Extret del text: Fins ara s'havia dit que la cóclea no tenia mecanisme o sistema del dolor però ara s'ha vist que les fibres tipus dos, les que conecten amb les cel.lules ciliades externes, són els responsables del dolor de la hiperacúsia. A nivel personal puc dir que quan un soroll supera la meva tolerància provoca un dolor elèctric primer, seguit d'una cremor al cap d'una estona i durant uns dies i seguit d'un dolor (com si fos un blau) durant els dies i setmanese següents de la cremor.
El text està dividit en tres parts (A, B i C). La part C explica el desenvolupament i la optimització de la teràpia que passa per realitzar teràpia sonora, TRT (teràpia de reeentreament del tinnitus), de l'eficàcia de pendre determinats medicaments..
El text també comenta això en refererncia a l'eficàcia de les teràpies sonores: "Formby va dir que calen més assajos controlats aleatoris (ACA) per avaluar l'eficàcia de tractaments acústics per a la hiperacusia. Formby (en premsa, 2015) va informar clinicament de l'expansió significativa del rang dinàmic auditiv i d'una major tolerància de so entre les persones amb discapacitat auditiva amb hiperacusia lleu en un assaig clínic aleatoritzat, controlat amb placebo d'un protocol implementat amb l'assessorament i de baix nivell de so de banda ampla generadors"
PART A:
Here is a summary of "Path A: Identification of Hyperacusis Mechanisms," discussed at the Hyperacusis Research event at ARO.
Materials were compiled by Fan-Gang Zeng, Professor of Otolaryngology, Anatomy & Neurobiology at the University of California, Irvine; Sarah Hayes, Neuroscience PhD candidate at SUNY Buffalo; and Jennifer Melcher, Associate Professor of Otology and Laryngology at Harvard Medical School and the Director of the MEEI Tinnitus Center.
A brief background of what we know:
• Hyperacusis definitions vary widely in published literature. Two examples are "abnormally strong response to moderate sound" and "abnormal reactions to sound, including excessive loudness, annoyance, fear and pain."
• How is hyperacusis identified in people? By means of questionnaires, case histories, Loudness Discomfort Levels (LDL’s), and Loudness Growth Functions. For LDL’s, some classify hyperacusis patients as those with LDL’s below 90dB, while others use 70 dB. Severe hyperacusis is defined by some at 60 dB or below.
• How is hyperacusis identified in animals (for animal models)? By using the Acoustic Startle Reflex, Reaction Time and Two-alternative Forced Choice.
• Epidemiological studies in the general population are insufficient.
The future of essential research work includes:
• Better sub-typing of hyperacusis patients (perhaps building from the four identified subcategories: loudness, annoyance, fear and pain).
• Better standards for LDL testing along with categorization of hyperacusis severity and objective tests such as startle reflex.
• Improved animal models addressing pain and other components of hyperacusis, along with the use of animal-model metrics that can also be used in humans (such as reaction time).
• Epidemiological studies to determine the prevalance of hyperacusis in the general population.
The photos show Fan-Gang Zeng and Sarah Hayes presenting, as well as the audience at our event.
PART B
One key topic for our Hyperacusis Research discussion at the ARO Ear Research conference was "Path B: Elucidation of Hyperacusis Mechanisms." Six researchers participated in a deep discussion of the possible mechanisms underlying hyperacusis.
The researchers were:
• Charlie Liberman, Professor of Otology and Laryngology, Harvard Medical School
• Paul Fuchs, Bordley Professor and Director of Research, Otolaryngology–Head and Neck Surgery, Johns Hopkins University School of Medicine
• Marlies Knipper, Professor, Hearing Research Centre, Eberhard Karls University Tübingen, Germany
• James Kaltenbach, Staff and Director of Otology Research, Cleveland Clinic
• Amanda Lauer, Assistant Professor, Johns Hopkins University School of Medicine
• Kelly Radziwon, PhD Student, SUNY Buffalo
Charlie Liberman led this topic in an effort to identify changes in cellular and neural populations leading to hyperacusis with pain. While it has been historically accepted that the cochlea (inner ear) does not have a pain sensory mechanism, recent discoveries have proven that there are pain nerve fibers that likely send pain signals to the brain under certain conditions.
