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Francart T.,Catholic University of Leuven | Francart T.,Bionics Institute | McDermott H.J.,Bionics Institute | McDermott H.J.,University of Melbourne
Ear and Hearing | Year: 2013

The addition of acoustic stimulation to electric stimulation via a cochlear implant has been shown to be advantageous for speech perception in noise, sound quality, music perception, and sound source localization. However, the signal processing and fitting procedures of current cochlear implants and hearing aids were developed independently, precluding several potential advantages of bimodal stimulation, such as improved sound source localization and binaural unmasking of speech in noise. While there is a large and increasing population of implantees who use a hearing aid, there are currently no generally accepted fitting methods for this configuration. It is not practical to fit current commercial devices to achieve optimal binaural loudness balance or optimal binaural cue transmission for arbitrary signals and levels. There are several promising experimental signal processing systems specifically designed for bimodal stimulation. In this article, basic psychophysical studies with electric acoustic stimulation are reviewed, along with the current state of the art in fitting, and experimental signal processing techniques for electric acoustic stimulation. Copyright © 2013 by Lippincott Williams & Wilkins. Source


Badawy R.A.B.,St. Vincents Hospital | Badawy R.A.B.,University of Melbourne | Lai A.,Bionics Institute | Vogrin S.J.,St. Vincents Hospital | And 3 more authors.
Neurology | Year: 2013

In the past, the cortex has for the most part been considered to be the site of seizure origin in the different forms of epilepsy. Findings from histopathologic, electrophysiologic, and brain imaging studies now provide ample evidence demonstrating that like normal cerebral function, epileptic seizures involve widespread network interactions between cortical and subcortical structures. These studies show that different forms of generalized and focal epileptiform discharges and seizures engage various subcortical structures in varying ways. This interaction has been the subject of many reviews and is not the focus of the current work. The aim of this review is to examine the evidence suggesting the possibility for some of the subcortical structures to initiate seizures independently and the clinical implications of this. © 2013 American Academy of Neurology. Source


Richardson R.T.,Bionics Institute | Atkinson P.J.,Stanford University
Expert Opinion on Biological Therapy | Year: 2015

Introduction: The sensory epithelium of the cochlea is a complex structure containing hair cells, supporting cells and auditory nerve endings, all of which degenerate after hearing loss in mammals. Biological approaches are being considered to preserve and restore the sensory epithelium after hearing loss. Of particular note is the ectopic expression of the Atoh1 gene, which has been shown to convert residual supporting cells into hair cells with restoration of function in some cases.Areas covered: In this review, hair cell development, spontaneous regeneration and hair cell regeneration mediated by Atoh1 gene therapy in the cochlea are discussed.Expert opinion: Gene therapy can be safely delivered locally to the inner ear and can be targeted to the sensory epithelium of the cochlea. Expression of the Atoh1 gene in supporting cells results in their transformation into cells with the appearance and function of immature hair cells but with the resulting loss of the original supporting cell. While the feasibility of Atoh1 gene therapy in the cochlea is largely dependent on the severity of the hearing loss, hearing restoration can be achieved in some situations. With further advances in Atoh1 gene therapy, hearing loss may not be as permanent as once thought. © 2014 Informa UK, Ltd. Source


Badawy R.A.B.,St. Vincents Hospital | Badawy R.A.B.,University of Melbourne | Vogrin S.J.,St. Vincents Hospital | Lai A.,Bionics Institute | And 2 more authors.
Epilepsia | Year: 2013

Purpose To investigate whether using transcranial magnetic stimulation (TMS) to derive if measures of cortical excitability changes can distinguish between various adolescent/adult-onset generalized epilepsy syndromes at different phases of the disorder. Methods One hundred thirty-seven patients with adolescent/adult-onset generalized epilepsy divided into juvenile myoclonic epilepsy, juvenile absence epilepsy, and generalized epilepsy with tonic-clonic seizures only were studied. The cohorts were further divided into drug naive-new onset, refractory, and seizure-free groups. Motor threshold (MT) and paired pulse TMS at short (2, 5, 10, 15 msec) and long (100-300 msec) interstimulus intervals (ISIs) were measured. Results were compared to those of 20 controls. Key Findings In the drug-naive cohorts MT was reduced (p < 0.05) and cortical excitability increased at 2 and 5 msec and 150, 250, and 300 msec ISIs (p < 0.01) in juvenile myoclonic epilepsy compared to other generalized epilepsy groups and controls. Cortical excitability increased to a lesser degree in other generalized epilepsy syndromes compared to controls, but those two syndromes were not distinguishable from one another. The changes in paired pulse TMS were more prominent in the groups with refractory seizures and very small in the groups who were seizure free. Significance There are syndrome specific changes in cortical excitability associated with generalized epilepsy. These changes are also dependent on seizure control with medication. Juvenile myoclonic epilepsy has a higher cortical excitability profile compared to other adolescent/adult-onset generalized epilepsy syndromes and can be clearly distinguished from them during all phases. © Wiley Periodicals, Inc. © 2013 International League Against Epilepsy. Source


Gilson M.,RIKEN | Gilson M.,University of Melbourne | Fukai T.,RIKEN | Burkitt A.N.,University of Melbourne | Burkitt A.N.,Bionics Institute
PLoS Computational Biology | Year: 2012

Spike-timing-dependent plasticity (STDP) has been observed in many brain areas such as sensory cortices, where it is hypothesized to structure synaptic connections between neurons. Previous studies have demonstrated how STDP can capture spiking information at short timescales using specific input configurations, such as coincident spiking, spike patterns and oscillatory spike trains. However, the corresponding computation in the case of arbitrary input signals is still unclear. This paper provides an overarching picture of the algorithm inherent to STDP, tying together many previous results for commonly used models of pairwise STDP. For a single neuron with plastic excitatory synapses, we show how STDP performs a spectral analysis on the temporal cross-correlograms between its afferent spike trains. The postsynaptic responses and STDP learning window determine kernel functions that specify how the neuron "sees" the input correlations. We thus denote this unsupervised learning scheme as 'kernel spectral component analysis' (kSCA). In particular, the whole input correlation structure must be considered since all plastic synapses compete with each other. We find that kSCA is enhanced when weight-dependent STDP induces gradual synaptic competition. For a spiking neuron with a "linear" response and pairwise STDP alone, we find that kSCA resembles principal component analysis (PCA). However, plain STDP does not isolate correlation sources in general, e.g., when they are mixed among the input spike trains. In other words, it does not perform independent component analysis (ICA). Tuning the neuron to a single correlation source can be achieved when STDP is paired with a homeostatic mechanism that reinforces the competition between synaptic inputs. Our results suggest that neuronal networks equipped with STDP can process signals encoded in the transient spiking activity at the timescales of tens of milliseconds for usual STDP. © 2012 Gilson et al. Source

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