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Robert F Burkard

Publications and source records attributed to Robert F Burkard.

11 recordsLinked to original sources
PubMed2005

Mapping the 40-Hz auditory steady-state response using current density reconstructions.

We mapped the 40-Hz aSSR from nine normal subjects using PET-independent low-resolution electroencephalographic tomography (LORETA) as well as PET-weighted LORETA and minimum norm (MinNorm) current density reconstructions. In grand mean data, PET-independent LORETA identified seven sites with peaks in current density in right temporal lobe, right brainstem/cerebellum, right parietal lobe, left cerebellum/temporal lobe, and right frontal lobe. PET-weighted LORETA found six of the same sites as the PET-independent LORETA: the right brainstem source was eliminated and two right-frontal sources were added. Both LORETA analyses revealed considerable phase dispersion across identified sources. In both LORETA analyses, the relative time course of activation measured from an arbitrary starting phase progressed from right temporal lobe to right mid-frontal lobe to right parietal-frontal to right inferior parietal and finally to left cerebellum and left temporal lobe. MinNorm analysis incorporating PET information identified sources in the same locations as specified in the PET data. These sources were synchronized, with their amplitudes peaking almost simultaneously. Both PET-independent and PET-weighted LORETA results suggest that the aSSR is: (1) the result of a reverberating network with two or more groups of sources that recurrently excite each other or (2) the result of sequential auditory processing through various levels of a hierarchical network. In contrast, the PET-weighted MinNorm results suggest that the 40-Hz response represents simultaneous activation over widely spaced areas of the brain, perhaps due to synchronization of gamma-band activity to a common neural clock.

Acoustic Stimulation↗
PubMed2004

PET imaging of the 40 Hz auditory steady state response.

The auditory steady state response (aSSR) is an oscillatory electrical potential recorded from the scalp induced by amplitude-modulated (AM) or click/tone burst stimuli. Its clinical utility has been limited by uncertainty regarding the specific areas of the brain involved in its generation. To identify the generators of the aSSR, 15O-water PET imaging was used to locate the regions of the brain activated by a steady 1 kHz pure tone, the same tone amplitude modulated (AM) at 40 Hz and the specific regions of the brain responsive to the AM component of the stimulus relative to the continuous tone. The continuous tone produced four clusters of activation. The boundaries of these activated clusters extended to include regions in left primary auditory cortex, right non-primary auditory cortex, left thalamus, and left cingulate. The AM tone produced three clusters of activation. The boundaries of these activated clusters extended to include primary auditory cortex bilaterally, left medial geniculate and right middle frontal gyrus. Two regions were specifically responsive to the AM component of the stimulus. These activated clusters extended to include the right anterior cingulate near frontal cortex and right auditory cortex. We conclude that cortical sites, including areas outside primary auditory cortex, are involved in generating the aSSR. There was an unexpected difference between morning and afternoon session scans that may reflect a pre- versus post-prandial state. These results support the hypothesis that a distributed resonating circuit mediates the generation of the aSSR.

Adult↗
PubMed2003

Noise-induced hearing loss in chinchillas pre-treated with glutathione monoethylester and R-PIA.

The protective effects of glutathione monoethylester (GEE) and GEE in combination with R-N6-phenylisopropyladenosine (R-PIA) were evaluated in the chinchilla when exposed to impulse (145 dB pSPL) or continuous (105 dB SPL, 4 kHz OB) noise. Six groups of 10 chinchillas were used as subjects. Before exposure to noise, the subjects were anesthetized, a 30 microl drop of drug was placed on the round window (GEE [50, 100, 150 mM], GEE 50 mM and R-PIA). Forty minutes later the subject was exposed to either impulse or continuous noise. The 50 mM treatment provided significant protection from impulse noise, but not from continuous noise exposure. The combination provided significant protection from both the continuous and impulse noise. In a separate set of experiments, glutathione (GSH) levels were measured in the perilymph. All the drug treatments elevated GSH levels. The results are discussed in terms of antioxidant treatments as a prophylactic measure against noise-induced hearing loss.

Adenosine↗
PubMed2003

Impaired gap encoding in aged mouse inferior colliculus at moderate but not high stimulus levels.

Age-related deterioration of auditory temporal acuity has been identified as a contributing factor in presbycusis. In the present study, the effects of aging and stimulus level on gap encoding and gap recovery functions were investigated by measuring near-field auditory evoked potentials in the inferior colliculus of eight 3 month old and eight 24 month old CBA/CaJ mice, in response to gap stimuli embedded in broadband noise (40, 60, and 80 dB SPL). Gap encoding was assessed by measuring latencies and amplitudes of peak features of the near-field response, and also with a procedure that calculated the root mean square of the response within specific time windows. The chief differences in gap encoding between young and old mice were longer gap thresholds, slower recovery functions, and longer response peak latencies for old mice at 60, but not 80 dB SPL, although the latency of the earliest measured peak remained delayed for this condition in the old compared with the young mice. These results demonstrate that age-related changes in temporal acuity may interact with stimulus level, and suggest that adequate amplification may be critically important for maintaining temporal acuity with advancing age.

Acoustic Stimulation↗
PubMed2003

Development of materials for the clinical assessment of speech recognition: the speech sound pattern discrimination test.

