OHC Disorder

Question 1

How is tuning of the basilar membrane improved?

Answer 1

• Improved by the cochlear amplifier, which is initiated by the outer hair cells
• Amplifies the traveling wave particularly at low intensities

Question 2

What is the electromotile response of the OHCs?

Answer 2

• OHCs move longitudinally in response to transmembrane voltage changes
• The electromotile capacity helps amplify the traveling wave, and underlies the cochlear amplifier
• OHCs are innervated by efferent auditory nerve fibers which helps regulate the electromotile response

Question 3

What is the cochlear amplifier?

Answer 3

• Physiologic process that amplifies the traveling wave
• Contributes to the characteristics of the cochlea’s nonlinear response, including sensitivity and frequency selectivity

Question 4

Where does the mechanical energy within the cochlea reside?

Answer 4

• Within the OHCs
• The electromotile response plays a role in reverse transduction
• Acoustical stimulation causes changes in the transmembrane voltage and the OHCs send mechanical energy back into the cochlea

Question 5

What is the theory of bidirectional transduction?

Answer 5

• Theorizes that the cochlea and OHCs participate in a high-gain feedback loop
• The cochlea is dependent on the forward transduction from the hair cells
• The bidirectional transduction contributes to the sensitivity and frequency selectivity of human hearing

Question 6

What causes hearing loss following OHC dysfunction?

Answer 6

• Loss of frequency sensitivity
• Reduced auditory sensations
• Abnormal loudness growth

Question 7

What is loudness recruitment?

Answer 7

• The unusual growth in loudness as the sensation level of a stimulus is increased
• Observed during word recognition and Acoustic reflex threshold assessment

Question 8

What was demonstrated in the human model with aspirin induced OHC dysfunction?

Answer 8

• Significant changes in frequency selectivity, even for small hearing losses (5 dB)
• Significant declines in hearing

Question 9

What was observed in the mouse model genetically engineered without prestin?

Answer 9

• Reduced OHC length
• Lack of electromotile response
• Loss of OHCs and IHCs in the basal region of the cochlea
• HOWEVER, OAEs were still measured

Question 10

What causes OAEs in humans?

Answer 10

OAEs are mediated by the cochlear amplifier

• OHCs produce sounds which are then transmitted in reverse to the external auditory meatus

Question 11

How does OHC dysfunction affect the ABR?

Answer 11

• Latencies of neural generators of the ABR require normal functioning IHCs and OHCs
• Wave I is generated by the distal portion of the auditory nerve and receives input from IHCs
• With OHC dysfunction, stimuli presented at greater intensities are needed to elicit hair cell excitation and to stimulate the auditory nerve and other auditory structures

Question 12

What ABR results are expected with OHC dysfunction?

Answer 12

• Prolonged Wave I at low intensities
• Wave I may be absent due to degree of hearing loss
• Latency-intensity functions are steeper for sensorineural hearing losses than for conductive losses

Question 13

What are the elements of the ECochG?

Answer 13

• Cochlear Microphonic
• Summating Potential
• Compound action potential

Question 14

What is the cochlear microphonic?

Answer 14

• Indicator of OHC function
• Closely resembles the stimulus and reflects the receptor currents of the OHCs with some inputs from the IHCs
• Basilar membrane vibrations and the OHCs contribute to the cochlear microphonic at low intensities
• Basilar membrane displacement and IHCs contribute to CM at high intensities