Virtually all ear research has been based on the main auditory nerve fibers (known as Type I) that send noise signals to the auditory parts of the brain from the Inner Hair Cells. It has been known for some time there was another type of nerve fibers (known as Type II), which are largely connected to the Outer Hair Cells. Their function has been unknown. Recent work shows that these Type II fibers are sensory mechanisms for pain.
As a basic scientist, Paul Fuchs has been studying these Type II fibers extensively, and recently proved that the fibers can be excited under certain tissue-damaging conditions, such as those that can occur from very loud noise exposures.
These concepts open a whole new dimension of research and lead to many questions in relationship to hyperacusis. How can we validate that these Type II fibers are activated in hyperacusis cases? What would cause the reactivation of these pain fibers at lower noise levels once someone has hyperacusis? What can be done to contain or stop the activation of the pain fibers that play a role in hyperacusis?
To answer these types of questions for Type II pain fibers, good animal models are needed. Amanda Lauer proposed the following for animal model studies: acoustic startle reflex, grooming, grimacing, and changes in home behavior.
Additional topics covered under the Path B mechanism discussion will be covered in an upcoming post.
PART C
• Better sub-typing of hyperacusis patients (perhaps building from the four identified subcategories: loudness, annoyance, fear and pain).
• Better standards for LDL testing along with categorization of hyperacusis severity and objective tests such as startle reflex.
• Improved animal models addressing pain and other components of hyperacusis, along with the use of animal-model metrics that can also be used in humans (such as reaction time).
• Epidemiological studies to determine the prevalance of hyperacusis in the general population.
The photos show Fan-Gang Zeng and Sarah Hayes presenting, as well as the audience at our event.
PART B
One key topic for our Hyperacusis Research discussion at the ARO Ear Research conference was "Path B: Elucidation of Hyperacusis Mechanisms." Six researchers participated in a deep discussion of the possible mechanisms underlying hyperacusis.
The researchers were:
• Charlie Liberman, Professor of Otology and Laryngology, Harvard Medical School
• Paul Fuchs, Bordley Professor and Director of Research, Otolaryngology–Head and Neck Surgery, Johns Hopkins University School of Medicine
• Marlies Knipper, Professor, Hearing Research Centre, Eberhard Karls University Tübingen, Germany
• James Kaltenbach, Staff and Director of Otology Research, Cleveland Clinic
• Amanda Lauer, Assistant Professor, Johns Hopkins University School of Medicine
• Kelly Radziwon, PhD Student, SUNY Buffalo
Charlie Liberman led this topic in an effort to identify changes in cellular and neural populations leading to hyperacusis with pain. While it has been historically accepted that the cochlea (inner ear) does not have a pain sensory mechanism, recent discoveries have proven that there are pain nerve fibers that likely send pain signals to the brain under certain conditions.
Virtually all ear research has been based on the main auditory nerve fibers (known as Type I) that send noise signals to the auditory parts of the brain from the Inner Hair Cells. It has been known for some time there was another type of nerve fibers (known as Type II), which are largely connected to the Outer Hair Cells. Their function has been unknown. Recent work shows that these Type II fibers are sensory mechanisms for pain.
As a basic scientist, Paul Fuchs has been studying these Type II fibers extensively, and recently proved that the fibers can be excited under certain tissue-damaging conditions, such as those that can occur from very loud noise exposures.
These concepts open a whole new dimension of research and lead to many questions in relationship to hyperacusis. How can we validate that these Type II fibers are activated in hyperacusis cases? What would cause the reactivation of these pain fibers at lower noise levels once someone has hyperacusis? What can be done to contain or stop the activation of the pain fibers that play a role in hyperacusis?
To answer these types of questions for Type II pain fibers, good animal models are needed. Amanda Lauer proposed the following for animal model studies: acoustic startle reflex, grooming, grimacing, and changes in home behavior.
Additional topics covered under the Path B mechanism discussion will be covered in an upcoming post.
PART C
We continue our coverage of our Roadmap to a Cure as discussed at the ARO research conference.
