Publication Abstracts -1999

Bourdette, D., Antel, J., Montgomery, E. (1999). Monitoring relapsing remitting multiple sclerosis patients. Journal of Neuroimmunology, 98:16-21. 

Department of Neurology, Oregon Health Sciences University, Department of Veterans Affairs Medical Center, Portland 97201, USA. dennis.bourdette@va.gov

The availability of safe and partially effective disease modifying therapies necessitates changes in how neurologists monitor patients with relapsing remitting multiple sclerosis (RRMS). Neurologists need to make the diagnosis of MS as soon as possible to be able to initiate therapy early in the course of disease. In deciding whom to treat, neurologists should consider information on disease activity and burden acquired from the neurologic history and examination and magnetic resonance imaging (MRI). Patients not on a disease modifying therapy should undergo yearly clinical assessments and periodic cerebral MRI to monitor for changes in disease activity. Patients on disease modifying therapy should undergo regular clinical assessments to monitor for side-effects and disease activity. Cerebral MRI scanning may also be useful in assessing patients on therapy, particularly when considering changes in therapy.

Dronkers, NF; Husted, DA; Deutsch, G; Taylor, MK; Saunders, GH & Merzenich, MM (1999). Lesion site as a predictor of improvement after "Fast ForWord" treatment in adult aphasic patients. Brain & Language 69, 450-452.

New treatment techniques for adult aphasic patients are always in demand.  Equally needed is information about the factors that might predict which patients will improve with certain treatments.  Such information can assist clinicians in choosing the most successful therapy for their patients.

One new technique, "Fast ForWord," has been shown to be successful in treating children with "language-based leanring impairments," a developmental disorder that affects a large percentage of language-disordered children (Merzenich et al., 1996; Tallal et al., 1996). These children are believed to have a temporal processing deficit that impairs their ability to identify stimuli presented at very short durations.  Certain speech sounds occur at speeds of around 40 ms and are difficult for these children to discriminate and sequence.  By slowing these sounds down to speeds that facilitate discrimination, the computer-based Fast ForWord technique appears to enable these children to detect, process, and learn these sounds, thus improving their language comprehension skills.  Performance on psychoacoustic measures of temporal processing also show improvement after Fast ForWord training.  It is believed that this training improves the brain's ability to respond to and process these rapidly presented stimuli.

While these results in developmentally language-disordered children are encouraging, it is not known why some children improve more than others. It is also not known how adult aphasic patients with acquired disorders might respond to this treatment technique.  The present study represents pilot work with 12 adult aphasic patients, both acute and chronic, with extensive speech, language, cognitive, neurologic, and neuroradiologic evaluations.  Specific questions included (1) whether Fast ForWord could significantly improve the language comprehension abilities of adult aphasic patients, (2) how potential benefits from Fast ForWord treatment would compare to those of conventional one-on-one speech therapy, and (3) whether psychophysical, functional/behavioral, and/or site-of-lesion measures could predict outcome with Fast ForWord treatment.

Fausti, S. A., Henry, J. A., Hayden, D., Phillips, D. S., Frey, R. H. (1999).  Intrasubject reliability of high-frequency (9-14kHz) thresholds tested separately vs following conventional frequency testing.  Journal of the American Academy of Audiology, 9:147-152.

Department of Veterans Affairs Medical Center, Portland, Oregon 97207, USA.

