Publications by authors named "Carol Bauer"

The search for an effective medication that will eliminate tinnitus has a long history. Currently, no drugs exist that universally cure tinnitus. Pharmacologic interventions that have been investigated can be divided into those that attempt to eliminate the perception of tinnitus, and those that are designed to treat the negative comorbidities associated with tinnitus, thereby mitigating tinnitus' negative impact on quality of life.

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Objectives: The goal of this study was to compare treatment outcomes for chronic bothersome tinnitus after Tinnitus Retraining Therapy (TRT) versus standard of care treatment (SC) and to determine the longevity of the effect over an 18-month period.

Study Design: A randomized controlled trial comparing TRT to SC for chronic tinnitus.

Methods: Adults with subjective, stable, bothersome chronic tinnitus associated with hearing loss amenable to aural rehabilitation with hearing aids were recruited.

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Animal model research has shown that the central features of tinnitus, the perception of sound without an acoustic correlate, include elevated spontaneous and stimulus-driven activity, enhanced burst-mode firing, decreased variance of inter-spike intervals, and distortion of tonotopic frequency representation. Less well documented are cell-specific correlates of tinnitus. Unipolar brush cell (UBC) alterations in animals with psychophysical evidence of tinnitus has recently been reported.

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Neuroscience of Tinnitus.

Neuroimaging Clin N Am

May 2016

Tinnitus is a consequence of changes in auditory and nonauditory neural networks following damage to the cochlea. Homeostatic compensatory mechanisms occur after hearing loss and these mechanisms alter the balance of excitatory and inhibitory neurotransmitters. In many individuals with hearing loss, chronic tinnitus and related phenomena emerge.

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Presented is a thematic review of animal tinnitus models from a functional perspective. Chronic tinnitus is a persistent subjective sound sensation, emergent typically after hearing loss. Although the sensation is experientially simple, it appears to have central a nervous system substrate of unexpected complexity that includes areas outside of those classically defined as auditory.

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The Tinnitus Research Consortium funded three clinical trials investigating treatments for chronic bothersome tinnitus at Southern Illinois University School of Medicine. The trials were designed to measure the subjective changes in tinnitus distress using standardized questionnaires and objective changes in tinnitus loudness using psychophysical matching procedures. The results of the first two trials have been published and are summarized here.

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The American Academy of Otolaryngology--Head and Neck Surgery Foundation (AAO-HNSF) has published a supplement to this issue featuring the new Clinical Practice Guideline: Tinnitus. To assist in implementing the guideline recommendations, this article summarizes the rationale, purpose, and key action statements. The 13 recommendations developed address the evaluation of patients with tinnitus, including selection and timing of diagnostic testing and specialty referral to identify potential underlying treatable pathology.

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Objective: Tinnitus is the perception of sound without an external source. More than 50 million people in the United States have reported experiencing tinnitus, resulting in an estimated prevalence of 10% to 15% in adults. Despite the high prevalence of tinnitus and its potential significant effect on quality of life, there are no evidence-based, multidisciplinary clinical practice guidelines to assist clinicians with management.

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Manganese enhanced magnetic resonance imaging (MEMRI) is a method used primarily in basic science experiments to advance the understanding of information processing in central nervous system pathways. With this mechanistic approach, manganese (Mn(2+)) acts as a calcium surrogate, whereby voltage-gated calcium channels allow for activity driven entry of Mn(2+) into neurons. The detection and quantification of neuronal activity via Mn(2+) accumulation is facilitated by "hemodynamic-independent contrast" using high resolution MRI scans.

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Article Synopsis
  • Chronic tinnitus currently lacks effective treatments, but identifying specific markers could help develop therapeutics, with recent studies suggesting glutamatergic blockade in the cerebellar paraflocculus may reduce symptoms.
  • In an experiment, the NMDA antagonist D-AP5 was infused into rats with noise-induced tinnitus, resulting in significant reduction of tinnitus symptoms within three days and lasting effects observed for 23 days post-treatment.
  • Neural activity assessments showed that D-AP5 treatment led to decreased activity in regions associated with tinnitus, indicating that NMDA-mediated glutamatergic transmission in the paraflocculus is crucial for chronic tinnitus in this rat model.
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Unipolar brush cells (UBCs) are excitatory interneurons found in the dorsal cochlear nucleus (DCN) and the granule cell layer of cerebellar cortex, being particularly evident in the paraflocculus (PFL) and flocculus (FL). UBCs receive glutamatergic inputs and make glutamatergic synapses with granule cells and other UBCs. It has been hypothesized that UBCs comprise local networks of tunable feed-forward amplifiers.