Path C: Development & Optimization of Therapy
Four researchers participated in this section by preparing or presenting materials associated with current hyperacusis therapies:
• Craig Formby, Graduate Research Professor, University of Alabama
• Susan Gold, Senior Audiologist (retired), University of Maryland Tinnitus & Hyperacusis Center
• Col. Mickra Hamilton, AuD – Director, Synchronicity Wellness; Individual Mobilization Augmentee (IMA) to the Executive Director, DOD, Hearing Center for Excellence
• Tanisha Hammill, MPH, MA, Hearing Center for Excellence (with support from Erin Sheffer, AuD)
Craig Formby introduced Path C, discussing the Development & Optimization of Therapies for hyperacusis. In his summary, Dr. Formby referenced the following therapies and noted in discussing severe cases of hyperacusis with pain that more research is needed for measuring the effectiveness of each therapy.
1. Counseling / Cognitive Behavioral Therapy – Usually combined with sound therapy.
2. Medications – Limited case studies have shown some benefit for Alprazolam (short-acting anxioltic) (Johnson et al., 1993); Carbamazepine (anti-convulsant/mood stabilizer) (Nields et al., 1999); Fluvoxamine/Fluoxetine (serotonin inhibitors) (Gopal et al., 2000); Citalopram (serotonin inhibitor).
3. Electrical Stimulation – All of this work has been tinnitus-centric, where various forms of Repetitive Transcranial Magnetic Stimulation are explored. This could also be tested for potential value to hyperacusis.
4. Sound Therapies – Included review of the following types:
• Continuous Low-Level Broadband Noise: Implemented with chronic use of bilateral sound generators per desensitization protocol described by Hazell & Sheldrake in 1992.
• Tinnitus Retraining Therapy: Combines Hazell & Sheldrake’s sound-therapy protocol with Jastreboff’s neurophysiological model and counseling principles.
• Desensitization/approximation approach to high-level broadband (pink) noise: Patient is exposed to progressively higher level sounds toward enhancing comfort and tolerance for higher sound levels from Vernon & Press, 1998.
• Hearing aids/combination devices for hearing-impaired hyperacusis patients.
• Loudness suppression: An application of extreme amplitude compression in an ear-worn device; some benefit seen for severely debilitated hyperacusis patients; advocated by Sammeth (2000) as an aid to facilitate TRT-based desensitization therapy.
• Neuromonics: Music-based treatment approach, including counseling, calling for repeated sessions of listening to proprietary stimulation over weeks to months; Davis (2007) reported enhanced LDLs and sound tolerance in tinnitus patients.
• Tailored Sound Therapy: Repeated daily listening sessions (~1-2 hrs, over a period of a few weeks) to a temporally complex, band-limited stimulus have been reported by Norena & Chery-Croze (2007) to improve the sound intolerance of tinnitus patients with hyperacusis.
Formby stated that randomized controlled trials (RCTs) are needed to evaluate efficacies of sound therapies for hyperacusis. Formby (in press, 2015) reported clinically significant expansion of the auditory dynamic range and enhanced sound tolerance among hearing-impaired persons with mild hyperacusis in a randomized, placebo-controlled, clinical trial of a protocol implemented with counseling and low-level broadband sound generators.
Susan Gold added information from her work at the University of Maryland Tinnitus & Hyperacusis Center. A key learning from her work is the clinical intake form, which included some questions on pain and the conditions under which pain persists. For example, does the pain exist only during a noise exposure or does it linger after the noise, and for how long does it linger? Susan Gold’s experience showed that patients who had pain linger until the next day were more severe than those who recovered by the next day and the treatment approach would be more extensive.
Dr. Mickra Hamilton was unable to make the event but sent a brief summary of her work on Taming the Autonomic Nervous System (ANS) as practiced at the Synchronicity Wellness Center. The physiological symptoms of ANS are addressed first, followed by neurofeedback after physiologic stress markers have improved, such as increased heart rate variability coherence. Auditory treatment includes custom communication devices that deliver therapy and also serve as hearing protection. Soundscapes are generally nature based with embedded heart rate variability breath paced tones specifically designed based on audiometric findings. Breath paced tones are based on individual resonant heart rate variability frequencies obtained during the psychophysiologic profile. Custom musician earplugs with multiple filters are also standard.