Retrospective analysis of hearing-threshold data from a multisite ototoxicity monitoring study identified an individualized range of predominantly high frequencies (> 8 kHz) that appeared to be highly sensitive to early threshold changes caused by ototoxicity. This suggested the potential for a limited-frequency monitoring protocol that could be conducted rapidly without compromising sensitivity to ototoxicity. Such testing would require high-frequency thresholds to be obtained independently, that is, without prior testing at conventional frequencies (0.25-8 kHz). This study was conducted to determine the test-retest reliability of isolated threshold testing in a "target" frequency range of high frequencies (9, 10, 11.2, 12.5, and 14 kHz) that represented a shortened ototoxicity monitoring test. Twenty normal-hearing subjects were evaluated over five sessions. During each session, subjects were tested in each of two conditions: (1) conventional frequencies (0.25-8 kHz) tested first, followed by target frequencies; and (2) target frequencies tested alone (isolation condition). Depending on test frequency, reliability of high-frequency thresholds was either unchanged or improved in the isolation condition. Although these results cannot be generalized to ill hospitalized patients, who may also have pre-existing hearing loss, they lay the groundwork for development of a time-saving limited-frequency test to monitor for ototoxicity in these patients.

Fausti, S. A., Henry, J. A., Helt, W. L., Phillips, D. S., Frey, R. H., Noffsinger, D., Larson, V. D., & Fowler, C. G. (1999). An individualized, sensitive frequncy range for early detection of ototoxicity. Ear and Hearing, 20:497-505. 

VA RR&D National Center for Rehabilitative Auditory Research, Department of Veterans Affairs Medical Center, Portland, Oregon.

OBJECTIVE: The aim of this study was to identify auditory frequencies at which serial threshold testing would provide the greatest sensitivity for early detection of ototoxicity. The overall objective is to develop a more time-efficient ototoxicity monitoring protocol. DESIGN: Threshold data were analyzed from 370 hospitalized patients treated with aminoglycoside antibiotics (AMGs) or cisplatin (CDDP) who received serial auditory monitoring before, during, and after treatment at conventional (0.25 to 8 kHz) and high (9 to 20 kHz) frequencies. RESULTS: For patients showing hearing changes due to ototoxicity, a frequency range was identified for its apparent high sensitivity to initial ototoxicity. This sensitive range is identified according to an individual's hearing threshold configuration, and is, therefore, unique for each patient. The range consists of five frequencies, generally separated by 1/6 octave, e.g., 8, 9, 10, 11.2, and 12.5 kHz. To determine frequencies and combinations of frequencies that were most often involved in ototoxicity detection, threshold data in the sensitive range were analyzed in detail. This analysis suggests that patients receiving treatment with AMG or CDDP can be monitored for hearing thresholds at only five frequencies, resulting in an 84% detection rate for AMG and 94% for CDDP compared with monitoring at all conventional and high frequencies. CONCLUSIONS: This comprehensive analysis supports earlier observations that a sensitive, limited frequency range exists in which serial threshold monitoring will provide early warning of ototoxicity before effects in the speech frequency range. This finding is now being evaluated in a prospective investigation.

Folmer, R. L., Griest, S. E., Meikle, M. B., & Martin, W. H. (1999). Tinnitus severity, loudness and depression. Otolaryngology Head and Neck Surgery, 121:48-51.

Oregon Hearing Research Center, Department of Otolaryngology, Oregon Health Sciences University, Portland 97201-3098, USA.

Answers to questionnaires filled out by 436 patients who visited our tinnitus clinic were analyzed. Patients were asked to report the presence or absence of depression and to rate the loudness and severity of their tinnitus. Responses to questions about tinnitus loudness and severity from 121 patients who reported current depression were compared with responses from 285 patients who reported no history of depression. There was no significant difference in reported loudness of tinnitus between patients with and without depression. However, patients with current depression scored significantly higher than patients without depression on all 12 questions relating to tinnitus severity. We conclude that depression and tinnitus severity are linked in some patients. Treatment of depression with medications and psychotherapy is likely to reduce tinnitus severity for many of these patients. 

Henry, J. A., & Meikle, M. B. (1999). Pulsed versus continuous tones for evaluation the loudness of tinnitus. Journal of the American Academy of Audiology, 10:261-272. 

National VA RR&D Center for Rehabilitative Auditory Research, Portland VA Medical Center, Oregon 97207, USA.

