Synaptic plasticity in depression: Molecular, cellular and functional correlates

Fuente: 

Progress in Neuro-Psychopharmacology and Biological Psychiatry

22 December 2012

• Author: W.N. Marsden^,

• Highclere Court, Woking, Surrey, GU21 2QP, UK

---

Abstract

Synaptic plasticity confers environmental adaptability through modification of the connectivity between neurons and neuronal circuits. 

This is achieved through changes to synapse-associated signaling systems and supported by complementary changes to cellular morphology and metabolism within the tripartite synapse. 

Mounting evidence suggests region-specific changes to synaptic form and function occur as a result of chronic stress and in depression. 

The prefrontal cortex (PFC) and hippocampus represent the best studied regions where functional and structural findings are consistent with a deficit in long-term potentiation (LTP), and neuronal and glial growth at excitatory synapses. 

Correlating these changes may be those to glutamate receptors (AMPARs and NMDARs), growth factor signaling (BDNF-TrkB) and several signal transduction pathways (NOS-NO, cAMP-PKA, Ras-ERK, PI3K-Akt, GSK-3, mTOR and CREB). 

In contrast other brain regions such as the amygdala may feature a somewhat opposite synaptic pathology including reduced inhibitory tone. 

Deficits in synaptic plasticity may further correlate disrupted brain redox and bioenergetics in stress and depression. 

Moreover, at a functional level region-specific changes to synaptic plasticity in depression may relate to maladapted neurocircuitry and parallel reduced cognitive control over negative emotion.

"The Promise of Cell Regeneration"

On October 3, 2011, Bryan Pollard represented Hyperacusis Research at the Summit on Hearing Restoration at the New York Academy of Medicine. 
This Summit was sponsored by the Hearing Health Foundation (formerly Deafness Research Foundation). 
It brought together the leaders in the field of cell regeneration research to discuss what needs to be accomplished for therapy for cell regeneration in the ear to become a reality. 

While this Summit did not relate directly to issues with Hyperacusis, the Hearing Restoration Project is an important effort because hair cell damage is still a possible consideration in the etiology of Hyperacusis. 
Also Hyperacusis Research is working together to sponsor a future research project with the Hearing Health Foundation.

Panel Discussion

The event started out with a panel discussion lead by Dr. Jon Lapook of the CBS Evening News. The members of the panel were: Dr. Sujana Chandrasekhar from New York Otology, Dr. Ed Rubel from the University of Washington, Dr. Stefan Heller from Stanford University and Dr. Andy Groves from Baylor College of Medicine. An interesting perspective from the panel discussion was how much less the NIH funds hearing research compared to cancer and other significant health issues. That was an important insight into possibly why it is even more difficult to get funding for hyperacusis since it represents only a fraction of the population with ear issues. 

Dr. Lopook referenced a recent news story highlighting the growing risk of hearing loss for children. 
There was a good question about why there were not more news stories on hearing challenges. Dr. Lopook described the significant challenge of getting even one deeper story of 5 or 6 minutes into the evening news every few weeks. 
Dr. Chandrasekhar gave a good overview the basic clinical types of cases she works with. She supports efforts with veterans who have hearing damage from the battle field. Dr. Rubel described the historical work that was accomplished to discover that birds and reptiles re-grow hair cells after damage. This gives a great model to study to understand why mammals are different since no mammal can re-grow hair cells after damage. Dr Heller gave a short description of how various types of stem cells can be used as a basis to initiate new hair cell growth.
 Finally Dr. Groves described briefly how hair cells grow. Each of these researchers gave a much more detailed description in their presentation.

How We Hear

The first speaker was Dr. George Gates who is on the board of the Hearing Health Foundation. His presentation gave a good overview of the basic ear function including the inner ear and hair cell function. He described how the outer hair cells (OHC) work from feedback signals to amplify quiet sounds. I asked a follow-up question about what other function the OHC has and he responded by describing that the OHC does provide some function to dampen loud sounds.

Hair Cell Regeneration

Dr. Rubel's presentation gave more details on birds and reptiles amazing hair cell recovery and re-growth from damage. For example, birds re-grow their hair cells in 22 days. His session ended with a question on Tinnitus. Another question related to both Tinnitus and Hyperacusis where a member of the audience referenced work in Germany to use lower level laser treatments to improve the condition of Tinnitus and Hyperacusis patients. No one on the panel was familiar with the work.

Barriers to Hair Cell Regeneration

Dr. Andy Groves presented details on hair cell regeneration that were highly technical. It appears there is a gene (P27) which won't allow hair cells to divide once cells are older. A key element to overcome this issue relates to Notch Signaling where one cell gives signals to the cell next to it which prevent the cell from changing into a different type of cell. Suffice it to say that there are some serious barriers to be overcome.

Stem Cells and Inner Ear Cell Regeneration

Dr. Heller described how stem cells work. He reviewed the 3 types of stem cells which enables various methods to obtain the needed building blocks. He then described how the process works to move from a stem cell to grow a specific type of cell such as a hair cell. This was also very technical and while occasional media stories make this sound like it is ready for prime time for certain diseases there are still huge barriers to overcome.

Conclusion

The key take-away is that while barriers remain large, the team felt overall that a real pathway is possible in the next decade or two. The most important aspect that relates to hyperacusis is that this research work will continue to drive the need for more detailed understanding of every inner ear component down to the molecular level. Every new piece of knowledge gained may further advance possible models relating to hyperacusis as long as we are connected to the work. For example, a key issue with hyperacusis is getting solid evidence for whether or not hyperacusis patients have hair cell damage. Currently all methods to truly establish hair cell damage can only be done on a destroyed cochlea. In a follow-up discussion, Dr. Heller described that recent advances in optical tomography may soon enable this diagnostic tool to be able to view inside a live cochlea. That breakthrough would enable many in the study of the inner ear to gain much needed understanding for modeling the inner ear and help to finally answer the question for damage for hyperacusis patients.
fuente:  http://hyperacusisresearch.org

Exercise-induced hypotension in autonomic disorders

• David A. Low^{a, b},
• Antonio C.L. da Nóbrega^c,
• Christopher J. Mathias^{a, b, ,}

• ^a Autonomic and Neurovascular Medicine Unit, Department of Medicine, Division of Brain Sciences, Faculty of Medicine, Imperial College London at St Mary's Hospital, UK
• ^b Autonomic Unit, National Hospital for Neurology & Neurosurgery, Queen Square/Division of Clinical Neurology, Institute of Neurology, University College London, London, UK
• ^c Department of Physiology and Pharmacology & Post-Graduate Program in Cardiovascular Sciences, Fluminense Federal University, Niterói, RJ, Brazil

 Abstract

The autonomic nervous system closely integrates a range of vital processes, including, cardiovascular function. 

