martes, 29 de noviembre de 2011

Dr. Cormillot | Acúfenos o tinnitus: el zumbido en los oídos



Fuente: http://comocurarelacufenorapidamente.com/dr-cormillot-acufenos-o-tinnitus-el-zumbido-en-los-oidos/

La foto-terapia Láser

La foto-terapia Láser se muestra como una excelente técnica en el tratamiento de Vértigos, Acúfenos o Tinnitus, hiperacusia, aumento y recuperación de la capacidad auditiva en hipoacusias neurosensoriales, etc...


¿Qué es la Foto-Terapia láser?

La foto-terapia láser es una técnica efectiva para el tratamiento de lesiones músculo-esqueléticas, artritis y otras dolencias en diferentes condiciones, utilizando luz monocromática en la región visible, entre el casi infrarrojo al ultravioleta, del espectro electromagnético y no solo por láseres convencionales, sino también por los nuevos emisores de luz láser LED.

Sorprende que la "bio-estimulación del láser" no siempre ha sido bien comprendida, y habitualmente hasta ahora, solamente admitida para tratamientos superficiales dermatológicos, cosméticos o estéticos.

Sin embargo existen muchas posibilidades de emplear las propiedades de la "bio-estimulación celular" en otras partes y órganos del cuerpo humano y entre muchas de ellas, especificamente también en el tratamiento de diversos trastornos de las estructuras del oído interno o cóclea.

Desde nuestra experiencia, la terapia láser para la estimulación celular del oído interno presenta actualmente los mejores resultados terapéuticos, en pacientes con vértigos, acúfenos o tinnitus, hiperacusia, sordera súbita, hipoacusias neurosensoriales y otros..., con mejorías completas e incluso remisión total en ciertos casos o con mejorías parciales.

La foto-terapia es la técnica de exponer o irradiar a algún órgano o parte del cuerpo, con una luz láser de potencia suficiente, capaz de provocar el esperado y ya conocido efecto foto-biológico a nivel celular.

La regeneración de las funciones celulares, en el caso del oído interno, es un fenómeno que se produce por un efecto foto-biológico que sucede en el metabolismo celular, al exponerlas a una irradiación de luz (energía) tipo láser.

El efecto foto-biológico

Se ha demostrado que celularmente se produce un efecto foto-biológico, cuando las células son irradiadas con la adecuada energía de una fuente de luz Láser.

Las respuestas biológicas de una misma célula son dependientes al tipo de Láser, a su longitud de onda, intensidad media, dosis de fluencia, luz continua o pulsada, etc...

Un elemento de las células, conocido y denominado mitocondria, se ha mostrado como un organelo fundamental para producir el mecanismo fotobiológico y universal de activación celular. Este mecanismo no ocurre, en cambio, en células que no contienen mitocondrias y que realizan su ciclo energético por glucólisis.

¿Qué riesgos tiene el láser?

La garantía y seguridad del tratamiento nos permite asegurar que:

1. El tratamiento es totalmente indoloro, sin molestias.

2. No existen efectos adversos ni contraindicaciones. No hay registrado ningún caso con daños accidentales o irreversibles, en los diez ultimos años. El láser apliacado es médicamente SEGURO y SIN RIESGOS.

3. Hay un alto grado de evoluciones positivas en todos los pacientes tratados. Algunos trastornos crónicos requieren mayor número de dosis (sesiones), aunque no siempre se puede pronosticar un progreso positivo o mejora suficiente en algunos casos.

Algunas evidencias científicasATP


El efecto térmico del láser no explica los fenómenos biológicos de la foto-terapia.
El descubrimiento de la característica "foto-receptora" de la enzima citocromo c oxidasa, puede explicar muchos de los fenómenos de recuperación celular observados con la foto-terapia.

Estudios han demostrado, que no existen efectos adversos con exposiciones de altas dosis de láser. Más aún, los autores han comprobado que se reduce el daño proteínico ante ciertos oxidantes químicos - farmacológicos.

El papel que desempeña la molécula ATP, resulta fundamental en la activación de los mecanismos bioquímicos de regeneración celular.

La regeneración celular es un mecanismo que es activado por la exposición a una luz láser.

La regeneración supone recuperar funciones perdidas o normalizar los procesos del metabolismo celular que estuviesen alterados.

Fuente: Otoclinica-centro Médico de Terapias Auditivas
http://www.otoclinica.es/noticia_ampliada.php?id_noticia=97
Pd. nuestro agradecimiento por su informacion sobre la FotoTerapia Laser al Dr.Dr. Tarsicio Martín, Otorrino de Otoclínica y Director del Centro Otoclínica Granada.

Acúfenos. Manual de Ayuda

Acúfenos. Manual de AYUDA



El tratamiento del acufeno ha sido siempre discutido y generalmente admitido por la clase médica de que tiene pocas posibilidades de solución. La teoría de la aceptación, el “tiene usted que habituarse a ello”, es la tónica general que el paciente suele escuchar cuando va a la mayoría de los centros médicos.

Aunque no existe un tratamiento único, en los últimos años, se han producido importantes cambios en el conocimiento y modo de entender los mecanismos que pueden provocar el acúfeno y en consecuencia se han desarrollado nuevas técnicas para tratar este problema.

En primer lugar hay que desenmascarar al acúfeno. Es decir hay que tratar de identificar cual es la causa u origen del acúfeno para proceder a diseñar la terapia y el modo de su abordaje.