Loudness balance techniques are commonly employed to match the loudness of tinnitus using either pulsed or continuous tones; however, it is not known whether the tone duration affects the observed loudness matches. In this study, hearing thresholds and tinnitus loudness matches were measured in 26 subjects with chronic tinnitus using both pulsed and continuous tones. Subjects' thresholds and loudness matches were determined at 11 frequencies between 0.5 and 10 kHz. No significant differences were found between pulsed versus continuous measures, either for thresholds or for loudness matches. There were, however, nine subjects (34.5% of the group) who showed relatively large differences (> or =10 dB) at one or more test frequencies. These "outlier" values did not show systematic trends; some were positive, some negative. In conclusion, studies employing group data appear to be comparable if group sizes are sufficiently large (e.g., > or =25 subjects). Studies employing smaller numbers of subjects may, however, be vulnerable to potential positive or negative biases introduced by one or more outliers.

Henry, J. A., Flick, C. L., Gilbert, A. M., Ellingson, R. M., & Fausti, S. A. (1999). Reliability of tinnitus loudness matches under procedural variation. Journal of the American Academy of Audiology, 10:502-520. 

National VA RR&D Center for Rehabilitative Auditory Research, Portland VA Medical Center, Oregon 97207, USA.

Repeated tinnitus loudness matches (LMs) were obtained to determine response reliability using a computer-automated technique with two procedural variations, fixed or random step sizes, to increase output level during the initial ascending series of tones at each frequency. Twenty subjects with stable, tonal tinnitus were evaluated with both methods during each of two sessions. Response instructions were displayed on a portable computer, and a pen device was used to make response choices that appeared on the touch-sensitive video monitor. For each method, hearing thresholds and LMs were obtained, with 1-dB resolution, at 1/3-octave frequencies from 1 to 16 kHz. Analyses revealed reliability of LMs to be equivalent between methods. LM data are reported in both dB SPL and dB SL, with the SPL values providing greater reliability both within and between sessions (all r's > or = .889, p's < or = .0001).

Jiang, Z. G., Qiu, J., Ren, T., & Nuttall, A. L. (1999). Membrane properties and the excitatory junction potentials in smooth muscle cells of cochlea spiral modiolar artery in guinea pigs. Hearing Research, 138:171-180. 

Oregon Hearing Research Center, NRC-04, Oregon Health Sciences University, Portland, OR 97201, USA. jiangz@ohsu.edu

Blood circulation changes in the inner ear play an important role in many physiological and pathological conditions of hearing function. The spiral modiolar artery (SMA) is the terminal artery to the cochlea. It was surrounded with nerve fibers immunostained by an antibody for tyrosine hydroxylase. By using intracellular recording techniques on the acutely isolated SMA, membrane properties of the smooth muscle cells and the neuromuscular transmission in this preparation were investigated. With minimum tension and normal extracellular K(+) concentration (5 mM), the majority of muscle cells showed a resting potential near -80 mV and an input resistance of about 8 MOmega. V/I plot showed an inward rectification in these cells. Barium (50-500 microM) caused strong depolarization and an increase in input resistance. Transmural electrical stimulation evoked stimulation intensity-dependent depolarizations (2-31 mV) following a short latency ( approximately 20 ms). The evoked potential by a low intensity stimulus was completely blocked by 1 microM tetrodotoxin. The potential and a depolarization induced by norepinephrine (10 microM) was usually partially (40-90%) blocked by alpha-receptor antagonists prazosin and/or idazoxan with concentrations up to 1 microM. Action potentials were observed when the depolarization was more than -40 mV. It is concluded that SMA smooth muscle cells, similar to those in other brain small arteries, highly express inward rectifying potassium channels; the cells receive catecholaminergic innervation, and stimulation of the nerves elicited an excitatory junction potential that is partially mediated by adrenergic receptors.

Meikle, M. B. (1999). A salute to bravery. Tinnitus Today.  Journal of the American Tinnitus Association, 24:14-15. 

