Neural phase-locking to temporal fluctuations is a fundamental and unique mechanism by which acoustic information is encoded by the auditory system. The perceptual role of this metabolically expensive mechanism, the neural phase-locking to temporal fine structure (TFS) in particular, is debated.Although hypothesized, it is unclear if auditory perceptual deficits in certain clinical populations are attributable to deficits in TFS coding. Efforts to uncover the role of TFS have been impeded by the fact that there are no established assays for quantifying the fidelity of TFS coding at the individual level. While many candidates have been proposed, for an assay to be useful, it should not only intrinsically depend on TFS coding, but should also have the property that individual differences in the assay reflect TFS coding per se over and beyond other sources of variance. Here, we evaluate a range of behavioral and electroencephalogram (EEG)-based measures as candidate individualized measures of TFS sensitivity. Our comparisons of behavioral and EEG-based metrics suggest that extraneous variables dominate both behavioral scores and EEG amplitude metrics, rendering them ineffective. After adjusting behavioral scores using lapse rates, and extracting latency or percent-growth metrics from EEG, interaural timing sensitivity measures exhibit robust behavior-EEG correlations. Together with the fact that unambiguous theoretical links can be made relating binaural measures and phase-locking to TFS, our results suggest that these "adjusted" binaural assays may be well-suited for quantifying individual TFS processing.

Animal models suggest that cochlear afferent nerve endings may be more vulnerable than sensory hair cells to damage from acoustic overexposure and aging. Because neural degeneration without hair-cell loss cannot be detected in standard clinical audiometry, whether such damage occurs in humans is hotly debated. Here, we address this debate through co-ordinated experiments in at-risk humans and a wild-type chinchilla model. Cochlear neuropathy leads to large and sustained reductions of the wideband middle-ear muscle reflex in chinchillas. Analogously, human wideband reflex measures revealed distinct damage patterns in middle age, and in young individuals with histories of high acoustic exposure. Analysis of an independent large public dataset and additional measurements using clinical equipment corroborated the patterns revealed by our targeted cross-species experiments. Taken together, our results suggest that cochlear neural damage is widespread even in populations with clinically normal hearing.

The nervous system adapts in many ways to changes in the statistics of the inputs it receives. An example of such plasticity observed in animal models is that central auditory neurons tend to retain their driven firing rate outputs despite reductions in cochlear input due to hearing loss or deafferentation. The perceptual consequences of such “central gain” are unknown; pathological versions of such gain are often hypothesized to underlie tinnitus and hyperacusis. To investigate central gain in humans, we designed an electroencephalogram (EEG)-based paradigm that concurrently elicits robust separable responses from different levels of the auditory pathway. Using this measure, we find that cortical responses are relatively invariant despite a large monotonic decrease in auditory nerve responses with age, and that this central gain is also associated with perceptual deficits in co-modulation processing. We then applied the same measures to a cohort of individuals with persistent tinnitus and to a third cohort where a week-long monaural conductive hearing loss was induced using silicone earplugs. Overall, our results suggest that central gain is ubiquitous in response to reduced peripheral input and may affect auditory scene analysis, but does not in itself account for tinnitus perception.

Neural phase-locking to temporal fluctuations is a fundamental and unique mechanism by which acoustic information is encoded by the auditory system. The perceptual role of this metabolically expensive mechanism, the neural phase-locking to temporal fine structure (TFS) in particular, is debated. Although hypothesized, it is unclear if auditory perceptual deficits in certain clinical populations are attributable to deficits in TFS coding. Efforts to uncover the role of TFS have been impeded by the fact that there are no established assays for quantifying the fidelity of TFS coding at the individual level. While many candidates have been proposed, for an assay to be useful, it should not only intrinsically depend on TFS coding, but should also have the property that individual differences in the assay reflect TFS coding per se over and beyond other sources of variance. Here, we evaluate a range of behavioral and electroencephalogram (EEG)-based measures as candidate individualized measures of TFS sensitivity. Our comparisons of behavioral and EEG-based metrics suggest that extraneous variables dominate both behavioral scores and EEG amplitude metrics, rendering them ineffective. After adjusting behavioral scores using lapse rates, and extracting latency or percent-growth metrics from EEG, interaural timing sensitivity measures exhibit robust behavior-EEG correlations. Together with the fact that unambiguous theoretical links can be made relating binaural measures and phase-locking to TFS, our results suggest that these "adjusted" binaural assays may be well-suited for quantifying individual TFS processing.