Context effects on phoneme categorization in children with dyslexia.

Research shows that, on average, children with dyslexia behave less categorically in phoneme categorization tasks. This study investigates three subtle ways that struggling readers may perform differently than their typically developing peers in this experimental context: sensitivity to the frequency distribution from which speech tokens are drawn, bias induced by previous stimulus presentations, and fatigue during the course of the task. We replicate findings that reading skill is related to categorical labeling, but we do not find evidence that sensitivity to the stimulus frequency distribution, the influence of previous stimulus presentations, and a measure of task engagement differs in children with dyslexia. It is, therefore, unlikely that the reliable relationship between reading skill and categorical labeling is attributable to artifacts of the task design, abnormal neural encoding, or executive function. Rather, categorical labeling may index a general feature of linguistic development whose causal relationship to literacy remains to be ascertained.

Categorical phoneme labeling in children with dyslexia does not depend on stimulus duration.

It is established that individuals with dyslexia are less consistent at auditory phoneme categorization than typical readers. One hypothesis attributes these differences in phoneme labeling to differences in auditory cue integration over time, suggesting that the performance of individuals with dyslexia would improve with longer exposure to informative phonetic cues. Here, the relationship between phoneme labeling and reading ability was investigated while manipulating the duration of steady-state auditory information available in a consonant-vowel syllable. Children with dyslexia obtained no more benefit from longer cues than did children with typical reading skills, suggesting that poor task performance is not explained by deficits in temporal integration or temporal sampling.

The development of biophysical models of the electrically stimulated auditory nerve: Single-node and cable models.

In the last few decades, biophysical models have emerged as a prominent tool in the study and improvement of cochlear implants, a neural prosthetic that restores a degree of sound perception to the profoundly deaf. Owing to the spatial phenomena associated with extracellular stimulation, these models have evolved to a relatively high degree of morphological and physiological detail: single-node models in the tradition of Hodgkin-Huxley are paired with cable descriptions of the auditory nerve fiber. No singular model has emerged as a frontrunner to the field; rather, parameter sets deriving from the channel kinetics and morphologies of numerous organisms (mammalian and otherwise) are combined and tuned to foster strong agreement with response properties observed in vivo, such as refractoriness, summation, and strength-duration relationships. Recently, biophysical models of the electrically stimulated auditory nerve have begun to incorporate adaptation and stochastic mechanisms, in order to better realize the goal of predicting realistic neural responses to a wide array of stimuli.

Simulating electrical modulation detection thresholds using a biophysical model of the auditory nerve.

Modulation detection thresholds (MDTs) assess listeners' sensitivity to changes in the temporal envelope of a signal and have been shown to strongly correlate with speech perception in cochlear implant users. MDTs are simulated with a stochastic model of a population of auditory nerve fibers that has been verified to accurately simulate a number of physiologically important temporal response properties. The procedure to estimate detection thresholds has previously been applied to stimulus discrimination tasks. The population model simulates the MDT-stimulus intensity relationship measured in cochlear implant users. The model also recreates the shape of the modulation transfer function and the relationship between MDTs and carrier rate. Discrimination based on fluctuations in synchronous firing activity predicts better performance at low carrier rates, but quantitative measures of modulation coding predict better neural representation of high carrier rate stimuli. Manipulating the number of fibers and a temporal integration parameter, the width of a sliding temporal integration window, varies properties of the MDTs, such as cutoff frequency and peak threshold. These results demonstrate the importance of using a multi-diameter fiber population in modeling the MDTs and demonstrate a wider applicability of this model to simulating behavioral performance in cochlear implant listeners.

Reading ability and phoneme categorization.

Dyslexia is associated with abnormal performance on many auditory psychophysics tasks, particularly those involving the categorization of speech sounds. However, it is debated whether those apparent auditory deficits arise from (a) reduced sensitivity to particular acoustic cues, (b) the difficulty of experimental tasks, or (c) unmodeled lapses of attention. Here we investigate the relationship between phoneme categorization and reading ability, with special attention to the nature of the cue encoding the phoneme contrast (static versus dynamic), differences in task paradigm difficulty, and methodological details of psychometric model fitting. We find a robust relationship between reading ability and categorization performance, show that task difficulty cannot fully explain that relationship, and provide evidence that the deficit is not restricted to dynamic cue contrasts, contrary to prior reports. Finally, we demonstrate that improved modeling of behavioral responses suggests that performance does differ between children with dyslexia and typical readers, but that the difference may be smaller than previously reported.

Simulated auditory nerve axon demyelination alters sensitivity and response timing to extracellular stimulation.

Since cochlear implant function involves direct depolarization of spiral ganglion neurons (SGNs) by applied current, SGN physiological health must be an important factor in cochlear implant (CI) outcomes. This expected relationship has, however, been difficult to confirm in implant recipients. Suggestively, animal studies have demonstrated both acute and progressive SGN ultrastructural changes (notably axon demyelination), even in the absence of soma death, and corresponding altered physiology following sensorineural deafening. Whether such demyelination occurs in humans and how such changes might impact CI function remains unknown. To approach this problem, we incorporated SGN demyelination into a biophysical model of extracellular stimulation of SGN fibers. Our approach enabled exploration of the entire parameter space corresponding to simulated myelin diameter and extent of fiber affected. All simulated fibers were stimulated distally with anodic monophasic, cathodic monophasic, anode-phase-first (AF) biphasic, and cathode-phase-first (CF) biphasic pulses from an extracellular disc electrode and monitored for spikes centrally. Not surprisingly, axon sensitivity generally decreased with demyelination, resulting in elevated thresholds, however, this effect was strongly non-uniform. Fibers with severe demyelination affecting only the most peripheral nodes responded nearly identically to normally myelinated fibers. Additionally, partial demyelination (<50%) yielded only minimal increases in threshold even when the entire fiber was impacted. The temporal effects of demyelination were more unexpected. Both latency and jitter of responses demonstrated resilience to modest changes but exhibited strongly non-monotonic and stimulus-dependent relationships to more profound demyelination. Normal, and modestly demyelinated fibers, were more sensitive to cathodic than anodic monophasic pulses and to CF than AF biphasic pulses, however, when demyelination was more severe these relative sensitivities were reversed. Comparison of threshold crossing between nodal segments demonstrated stimulus-dependent shifts in action potential initiation with different fiber demyelination states. For some demyelination scenarios, both phases of biphasic pulses could initiate action potentials at threshold resulting in bimodal latency and initiation site distributions and dramatically increased jitter. In summary, simulated demyelination leads to complex changes in fiber sensitivity and spike timing, mediated by alterations in action potential initiation site and slowed action potential conduction due to non-uniformities in the electrical properties of axons. Such demyelination-induced changes, if present in implantees, would have profound implications for the detection of fine temporal cues but not disrupt cues on the time scale of speech envelopes. These simulation results highlight the importance of exploring the SGN ultrastructural changes caused by a given etiology of hearing loss to more accurately predict cochlear implantation outcomes.