Merzenich, MM; Saunders, GH; Jenkins, WM; Miller, S; Peterson, B & Tallal, P. Pervasive Developmental Disorders: Listening Training and Language Abilities in The Changing Neuron System Neurobehavioral Consequences of Early Brain Disorders. Broman SH & Fletcher JM (Eds.) Oxford Press.

By definition, children diagnosed with pervasive developmental disorders (PDD, autistic [PDD-A]; pervasive developmental disorder-not otherwise specified [PPD-NOS]) have severe language impairments.  Some scientists have argued that their especially severe early receptive language difficulties, resulting in the predominance of a thinking-in-pictures rather than a thinking-in-words cognition, are at the core of their complex panoply of neurobehavioral deficits.  Others have argued that language difficulties are one of many parallel and substantially independent deficits or "principal factors" that can have widely variable expressions in this population.

Twin studies have shown that nearly all monozygotes of children with PDD-A and PDD-NOS have language impairments, but that the language (and other neurobehavioral) deficits of the identical twin are commonly of a different severity and can be expressed in moderate form.  It has long been argued that children can also develop PDD-like symptoms, including a correspondingly severe language impairment form a variety of other inherited and postnatal neurological causes, such as intrauterine rubella, tuberous sclerosis, herpes simplex encephalitis, phenylketonuria, or fragile-X syndrome. While these children may comprise only a small fraction of individuals identified as "autistic" they raise a very important question: What do these inherited and disease-induced conditions have in common that could result in such similar expressions of very severe language impairment? Moreover, how do the language impairment of children with PDDs relate to the often milder language impairments of their siblings or monozygotic twins- or to the neurological origins and expressions of language deficits in children with less severe impairments, in general?  Are the language impairments of children with PDDs on a neurological continuum with those of children with specific language impairments (SLIs)? Can similar remedial training strategies be expected to ameliorate speech and language usage in both populations? This current study is a part of an extended series of experiments that are designed to address these important questions.

Mitchell, C. R., Kempton, J. B., Creedon, T. A., & Trune, D. R. (1999). Using  56-stimulus train for the rapid acquisition of auditory brainstem responses. Audiology and Neuro-Otology, 4:80-87. 

National Center for Rehabilitative Auditory Research, Portland, OR, USA.

To further develop a multiple stimulus method for the rapid acquisition of auditory brainstem responses (ABRs), a 56-stimulus train was tested in mice. Stimuli in the train were tone bursts spaced at 0.5-octave intervals from 4 to 32 kHz. ABR thresholds, latency-intensity and amplitude-intensity functions were obtained using stimuli presented singly (one at a time) and using the 56-stimulus train. Responses from stimuli presented singly and those obtained using the 56-stimulus train were compared. There were no significant differences in thresholds (0.01 level) and very small differences in response latencies and amplitudes. These findings demonstrate the feasibility of multiple stimulus trains for the rapid acquisition of ABRs.

Noffsinger, D., & Martinez, C. (1999). Differential diagnosis of central auditory system disorders. In F. Canalis & P. Lambert (Eds.), The Ear: A Textbook of Otology (pp. 251-264). Lipincott-Raven, New York. 

Nuttall, A. L. (1999). Sound-induced cochlear ischemia/hypoxia as a Mechanism of Hearing Loss: A Review, Laryngology and Otology. Noise and Health Journal, 5:17-31.

Oregon Hearing Research Centre, NRC04, Department of Otolaryngology/Head & Neck Surgery, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Rd., Portland, OR 97201-3098, USA., Email: nuttall@ohsu.edu

This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that decreased cochlear blood flow can be demonstrated and measured by laser Doppler flowmetry and by direct observation of cochlear microvessels. Oxygen levels also decline and possibly to a greater degree than blood flow. There is also evidence that in certain circumstances sound can increase blood flow. Reduced blood flow, or reduced oxygenation, is critically important in an organ system with high energy needs like the cochlea. Therefore, a second hypothesis, that sound-induced reduction in CBF represents a functional ischemia, will be explored in examining the relevance of traditional ischemia/reperfusion models to cochlear damage. It is found that reactive oxygen species (free radicals and oxidizing ions) are present in sound-induced hearing loss and thus there is evidence that an ischemia/reperfusion type of injury occurs during loud sound exposures. 