Existen o hay muchas y variadas causas fisiopatológicas que pueden producir la sensación del acúfeno y por ello, es imprescindible una exploración médica y audiológica. Solo así se puede empezar, con un conocimiento del tipo de acúfeno al que nos enfrentamos. Un diagnóstico puede incluir una exploración auditiva para conocer, de una parte, el nivel sonoro del acúfeno, frecuencias principales de perturbación, posibles “puntos gatillo” de modulación, nivel de hiperacusia y otras variables audiométricas y patológicas del oído o de la anatomía muscular del cuello y cabeza. Pero también puede ser necesario, un análisis de los factores de riesgo cardiovasculares o antecedentes personales, detectando enfermedades circulatorias o metabólicas, u otros trastornos hormonales.

Recomendaciones y Pasos a Seguir por el afectado con Acúfenos.

1. No se alarme. Si es la primera vez que acaba de sentir ese sonido de forma espontánea, sin aparente causa, lo primero mantenga la calma. Debe usted saber que el sonido “aberrante” que escucha, es un síntoma y no es una enfermedad. Pero al igual que en otros síntomas es conveniente y necesario consultar con un médico especialista.

2. Solicite cita con su especialista. Si ya acudió al mismo y piensa que no obtuvo una respuesta convincente, solicite una segunda opinión. Aún así, aunque le hubieren indicado que, no hay cura, que no hay solución para su problema, nosotros no estamos de acuerdo. Tiene usted que saber que Si hay tratamientos, hay solución. “Y lo decimos con conocimiento de causa”.

3. No existe un tratamiento único contra los acúfenos que esté validado como universal. Y esto es lógico, porque no todos los acúfenos tienen la misma causa. Cada persona puede padecer acúfenos por diferentes problemas auditivos, por distintos cambios en su metabolismo y/o por diferentes problemas vasculares, por causas diversas de mal-funciones músculo esqueléticas, por alteraciones hormonales, etc..

4. Un diagnóstico oportuno y preciso es siempre necesario. Pero un diagnóstico acertado no es fácil y en todo caso en muchas ocasiones es muy complejo. Tenga paciencia controle su estrés y no se agobie; ese proceder empeorará todavía más el síntoma del acúfeno

5. Según qué tipo de tinnitus o acúfeno se trate, es decir dependiendo de su origen, la terapia elegida puede ser completamente ineficaz o viceversa. Pero no se desanime. A veces una terapia y decisión tan simple como un cambio de dieta y hábito de vida produce el efecto deseado; es decir que la alimentación puede hacer que el acúfeno remita a valores de percepción no molestos o incluso a su remisión total. Créalo es cierto que un tratamiento con cambio de alimentación, produce o equivale a un tratamiento con fármacos.

Pero ¿Cómo decidir cuál es mi terapia?

6. En una Unidad Médica especialista en el tratamiento de Acúfenos, con metodología y dedicación, el abordaje del acúfeno puede y debe ser tratado por un equipo multidisciplinar. La exploración y diagnóstico es lo más importante y en ocasiones, ya lo mencionamos, esto es complejo y requiere la intervención de varios especialistas médicos, audiólogos, psicólogos, etc...

7. Después de la exploración, estudio y valoración del trastorno, se toma la decisión de cuál es la terapia adecuada. No obstante en ocasiones se utiliza el método de prueba y error. (El método se inicia por aquella que se cree puede ser la eficaz; si no resulta así, se prueba con otra). Sin embargo esta metodología, no debe ser seguida indiscriminadamente por las personas afectadas sin un control médico. Y sabemos que ese es el modo de proceder de muchos pacientes, que muestran gran ansiedad por resolver su problema. Prueban y prueban sin control todo aquello que localizan. Este proceder sin control médico no es recomendable, ya que puede ocasionar mayores empeoramientos sin solución posterior.

8. La foto-terapia láser es una técnica que resulta eficaz sólo, en ciertos casos de “tinnitus o acúfenos”, cuando está originado en el oído interno. Son estos los más habituales, cierto, pero hay otras causas en las que se requiere el uso de otras terapias, tales como Neuromodulación, Terapia de Estimulación Acústica (TEA), Terapia Alimentaria/ o Farmacológica, Terapia Transcraneal Magnética, Terapia de Entrenamiento y habituación psicológica (TRT. Tinnitus Retraining Therapy), etc…

9. La terapia de láser actúa biológicamente, con mecanismos propios físico-químicos y sus efectos son equivalentes a los de un fármaco, pero sin crear otros efectos secundarios o adversos.

10. La terapia láser permite garantizar en el 50-55% de todos los casos de acúfenos, una recuperación contrastable por la mejoría del perfil audiológico de la persona tratada. Sin embargo existen otros casos de acúfenos cuya etiología u origen no es solucionable con la técnica de foto-terapia. Y en estos casos hay que utilizar otras técnicas terapéuticas, que también consiguen la remisión total o parcial del acúfeno. Pregunte a su médico cuando esto sea así o explíquenos su caso en una consulta informativa sin coste para usted. Pida una cita con nuestro Equipo Médico en OTOCLINICA, en el número 900 101 651 (llamada gratuita).

En nuestros Centros nos resistimos a tener que admitir el sentimiento general habitual, - “No hay solución, hay que acostumbrarse”. Le recordamos que existen varios otros tratamientos que pueden ser utilizados para encontrar la solución al problema del acúfeno, porque se ha comprobado que “si hay tratamientos, hay una posible solución también para Usted”.

El Equipo Médico
OTOCLINICA


Fuente: Material tomado, con permiso de OTOCLINICA, Centro médico de terapias auditivas, de España.