Physical activity, or exercise, requires a range of integrated autonomic and cardiovascular adjustments in order to maintain homeostasis. 

Pathological conditions that result in dysfunction of the autonomic nervous system, such as autonomic failure, can therefore jeopardize the control of blood pressure resulting in hypotension and have serious implications for health. 

Exercise induced hypotension, defined as a ≥ 10 mm Hg fall in systolic blood pressure during exercise, can be a significant symptom/event for autonomic failure, as well as other autonomic disorder, patients, including, Multiple System Atrophy and Spinal Cord Injury, and can reduce physical capacity, orthostatic tolerance, result in falls, complicate management and reduce quality of life. 

The likely mechanisms do not appear to be an altered cardiac output or active muscle vasodilation response to exercise, but rather, a lack of and/or a blunted increase in sympathetic nerve activity during exercise and/or excessive vasodilation in the splanchnic circulation.

The severity of exercise induced hypotension seems to be higher during dynamic relative to static exercise. 

The possible management strategies for exercise induced hypotension include both non-pharmacological, e.g., reducing risk factors, and pharmacological measures, such as sympathomimetics, but studies on other pharmacological agents are limited.

 

fuetne : Autonomic Neuroscience

Volume 171, Issues 1–2, 2 November 2012, Pages 66–78

EPFL and Harvard Seek to Uncover Details Behind Hearing Loss

Monday, October 22nd 2012

What actually causes hearing loss in humans? And what are the best therapeutic approaches to this problem? 

Modern medicine hasn't yet been able to provide doctors with the right answers in many cases, because there has been no way to observe the tissue of the inner ear, without destroying it.

This situation was the starting point for a team of scientists from EPFL's School of Engineering (STI) and Harvard Medical School. They have been presented recently at the Bertarelli Symposium at EPFL, and will also appear in the online and print version of the Journal Of Biomedical Optics. 

Observing without destroying
The team's new optical method is groundbreaking in that it provides extremely clear images of inner ear tissue without any need for fluorescent labeling of the cells with antibiotics, proteins and other fluorescent markers that are usually used to "color" the targeted cells. 

This represents an enormous advantage compared with the traditional microscopic methods considered in recent years, which require fluorochrome markers and are therefore impossible to use in clinical practice.

"The markers irreversibly damage the tissue, which skews the analyses," said Xin Yang, co-author of the article and a doctoral assistant in Demetri Psaltis's Optics Laboratory (LO) at EPFL.

As for Magnetic Resonance Imaging (MRI), its resolution is inadequate for observing deep tissue cells.

"MRIs can't get beyond 40 microns (a micron equals one thousandth of a millimeter) and the cells we're looking at are on the order of two microns," said Yang.

Autofluorescent cells
To overcome the various obstacles in their path, the team takes advantage of the autofluorescence of the cells in the cochlea.

Autofluorescence refers to a phenomenon where certain cells tend to remit light after absorbing it. 

This phenomenon makes it possible to do without external fluorescent markers. 

The principle is simple: a laser is aimed at a specific target, causing the absorption of the photons by the cells' molecules. 

This excites the electrons, and a photon is emitted in return. 

These photons are then analyzed, providing a high quality image.
"To achieve better penetration into the tissue and a higher resolution 3D image, we use a method called two-photon microscopy," said Yang. 

A new method for endoscopic exams?
To test their approach experimentally the team used two populations of mice. 

One of the two groups was exposed to sounds that caused permanent damage to the inner ears, while the second group experienced a normal environment. 

The mice in both groups were then put down and their cochleas were removed. 

The scientists used their laser method and compared the results they obtained from each group.

"Among subjects exposed to the sounds, we observed irregularities in the way the cells were aligned and even some missing cells," said Yang.

Fuente: http://www.healthyhearing.com/

Improvements in Sensorineural Hearing Loss After Cord Blood Transplant in Patients With Mucopolysaccharidosis

Authors

Victor Da Costa, MD; Gwendolyn O’Grady, PhD, MS; Laura Jackson, AuD; David Kaylie, MD, MS; Eileen Raynor, MD

Fuente de la imagen: http://annareula.blogspot.com.ar/2010_12_01_archive.html

ABSTRACT

Objective  To objectively determine changes in sensorineural hearing in children with mucopolysaccharidosis (MPS) by comparing audiological data before and after hematopoietic stem cell transplantation (HSCT).

Design  Retrospective medical chart analysis.
Setting  Tertiary referral hospital.
Patients  Thirty pediatric patients with the diagnosis of MPS who underwent HSCT and had audiological data before and after HSCT. Data were extracted from medical charts for patients seen at our institution from January 1, 1999, to December 1, 2009.

Main Outcomes Measures  Hearing was assessed using behavioral audiometry testing and auditory brainstem responses (ABR) before and after HSCT. Patient demographics, diagnosis, and age at HSCT were also evaluated.

Results  Thirty patients with MPS were included. Four (13%) had MPS type 3a, 2 (7%) had MPS type 2, and 24 (80%) had MPS type 1.

The average age at HSCT was 19 months (range, 5-44 months).

Hearing improvement was evaluated by audiogram (20 patients), ABR (8 patients), and qualitative measures (30 patients).

On average, patients did not show improvement on audiogram (P = .28; paired t test).

The ABR click threshold improved 19 dB on average (P < .001). Qualitatively, 3 patients had normal hearing before and after HSCT. Of the remaining 27 patients, 20 (67%) showed improvement in sensorineural hearing (P < .001).

Five (17%) had hearing loss and did not improve.

Two (7%) had worsening hearing.

Hematopoietic stem cell transplantation at the age of 25 months or younger was significantly correlated with hearing improvement (P = .03).

Conclusions  Hematopoietic stem cell transplantation may provide improvement in MPS-associated sensorineural hearing loss.

Hearing improvement is more likely to occur in patients who undergo transplantation at 25 months or younger.

Fuente:  Arch Otolaryngol Head Neck Surg. 2012;138(11):1071-1076. 
doi:10.1001/jamaoto.2013.597.

Granddaughter's somersault treats cupulolithiasis of the horizontal semicircular canal

Authors

• Dirk Czesnik, MD^, ,
• David Liebetanz, MD

• Department of Clinical Neurophysiology, Medical School Göttingen, Georg-August-University of Göttingen, Robert-Koch-Str. 40, Göttingen, Germany

---

Abstract

We report on a 61-year-old woman with cupulolithiasis of the right horizontal semicircular canal, which is usually difficult to treat. 

