Publications by authors named "Brozoski T"

Tinnitus impacts between 10-20% of the population. Individuals most troubled by their tinnitus have their attention bound to and are distracted by, their tinnitus percept. While numerous treatments to ameliorate tinnitus have been tried, no therapeutic approach has been clinically accepted.

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Objective: To examine how 1Hz and 10Hz rTMS temporarily influence ratings of tinnitus loudness, annoyance, and awareness. The thalamocortical dysrhythmia (TCD) model of tinnitus was tested by examining changes in spectral power and coherence of resting state EEGs from baseline to each phase of treatment and correlating these data with change in tinnitus.

Methods: Nineteen participants completed a double-blind, placebo (sham rTMS) controlled, within-subjects study with crossover between the two active rTMS treatment conditions.

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Animal models have significantly contributed to understanding the pathophysiology of chronic subjective tinnitus. They are useful because they control etiology, which in humans is heterogeneous; employ random group assignment; and often use methods not permissible in human studies. Animal models can be broadly categorized as either operant or reflexive, based on methodology.

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Attention may be an important factor in tinnitus. Individuals most disturbed by their tinnitus differ from those who are not in terms of attention allocation. This study used an operant-conditioning animal model to examine the interaction between tinnitus and auditory vigilant attention as well as auditory selective attention.

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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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Article Synopsis
  • SUDEP (sudden unexpected death in epilepsy) is a significant risk for epilepsy patients, often linked to generalized seizures and respiratory failure before death.
  • In a study using DBA/1 mice, researchers examined brain changes during seizure-induced respiratory arrest (S-IRA) through manganese-enhanced MRI, finding increased activity in specific brain structures associated with auditory, sensorimotor-limbic, and respiratory networks.
  • The findings reveal that while some brain regions activated compensatory responses to apnea during S-IRA, they were insufficient to prevent death, mirroring observations in human SUDEP cases.
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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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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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Purpose: Hyperacusis can be extremely debilitating, and at present, there is no cure. In this detailed review of the field, we consolidate present knowledge in the hope of facilitating future research.

Method: We review and reference the literature on hyperacusis and related areas.

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Introduction: Sensorineural hearing loss (HL) is becoming a global phenomenon at an alarming rate. Nearly 600 million people have been estimated to have significant HL in at least one ear. There are several different causes of sensorineural HL included in this review of new investigational drugs for HL.

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Tinnitus is an auditory percept without an environmental acoustic correlate. Contemporary tinnitus models hypothesize tinnitus to be a consequence of maladaptive plasticity-induced disturbance of excitation-inhibition homeostasis, possibly convergent on medial geniculate body (MGB, auditory thalamus) and related neuronal networks. The MGB is an obligate acoustic relay in a unique position to gate auditory signals to higher-order auditory and limbic centres.

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Purpose: Hyperacusis can be extremely debilitating, and at present, there is no cure. We provide an overview of the field, and possible related areas, in the hope of facilitating future research.

Method: We review and reference literature on hyperacusis and related areas.

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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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Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central auditory system. Sensory thalamic structures show high levels of non-desensitizing extrasynaptic GABAA receptors (GABAARs) and a reduction in the redundancy of coded information. The present study compared the inhibitory potency of GABA acting at GABAARs between the inferior colliculus (IC) and the medial geniculate body (MGB) using quantitative in vivo, in vitro, and ex vivo experimental approaches.

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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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The auditory brainstem response (ABR) is an acoustically evoked potential commonly used to determine hearing sensitivity in laboratory animals. Both isoflurane and ketamine/xylazine anesthesia are commonly used to immobilize animals during ABR procedures. Hearing threshold determination is often the primary interest.

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Tinnitus perception depends on the presence of its neural correlates within the auditory neuraxis and associated structures. Targeting specific circuits and receptors within the central nervous system in an effort to relieve the perception of tinnitus and its impact on one's emotional and mental state has become a focus of tinnitus research. One approach is to upregulate endogenous inhibitory neurotransmitter levels (e.

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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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Tinnitus is a phantom auditory sensation experienced by up to 14% of the United States population with a smaller percentage experiencing decreased quality of life. A compelling hypothesis is that tinnitus results from a maladaptive plastic net down-regulation of inhibitory amino acid neurotransmission in the central auditory pathway. This loss of inhibition may be a compensatory response to loss of afferent input such as that caused by acoustic insult and/or age-related hearing loss, the most common causes of tinnitus in people.

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Recent studies suggested that acute sound exposure resulting in a temporary threshold shift in young adult animals within a series of maladaptive plasticity changes in central auditory structures. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is involved in post-trauma peripheral hair cell and spiral ganglion cell survival and has been shown to modulate synaptic strength in cochlear nucleus following sound exposure. The present study evaluated levels of BDNF and its receptor (tyrosine kinase B, [TrkB]) in the dorsal cochlear nucleus (DCN) following a unilateral moderate sound exposure in young (7-8 months) and aged (28-29 months) Fischer Brown Norway (FBN) rats.

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