Pd. Nuestro agradecimiento a Joaquín Prósper, Director Clínico,OTOCLINICA, Centro Médico de Terapias Auditivas.
Príncipe de Vergara, 57, 1C, 28006 Madrid

email: consulta@otoclinica.es
web: www.otoclinica.es
Tel: (+34) 915 648 744

lunes, 28 de noviembre de 2011

Progress in Hair Cell Regeneration

HEARING LOSS – A BRIEF HISTORY


January 2001

As most of our readers probably know, most hearing loss is caused by deterioration of the hair cells in the cochlea.

The hair cells move in response to acoustic energy entering the ear, and stimulate the auditory nerve with information regarding the characteristics of the incoming sound.

Drugs, heredity, or loud noises can damage or destroy the hair cells, resulting in hearing loss.

We have known for some time that some animals (including many birds) can spontaneously regenerate damaged hair cells, but regeneration has never been observed in mammals – until now.

The August 26, 2000 Issue of the British medical Journal Lancet reported successful regeneration of hair cells in a postnatal rat cochlea by introducing a particular gene (Math1) to the cochlea. Researcher Wei-Qiang Gao (Genentech, San Francisco, CA,USA) points out, “It wasn’t just a few hair cells–we had several hundred, so it’s robust production”.

The next step in the investigation is to determine whether similar techniques can regenerate hair cells in mature rats. Success in these experiments would bode well for eventual hair cell regeneration in humans.

Another possibility to replace damaged hair cells is transplantation.

Matthew Holley (University of Bristol, UK) and his colleagues have developed an “ear in a test tube”, in which they have successfully grown mouse hair cells. Future advances may allow growth and transplantation of human hair cells.

Hair Cell Regeneration Update from the House Ear Institute – August 2001

The House Ear Institute has been actively involved in the research on hair cell regeneration. They are pursuing two complementary strategies in hopes of understanding the regeneration process and how to induce it in humans. Here’s a link to an article describing their recent work. http://www.hei.org/research/projects/cmb/haircellchall.htm

In vitro growth and differentiation of mammalian sensory hair cell progenitors: a requirement for EGF and periotic mesenchyme –

aGonda Department of Cell and Molecular Biology, House Ear Institute,
bCenter for Basic Neuroscience, University of Texas Southwestern Medical Center,
cDepartment of Cell and Neurobiology, University of Southern California Medical School,

24 September 2003; The sensory hair cells and supporting cells of the organ of Corti are generated by a precise program of coordinated cell division and differentiation.

Since no regeneration occurs in the mature organ of Corti, loss of hair cells leads to deafness.

To investigate the molecular basis of hair cell differentiation and their lack of regeneration, we have established a dissociated cell culture system in which sensory hair cells and supporting cells can be generated from mitotic precursors.


By incorporating a Math1-GFP transgene expressed exclusively in hair cells, we have used this system to characterize the conditions required for the growth and differentiation of hair cells in culture.

These conditions include a requirement for epidermal growth factor, as well as the presence of periotic mesenchymal cells.

Lastly, we show that early postnatal cochlear tissue also contains cells that can divide and generate new sensory hair cells in vitro.

Europe Issues Patent on Hearing Loss Treatment – October 2003

Editor: Here’s more breaking news on hair cell regeneration.



Sound Pharmaceuticals has been issued a European patent for its hair cell regeneration treatment.

Note that this development is only part of the required solution, and it doesn’t mean that a treatment will be widely available next week. But I think it is a big step towards viable hair cell regeneration.

Here’s the press release: Sound Pharmaceuticals, Inc. (SPI) announced that its patent “Method for the treatment of diseases or disorders of the inner ear” has issued in Europe, effective Oct. 1, 2003.

SPI has developed a novel strategy to stimulate auditory hair cell regeneration using proprietary cell cycle inhibition technology.

Typically, auditory hair cells in mammals are not replaced when injured or lost. This results in permanent and often progressive sensorineural hearing a disease that affects over 30 million in the US.

In non-mammals like birds, hair cell regeneration occurs through the spontaneous proliferation of the adjacent supporting cell.

These newly proliferating supporting cells can go on to become replacement hair cells.

However in mammals, auditory supporting cells do not proliferate or regenerate into hair cells even in the presence of growth factors.

SPI identified that p27Kip1, a cyclin dependent kinase inhibitor, prevents supporting cells from proliferating after embryogenesis.

Compounds developed by SPI to inhibit p27Kip1 have been shown to stimulate supporting cell proliferation after drug or noise induced hair cell loss.

“We are the only group that has demonstrated the ability to stimulate proliferative regeneration in the cochlea of mammals” says Dr. Jonathan Kil, President & CEO. “It is anticipated that this revolutionary technology will be critical in developing treatments to restore hearing in humans.”

Sound Pharmaceuticals, Inc. is a drug development company focused on treating hearing loss.

To date, Sound Pharmaceuticals’ drug discovery program has identified targets for the prevention of hearing loss and for the improvement of hearing in individuals with hearing loss.

For more information please visit http://www.soundpharmaceuticals.com

Transplantation of bone marrow stromal cells into the cochlea of chinchillas – 19 January 2004 – Volume 15 – Issue 1 – pp 1-4, Auditory and Vestibular Systems – Survival, migrational mobility and differentiation of autologous marrow cells in damaged cochlea suggest their potential as transplants for treatment of various degenerative inner ear diseases.

Promising Research on Hair Cell Regeneration – October 2004

Editor: For people interested in hearing loss “cures”, hair cell regeneration is the current best bet. It appears that virtually all animals except mammals regenerate hair cells on a routine basis.

Dr. Edwin W. Rubel [Virginia Merrill Bloedel Professor of Hearing Science, Virginia Merrill Bloedel Hearing Research Center, Otolaryngology-Head and Neck Surgery, Physiology and Biophysics, Psychology (Adjunct)] and his colleagues are among the researchers on the forefront of this exciting technology.