The patient reported that several years ago, similar symptoms relieved completely after having performed several somersaults together with her granddaughter. 

This time, repetitive somersaults were again effective to treat her benign paroxysmal positional vertigo. 

Acceleration during a somersault may induce an intracanalicular force strong enough to detach otoconia debris from the cupula.

Rolling may then promote their reentrance into the utricle. This case suggests that repetitive somersaults may be an alternative treatment of cupulolithiasis of the horizontal semicircular canal.

Body rotation (A) and rotation of the horizontal semicircular canal during a somersault (B; lateral view). 
The gray line illustrates the position of horizontal semicircular canal. 
(C) The left picture illustrates how acceleration in the forward-facing direction during the somersault induce an intracanalicular force strong enough to detach otoconia debris from the cupula. 
The right picture demonstrates how ongoing rolling may move loose otoconia debris back into the utricle.

Fuente:

American Journal of Otolaryngology

Volume 34, Issue 1, January–February 2013, Pages 72–74

Progressive hearing loss following acquired cytomegalovirus infection in an immunocompromised child

---

Abstract

We report a rare case of progressive hearing loss after acquired CMV infection in a child with Langerhans cell histiocytosis (LCH).

 A 5-month-old female was diagnosed as having LCH. When she was 14 months old, she received an unrelated donor umbilical cord blood transfusion for the treatment of intractable LCH. 

CMV infection was confirmed after the blood transfusion. 

Because her own umbilical cord had no CMV, the CMV infection was not congenital. 

When she was 7 years old, mixed hearing loss was noted with bilateral otitis media with effusion. 

After that time, the sensorineural hearing loss progressed to bilateral profound hearing loss over 3 years. 

Three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging with gadolinium contrast enhancement revealed a high intensity area in the inner ear that suggested bilateral labyrinthitis. 

  3D-FLAIR MRI after intervenous gadolinium administration. 

A was taken when she was 8 years old, and B was when she was 11 years old. 

The gadolinium enhancement of the internal auditory canal indicated by arrows was stronger in B than in A.

 This case demonstrates the possibility that, under the immunodeficiency, the acquired CMV infection causes progressive sensorineural hearing loss.

 Authors:

• Ken Kato, MD^{a, ,} ,
• Hironao Otake, MD, PhD^a,
• Mitsuhiko Tagaya, MD, PhD^a,
• Yoshiyuki Takahashi, MD, PhD^b,
• Yoshinori Ito, MD, PhD^b,
• Asahito Hama, MD, PhD^b,
• Hideki Muramatsu, MD, PhD^b,
• Seiji Kojima, MD, PhD^b,
• Shinji Naganawa, MD, PhD^c,
• Tsutomu Nakashima, MD, PhD^a

• ^a Department of Otorhinolaryngology, Nagoya University Graduate School of Medicine, 65, Tsurumai-cho, Showa-ku, Nagoya, Japan
• ^b Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan
• ^c Department of Radiology, Nagoya University Graduate School of Medicine, Nagoya, Japan

  

• fuente: American Journal of Otolaryngology.
  Volume 34, Issue 1, January–February 2013, Pages 89–92

tratamiento de urgencia del acúfeno

En el libro "el acúfeno como señal de malestar"
los autores

Miguel A. López González
Bioquímico
Otorrinolaringólogo
Hospital Universitario Virgen del Rocío
Sevilla
Francisco Esteban Ortega
Jefe de Servicio de Otorrinolaringología
Hospital Universitario Virgen del Rocío
Sevilla
Profesor Numerario de Otorrinolaringología
Universidad de Sevilla


nos señalan

Tratamiento de urgencia del acúfeno 

donde aparte de la medicación , resalto que los autores recomiendan terapia cognitiva-conductual,

 Ante cuadros de pacientes que solicitan asistencia de urgencia 
debido al síntoma acúfeno, se puede administrar medicación específica
junto con terapia conductual. 


Dexclorfeniramina

 
Una gragea de 6 mg como dosis inicial, continuando con 2 mg (un
comprimido) cada 8 horas hasta la disminución o desaparición del
acúfeno.
Alternativamente, una ampolla de 5 mg intramuscular, continuando
con 2 mg (un comprimido) cada 8 horas.

Sulpirida 

Un comprimido de 200 mg como dosis inicial, continuando con 50
mg (una cápsula) cada 8 horas hasta la disminución o desaparición
del malestar.
Alternativamente, una ampolla de 100 mg intramuscular,
continuando con 50 mg (una cápsula) cada 8 horas.

Diazepam 

 
Un comprimido de 25 mg como dosis inicial, continuando con 5 mg
(un comprimido) cada 8 horas hasta la disminución o desaparición
del malestar.
Alternativamente, una ampolla de 10 mg intramuscular como dosis
inicial, continuando con 5 mg (un comprimido) cada 8 horas.

Juntamente con la medicación, hay que realizar una terapia cognitiva-conductual que va a ser la que resuelva el caso definitivamente.

 Se investigarán los factores biopsicosociales incidentes para conseguir 
mediante los cambios pertinentes en la actitud o afrontamiento de los 
eventos, por parte del paciente, la superación o aceptación de sus 
circunstancias.  

Publicado por OTIN en 20:32
Fuente: Blog la puerta de la esperanza
 http://otinylucas.blogspot.com.ar/2012/12/tratamiento-de-urgencia-del-acufeno.html 

Recetas de cocina para los acúfenos. Arroz con delicias al tínnitus

Arroz con delicias al tínnitus

Ingredientes:

1. tres vasitos de arroz redondo, calidad extra. 

2. El mejor arroz el redondo, el de toda la vida
3. 6 vasitos de caldo vegetal
4. 1 zanahoria
5. 1 calabacín
6. 6 champiñones
7. jamon serrano en tacos pequeños
8. pimienta molida
9. aceite de oliva
10. sal

paciencia y buen hacer, tiempo 25 minutos, dificultad fácil
esta receta te aporta:

1. MELATONINA
2. ZINC
3. MAGNESIO
4. VITAMINA B3

alimentos excelentes para tratar el acúfeno, antioxidantes de la células ciliadas
Mientras cocinas esta receta, ponte en la casa música ambiental, suave, relajante para tratar tu hiperacusia.

