Biomedical subjects

Paul W F Poon

Publications and source records attributed to Paul W F Poon.

5 recordsLinked to original sources

PubMed2006

Functional connections between auditory cortical fields in humans revealed by Granger causality analysis of intra-cranial evoked potentials to sounds: comparison of two methods.

Knowledge of neural interactions amongst cortical sites is important for understanding higher brain function. We studied such interactions using Granger causality (GC) to analyze auditory event-related potentials (ERPs) recorded directly and simultaneously from two physiologically identified and functionally interconnected auditory areas of cerebral cortex in human neurosurgical patients. Two methods of GC analysis were used and the results compared. Both approaches involved adaptive autoregressive modeling but differed from each other in other ways. Results obtained by using the two methods also differed. Fewer false-positive results were obtained using the method that suppressed the ERP non-stationarity and that expressed the GC as the sum of model coefficients, which suggests that this is the more appropriate approach for analyzing ERPs recorded directly from the human cortex.

Auditory Cortex↗

PubMed2006

Real-time data-reusing adaptive learning of a radial basis function network for tracking evoked potentials.

Tracking variations in both the latency and amplitude of evoked potential (EP) is important in quantifying properties of the nervous system. Adaptive filtering is a powerful tool for tracking such variations. In this paper, a data-reusing non-linear adaptive filtering method, based on a radial basis function network (RBFN), is implemented to estimate EP. The RBFN consists of an input layer of source nodes, a single hidden layer of non-linear processing units and an output layer of linear weights. It has built-in nonlinear activation functions that allow learning of function mappings. Moreover, it produces satisfactory estimates of signals against a background noise without a priori knowledge of the signal, provided that the signal and noise are independent. In clinical situations where EP responses change rapidly, the convergence rate of the algorithm becomes a critical factor. A carefully designed data-reusing RBFN can accelerate the convergence rate markedly and, thus, enhance its performance. Both theoretical analysis and simulation results support the improved performance of our new algorithm.

Adolescent↗

PubMed2003

Long-term changes of response in the inferior colliculus of senescence accelerated mice after early sound exposure.

Early sound exposure could alter auditory sensitivity in young animals. For example, the distribution of frequency tuning at the midbrain inferior colliculus (IC) is altered following early exposure to a tone at a moderate intensity level. Whether such neonatal change is still present in the old animals remains unknown. We studied the long-term effects of early sound exposure using a mutant strain of mice expressing accelerated senescence (SAM). Experimental animals were first exposed to a 9-kHz tone (53 dB sound pressure level (SPL)) for 30 days (10 h/day) after birth. Control animals received no tones. At the age of 15 months, responses of single IC units to sounds were studied electrophysiologically under urethane anesthesia. In the control group, we found an overall reduction in sensitivity to tones particularly at high frequencies, in comparison with normal non-senescent mice. Moreover, neurons exhibited increased spontaneous activities. These signs are consistent with accelerated senescence. Early sound exposure produced two effects in the experimental group. Firstly, IC units showed an apparent 'clustering' of best frequencies towards the frequency of the exposing tone (i.e., 9 kHz). Secondly, there was a further loss in sensitivity to tones particularly at high frequencies. Results suggest that early sound exposure has produced a long-lasting effect on frequency tuning of IC neurons. Acoustic overstimulation early in life may also accelerate the senescence of neurons or structures in the auditory system.

Acoustic Stimulation↗

PubMed2003

Early postnatal sound exposure induces lasting neuronal changes in the inferior colliculus of senescence accelerated mice (SAMP8): a morphometric study on GABAergic neurons and NMDA expression.

Senescence-acceleration-prone mice (SAMP8) provide a model to study the influence of early postnatal sound exposure upon the aging auditory midbrain. SAMP8 were exposed to a 9-kHz monotone of either 53- or 65-dB sound pressure level during the first 30 postnatal days, the neurons in the auditory midbrain responding selectively to 9 kHz were localized by c-fos immunohistochemistry and the following parameters were compared to control SAMP8 not exposed to sound: mortality after sound exposure, dendritic spine density, and quantitative neurochemical alterations in this 9-kHz isofrequency lamina. For morphometric analysis, animals were examined at 1, 4, and 8 months of age. Serial sections of the inferior colliculus were Golgi impregnated or stained immunohistochemically for the expression of epsilon1 subunit of NMDA receptor or GABA. Mortality after exposure to 53 dB was the same as in controls, but was markedly increased from 7 months of age onward after postnatal exposure to 65 dB. No gross morphological alterations were observed in the auditory midbrain after sound exposure. However, sound exposure to 53 or 65 dB significantly reduced dendritic spine density by 11% at 4 months or by 11-17% both at 1 and 4 months of age, respectively. The effect of sound exposure upon neurons expressing the NMDAepsilon1 subunit was dose-dependent. Increasing with age until 4 months in control mice and remaining essentially stable thereafter, the percentage of NMDAepsilon1-immunoreactive neurons was significantly elevated by 40-66% in 1- and 8-month-old SAMP8 exposed to 53 dB, whereas no significant effect of 65 dB was apparent. The proportion of GABAergic cells declined with age in controls. It was significantly decreased at 1 month after 53 and 65 dB sound exposure. In contrast, it was elevated at later stages, being significantly increased at 4 months after exposure to 53 dB and at 8 months after exposure to 65 dB. The total cell number in the 9-kHz isofrequency lamina of SAMP8 decreased with age, but was not affected by exposure to either 53 or 65 dB. The present results indicate that early postnatal exposure to a monotone of mild intensity has long-term effects upon the aging auditory brain stem. Some of the changes induced by sound exposure, e.g., decline in spine density, are interpreted as accelerations of the normal aging process, whereas other effects, e.g., increased NMDAepsilon1 expression after 53 dB and elevated GABA expression after both 53 and 65 dB, are not merely explicable by accelerated aging.

Acoustic Stimulation↗

PubMed2002

Adaptive filtering of evoked potentials with radial-basis-function neural network prefilter.

Evoked potentials (EPs) are time-varying signals typically buried in relatively large background noise. To extract the EP more effectively from noise, we had previously developed an approach using an adaptive signal enhancer (ASE) (Chen et al., 1995). ASE requires a proper reference input signal for its optimal performance. Ensemble- and moving window-averages were formerly used with good results. In this paper, we present a new method to provide even more effective reference inputs for the ASE. Specifically, a Gaussian radial basis function neural network (RBFNN) was used to preprocess raw EP signals before serving as the reference input. Since the RBFNN has built-in nonlinear activation functions that enable it to closely fit any function mapping, the output of RBFNN can effectively track the signal variations of EP. Results confirmed the superior performance of ASE with RBFNN over the previous method.

Algorithms↗