Pictured: Craig Formby, Mickra Hamilton
Path C: Development & Optimization of Therapy
Four researchers participated in this section by preparing or presenting materials associated with current hyperacusis therapies:
• Craig Formby, Graduate Research Professor, University of Alabama
• Susan Gold, Senior Audiologist (retired), University of Maryland Tinnitus & Hyperacusis Center
• Col. Mickra Hamilton, AuD – Director, Synchronicity Wellness; Individual Mobilization Augmentee (IMA) to the Executive Director, DOD, Hearing Center for Excellence
• Tanisha Hammill, MPH, MA, Hearing Center for Excellence (with support from Erin Sheffer, AuD)
Craig Formby introduced Path C, discussing the Development & Optimization of Therapies for hyperacusis. In his summary, Dr. Formby referenced the following therapies and noted in discussing severe cases of hyperacusis with pain that more research is needed for measuring the effectiveness of each therapy.
1. Counseling / Cognitive Behavioral Therapy – Usually combined with sound therapy.
2. Medications – Limited case studies have shown some benefit for Alprazolam (short-acting anxioltic) (Johnson et al., 1993); Carbamazepine (anti-convulsant/mood stabilizer) (Nields et al., 1999); Fluvoxamine/Fluoxetine (serotonin inhibitors) (Gopal et al., 2000); Citalopram (serotonin inhibitor).
3. Electrical Stimulation – All of this work has been tinnitus-centric, where various forms of Repetitive Transcranial Magnetic Stimulation are explored. This could also be tested for potential value to hyperacusis.
4. Sound Therapies – Included review of the following types:
• Continuous Low-Level Broadband Noise: Implemented with chronic use of bilateral sound generators per desensitization protocol described by Hazell & Sheldrake in 1992.
• Tinnitus Retraining Therapy: Combines Hazell & Sheldrake’s sound-therapy protocol with Jastreboff’s neurophysiological model and counseling principles.
• Desensitization/approximation approach to high-level broadband (pink) noise: Patient is exposed to progressively higher level sounds toward enhancing comfort and tolerance for higher sound levels from Vernon & Press, 1998.
• Hearing aids/combination devices for hearing-impaired hyperacusis patients.
• Loudness suppression: An application of extreme amplitude compression in an ear-worn device; some benefit seen for severely debilitated hyperacusis patients; advocated by Sammeth (2000) as an aid to facilitate TRT-based desensitization therapy.
• Neuromonics: Music-based treatment approach, including counseling, calling for repeated sessions of listening to proprietary stimulation over weeks to months; Davis (2007) reported enhanced LDLs and sound tolerance in tinnitus patients.
• Tailored Sound Therapy: Repeated daily listening sessions (~1-2 hrs, over a period of a few weeks) to a temporally complex, band-limited stimulus have been reported by Norena & Chery-Croze (2007) to improve the sound intolerance of tinnitus patients with hyperacusis.
Formby stated that randomized controlled trials (RCTs) are needed to evaluate efficacies of sound therapies for hyperacusis. Formby (in press, 2015) reported clinically significant expansion of the auditory dynamic range and enhanced sound tolerance among hearing-impaired persons with mild hyperacusis in a randomized, placebo-controlled, clinical trial of a protocol implemented with counseling and low-level broadband sound generators.
Susan Gold added information from her work at the University of Maryland Tinnitus & Hyperacusis Center. A key learning from her work is the clinical intake form, which included some questions on pain and the conditions under which pain persists. For example, does the pain exist only during a noise exposure or does it linger after the noise, and for how long does it linger? Susan Gold’s experience showed that patients who had pain linger until the next day were more severe than those who recovered by the next day and the treatment approach would be more extensive.
Dr. Mickra Hamilton was unable to make the event but sent a brief summary of her work on Taming the Autonomic Nervous System (ANS) as practiced at the Synchronicity Wellness Center. The physiological symptoms of ANS are addressed first, followed by neurofeedback after physiologic stress markers have improved, such as increased heart rate variability coherence. Auditory treatment includes custom communication devices that deliver therapy and also serve as hearing protection. Soundscapes are generally nature based with embedded heart rate variability breath paced tones specifically designed based on audiometric findings. Breath paced tones are based on individual resonant heart rate variability frequencies obtained during the psychophysiologic profile. Custom musician earplugs with multiple filters are also standard.
Pictured: Craig Formby, Mickra Hamilton
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