The purpose of this investigation was to evaluate the validity and reliability of materials designed for an assessment procedure capable of making meaningful distinctions in speech recognition ability among individuals having mild-to-moderate hearing losses. Sets of phonetic contrasts were presented within sentence contexts to 53 listeners (22 normal hearing, 31 hearing impaired) in 4 listening conditions (quiet and with background competition at signal-to-noise ratios of +5, 0, and -5 dB). The listeners were asked to discriminate pairs of sentences (e.g., "The man hid the dog" and "The man hit the dog") using same-different judgments. Their performances were analyzed in a manner enabling comparisons among items in terms of the classification of phonetic contrasts. Listener performance was also compared to performance on a set of independent variables, including the W-22 and QuickSIN speech tests, high-frequency hearing loss, speech reception threshold, listener age, and others. Results indicated that the new materials distinguished the normal-hearing from the hearing-impaired group and that listener performance (a) declined about 17% for each 5 dB decrement in SNR and (b) was influenced by the phonetic content of items in a manner similar to that reported by G. A. Miller and P. E. Nicely (1955). The performances of the hearing-impaired listeners were much more strongly related to high-frequency hearing loss, listener age, and other variables than were their performances on either the W-22 or QuickSIN tests. These findings are discussed with specific reference to the use of a mathematical model (i.e., the Rasch model for person measurement) for scaling items along a continuum of difficulty. The mathematical model and associated item difficulty values will serve as the basis for construction of a clinically useful computerized, adaptive test of speech recognition ability known as the Speech Sound Pattern Discrimination Test (Bochner, J., Garrison, W., Palmer, L., MacKenzie, D., & Braveman, A., 1997).

Adult↗
PubMed2002

Tinnitus.

Explore the source record for details and available documents.

Algorithms↗
PubMed2002

Stimulus and recording variables and their effects on mammalian vestibular evoked potentials.

Linear vestibular evoked potentials (VsEPs) measure the collective neural activity of the gravity receptor organs in the inner ear that respond to linear acceleration transients. The present study examined the effects of electrode placement, analog filtering, stimulus polarity and stimulus rate on linear VsEP thresholds, latencies and amplitudes recorded from mice. Two electrode-recording montages were evaluated, rostral (forebrain) to 'mastoid' and caudal (cerebellum) to 'mastoid'. VsEP thresholds and peak latencies were identical between the two recording sites; however, peak amplitudes were larger for the caudal recording montage. VsEPs were also affected by filtering. Results suggest optimum high pass filter cutoff at 100-300 Hz, and low pass filter cutoff at 10,000 Hz. To evaluate stimulus rate, linear jerk pulses were presented at 9.2, 16, 25, 40 and 80 Hz. At 80 Hz, mean latencies were longer (0.350-0.450 ms) and mean amplitudes reduced (0.8-1.8 microV) for all response peaks. In 50% of animals, late peaks (P3, N3) disappeared at 80 Hz. The results offer options for VsEP recording protocols.

Animals↗
PubMed2002

Brain imaging of the effects of lidocaine on tinnitus.

Using a single-blind placebo-controlled design, we mapped lidocaine related changes in neural activity, measured by regional cerebral blood flow (rCBF) with (15)O-H(2)O positron emission tomography. Intravenous lidocaine produced both increases and decreases in the loudness of tinnitus. The change in tinnitus loudness was associated with a statistically significant change in neural activity in the right temporal lobe in auditory association cortex. Decreases in tinnitus loudness resulted in larger changes in rCBF than increases. The unilateral activation pattern associated with tinnitus, in contrast with the bilateral activation produced by a real sound, suggests that tinnitus originates in the central auditory system rather than the cochlea. In addition, generalized lidocaine effects were found in the basal ganglia, thalamus, and a region spanning the Rolandic fissure.

Acoustic Stimulation↗
PubMed2002

A comparison of the effects of broadband masking noise on the auditory brainstem response in young and older adults.

We examined the effects of ipsilateral-direct, continuous, broadband noise on auditory brainstem response (ABR) wave I and V latencies and amplitudes in young adult versus older adult humans. It was hypothesized that age might influence the effects of masking noise on ABR peak latencies and/or amplitudes, given the frequent complaint of older persons' ability to process speech in background noise. Young adults had hearing thresholds of 20 dB HL or better for the octave frequencies from 250 to 8,000 Hz. A subset of older study participants had thresholds of 20 dB HL or better across frequency, but others had thresholds up to 45 dB HL. All data were collected and analyzed with a Nicolet Bravo. An electrode was placed on the tympanic membrane (as well as on high forehead and contralateral mastoid), and a click level of 115 dB pSPL was used to maximize wave I amplitude. Masker conditions included a no-noise control and noise levels ranging from 20 to 70 dB effective masking, in 10 dB steps. With increasing noise level, both age groups showed minimal changes in wave I latency, but substantial increases in wave V latency and I-V interval. Peak amplitudes decreased with increasing noise level. Mean amplitudes were smaller for the older group, most notably for wave I. Mean peak latencies were greater in the older group, but the I-V interval was similar across age groups, as was the change in peak latencies and I-V interval across noise level. ABR parameters for the older adults with hearing meeting the 20-dB HL criterion at all frequencies (older-better) were compared to those who didn't meet this criterion (older-worse). Mean wave I latency was greater and wave V latency and I-V interval were smaller for the older-worse group at all noise levels. Mean wave I and V amplitudes were similar for the older-better and older-worse groups. In participants with normal or near-normal hearing, ABR changes with increasing age included small latency increases and a substantial reduction in wave I amplitude. The effects of ipsilateral-direct masking noise on the click-evoked ABR are similar for young and older adults.

Adult↗