Nuttall, A. L., Guo, M., & Ren, T. (1999). The radial pattern of basilar membrane motion evoked by electric stimulation of the cochlea. Hearing Research, 131:39-46. 

Oregon Hearing Research Center, Department of Otolaryngology/Head and Neck Surgery, Oregon Health Sciences University, Portland 97201-3098, USA.

Electric current applied to the cochlea can evoke in situ electromotile responses of the organ of Corti. These nonsound-generated responses can give insight into the mechanics of the organ as the putative forces produced by outer hair cells (OHC) must couple to the modes of vibration of the basilar membrane (BM). In this study, platinum-iridium wire electrodes were positioned into the scala vestibuli and scala tympani of the first cochlear turn in the guinea pig. Current (1.5 ms rectangular-shaped pulses) was applied to these electrodes at levels to 500 microA peak. A laser Doppler velocimeter was used to record the velocity or displacement of the basilar membrane at the tonotopic 18 kHz place via an opening into the scala tympani of the first cochlear turn. Beads were positioned across the width of the BM so that the velocity or displacement of the BM could be studied in the radial direction. It was found that the current pulses evoked linear displacements of up to 2 nm for current levels of 500 microA (higher levels were damaging to the organ of Corti). The pattern of motion across the width of the BM was such that maximum displacement and velocity was located near the first row of OHCs and the position of the outer pillar cell footplate. The BM motion was biphasic in that the zona arcuata moved in the opposite direction to that of the zona pectinata. The results of this study demonstrate that the level of force produced by OHCs is effective in moving the BM and that the distribution of force within the organ of Corti leads to a multimodal motion pattern of the BM for this experimentally artificial means of evoking OHC motion.

Pillers, D. M., Duncan, N. M., Dwinnell, S. J., Rash, S. M., Kempton, J. B., & Trune, D. R. (1999). Normal cochlear function in mdx and mdxCv3 Duchenne muscular dystrophy mouse models. Laryngoscope, 109:1310-1312. 

Department of Pediatrics, Oregon Child Health Research Center, Doernbecher Children's Hospital, Oregon Health Sciences University, Portland 97201-3042, USA. pillersd@ohsu.edu

OBJECTIVES/HYPOTHESIS: Sensorineural hearing loss has been found in association with inherited muscular dystrophies in humans and in mouse models. An increased brainstem auditory evoked response threshold has been previously reported in the dystrophin-deficient mdx mouse model for Duchenne muscular dystrophy, suggesting that full-length dystrophin (Dp427) is involved in hearing. The objective of the present study was to confirm cochlear dysfunction with this gene defect and determine whether the shorter carboxyl terminus isoforms of dystrophin are also critical in maintaining normal hearing. STUDY DESIGN: Case controlled. Animal model. METHODS: Auditory brainstem response (ABR) audiometry to pure tones was used to evaluate cochlear function. Fourteen mdx, 4 mdx(Cv3), and 13 age-matched control (C57BL/6J and C57BL/10ScSn) male mice were tested at 5 weeks and 11 weeks of age. The ABR thresholds to tone-burst stimuli at 4, 8, 16, and 32 kHz were obtained for each ear and statistically compared (ANOVA) for potential group differences. RESULTS: Both mdx and mdx(Cv3) mice demonstrated normal ABR thresholds when compared with controls. CONCLUSIONS: Both mdx and mdx(Cv3) mouse models have normal hearing by ABR. The authors' data suggest that dystrophin and its carboxyl terminus isoforms do not play a critical role in hearing in the mouse. This was unexpected, as previous studies using the brainstem auditory evoked response method suggested that the mdx mouse has an increased threshold for hearing.

