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 14th 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.
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