“Hearing Review” recently published an interview of Dr. Rubel along with a synopsis of the research status. Here’s one question and answer from the interview. The complete article is available at: http://www.hearingreview.com/Articles.ASP?articleid=H0410F01

Hearing Review: If hair cell regeneration is indeed possible, do you think this science will ever progress to a point where there will be full restoration of hair cells, or do you think that it’s far more likely we would see a partial restoration of hair cells in the inner ear?

Rubel: In my opinion, it’s not a question of if we will regenerate, restore, or protect hair cells, it’s a question of when. Because we now know that it’s possible, it’s only a matter of time until we can apply this science to humans. My best prediction is 10-20 years. I certainly hope to see it in my lifetime.

With respect to the degree of hair cell regeneration or restoration, my gut feeling is that it will all depend on what type of hearing loss a person has to begin with. One possibility for regeneration are people who have complete loss of hair cells due to some genetic anomaly, ototoxins, aminoglycosides, etc.

In these cases, hearing care professionals may someday have a choice between recommending a cochlear implant versus an approach for growing enough hair cells where hearing aids could be used more effectively and provide much more acoustic information to that patient.

As another example, you might see a patient who has a 50% loss of their outer hair cells. In this case, maybe we will be able to stimulate the regrowth and replacement of these “cochlear amplifier” cells.

Stem-cell researchers hope for deafness cure within 15 years – November 2004

Editor: “The Scotsman” is reporting on research at Sheffield University that may enable hearing restoration in the foreseeable future. Here are excerpts from the story. For the complete article, please point your browser to http://news.scotsman.com/uk.cfm?id=1346202004 SCIENTISTS hope that stem-cell research could lead to a cure for deafness in as little as ten years.

Researchers from Sheffield University are using embryonic stem cells in efforts to grow new cells in the inner ear. Although in its early stages, the team from Sheffield University hopes it could lead to a cure for deafness in ten to 15 years. Dr Rivolta added that his team hoped to undertake the first tests on animals in two years. “It could then be possible to do human trials in three to four years, but that would depend on the animal trials.”

Stem cells could cure deafness in ten years.

Scientists at Britain’s Sheffield University are hoping that stem cell research could lead to a cure for deafness within ten years!

Laboratory tests have demonstrated that embryonic stem cells have the capability to regrow in damaged areas; animal testing is planned within two years. Here’s the full story.

Survey and research on acute severe hearing disorders.

Study on the expression of cells similar to internal ear stem cell after acute acoustic trauma using a nestin GFP rat. – 2005 Rats that co-expressed nestin and GFP (green fluorescent protein) were used to study whether the presence of cells similar to internal ear stem cell could be identified using nestin, a filament of an intermediate size, as a marker.

In the cochlea of 4-week-old nestin-GRP rats, nestin-positive cells were observed only in spiral ganglion cells but not in the sensory epithelial cell layer comprising hair cells and supprt cells of Corti organ.


A very small number of nestin-positive cells were observed inside the Corti organ in the cochlea of the rats loaded with band noise at 4 kHz and 125 dB for two hours. Cells similar to internal ear stem cell are deemed likely to differentiate to support cells or hair cells. Regeneration therapy of cochlea hair cells was suggested to be possible.

Stem Cells May Be Key To Deafness Cure – August 2006

In a dusty, cluttered lab at Stanford University, a team of young scientists is on a quest. Curing deafness is the goal, reports CBS News correspondent Elizabeth Kaledin, and Stefan Heller says stem cells hold the key. Heller and his entire team were recruited away from Harvard, and they’ve made a breakthrough discovery: They’ve found that stem cells have the capacity to regenerate in the inner ear. Full Story

Stem cell based therapy to restore nearly normal hearing Nov 2006 – hearing in humans. The current review focuses on stem cell-based therapy with particular emphasis to summarize …. restored hearing loss, which demonstrates their potential ….

First blood and bone stem cell research on deafness – December 2006 – Deafness Research UK is funding a new research programme that will be the first to try and develop a cure for deafness using stem cells taken from umbilical cord blood or bone marrow.

This three-year project will be based in the Centre for Stem Cell Biology at the University of Sheffield and has been made possible by a £126,000 charitable donation from GlaxoSmithKline (GSK).

It will be the first research to use these promising new lines of stem cells, which are less controversial than stem cells derived from human embryos, in the search for a cure for deafness. Full Story

COSM 2007: Triological Society – Stem Cell and Genetic Therapies for Hair Cell-Related Hearing Loss

Neil Segil, PhD, from the House Ear Institute, discussed the potential of hair cell regeneration with endogenous progenitor cells—specifically supporting cells. In mice, Dr. Segil’s team tested the capacity of cochlear supporting cells to divide and transdifferentiate by using green fluorescent markers expressed only in supporting cells in the inner ear. With the resulting purified supporting cells, the scientists discovered that the cells were still capable of self-division. And, although these cells normally wouldn’t actively divide, under the culture conditions in the lab, they did.

“If we keep these cells in culture for six days, some of the cells begin to differentiate as hair cells,” he said, adding that they have not yet identified the stimulus for the division. What they did determine is that self-division is age-dependent, in early cells.

It is important, Dr. Segil said, to further test whether self-division can be stimulated in mature cells.

In another study, Dr. Segil’s team is targeting one pathway that keeps cells next to each other from differentiating as the same cell type.


They believe that supporting cells are being actively inhibited from becoming hair cells by this pathway. Additional projects look at cell differentiation to better understand the process by which the supporting cell differentiated state is maintained.