Reagan, L. P., Magarinos, A. M., Lucas, L. R.,Van Buren, A., McCall, A. L., & McEwen, B. S. (1999). Streptozotocin-induced diabetes regulation of GLUT3 glucose transporter in rat hippocampus: absence of modulation by stress. American Journal of Physiology, 276:E879-E886. 

Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10021, USA.

Previous studies from our laboratory have demonstrated that chronic stress produces molecular, morphological, and ultrastructural changes in the rat hippocampus that are accompanied by cognitive deficits. Glucocorticoid attenuation of glucose utilization is proposed to be one of the causative factors involved in stress-induced changes in the hippocampus, producing an energy-compromised environment that may make hippocampal neuronal populations more vulnerable to neurotoxic insults. Similarly, diabetes potentiates neuronal damage in acute neurotoxic events, such as ischemia and stroke. Accordingly, the current study examined the regulation of the neuron-specific glucose transporter, GLUT-3, in the hippocampus of streptozotocin-induced diabetic rats subjected to restraint stress. Diabetes leads to significant increases in GLUT-3 mRNA and protein expression in the hippocampus, increases that are not affected by stress. Collectively, these results suggest that streptozotocin-induced increases in GLUT-3 mRNA and protein expression in the hippocampus may represent a compensatory mechanism to increase glucose utilization during diabetes and also suggest that modulation of GLUT-3 expression is not responsible for glucocorticoid impairment of glucose utilization.

Takayanagi, S., Kreiman, J., & Dirks, D.  (1999).  Effects of unnatural pauses on speech intelligibility.  Proceedings of the 14^th International Congress of Phonetic Sciences, V2:865-868. 

Trune, D. R., Wobig, R. J., Kempton, J. B., & Hefeneider, S. H. (1999). Steroid treatment in young MRL MpJ-Faslpr autoimmune mice prevents cochlear dysfunction. Hearing Research, 137:167-173. 

Oregon Hearing Research Center, Department of Otolaryngology - Head and Neck Surgery, Oregon Health Sciences University, NRC04, 3181 SW Sam Jackson Park Road, Portland, OR 97201-3098, USA. truned@ohsu.edu

Corticosteroid therapy reverses clinical autoimmune sensorineural hearing loss, although little is known of how steroids restore normal auditory function. If suppression of systemic autoimmune processes underlies hearing restoration, then preventing autoimmune symptoms from developing should prevent cochlear dysfunction. MRL. MpJ-Fas(lpr) autoimmune mice were used to test this potential mechanism by initiating oral prednisolone treatment at 6 weeks of age, prior to autoimmune disease and hearing loss onset. The steroid treatment group was given prednisolone in their drinking water, while untreated controls were given tap water. Treatment continued for 7 months with periodic evaluations of cochlear function with auditory brainstem response (ABR) audiometry. Autoimmune mice given the steroid lived longer and did not develop levels of serum immune complexes seen in their untreated controls. Also, their ABR thresholds remained near normal throughout the 7 months of treatment, while untreated controls showed progressive threshold elevations typical for autoimmune disease. This correlation of suppressed systemic autoimmune activity and maintenance of normal cochlear function identifies one potential mechanism for autoimmune hearing loss and hearing restoration with steroid therapy. The autoimmune mouse should serve as a valuable model for future studies of the cochlear mechanisms responsive to steroid treatment in autoimmune hearing loss.

Trune, D. R., Wobig, R. J., Kempton, J. B., & Hefeneider, S. H. (1999). Steroid therapy improves cochlear function in the C3H.   MRL-Faslpr autoimmune mouse. Hearing Research, 137:160-166. 