Modo de hacer

En una sartén mediana, ponemos dos cucharaditas de aceite de oliva virgen extra, a fuego bajo.
Mientras tanto pelamos la zanahoria y la partimos muy fina, así como el calabacín también finamente picado, y los champiñones.
Añadimos la zanahoria y la dejamos pochar a fuego bajo-moderado, después de cinco minutos se añade el calabacin, y cuando pase un ratito añades por ultimo el champiñon y salpimentas al gusto.

Retiras en un plato las verduras fritas.

En la misma sarten añades el arroz que previamente habrás lavado en agua fría  lo rehogas en el aceite de las verduras a fuego moderado durante 3 minutos sin dejar de remover, pones el fuego a máxima potencia y añades los 6 vasitos de caldo, cuando empiece a hervir, lo bajas a fuego moderado-suave. El arroz redondo necesita 15 minutos para estar listo, cuando falten 5 minutos para terminar su cocción añades todas las verduras, y mezclas bien con el arroz.  Pasados los 15 minutos, apagas el fuego, y añades los taquitos de jamón (no antes pues se quedarían duros, al final de la receta recuerda), cubres con un paño de tela, mojado levemente con agua y dejas reposar 10 minutos.

Buen provecho

Bebida recomendadacerveza de trigo suave, ligera, afrutada

cava 

Publicado por OTIN en 18:39
Fuente:  http://otinylucas.blogspot.com.ar/2012/12/recetas-de-cocina-para-los-acufenos.html

Nuevas pistas sobre el origen del autismo abre el camino a nuevos tratamientos

Tras identificar una síntesis particular de una determinada proteína, científicos de Canadá pudieron revertir algunos síntomas en ratones. Según los expertos, se abre el camino hacia nuevas terapéuticas, incluso farmacológicas.

La noticia se publicó en Nature y está dando la vuelta al mundo: la evidencia directa de que una alteración en la síntesis de proteínas puede provocar comportamientos autistas en ratones abre una posible vía para identificar nuevas dianas terapéuticas para los síndrome relacionados con el espectro autista.

Los investigadores de la Universidad McGill y la Universidad de Montreal (Canadá) aseguran haber identificado un vínculo crucial entre la síntesis de proteínas y los trastornos del espectro autista, un hallazgo que, a su juicio, puede impulsar el desarrollo nuevas vías terapéuticas.

La regulación de la síntesis de proteínas, también conocida como ARNm, es el proceso por el cual las células fabrican proteínas. Este mecanismo, explican los investigadores, está involucrado en todos los aspectos de la función celular y del organismo. Los investigadores encontraron que la síntesis anormalmente elevada de un grupo de proteínas neuronales, llamadas neuroliginas, causa síntomas similares a los que se diagnostica en los casos de trastornos del espectro autista.

El estudio reveló que las conductas asociadas al autismo pueden ser rectificadas en los ratones adultos con compuestos que inhiben la síntesis de proteína, o con una terapia génica que tenga como diana la neuroliginas.

El equipo estaba investigando, en realidad, el papel de la síntesis de proteínas en la etiología del cáncer, y vieron con sorpresa que mecanismos similares a los que investigan pueden estar asociados en el desarrollo del autismo.

Según explica el profesor Nahum Sonenberg, del Departamento de Bioquímica de McGill, Facultad de Medicina y el Centro de Investigación del Cáncer Goodman, emplearon un modelo de ratón en el que se eliminó un gen clave que controla el inicio de la síntesis de proteínas. "Vimos que se incrementaba la producción de neuroliginas, proteínas importantes en la formación y regulación de las conexiones conocidas como sinapsis entre las células neuronales en el cerebro y esenciales para el mantenimiento del equilibrio en la transmisión de información de una neurona a otra".

El trabajo, subrayan, es el primero en relacionar la traducción de control de neuroliginas con la alteración de la función sináptica y los comportamientos similares al autismo en ratones.

Neurodesarrollo
Los trastornos del espectro autista abarcan una amplia gama de enfermedades del neurodesarrollo que afectan a tres áreas de comportamiento: interacción social, comunicación y comportamientos e intereses restringidos, repetitivos y estereotipados.
Se calcula que entre 4 y 20 de cada 10.000 niños de la población general padecen un trastorno del espectro autista. Generalmente es cuatro a cinco veces más frecuente en niños que en niñas, y no se asocia con ningún grupo socioeconómico. Generalmente se detecta en los primeros 2 o 3 años de la vida del niño.

Fuente: Nature

Nuevos avances sobre el tinnitus

Las investigaciones acerca del tinnitus o acúfenos han proporcionado importantes hallazgos durante el último año sobre el tinnitus.

Se ha descubierto que el riesgo de padecer tinnitus o acúfenos es mayor bajo estrés. 
Otro estudio demuestra que el tinnitus lo produce el propio cerebro para compensar la existencia de una pérdida de audición. 
En cuanto a los tratamientos, la terapia que se basa en la aceptación y la conciencia plena ayuda al paciente a convivir con el tinnitus. 
Se ha demostrado también que la terapia a través de internet es prácticamente igual de efectiva que las terapias de grupo presenciales. 
Asimismo, la terapia de reinicio acústico coordinado ayuda a reducir la intensidad y las molestias del tinnitus. Por último, un estudio británico pone de manifiesto que cuatro de cada diez personas encuestadas desconocen lo que es el tinnitus.

La incidencia de tinnitus se duplica bajo estrés

Los expertos creen que existe una relación directa entre el tinnitus y el estrés. La incidencia de los casos de tinnitus se duplica en personas que sufren estrés, según indica un estudio realizado por el Instituto Karolinska en Suecia.

“Descubrimos que el tinnitus afectaba 2,5 veces más a personas que estaban en situaciones de estrés prolongadas”, explica el Profesor Barbera Canlon, investigador jefe del estudio.

Más que un problema de audición

Los investigadores han descubierto que el cerebro es el responsable del pitido de oídos que produce el tinnitus, como estrategia para compensar la existencia de una pérdida de audición.
Según el estudio realizado en el Centro Médico de la Universidad de Georgetown, en Estados Unidos, el tinnitus no se produce solo por un efecto oclusivo o daño en el oído, sino que es el resultado fallido del propio cerebro por recuperarse.

Elegir la terapia apropiada

Según una tesis doctoral en psicología presentada en Suecia, la terapia basada en la aceptación y la conciencia plena puede servir para aprender a convivir con el tinnitus. Esta técnica busca generar una nueva actitud hacia el tinnitus, para evitar que los síntomas consuman la vida del paciente. Este método se denomina Terapia de Aceptación y Compromiso.