Tech Could End Deafness – February 2007

“We have a good chance of getting normal hearing back in normal ears,” said Richard Schmiedt, an otolaryngology professor at the Medical University of South Carolina. The stem-cell approach involves restoring the tiny “hair cells” in the ear that convert sound into electrical impulses.

When the cells die, people permanently lose their hearing. Bringing back the cells through stem-cell transplants, along with a shock of electricity, could restore hearing, scientists say.

At Stanford University, professor Stefan Heller, who discovered stem cells in the inner ear, believes they can be used to cure deafness in mice within five years. Heller and his colleagues are trying to learn from birds, which do not become deaf, the secret genetic recipe for warding off hearing loss. Full Story

The Miracle of Hair Cells and Prospects for Regrowth – June 2007

Here’s a great article that explains the structure and function of inner and outer hair cells and also looks at some of the research into regrowing these cells. If you’re interested in this topic, it’s very much worth the read! Full Story

Stem Cell Therapy Recovers Lost Hearing – June 2007

Stem cells injected into the inner ear survived in half of the injured rats, where they migrated away from the site of injection toward the injured region within the inner ear.

These stem cells divided in the new environment and expressed several proteins necessary for hearing, suggesting tissue-specific differentiation. Further, transplanted cells that migrated to the damaged area of the inner ear displayed shape similar to that of cochlear fibrocytes.


Importantly, transplanted rats exhibited faster recovery from hearing loss, particularly in the high frequency range, which is difficult to restore by natural regeneration.

Stem cell migration into the damaged area of the inner ear improved hearing of high frequency sound (40 kHz) by 23% compared to natural recovery in untreated animals. Full Story

Genes In Human Inner Ear Cells Restored – June 2007

Dr. Jeffrey Holt, associate professor of neuroscience and otolaryngology at UVa, and his research team, including Dr. Bradley Kesser, an assistant professor of otolaryngology, targeted a gene known as KCNQ4, which causes genetic hearing loss in humans when mutated.

They engineered a correct form of the gene and created a gene therapy delivery system that successfully transferred the KCNQ4 gene into human hair cells harvested from the inner ears of patients with hearing loss.

“Our results show that gene therapy reagents are effective in human inner ear tissue.

Taken together with the results from another group of scientists who showed that similar gene therapy compounds can produce new hair cells and restore hearing function in guinea pigs suggest that the future of gene therapy in the human inner ear is sound,” Holt said. Full Story

Researchers Develop New Method of Growing Hair Cells – November 2007 – Researchers at the University of Virginia have developed a new method of growing inner-ear hair cells that will aid research to help people regain their hearing.


Dr. Jeffrey T. Corwin, a professor of neuroscience at the UVa Health System, and Dr. Zhengqing Hu, a neuroscience research assistant, have been growing cells from inner ears of chicken embryos.

They hope to extend that knowledge to re-grow the inner-ear hair cells of humans. Mammals grow inner-ear hair cells only before they are born, unlike amphibians and birds, which can re-grow damaged or lost cells.

These unique structures are lost over time as mammals age, or if they contract certain infections or undergo trauma.

The loss of inner-ear hair cells results in hearing loss and balance impairment.

Hu and Corwin’s process is able to grow chicken inner-ear hair cells in a laboratory setting. Full Story

Mesenchymal Stem Cell Transplantation Accelerates Hearing Recovery through the Repair of Injured Cochlear Fibrocytes – (American Journal of Pathology. 2007;171:214-226.) DOI: 10.2353/ajpath.2007.060948 – From the Laboratory of Auditory Disorders* and Division of Hearing and Balance Research, National Institute of Sensory Organs, and the Department of Plastic Surgery, National Tokyo Medical Center, Tokyo, Japan – Cochlear fibrocytes play important roles in normal hearing as well as in several types of sensorineural hearing loss attributable to inner ear homeostasis disorders.


Recently, we developed a novel rat model of acute sensorineural hearing loss attributable to fibrocyte dysfunction induced by a mitochondrial toxin. In this model, we demonstrate active regeneration of the cochlear fibrocytes after severe focal apoptosis without any changes in the organ of Corti.


To rescue the residual hearing loss, we transplanted mesenchymal stem cells into the lateral semicircular canal; a number of these stem cells were then detected in the injured area in the lateral wall.


Rats with transplanted mesenchymal stem cells in the lateral wall demonstrated a significantly higher hearing recovery ratio than controls.

The mesenchymal stem cells in the lateral wall also showed connexin 26 and connexin 30 immunostaining reminiscent of gap junctions between neighboring cells.

These results indicate that reorganization of the cochlear fibrocytes leads to hearing recovery after acute sensorineural hearing loss in this model and suggest that mesenchymal stem cell transplantation into the inner ear may be a promising therapy for patients with sensorineural hearing loss attributable to degeneration of cochlear fibrocytes.

Directed differentiation of mouse cochlear neural progenitors in vitro- 18 June 2008 – Departments of 1Otolaryngology and 2Neurosurgery, 3Graduate Program in Neuroscience, 4Stem Cell Institute, and 5Bioengineering, University of Minnesota, Minneapolis, Minnesota – Multipotent cochlear neural progenitors (CNPs) in the organ of Corti hold the promise for cell replacement in degenerative hearing disorders.

However, not much is known about the CNPs and the specific conditions for their differentiation. Here we isolate the CNPs from the postnatal day 1 organ of Corti in mice and demonstrate their capability to self-renew and to differentiate into hair cell-like and neuronal cell-like phenotypes under the guidance of sonic hedgehog (SHH), epidermal growth factor (EGF), retinoic acid (RA), and brain-derived neurotrophic factor (BDNF), herein termed SERB (abbreviation of SHH, EGF, RA, and BDNF) in an asymmetric or symmetric manner from clonal isolates.