Oregon Hearing Research Center, Department of Otolaryngology - Head and Neck Surgery, Oregon Health Sciences University, NRC04, 3181 SW Sam Jackson Park Road, Portland, OR 97201-3098, USA. truned@ohsu.edu

Corticosteroid therapy is used to reverse autoimmune sensorineural hearing loss, although little is known of the mechanism by which this occurs. This has been due to the lack of a suitable animal model with spontaneous hearing loss that is steroid responsive. The present study examined the effects of prednisolone treatment on auditory thresholds in the MRL.MpJ-Fas(lpr) autoimmune mouse to determine its suitability as such a model. Autoimmune mice at 3.5-4. 5 months of age were evaluated by pure-tone auditory brainstem response (ABR) to establish threshold elevations due to the disease. The steroid treatment group was then given prednisolone in their drinking water for 2.5 months, while untreated controls were given tap water. Significantly more steroid treated mice survived to the time of post-treatment ABR evaluation. Half of the steroid treated ears demonstrated either improvement or no change in cochlear function compared to only 25% in the untreated controls. Overall, cochlear thresholds in the untreated controls increased by 14.7 dB, whereas no significant threshold increase was seen in the steroid treated group (4.3 dB) over the treatment period. No qualitative anatomical differences were seen in the ears of those mice surviving to the end of the study. These findings establish the autoimmune mouse as a model for studies of steroid responsive mechanisms within the ear. This could apply to autoimmune sensorineural hearing loss, as well as any hearing disorder for which steroid therapy is recommended.

Uchida, Y., Lilly, D. J., & Meikle, M. B. (1999). Cross language speech intelligibility in noise: A comparison on the aspect of language dominance. Journal of the Acoustical Society of America, 106:2151-2154. 

Yasue Uchida (Dept. of Otorhinolaryngology, Nagoya Univ. School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550 Japan, yasueu@nils.go.jp), David J. Lilly (Veteran Administration Natl. Ctr. For Rehabilitative Auditory Res., Portland, OR), and Mary B. Meikle (Oregon Hearing Res. Ctr., Portland, OR)

The purpose of this study is to obtain information about the influence of language characteristics on the results of speech intelligibility in two different languages: English and Japanese.  This study investigates the speech intelligibility of both English and Japanese under quiet and nosiy situation on 14 bilingual subjects aged 23 to 42 years with normal hearing. As test materials, the CID W-22 word lists which are meaningful monosyllables are used for English and the 57-S word lists which are nonsense monosyllables are used for Japanese.  The subjects whose dominant language is English are 6. Results show that percentage-correct of speech intelligibility is higher in Japanese than in English at lower intensity and noisy situation. This advantage in Japanese is seen regardless of the language dominance.  It is considered that the phonetic characteristics and the simple structure of Japanese can make it relatively resistant to the hard listening condition. [Work supported in part by Japan Foundation for Aging and Health.]

Wobig, R. J., Kempton, J. B., & Trune, D. R. (1999). Steroid responsive cochlear dysfunction in the MRL/lpr autoimmune mouse. Otolaryngology Head & Neck Surgery, 121:344-347. 

Department of Otolaryngology-Head and Neck Surgery, Oregon Hearing Research Center, Oregon Health Sciences University, Portland, 97201-3098, USA.

Corticosteroids historically have been used to treat autoimmune sensorineural hearing loss, although little is known of how steroids restore normal inner ear function. Therefore, to identify a potential model for this field of research, this study examined the effects of prednisolone on auditory brain stem response thresholds in the MRL/lpr mouse model of autoimmune sensorineural hearing loss. Mice treated with prednisolone after auditory threshold elevations demonstrated significant improvement and stabilization of thresholds compared with untreated controls. MRL/lpr mice treated with steroids before the onset of autoimmune disease and cochlear dysfunction demonstrated decreased serum immune complexes, higher survival rates, and lower auditory thresholds compared with untreated controls. These positive results suggest the autoimmune mouse may be useful for studies of steroid-responsive mechanisms of the cochlea in autoimmune sensorineural hearing loss, as well as any hearing disorder in which steroid therapy is currently used.