
exposure to music
was statistically
significant (p= 0.029)
 Main effect of
audiometric groups
was not statistically
significant (p>0.05)
1
2
3
4
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Results
continue…
• Main effect of music
exposure: DPgram
 Frequency range (2-4
kHz): F (3, 44) = 4.78,
p= 0.006
 Frequency range (4-8
kHz): F (3, 44) =
2.884, p= 0.046
• Main effect of
audiometric groups:
No statistically
significant effect found
1
2
3
4
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DPOAEs in 3 Audiometric
Configurations
DPgram: 2-8 kHz (9 data points/octave)
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Discussion
• No effect of audiometric
configurations on
DPOAEs
• Observation can be
attributed to:
 DPOAE recording
limitations and/or
 Physiological basis
Standing Waves in the Ear Canal
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Damage to
OHCs
Elevated audiometric
thresholds and
comparatively poor
DPOAEs
(Bhagat et al.,
2010;
Hofstetter,
Ding, Powers,
& Salvi, 1997;
Ozturan,
Jerger, Lew, &
Lynch, 1996)
Damage to
Stria
Vascularis
Elevated audiometric
thresholds and
comparatively better
DPOAEs
(Mills, Norton, &
Rubel, 1993;
Gates et al.,
2002)
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Conclusion
• Musicians with higher music exposure are likely
to show reduction in DPOAE amplitude
• Further research in required to investigate
DPOAEs in musicians with the 4-6 kHz
audiometric notch
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Future Research
• DPOAE recording using advance calibration
technique
• A well-defined control group of non-musicians
may improve sensitivity of the future studies
• Animal study to validate potential subphenotypes
• Validate the music exposure survey
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References
Bhagat, S. P., Bass, J. K., White, S. T., Qaddoumi, I., Wilson, M. W., Wu, J., & Rodriguez-Galindo, C. (2010). Monitoring
carboplatin ototoxicity with distortion-product otoacoustic emissions in children with retinoblastoma. International
Journal of Pediatric Otorhinolaryngology, 74(10), 1156-1163.
Gates, G. A., Mills, D., Nam, B. H., D'Agostino, R., & Rubel, E. W. (2002). Effects of age on the distortion product
otoacoustic emission growth functions. Hearing Research, 163(1-2), 53-60.
Hofstetter, P., Ding, D., Powers, N., & Salvi, R. (1997). Quantitative relationship of carboplatin dose to magnitude of inner
and outer hair cell loss and the reduction in distortion product otoacoustic emission amplitude in chinchillas.
Hearing Research,112(1-2), 199-215.
Mills, D. M., Norton, S. J., & Rubel, E. W. (1993). Vulnerability and adaptation of distortion product otoacoustic emissions
to endocochlear potential variation. Journal of The Acoustical Society of America, 94(4), 2108-2122.
Ozturan, O., Jerger, J., Lew, H., & Lynch, G. R. (1996). Monitoring of cisplatin ototoxicity by distortion-product
otoacoustic emissions. Auris Nasus Larynx, 23, 147-151.
Phillips, S. L., Mace, S. T., Richter, S. J., Morehouse, R., Henrich, V. C. (2012). Genetic Bases of Noise Induced Hearing
Loss. Podium presentation at the American Auditory Society conference, Scottsdale, Arizona, March.
Schulze, T.G., McMahon, F.J. 2004. Defining the phenotype in human genetic studies: Forward genetics and reverse
phenotyping. Hum. Hered., 58, 131-138.
Sliwinska-Kowalska, M., & Pawelczyk, M. (2013). Contribution of genetic factors to noise-induced hearing loss: a human
studies review. Mutation Research, 752(1), 61-65.
Van Laer, L., Carlsson, P., Ottschytsch, N., Bondeson, M., Konings, A., Vandevelde, A., & Dieltjens, N. (2006). The
contribution of genes involved in potassium-recycling in the inner ear to noise-induced hearing loss. Human
Mutation, 27(8), 786-795.
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