Differentiation of CNPs into hair cells by SERB was dependent on the ERK signaling pathway, whereas the differentiation of CNPs into neurons by SERB was not.

This work develops a new in vitro methodology for the maintenance and self-regeneration of CNPs for future design of regenerative strategies for hearing disorders.

Novel approaches to treating sensorineural hearing loss. Auditory genetics and necessary factors for stem cell transplant.

2008 Aug;14(8):RA114-25. Sensorineural hearing loss is a chronic disease, with a serious impact on human communication and quality of life.


Exposure to various factors can lead to irreversible hearing impairment, as the auditory epithelium in humans comprises terminally differentiated cells. By contrast, the inner ear of lower vertebrates and invertebrates shows regenerative capacity.


Efforts to regenerate the damaged human inner ear may involve renewed cell proliferation, or transplanting cells that can differentiate into sensory cells. Literature review.


Animal studies, in vitro studies, retrospective-cohort studies, community-based case-controls, clinical guidelines, and review articles. Embryonic stem cells, inner ear stem cells, and stem cells from other tissues (i.e., neural tissue, hematopoietic system) may be candidates for restoring the auditory epithelium.

Transcriptional regulation of p27kip1 is the primary determinant of terminal mitosis and the final number of postmitotic progenitors of hair and supporting cells.

Basic helix-loop-helix transcription factor Math1 was found to be necessary and sufficient for the production of auditory hair cells.

Notch signaling seems to play a major role in the regulation of Math1, through lateral inhibition. Brn3c, Gfi1, and Barhl1 are also specific transcription factors that have been implicated in hair cell maintenance and consequent survival.

Evidence concerning development, maintenance, and regeneration of hair cells is still at an embryonic stage. Combined data, as attempted in the present study, will lead to a more successful management of deafness.

Sensory Cell Regeneration and Stem Cells: What We Have Already Achieved in the Management of Deafness – Otology & Neurotology: September 2008 – Volume 29 – Issue 6 – pp 758-768, doi: 10.1097/MAO.0b013e31817fdfad – There is an already exciting progress in the fields of sensory cell regeneration and SC research in an attempt to restore hearing or prevent deafness.


However, further understanding of the underlying mechanisms of auditory genetics, continuing investigation of the human genome, refinement of the delivering techniques, and specification of the therapeutic strategies have to be developed before functional regeneration of the cochlea can be achieved in clinical practice.

Umbilical Stem Cells May Repair Damaged Cochlear Hair Cells – September 2008

According to an Italian research team publishing their findings in the current issue of Cell Transplantation (17:6), hearing loss due to cochlear damage may be repaired by transplantation of human umbilical cord hematopoietic stem cells (HSC) since they show that a small number migrated to the damaged cochlea and repaired sensory hair cells and neurons.

For their study, the team used animal models in which permanent hearing loss had been induced by intense noise, chemical toxicity or both.

Cochlear regeneration was only observed in animal groups that received HSC transplants.

Researchers used sensitive tracing methods to determine if the transplanted cells were capable of migrating to the cochlea and evaluated whether the cells could contribute to regenerating neurons and sensory tissue in the cochlea. Full Story

Researchers Make in Vitro Inner Ear Hair Cells – November 2008

Iranian researchers managed to successfully extract bone marrow stem cells from rodents and produce in vitro inner ear hair cells. “In this two-year project, researchers cultured and produced inner ear hair cells, a procedure which is not commonly performed in other countries,” research team-leader, Mohammad Farhadi told the Iranian students news agency.

Farhadi reported that injecting the resulted cells into deaf mice has successfully tackled hearing loss in them. Full Story

New Stem Cell Therapy May Lead To Treatment For Deafness – ScienceDaily (Mar. 23, 2009) — Deafness affects more than 250 million people worldwide. It typically involves the loss of sensory receptors, called hair cells, for their “tufts” of hair-like protrusions, and their associated neurons.


The transplantation of stem cells that are capable of producing functional cell types might be a promising treatment for hearing impairment, but no human candidate cell type has been available to develop this technology.

A new study led by Dr. Marcelo N. Rivolta of the University of Sheffield has successfully isolated human auditory stem cells from fetal cochleae (the auditory portion of the inner ear) and found they had the capacity to differentiate into sensory hair cells and neurons…”The results are the first in vitro renewable stem cell system derived from the human auditory organ and have the potential for a variety of applications, such as studying the development of human cochlear neurons and hair cells, as models for drug screening and helping to develop cell-based therapies for deafness,” say the authors.

Stem cells may help deaf people hear – April 2009 – Stem cells may help deaf people hear again, according to early stage research by British scientists. A team at the University of Sheffield said on Thursday they had discovered how to turn stem cells into ones that behave like sensory hair cells or auditory neurons, which could then be surgically inserted into the ear to restore lost hearing. Lead researcher Marcelo Rivolta said the approach, which is being tested on animals, held significant potential but was a long way from being offered to patients. Full Story

Hair Cell Regeneration – How It Works and What It Means for Audiologists – May 2009 – Twenty years have passed since the discovery of hair cell regeneration in birds (Corwin & Cotanche, 1988; Ryals & Rubel, 1988).

The initial excitement caused by this discovery has been followed by steady progress in understanding the fundamental mechanisms that recently culminated in research evidence of hair cell regeneration in both the auditory and vestibular portions of the mammalian inner ear (Kawamoto et al., 2003; Izumikawa et al., 2005; Staecker et al., 2007).