Terapia a través de internet

Investigadores de la Universidad Johannes Gutenberg en Alemania y de la Universidad de Linköping en Suecia trataron a un grupo de pacientes con tinnitus de moderado a severo con distintos tipos de terapias, durante un periodo de diez semanas. Los resultados del estudio ponen de manifiesto que la terapia a través de internet es igual de efectiva que la terapia de grupo presencial.
Al comparar los resultados con el grupo de control, cuyos sujetos solo participaron en un foro online, se observó que los pacientes que siguieron la terapia a través de internet o participaron en la terapia de grupo podían controlar mejor los síntomas del molesto sonido del tinnitus que perciben en sus oídos.

Terapia de reinicio acústico coordinado

Un ensayo clínico ha demostrado que una terapia denominada neuromodulación de reinicio acústico coordinado (Acoustic Coordinated Reset, en inglés), reduce la intensidad y el malestar que produce el tinnitus en siete de cada diez pacientes. Este estudio comparaba los resultados de la terapia de reinicio acústico coordinado con un tratamiento placebo de control en 63 pacientes con tinnitus de larga duración.

En el ensayo clínico, los pacientes tenían que llevar unos auriculares especiales durante varias horas al día. Los auriculares emitían una serie de tonos ajustados de acuerdo a la frecuencia característica del tinnitus del paciente. De esa forma, se pretendía interrumpir los patrones rítmicos del ruido del tinnitus que producen las células del nervio auditivo del cerebro.

Cuatro de cada diez desconocen lo que es el tinnitus

Por último, un estudio realizado por la organización británica de discapacitados auditivos “Action on Hearing loss” (Acción ante la Pérdida de Audición), revela que el 39% de los encuestados desconocían lo que era el tinnitus o acúfenos, y el 22% pensaba incluso que consistía en tener alergia al metal.
Para mas informacion sigua estos links
El tinnitus afecta hasta 2.5 veces mas a personas con estres
Tinnitus: Mas que una problema de audicion
Hacer frente al tinnitus depende de la terapia adecuada
La terapia para el tinnitus a traves de internet resulta util
La terapiad de reinicio acustico coordinado (ACR) ayuda a reducir los sintomas del tinnitus
Cuatro de cada diez desconocen lo que es el tinnitus

Fuente:  http://www.spanish.hear-it.org/Nuevos-avances-sobre-el-tinnitus
Julio de 2012

The Worst Noises in the World: Why We Recoil at Unpleasant Sounds

ScienceDaily (Oct. 12, 2012) — Heightened activity between the emotional and auditory parts of the brain explains why the sound of chalk on a blackboard or a knife on a bottle is so unpleasant.

 ScienceDaily (12 de octubre de 2012) - Una mayor actividad entre las partes emocionales y auditivas del cerebro explica por qué el sonido de la tiza en una pizarra o un cuchillo en una botella es tan desagradable.

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In a study published today in the Journal of Neuroscience and funded by the Wellcome Trust, Newcastle University scientists reveal the interaction between the region of the brain that processes sound, the auditory cortex, and the amygdala, which is active in the processing of negative emotions when we hear unpleasant sounds.

Brain imaging has shown that when we hear an unpleasant noise the amygdala modulates the response of the auditory cortex heightening activity and provoking our negative reaction.

"It appears there is something very primitive kicking in," says Dr Sukhbinder Kumar, the paper's author from Newcastle University. "It's a possible distress signal from the amygdala to the auditory cortex."

Researchers at the Wellcome Trust Centre for Neuroimaging at UCL and Newcastle University used functional magnetic resonance imaging (fMRI) to examine how the brains of 13 volunteers responded to a range of sounds. 

Listening to the noises inside the scanner they rated them from the most unpleasant -- the sound of knife on a bottle -- to pleasing -- bubbling water. 

Researchers were then able to study the brain response to each type of sound.

Researchers found that the activity of the amygdala and the auditory cortex varied in direct relation to the ratings of perceived unpleasantness given by the subjects. 

The emotional part of the brain, the amygdala, in effect takes charge and modulates the activity of the auditory part of the brain so that our perception of a highly unpleasant sound, such as a knife on a bottle, is heightened as compared to a soothing sound, such as bubbling water.

Analysis of the acoustic features of the sounds found that anything in the frequency range of around 2,000 to 5,000 Hz was found to be unpleasant. 

Dr Kumar explains: "This is the frequency range where our ears are most sensitive. 

Although there's still much debate as to why our ears are most sensitive in this range, it does include sounds of screams which we find intrinsically unpleasant."

Scientifically, a better understanding of the brain's reaction to noise could help our understanding of medical conditions where people have a decreased sound tolerance such as hyperacusis, misophonia (literally a "hatred of sound") and autism when there is sensitivity to noise.
Professor Tim Griffiths from Newcastle University, who led the study, says: "This work sheds new light on the interaction of the amygdala and the auditory cortex. 

This might be a new inroad into emotional disorders and disorders like tinnitus and migraine in which there seems to be heightened perception of the unpleasant aspects of sounds."

Most Unpleasant Sounds

Rating 74 sounds, people found the most unpleasant noises to be:

1. Knife on a bottle
2. Fork on a glass
3. Chalk on a blackboard
4. Ruler on a bottle
5. Nails on a blackboard
6. Female scream
7. Anglegrinder
8. Brakes on a cycle squealing
9. Baby crying
10. Electric drill

Least Unpleasant Sounds

• Applause
• Baby laughing
• Thunder
• Water flowing

 
Fuente:  
http://www.sciencedaily.com

Medical Devices Powered by the Ear Itself

ScienceDaily (Nov. 8, 2012) — 
For the first time, researchers power an implantable electronic device using an electrical potential -- a natural battery -- deep in the inner ear.

Por primera vez, los investigadores alimentan un dispositivo implantable electrónico utilizando un potencial eléctrico - una batería natural - profunda  del propio oído interno.

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The chip is small enough to fit in the cavity of the middle ear. (Credit: Patrick P. Mercier)

Deep in the inner ear of mammals is a natural battery -- a chamber filled with ions that produces an electrical potential to drive neural signals. 
In a recent issue of the journal Nature Biotechnology, a team of researchers from MIT, the Massachusetts Eye and Ear Infirmary (MEEI) and the Harvard-MIT Division of Health Sciences and Technology (HST) demonstrate for the first time that this battery could power implantable electronic devices without impairing hearing.
The devices could monitor biological activity in the ears of people with hearing or balance impairments, or responses to therapies.

Eventually, they might even deliver therapies themselves.
In experiments, Konstantina Stankovic, an otologic surgeon at MEEI, and HST graduate student Andrew Lysaght implanted electrodes in the biological batteries in guinea pigs' ears. 

