Electrophysiological Evidence of the Basilar-Membrane Travelling Wave and Frequency Place Coding of Sound in Cochlear Implant Recipients.

AIM: To obtain direct evidence for the cochlear travelling wave in humans by performing electrocochleography from within the cochlea in subjects implanted with an auditory prosthesis. BACKGROUND: Sound induces a travelling wave that propagates along the basilar membrane, exhibiting cochleotopic tuning with a frequency-dependent phase delay. To date, evoked potentials and psychophysical experiments have supported the presence of the travelling wave in humans, but direct measurements have not been made. METHODS: Electrical potentials in response to rarefaction and condensation acoustic tone bursts were recorded from multiple sites along the human cochlea, directly from a cochlear implant electrode during, and immediately after, its insertion. These recordings were made from individuals with residual hearing. RESULTS: Electrocochleography was recorded from 11 intracochlear electrodes in 7 ears from 6 subjects, with detectable responses on all electrodes in 5 ears. Cochleotopic tuning and frequency-dependent phase delay of the cochlear microphonic were demonstrated. The response latencies were slightly shorter than those anticipated which we attribute to the subjects' hearing loss. CONCLUSIONS: Direct evidence for the travelling wave was observed. Electrocochleography from cochlear implant electrodes provides site-specific information on hair cell and neural function of the cochlea with potential diagnostic value.

Altered attentional filters in subjects with graded levels of sensorineural hearing loss.

Near-threshold tones (targets) in noise that are preceded by cues of the same frequency or occur with a high probability are detected better than tones of other frequencies that may occur with a lower probability (probes); the better detection of targets than probes defines the attentional filter. We measured attentional filters using a cued probe-signal procedure with a two-interval forced-choice (2IFC) method in normal-hearing subjects (N = 15) and subjects with sensorineural hearing loss (SNHL; N = 14) with a range of hearing levels. Attentional filters were altered in SNHL subjects, who detected low-frequency probes as well as targets at all hearing levels and who detected high-frequency probes increasingly well with increasing hearing level. These effects were present in both intervals of the 2IFC procedure. As auditory filters measured psychophysically are typically asymmetric in subjects with SNHL, these results suggest that the signal frequencies affected by the attentional filter are governed by the shapes of the auditory filters at and around the cue frequency. The normal-hearing subjects showed the expected attentional filters in the first interval and shallower filters in the second interval, suggesting that the cue-evoked attentional process is transient. In the first interval, both low- and high-frequency probes were detected better as hearing level increased over a narrow range (from -5 to 10 dB at the target frequency), with a resultant loss of attentional filtering. This finding adds to observations of variable auditory function in individuals with clinically normal hearing thresholds established by audiometry.

Spontaneous hyperactivity in the auditory midbrain: relationship to afferent input.

Hyperactivity in the form of increased spontaneous firing rates of single neurons develops in the guinea pig inferior colliculus (IC) after unilateral loud sound exposures that result in behavioural signs of tinnitus. The hyperactivity is found in those parts of the topographic frequency map in the IC where neurons possess characteristic frequencies (CFs) closely related to the region in the cochlea where lasting sensitivity changes occur as a result of the loud sound exposure. The observed hyperactivity could be endogenous to the IC, or it could be driven by hyperactivity at lower stages of the auditory pathway. In addition to the dorsal cochlear nucleus (DCN) hyperactivity reported by others, specific cell types in the ventral cochlear nucleus (VCN) also show hyperactivity in this animal model suggesting that increased drive from several regions of the lower brainstem could contribute to the observed hyperactivity in the midbrain. In addition, spontaneous afferent drive from the cochlea itself is necessary for the maintenance of hyperactivity up to about 8 weeks post cochlear trauma. After 8 weeks however, IC hyperactivity becomes less dependent on cochlear input, suggesting that central neurons transition from a state of hyperexcitability to a state in which they generate their own endogenous firing. The results suggest that there might be a "therapeutic window" for early-onset tinnitus, using treatments that reduce cochlear afferent firing.