Clinical audiologists are faced with the responsibility of translating these basic science findings into potential patient application.

They raise important questions: When will hair cell regeneration be a reality for my patients? What will be the measures of candidacy? What will the impact of hair cell regeneration be in my patients who use or are candidates for hearing aids or other amplification devices? Will hearing aids or cochlear implants continue to be needed in the face of hair cell regeneration?

Full Story: Regrowing Hair Cells in the Human Cochlea – June 2009

More than 20 years ago, Douglas Cotanche, PhD, then at the Medical University of South Carolina and now affiliated with Children’s Hospital Boston, discovered that the hair cells within the chick cochlea were capable of a “significant amount of recovery and regeneration” following acoustic trauma.1

His unexpected discovery began a cascade of research on the question of whether hair cells within the human cochlea could someday achieve the same regenerative results.

If and when this happens, many of the causes of hearing loss in humans, from noise to aging, can finally be resolved without the need for hearing aids or cochlear implants.


Although steady progress has been made in understanding the mechanisms underlying hair cell regeneration, human subjects have yet to participate in clinical trials concerned with regrowing hair cells. Such trials may still be years away. Let’s look at a sampling of the research in 2008, which moves us ever closer to the goal of restoring hearing in this most natural way. Full Story

Can a Tiny Fish Save Your Ears? – August 2009

For many people, loss of hearing is irreversible. For scientists trying to figure out what can be done about that, one answer may lie-or swim, actually-in freshwater aquariums.

About one of every 10 Americans suffers from hearing impairment, according to a survey conducted by the Better Hearing Institute, a nonprofit advocacy group.

By far the most common cause of hearing loss is damage to the so-called hair cells in the inner ear as a result of excessive noise, certain illnesses and drugs, and simple aging.


The problem is that once hair cells die, humans (like other mammals) aren’t able to grow new ones.

In recent years, a research team at the University of Washington in Seattle has been working on finding a way to resolve that problem in experiments involving the zebrafish, a common aquarium denizen.

The zebrafish, like many aquatic creatures, has clusters of hair cells running along the outside of its body that help sense vibrations in the water, working in a similar way to hair cells in the human inner ear.

But unlike humans, zebrafish are able to regenerate their damaged hair cells. Researchers hope their work can unlock secrets to protect human hair cells from becoming damaged and to stimulate the cells to regenerate.

Full Story:Cord Blood Stem Cells Repair Mouse Inner Ear – August 2009

Results: The authors found that HSC migrated and engrafted into the cochlea of the deaf mice and that the levels of engraftment correlated with both the severity of damage and the treatment dose.

Analysis at 60 days post-treatment showed that the mice in the HSC treatment group had well-repaired cochlea with dramatic hair cell regrowth, while control mice showed no sign of repair or hair cell regeneration.

Conclusion: The study shows dramatic repair of cochlear damage in mice after intravenous infusion of cord blood HSC, suggesting a potential therapeutic strategy using cord blood stem cells in hearing rehabilitation therapies. Full Story

Regeneration of the mammalian inner ear sensory epithelium – Oct 2009 – …focus on ‘self-repair’ of the mammalian inner ear sensory epithelium, including recruiting the in-situ proliferation and differentiation of endogenous cells at the damaged site and the autologous transplantation

and finally…

Stem Cells Cure Hearing Loss? – November 2009 – Chloe had to travel outside of the United States for stem cell treatment for her hearing disorder.

Chloe’s hearing was tested two months after the procedure was completed on October 16, 2009.

The results were spectacular. The left ear improved to 50% from 0%. The right ear gained almost complete hearing. http://repairstemcell.wordpress.com/2009/11/05/stem-cells-heal-hearing-loss/

(much thanks to hearinglossweb.com for compiling many of these articles!)

To find out if you are a candidate for stem cell therapy for your hearing disorder, contact me at dsgrano@gmail.com –

The information is free and there is no obligation.

Autor: David Granovsky
Fuente:The Stem Cell Blog
http://repairstemcell.wordpress.com/2009/11/16/hearing-loss-%E2%80%93-a-brief-history/

Nestin-expressing cells in the developing, mature and noise-exposed cochlear epithelium

Reiko Watanabea, c, Maria H. Morellb, d, Josef M. Millera, Ariane Kanickia, K. Sue O'Sheab, Richard A. Altschulera, b, Yehoash Raphaela, Corresponding Author Contact Information, E-mail The Corresponding Author

a Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, MI 48109-5648, USA
b Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109-5648, USA
c Department of Otolaryngology, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-0016, Japan
d Instituto de Parasitologia y Biomedicina López Neyra, 18100 Armilla, Granada, Spain

Available online 20 November 2011.


Abstract

The auditory sensory epithelium in non-mammalian vertebrates can replace lost hair cells by transdifferentiation of supporting cells, but this regenerative ability is lost in the mammalian cochlea.


Future cell-based treatment of hearing loss may depend on stem cell transplantation or on transdifferentiation of endogenous cells in the cochlea.

For both approaches, identification of cells with stem cell features within the mature cochlea may be useful.

Here we use a Nestin-β-gal mouse to examine the presence of Nestin positive cells in the mature auditory epithelium, and determine how overstimulation of the ear impacts these cells.

Nestin positive cells were found in the apical turn of the cochlea lateral to the outer hair cell area.

This pattern of expression persisted into mature age.


The area of Nestin positive cells was increased after the noise lesion.


This increase in area coincided with an increase in expression of the Nestin mRNA. The data suggest that cells with potential stem cell features remain in the mature mammalian cochlea, restricted to the apical turn, and that an additional set of signals is necessary to trigger their contribution to cell replacement therapy in the ear.