Attached to the electrodes were low-power electronic devices developed by MIT's Microsystems Technology Laboratories (MTL). 

After the implantation, the guinea pigs responded normally to hearing tests, and the devices were able to wirelessly transmit data about the chemical conditions of the ear to an external receiver.

"In the past, people have thought that the space where the high potential is located is inaccessible for implantable devices, because potentially it's very dangerous if you encroach on it," Stankovic says.

 "We have known for 60 years that this battery exists and that it's really important for normal hearing, but nobody has attempted to use this battery to power useful electronics."

The ear converts a mechanical force -- the vibration of the eardrum -- into an electrochemical signal that can be processed by the brain; the biological battery is the source of that signal's current. 

Located in the part of the ear called the cochlea, the battery chamber is divided by a membrane, some of whose cells are specialized to pump ions. 

An imbalance of potassium and sodium ions on opposite sides of the membrane, together with the particular arrangement of the pumps, creates an electrical voltage.

Although the voltage is the highest in the body (outside of individual cells, at least), it's still very low. 

Moreover, in order not to disrupt hearing, a device powered by the biological battery can harvest only a small fraction of its power.

Low-power chips, however, are precisely the area of expertise of Anantha Chandrakasan's group at MTL.
The MTL researchers -- Chandrakasan, who heads MIT's Department of Electrical Engineering and Computer Science; his former graduate student Patrick Mercier, who's now an assistant professor at the University of California at San Diego; and Saurav Bandyopadhyay, a graduate student in Chandrakasan's group -- equipped their chip with an ultralow-power radio transmitter: After all, an implantable medical monitor wouldn't be much use if there were no way to retrieve its measurements.

But while the radio is much more efficient than those found in cellphones, it still couldn't run directly on the biological battery. 

So the MTL chip also includes power-conversion circuitry -- like that in the boxy converters at the ends of many electronic devices' power cables -- that gradually builds up charge in a capacitor. 

The voltage of the biological battery fluctuates, but it would take the control circuit somewhere between 40 seconds and four minutes to amass enough charge to power the radio. 

The frequency of the signal was thus itself an indication of the electrochemical properties of the inner ear.


To reduce its power consumption, the control circuit had to be drastically simplified, but like the radio, it still required a higher voltage than the biological battery could provide. 

Once the control circuit was up and running, it could drive itself; the problem was getting it up and running.


The MTL researchers solve that problem with a one-time burst of radio waves. "In the very beginning, we need to kick-start it," Chandrakasan says. "Once we do that, we can be self-sustaining. The control runs off the output."

Stankovic, who still maintains an affiliation with HST, and Lysaght implanted electrodes attached to the MTL chip on both sides of the membrane in the biological battery of each guinea pig's ear. 

In the experiments, the chip itself remained outside the guinea pig's body, but it's small enough to nestle in the cavity of the middle ear.
Cliff Megerian, chairman of the otolaryngology department at Case Western Reserve University, says that he sees three possible applications of the researchers' work: in cochlear implants, diagnostics and implantable hearing aids. 

"The fact that you can generate the power for a low voltage from the cochlea itself raises the possibility of using that as a power source to drive a cochlear implant," Megerian says. 

"Imagine if we were able to measure that voltage in various disease states. 

There would potentially be a diagnostic algorithm for aberrations in that electrical output."
"I'm not ready to say that the present iteration of this technology is ready," Megerian cautions. 

But he adds that, "If we could tap into the natural power source of the cochlea, it could potentially be a driver behind the amplification technology of the future."

The work was funded in part by the Focus Center Research Program, the National Institute on Deafness and Other Communication Disorders, and the Bertarelli Foundation.

Key words: electrical, potential, inner ear, deep,journal Nature Biotechnology,MIT,Konstantina, Stankovic, Andrew, Lysaght,Anantha Chandrakasan, Patrik Mercier, Saurav Bandyopadhyay,Cliff Megerian,Case Western Reserve University,Focus Center Research Program, the National Institute on Deafness and Other Communication Disorders, and the Bertarelli Foundation.

Fuente:  
http://www.sciencedaily.com/releases/2012/11/121108151730.htm

Hearing Health Summit

"The Promise of Cell Regeneration"

On October 3, 2011, Bryan Pollard represented Hyperacusis Research at the Summit on Hearing Restoration at the New York Academy of Medicine. 
This Summit was sponsored by the Hearing Health Foundation (formerly Deafness Research Foundation). It brought together the leaders in the field of cell regeneration research to discuss what needs to be accomplished for therapy for cell regeneration in the ear to become a reality. 
Learn more about Hearing Health Foundation's ground-breaking Hearing Restoration Project. 
While this Summit did not relate directly to issues with Hyperacusis, the Hearing Restoration Project is an important effort because hair cell damage is still a possible consideration in the etiology of Hyperacusis. 
Also Hyperacusis Research is working together to sponsor a future research project with the Hearing Health Foundation.

Panel Discussion

 
















The event started out with a panel discussion lead by Dr. Jon Lapook of the CBS Evening News. 

The members of the panel were: Dr. Sujana Chandrasekhar from New York Otology, Dr. Ed Rubel from the University of Washington, Dr. Stefan Heller from Stanford University and Dr. Andy Groves from Baylor College of Medicine. 

 An interesting perspective from the panel discussion was how much less the NIH funds hearing research compared to cancer and other significant health issues. 

That was an important insight into possibly why it is even more difficult to get funding for hyperacusis since it represents only a fraction of the population with ear issues. 

Dr. Lopook referenced a recent news story highlighting the growing risk of hearing loss for children. There was a good question about why there were not more news stories on hearing challenges. 
Dr. Lopook described the significant challenge of getting even one deeper story of 5 or 6 minutes into the evening news every few weeks.
Dr. Chandrasekhar gave a good overview the basic clinical types of cases she works with. She supports efforts with veterans who have hearing damage from the battle field.

Dr. Rubel described the historical work that was accomplished to discover that birds and reptiles re-grow hair cells after damage. 

This gives a great model to study to understand why mammals are different since no mammal can re-grow hair cells after damage. 

Dr Heller gave a short description of how various types of stem cells can be used as a basis to initiate new hair cell growth. Finally Dr. Groves described briefly how hair cells grow. Each of these researchers gave a much more detailed description in their presentation.

How We Hear

The first speaker was Dr. George Gates who is on the board of the Hearing Health Foundation. His presentation gave a good overview of the basic ear function including the inner ear and hair cell function.

