J Am Acad Audiol 2020; 31(08): C1-C2
DOI: 10.1055/s-0040-1722796
JAAA CEU Program

JAAA CEU Program


    The questions below refer to Campbell, Nielsen, Bean, and LaBrec, “Auditory Gating in Hearing Loss,” pages 559–565.

    Learner Outcomes

    Readers of this article should be able to:

    • Understand why hearing loss may decrease sensory inhibition and describe why auditory gating is a useful measure of this defi cit.

    • Identify the cortical auditory evoked potential (CAEP) gating component that is reflective of decreased inhibition in hearing loss, as well as the underlying cortical inhibitory networks that are active in adults with “normal” hearing and atypical in adults with hearing loss.


    CEU Questions

    1. Which auditory gating component is typically considered a biomarker of decreased sensory inhibition?

      • P50

      • N1

      • P2

    2. Hearing loss may decrease sensory inhibition through:

      • Increased central gain at the level of the cortex

      • Decreased fi ring in peripheral excitatory neurons

      • Peripheral deaff erentation resulting in a reduction of inhibitory inputs

    3. How was auditory gating quantifi ed in this study?

      • CAEP amplitude gating ratio and diff erence values

      • Current density reconstructions via sLORETA

      • CAEP gating component latencies

    4. How did the P2 gating component reflect decreased inhibition in hearing loss?

      • The amplitude gating ratio was lower in the hearingloss group

      • The amplitude diff erence value was lower in the “normal-hearing” group

      • The amplitude gating indices correlated with hearingloss severity

    5. What key inhibitory source underlying the P50 gating component was absent in the hearing-loss group?

      • Frontal cortex

      • Prefrontal cortex

      • Temporal cortex

    6. What key inhibitory source underlying the P2 gating component was absent in the hearing-loss group?

      • Frontal cortex

      • Prefrontal cortex

      • Temporal cortex

    7. Why might typical gating function, as observed through CAEP amplitude indices, have been absent in the “normal-hearing” group?

      • The sample size was too small

      • The stimulus was presented near threshold

      • The age range was higher than previous studies in that lab

    8. Which CAEP component appears to be consistently reflective of central auditory plasticity in adult-acquired hearing loss?

      • P50

      • N1

      • P2

    9. What compensatory behavior might such plasticity be associated with?

      • Eff ortful listening

      • Avoidance

      • Enhanced speech perception in background noise

    10. What is a possible hypothesis for the absence of key inhibitory networks observed in the hearing-loss group?

      • Cross-modal reorganization of early visual processing to the temporal cortex

      • Cortical resource reallocation of early auditory processing to the frontal cortex

      • Heightened activation of the parietal cortex


    No conflict of interest has been declared by the author(s).

    Publication History

    Article published online:
    24 December 2020

    © 2020. American Academy of Audiology. This article is published by Thieme.

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