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The role of the cerebellum in auditory processing is largely unknown. Recently it was shown that rats with psychophysical evidence of tinnitus had significantly elevated neural activity in the paraflocculus of the cerebellum (PFL), as indicated by functional imaging. It was further shown that PFL activity was not elevated in normal rats listening to a tinnitus-like sound.

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Chronic tinnitus is a common condition with a high burden of disease. While many different treatments are used in clinical practice, the evidence for the efficacy of these treatments is low and the variance of treatment response between individuals is high. This is most likely due to the great heterogeneity of tinnitus with respect to clinical features as well as underlying pathophysiological mechanisms.

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Damage to the auditory system following high-level sound exposure reduces afferent input. Homeostatic mechanisms appear to compensate for the loss. Overcompensation may produce the sensation of sound without an objective physical correlate, i.

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Article Synopsis
  • Research on chronic tinnitus suggests it may stem from compensatory processes in the brain due to lost sound input, particularly involving elevated neural activity in the dorsal cochlear nucleus (DCN).
  • While previous studies showed that damaging the DCN didn't reduce tinnitus in established cases, this research found that preemptive lesions to the DCN could prevent tinnitus from developing after noise exposure.
  • The study proposes that the DCN acts as a trigger for tinnitus rather than its long-term cause, with changes in neural circuits potentially leading to ongoing abnormal activity that signals chronic tinnitus.
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Objectives: Subjective tinnitus is the sensation of hearing a sound in the absence of an external stimulus. Although an estimated 30 million Americans experience chronic tinnitus, only a small percentage are significantly bothered by the sensation. However, this population is currently in need of effective therapy that reduces the impact of tinnitus.

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Loss of central inhibition has been hypothesized to underpin tinnitus and impact auditory acuity. Taurine, a partial agonist at inhibitory glycine and γ-amino butyric acid receptors, was added to the daily diet of rats to examine its effects on chronic tinnitus and normal auditory discrimination. Eight rats were unilaterally exposed once to a loud sound to induce tinnitus.

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Objective: Atrial natriuretic peptide (ANP) is a key regulator in the homeostasis of water excretion and has emerged as an important prognostic marker for symptomatic chronic heart failure (CHF). The stability of ANP represents a crucial factor in assessing its use as a cardiac biomarker. Accordingly, we assessed the stability of ANP in blood samples collected from healthy controls and CHF subjects for a 12 month period.

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A longstanding hypothesis is that tinnitus, the perception of sound without an external acoustic source, is triggered by a distinctive pattern of cochlear hair cell (HC) damage and that this subsequently leads to altered neural activity in the central auditory pathway. This hypothesis was tested by assessing behavioral evidence of tinnitus and spontaneous neural activity in the inferior colliculus (IC) after unilateral cochlear trauma. Chinchillas were assigned to four cochlear treatment groups.

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Gabapentin.

Prog Brain Res

January 2008

Several lines of evidence suggest that loss of central inhibition after deprivation of input from the ear (peripheral deafferentation) may be one cause of chronic tinnitus. Aging and acoustic trauma, the two most common causes of peripheral damage to the auditory system, each decrease input to central auditory structures. Loss of input to tonic inhibitory systems would release excitatory structures from inhibitory regulation.

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Acoustic trauma not only produces temporary and permanent hearing loss but is a common cause of chronic tinnitus. Recent work indicated a possible role for the transient receptor potential channel vanilloid subfamily type 1 (TRPV1) in modulating the effects of cochlear injury. In our research, we investigated the effects of acoustic damage on TRPV1 expression in spiral ganglion neurons of adult rats.

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Chronic tinnitus affects millions of people, but the mechanisms responsible for the development of this abnormal sensory state remain poorly understood. This study examined the type and extent of cochlear damage that occurs after acoustic trauma sufficient to induce chronic tinnitus in rats. Tinnitus was evaluated by using a conditioned suppression method of behavioral testing.

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The pathophysiology of tinnitus, the perception of sound in the absence of acoustic stimulation, is largely unknown, although several lines of research implicate long-term neuroplastic loss of inhibition. The evidence to date suggests that the neuroplastic alterations are likely to be found in multiple brain structures. The present study used manganese-enhanced magnetic resonance imaging (MEMRI) to assess the pattern of neural activity in the central auditory pathway of rats with psychophysical evidence of chronic acoustic-exposure-induced tinnitus.

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