He described how the outer hair cells (OHC) work from feedback signals to amplify quiet sounds. I asked a follow-up question about what other function the OHC has and he responded by describing that the OHC does provide some function to dampen loud sounds.

Hair Cell Regeneration

Dr. Rubel's presentation gave more details on birds and reptiles amazing hair cell recovery and re-growth from damage. 

For example, birds re-grow their hair cells in 22 days. His session ended with a question on Tinnitus. Another question related to both Tinnitus and Hyperacusis where a member of the audience referenced work in Germany to use lower level laser treatments to improve the condition of Tinnitus and Hyperacusis patients. No one on the panel was familiar with the work.

Barriers to Hair Cell Regeneration

Dr. Andy Groves presented details on hair cell regeneration that were highly technical. It appears there is a gene (P27) which won't allow hair cells to divide once cells are older. 

 A key element to overcome this issue relates to Notch Signaling where one cell gives signals to the cell next to it which prevent the cell from changing into a different type of cell. Suffice it to say that there are some serious barriers to be overcome.

Stem Cells and Inner Ear Cell Regeneration

Dr. Heller described how stem cells work. He reviewed the 3 types of stem cells which enables various methods to obtain the needed building blocks. 

He then described how the process works to move from a stem cell to grow a specific type of cell such as a hair cell. 

This was also very technical and while occasional media stories make this sound like it is ready for prime time for certain diseases there are still huge barriers to overcome.

Conclusion

The key take-away is that while barriers remain large, the team felt overall that a real pathway is possible in the next decade or two. 

The most important aspect that relates to hyperacusis is that this research work will continue to drive the need for more detailed understanding of every inner ear component down to the molecular level. 

Every new piece of knowledge gained may further advance possible models relating to hyperacusis as long as we are connected to the work. 

For example, a key issue with hyperacusis is getting solid evidence for whether or not hyperacusis patients have hair cell damage. 

Currently all methods to truly establish hair cell damage can only be done on a destroyed cochlea. In a follow-up discussion, 

Dr. Heller described that recent advances in optical tomography may soon enable this diagnostic tool to be able to view inside a live cochlea. 

That breakthrough would enable many in the study of the inner ear to gain much needed understanding for modeling the inner ear and help to finally answer the question for damage for hyperacusis patients.

fuente: Hyperacusis Research

Product Experiences

There are inexpensive consumer level sound meters such as the Scosche - SPL Meter that can give you the sound dB level of any product. Also, there are now app's to add to a smart phone to enable any phone to provide sound dB levels – although this will tend to be less accurate than a dedicated meter. Click here for an iphone sound meter app. Since consumer level sound meters don't provide a way to test frequency, hearing from the experiences of others is a helpful way to make better choices. Please share your product experiences in the comment section below. Please include sound dB levels if you have measured it or if the manufacturer provides a level based on their tests.


Fuente: http://hyperacusisresearch.org/index.php?option=com_content&view=category&layout=blog&id=13&Itemid=64

Nota, hay un video en youtube de este equipo

 <iframe width="640" height="360" src="http://www.youtube.com/embed/JGAFmAALjJQ" frameborder="0" allowfullscreen></iframe>

 fuente:http://www.youtube.com/watch?v=JGAFmAALjJQ

Hyperacusis Research

The list of possibilities for hyperacusis mechanisms is still quite large. 

To narrow the discussion, we focus primarily on cases induced by acoustic trauma.

It is natural then to start with the middle ear function for possible models. 

The stapedius muscle is responsible for sound attenuation by dampening the vibration of the stapes. 

Since many hyperacusis patients appear to have a normal stapedial reflex test (by current testing methods), there are very few works on the topic. 

In a work on the "Functional Model of the Middle Ear Ossicles," the authors suggest a mechanism of how paralysis of the stapedius muscle, caused by an injury to the facial nerve, results in hyperacusis. 

Further insights might be gained by a deeper analysis and possible advancement of the various acoustic reflex testing methods comparing a hyperacusis population to a control group.

Many possible mechanisms for hyperacusis start in the cochlea. Baguley and Andersson's book references Sahley and Nodar's 2001 article on "A Biochemical Model of Peripheral Tinnitus." 

A summary from their abstract states: "Naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes. 

In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear NMDA receptors. 

This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds. 

It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism." 

They propose this spontaneous activity leads to the perception of tinnitus and that the perceived intensity of sound may increase resulting in hyperacusis. 

This work is an example of where model associations between tinnitus and hyperacusis can be difficult. 

It would be far better to have an analysis of similar causal mechanisms purely in relationship to hyperacusis.

There are a wide range of supporting hyperacusis works describing the connections to the cochlea. 

The case of a musician who had his cochlea destroyed in a mostly deaf ear to relieve his symptoms is interesting as later works suggest such a radical measure may not impact the problem.

Some works suggest an abnormality of outer hair cell (OHC) function. 

In a work entitled "DPOAE in Tinnitus Patients with Cochlear Hearing Loss considering Hyperacusis and Misophonia," the authors promote the model that the OHC's are the most probable place generating tinnitus. 

They find that decreasing of otoemission "DPOAE amplitudes in patients with cochlear hearing loss and tinnitus suggests significant role of OHC pathology, unbalanced by IHC injury in generation of tinnitus in patients with hearing loss of cochlear localization.


DPOAE fine structure provides us the additional information about DPOAE amplitude recorded in two points per octave, spreading the amount of frequencies f2, where differences are noticed in comparison of two groups - tinnitus patients and control.

Function growth rate cannot be the only parameter in estimation of DPOAE in tinnitus patients with cochlear hearing loss, also including subjects with hyperacusis and misophony. 

Hyperacusis has important influence on DPOAE amplitude, increases essentially amplitude of DPOAE in the examined group of tinnitus patients.

" Another work focused on the OHC's impact from 1996 is entitled "Nonlinearity of mechanoelectrical transduction of outer hair cells as the source of nonlinear basilar-membrane motion and loudness recruitment." 

According to the experiment's data and "the feedback concept of outer hair cell action, disruption of the mechanoelectrical transduction of OHC leads to both a reduction of gain and linearizing of the response; that is, to both hearing loss and loudness recruitment.

" Since recruitment and hyperacusis are quite different, this model should not be extented to hyperacusis. 

However, since most OHC works were not primarily focused on hyperacusis, it may be useful to have a dedicated project that can conclusively prove OHC function in typical hyperacusis patients.


Dr. J. A. Vernon at the Oregon Health and Science University provided a basic clinical overview in 2002 entitled "Hyperacusis: Testing, Treatments, and a Possible Mechanism." He describes background information on the topic and the pink noise treatment program he has used for patients. 

