| Home > Departments > Center for Experimental Medicine > Department of Neurophysiology and Pathophysiology > Auditory Neurophysiology
Research Group:
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| [head of group:] | |||||
| Prof. Dr. Andrej Kral Professor of Neurophysiology Adjunct Professor of Neuroscience The University of Texas at Dallas |
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| [group members:] | |||||
| Dr. Peter Hubka Senior Scientist |
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| MSc Emilie Syed Doctoral candidate |
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| Cand.med. Melanie Ferreira Caetano Doctoral candidate |
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| Dorrit Schiemann Technician |
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| [neurophysiology of cochlear implants:] | |||||
Neuroprosthetic  devices represent an artificial equipment used to stimulate neural structures in order to compensate for neural deficits. Our Institute is working in this area on two topics: therapy of motor disorders related to Parkinson's disease and cochlear implants.Cochlear implants are devices used for electrical stimulation of the auditory nerve in deaf subjects. Using these devices the majority of subjects with a non-functional cochlea can learn to recognize speech and communicate acoustically without additional non-acoustic help. Our group is working on the understanding of the neurophysiological processes in electrical stimulation of the auditory nerve. |
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 Deafness itself induces a massive change in the functional properties of auditory nerve fibres: they loose the spontaneous activity. When auditory nerve fibres are stimulated electrically, the temporal jitter of the responses is very small when compared to acoustical stimulation of a hearing cochlea. One consequence of these processes is the reduction in the dynamic range of the responses: the fibres can "code" only changes of intensity in the range of ~ 3-10 dB, compared to 40-80 dB in a "hearing" auditory nerve (review in Hartmann and Kral, 2004, see below). One additional problem in cochlear implant stimulation is the spread of the electrical field in the cochlea during stimulation. A hearing auditory system is very sensitive to changes in the position of the most excited region in the cochlea: a change in position of this region in the order of few hair cells (order of tenths of µm) induces a perceptual change! Auditory nerve fibres have therefore sharp threshold curves. Such curves can by no means be replicated with electrical stimulation, although the electrical field can be substantially sharpened by "beam forming" using tripolar configuration of stimulation electrodes. Fortunately, in the spectral range of speech (up to 5 kHz), the temporal code is more important for decoding of stimuli in the central auditory system. |
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| The technology of cochlear implants has progressed so far that electrical stimulation is possible also in subjects with residual hearing. In these patients, a combined electrical (via cochlear implants) and acoustical (via high-power hearing aids) stimulation (electroacoustic stimulation) is possible. We investigate what type of interactions between the acoustic and electric stimulation takes place in a cochlear with residual hearing, and how to adjust the stimulation strategy to comply to these interactions. | |||||
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| [cortical consequences of auditory deprivation - deafness:] | |||||
| The processing elements of the nervous systems are synaptic contacts: here information is stored and processed. The synapses of the cerebral cortex show extensive development after birth: Synaptic densities increase during early postnatal life (human: 1st - 2nd year; so-called late synaptogenesis). Then, a peak in synaptic densities is achieved (synaptic overshoot), followed by a slow but extensive decrease in synaptic densities (synaptic elimination, "pruning"). At the same time, children develop increasingly complex cognitive abilities. Is this developmental process dependent on experience, as the synaptic selection hypothesis suggests, or is this process the consequence of the genetically-predetermined program? Research in the visual system of cats and monkeys with reversible blindness (eyelid suture) showed that at least certain aspects of this process are dependent on experience. Unfortunately, methods for reversible deprivation were not available in the auditory system: suturing the external auditory canal does not lead to complete deafness and does not affect perception of self-generated sounds at all. Pharmacological deafening is irreversible. After cochlear implants became available also for clinical purposes, the question of auditory deprivation regained clinical and scientific interest: can we implant prelingually deaf children (deaf before birth or before acquiring language competence) and initiate the development of language competence via cochlear implants? It was shown that this is indeed possible, provided an early cochlear implantation (before age 5, today implantation is recommended even before age 2). But why is there any sensitive period in this process? What is the consequence of early deafness on the postnatal developmental process? Which aspects of this development are genetically determined, and which require sensory experience to develop? These are the current topics of our work. |
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All objects have multimodal character, i.e. they represent a stimulus for several of our sensory systems. All sensory systems are specific in many aspects, and these include also the characteristics of the evoked neural activity. E.g. the auditory systems shows very precise temporal features: the cochlea is able to follow changes of air pressure in the order of µsec., whereas the retinal is more than 1000 time "slower". Consequently, response characteristics at the cortical level differ between different senses. Despite of this, the information from the sensory systems has to fuse to one multimodal representation of objects. How does this take place in the brain? And where? Certain aspects of this question have been addressed by imaging techniques, and our EEG/MEG group is also addressing them. A precondition for understanding of multimodal representation is the understanding of how brain areas from different modalities cooperate, and how this cooperation can be affected by experience. In our pilot experiment we addressed the question whether in a deaf auditory system the primary auditory cortex takes over visual functions. There has been a considerable debate of this topic, although it has repeatedly been demonstrated that higher-order auditory areas take over visual functions in deafness. Our first results indicate that the primary auditory cortex does not cross-modally reorganize, which contrasts with the strong reorganization in secondary areas. That makes it plausible to think that deafness leads to a de-coupling of primary from higher-order auditory areas. This hypothesis is in the focus of our current experimental work. |
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