Prediction and control of neural responses to pulsatile electrical stimulation

Department of Otolaryngology, University of Melbourne, 32 Gisborne Street, East Melbourne, 3002, Australia.
Journal of Neural Engineering (Impact Factor: 3.3). 03/2012; 9(2):026023. DOI: 10.1088/1741-2560/9/2/026023
Source: PubMed


This paper aims to predict and control the probability of firing of a neuron in response to pulsatile electrical stimulation of the type delivered by neural prostheses such as the cochlear implant, bionic eye or in deep brain stimulation. Using the cochlear implant as a model, we developed an efficient computational model that predicts the responses of auditory nerve fibers to electrical stimulation and evaluated the model's accuracy by comparing the model output with pooled responses from a group of guinea pig auditory nerve fibers. It was found that the model accurately predicted the changes in neural firing probability over time to constant and variable amplitude electrical pulse trains, including speech-derived signals, delivered at rates up to 889 pulses s(-1). A simplified version of the model that did not incorporate adaptation was used to adaptively predict, within its limitations, the pulsatile electrical stimulus required to cause a desired response from neurons up to 250 pulses s(-1). Future stimulation strategies for cochlear implants and other neural prostheses may be enhanced using similar models that account for the way that neural responses are altered by previous stimulation.

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    ABSTRACT: Successful cochlear implant performance requires adequate responsiveness of the auditory nerve to prolonged pulsatile electrical stimulation. Degeneration of the auditory nerve as a result of severe hair cell loss could considerably compromise this ability. The main objective of this study was to characterize the recovery of the electrically stimulated auditory nerve, as well as to evaluate possible changes caused by deafness-induced degeneration. To this end we studied temporal responsiveness of the auditory nerve in a guinea pig model of sensorineural hearing loss. Using masker-probe and pulse train paradigms we compared electrically evoked compound action potentials (eCAPs) in normal-hearing animals with those in animals with moderate (two weeks after ototoxic treatment) and severe (six weeks after ototoxic treatment) loss of spiral ganglion cells (SGCs). Masker-probe interval and pulse train inter-pulse interval was varied from 0.3 to 16 ms. Whereas recovery assessed with masker-probe was roughly similar for normal-hearing and both groups of deafened animals, it was considerably faster for six weeks deaf animals (τ ≈ 1.2 ms) than for two weeks deaf or normal-hearing animals (τ ≈ 3-4 ms) when 100-ms pulse trains were applied. Latency increased with decreasing inter-pulse intervals, and this was more pronounced with pulse trains than with masker-probe stimulation. With high frequency pulse train stimulation eCAP amplitudes were modulated for deafened animals, meaning that amplitudes for odd pulse numbers were larger than for even pulses. The relative refractory period (τ) and the modulation depth of the eCAP amplitude for pulse trains, as well as the latency increase for both paradigms significantly correlated with quantified measures of auditory nerve degeneration (size and packing density of SGCs). In addition to these findings, separate masker-probe recovery functions for the eCAP N1 and N2 peaks displayed a robust non-monotonic or shoulder-shaped course in all animals. The time interval between the N1 and N2 correlated with neuronal refractoriness, suggesting that the N2 peak reflects a second firing of part of the SGC population. We conclude that – compared to the commonly used masker-probe recovery functions – recovery functions obtained with pulse train stimulation may provide a means to augment differences and, by doing so, to more potently discriminate between auditory nerve conditions.
    Hearing Research 01/2015; 321:12-24. DOI:10.1016/j.heares.2015.01.001 · 2.97 Impact Factor

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