He concludes with a brief summary of the model often accepted for the cause: "It appears that the normal function of the olivocochlear bundle, which supplies efferent innervation to the cochlea, is to exert a suppressive or inhibitor effect upon responses to incoming sounds. 

If these efferent nerves are not performing normally it seems somewhat reasonable to propose that all sounds might be perceived as being louder than usual."

One classic work that led to moving beyond the cochlea is a paper from 2000 by Salvi, Wang, and Ding at University of Buffalo entitled: "Auditory plasticity and hyperactivity following cochlear damage." 

In it they describe some of the "functional changes that occur in the central auditory pathway after the cochlea is damaged by acoustic overstimulation or by carboplatin, an ototoxic drug that selectively destroys inner hair cells (IHCs). 

Acoustic trauma typically impairs the sensitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea.

Surprisingly, our results show that restricted cochlear damage enhances neural activity in the central auditory pathway. 

Despite a reduction in the auditory-nerve compound action potential (CAP), the local field potential from the inferior colliculus (IC) increases at a faster than normal rate and its maximum amplitude is enhanced at frequencies below the region of hearing loss. 

To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal cochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF). 

Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition. 

Selective IHC loss reduces the amplitude of the CAP without affecting the threshold and tuning of the remaining auditory nerve fibers. 

Although the output of the cochlea is reduced in proportion to the amount of IHC loss, the IC response shows only a modest amplitude reduction, and remarkably, the response of the auditory cortex is enhanced. 

These results suggest that the gain of the central auditory pathway can be up- or down regulated to compensate for the amount of neural activity from the cochlea." 

Although this work is centered on hearing loss, there are some important details which may relate to hyperacusis. 

 Figure 3 C from their initial experiment where chinchillas were exposed to 105db for 5 days shows the overshoot of the IC amplitude just above the 60dB level which exceeds the pre-exposure levels by a significant amount.


In another experiment where the IHC's only were selectively destroyed resulting in a similar reduction in output of the cochlea (lower CAP), the authors also find an increase in AC amplitude. 

Thus they propose that a mechanism for tinnitus could be "the loss of lateral inhibition that unmasks pre-existing neural circuits within the auditory pathway." 

Additionally they state that since "neural activity is enhanced and that amplitude grows at an abnormally rapid rate following cochlear damage, it seems plausible that recruitment and hyperacusis originate in the central auditory pathway.}

 While the model seems to fit well for recruitment, it does not fit as well for typical hyperacusis patients since they often have normal audiograms and do not have hearing loss in the lower thresholds. 

Additionally, the work is entirely based on a scenario created by hair cell damage (either IHC and OHC or both) which further supports the need to establish if typical hyperacusis patients have hair cell damage.


In their book (latest version from 2008) entitled Tinnitus Retraining Therapy, Dr. Jastreboff and Dr. Hazell devote the second chapter to "The neurophysiological model of tinnitus and decreased sound tolerance.

" Their primary theory is called the "discordant dysfunction (damage) theory." They postulate that "the tinnitus signal originates in the inner ear when one type of sensory cell, OHC, is more dysfunctional than the other type of sensory cells, IHC, at the same area of the basilar membrane in the cochlea. 

When neurons in the dorsal cochlear nuclei receive excitation from IHC but not from the damaged OHC, then an imbalance occurs at this level of the auditory system. 

This, in turn, causes abnormal activity in the form of burst of high-frequency neuronal discharges, which, after amplification within the auditory system are perceived as tinnitus." 

It is interesting to contrast the theory here focused on OHC loss compared to Salvi's work that was more focused on IHC loss. 

On the issue of detectable hearing loss for tinnitus, they state that "20% of patients with tinnitus have normal hearing. 

This is because changes are too small to be detectable on a standard audiogram." 

A key point to note here is that there is a wide frequency range above the normal 8000Hz range of standard audiograms that could be explored to help confirm these possibilities. In moving from the model above on tinnitus to the model associated with hyperacusis, Jastreboff is less detailed. 

The book simply states that "the model predicts that a relatively high percentage of tinnitus patients should exhibit increased sensitivity to external sound, that is decreased sound tolerance. 

This is what one would expect from the increased auditory gain, or the combination of an increased gain and some even minor dysfunction of the inner ear.

" Later it is further explained that in hyperacusis, "the external signal undergoes abnormal enhancement/amplification within the subconscious auditory pathways and only secondarily activates the limbic and autonomic nervous systems.

" The opportunity for further works here is similar to above models: prove the functional capabilities of the OHC's in hyperacusis patients.
In 2003, Formby, Sherlock, and Gold presented a paper focused on proving the central gain control process entitled: "Adaptive plasticity of loudness induced by chronic attenuation and enhancement of the acoustic background."

In it the authors show that "after continuous, 2-week earplugging and low-level noise treatments that listeners become more and less sensitive, respectively, to the loudness of sounds. 

This simple demonstration of adaptive plasticity is consistent with modification of a theoretical gain control process, which is the basis for desensitizing sound therapies used in treating hyperacusis and related sound tolerance problems." 

The specific mechanism of adaptive plasticity is not proposed. While the loudness judgments using the Contour Test of Loudness Perception in the work is helpful, another key component for direct comparison to hyperacusis would have been actual levels and types of pain the participants experienced when exposed back to everyday loud noises. 

More specifically did the participants experience pain for the days following the experiment.

Additional opportunities for research relate to a more detailed assessment of hyperacusis patients' symptoms. 

Most surveys are trying to establish whether or not a person has hyperacusis. 

Baugley has summarized some of these prevalence surveys which show a wide range of results from 8-9% in a Swedish study to 15% in a Polish study. 

He also summarizes the following finding: "Among patients attending tinnitus clinics with a primary complaint of tinnitus the prevalence of hyperacusis is about 40%; and in patients with a primary complaint of hyperacusis the prevalence of tinnitus has been reported as 86%". 

Beyond the issue of lack of standardization in questionnaires (one by Khalfa is presented as a possible standard), the more important detail for researches is a detailed guide of symptoms beyond life impacts. 

For example, with many neuropathies the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) Pain Scale is used. 

Similarly, in hyperacusis it would be helpful to know the level of pain severity, the type of pain such as throbbing, constant, random, the location of pain, the length of pain and timing after excessive noise exposure. 

This may yield possible measurable impacts. These results may add insights to psychological mechanisms and models associated with hyperacusis.

Fuente: http://hyperacusisresearch.org/index.php?option=com_content&view=article&id=16:hearing-protection&catid=5:research&Itemid=71