As such, this population of cells could serve to generate cochlear stem cells for research and potential therapy, and may be a target for treatments based on induced transdifferentiation of endogenous cochlear cells.

Keywords: Cochlea; Nestin; Deafness; Development; Mouse; Stem cell; Acoustic trauma
Article Outline

Corresponding Author Contact InformationCorresponding author at: MSRB-3 Rm. 9220B, 1150 W. Med. Cntr. Dr., Ann Arbor, MI 48109-5648, USA.

Fuente: Molecular and Cellular Neuroscience
doi:10.1016/j.mcn.2011.11.001

Longitudinal hypothalamic–pituitary–adrenal axis trait and state effects in recurrent depression

Authors.
Anja Loka, Corresponding Author Contact Information, 1, E-mail The Corresponding Author, Roel J.T. Mockinga, 1, Henricus G. Ruhéa, Ieke Vissera, Maarten W.J. Koetera, Johanna Assiesa, Claudi L.H. Bocktingb, Miranda Olffc, Aart H. Schenea
Purchase
a Program for Mood Disorders, Department of Psychiatry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
b Department of Clinical and Experimental Psychology, University of Groningen, Groningen, The Netherlands
c Center for Psychological Trauma, Department of Psychiatry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Available online 17 November 2011.
Summary
Background

Hypothalamic–pituitary–adrenal (HPA)-axis hyperactivity has been observed in (recurrent) major depressive disorder (MDD), although inconsistently and mainly cross-sectional.

Longitudinal studies clarifying state-trait issues are lacking.

We aimed to determine whether HPA-axis (hyper)activity in recurrent MDD is:

(I) reflecting a persistent trait;
(II) influenced by depressive state;
(III) associated with stress or previous episodes;
(IV) associated with recurrence; and
(V) influenced by cognitive therapy.


Methods

We included 187 remitted highly recurrent MDD-patients (mean number of previous episodes: 6.3), participating in a randomized-controlled-trial investigating the preventive effect of additional cognitive therapy on recurrence.

In an add-on two-staged patient-control and prospective-cohort design, we first cross-sectionally compared patients’ salivary morning and evening cortisol concentrations with 72 age- and sex-matched controls, and subsequently longitudinally followed-up the patients with repeated measures after three months and two years.


Results

Patients had higher cortisol concentrations than controls (p < .001), which did not change by MDD-episodes during follow-up. HPA-axis activity had no relation with daily hassles or childhood life events.

Cortisol concentrations were lower in patients with more previous episodes (p = .047), but not associated with recurrence(s) during follow-up. Finally, randomly assigned cognitive therapy at study-entry enhanced cortisol declines over the day throughout the two-year follow-up (p = .052).


Conclusions

Our results indicate that remitted recurrent MDD-patients have a persistent trait of increased cortisol concentrations, irrespective of stress.

In combination with our finding that patients’ cortisol concentrations do not change during new MDD-episodes (and thus not represent epiphenomenal or state-effects), our results support that hypercortisolemia fulfills the state-independence criterion for an endophenotype for recurrent depression.

Keywords: Depressive disorder; Major; Recurrence; Hypothalamo-hypophyseal system; Pituitary–adrenal system; Glucocorticoids; Saliva; Cohort studies; Case–control studies; Randomized controlled trial; Cognitive therapy


Corresponding Author Contact InformationCorresponding author at: Department of Psychiatry, Academic Medical Center, Meibergdreef 5, Amsterdam 1105 AZ, The Netherlands. Tel.: +31 205669111.

Fuente: Psychoneuroendocrinology
doi:10.1016/j.psyneuen.2011.10.005

Genetics of temporal lobe epilepsy

Su-Kyeong Hwang, Shinichi Hirose Corresponding Author Contact Information, E-mail The Corresponding Author

Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
Central Research Institute for the Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan


Abstract

The most common partial epilepsy, temporal lobe epilepsy (TLE) consists of a heterogeneous group of seizure disorders originating in the temporal lobe.

TLE had been thought to develop as a result of acquired structural problems in the temporal lobe.

During the past two decades, there has been growing evidence of the important influence of genetic factors, and familial and non-lesional TLE have been increasingly described.

Here, we focus on the genetics of TLE and review related genes which have been studied recently.

Although its molecular mechanisms are still poorly understood, TLE genetics is a fertile field, awaiting more research.

Keywords: Temporal lobe epilepsy; Genetics; Mutation; ADLTE; FMTLE; FPEVF
Article Outline

1. Introduction
2. Autosomal dominant lateral temporal lobe epilepsy (ADLTE)
2.1. LGI1: the only confirmed causal gene for ADLTE
3. Familial mesial temporal lobe epilepsy (FMTLE)
3.1. A number of candidate genes and loci have been suggested
3.2. FMTLE with hippocampal sclerosis
3.3. FMTLE with febrile seizures
3.4. Genetic markers for pharmacoresistant MTLE
4. Familial partial epilepsy with variable foci (FPEVF)
4.1. Two loci for FPEVF have been identified
5. Animal experiments
6. Gene therapy
7. Discussion
8. Summary
Acknowledgements
References


Corresponding Author Contact InformationCorresponding author. Address: Department of Pediatrics, School of Medicine, Fukuoka University, 45-1, 7-chome Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Tel.: +81 92 801 1011; fax: +81 92 862 6955.

Fuente: Brain and Development
doi:10.1016/j.braindev.2011.10.008
Available online 20 November 2011.

Home Remedies For Tinnitus, Easy And Simple Natural Cure

Tinnitus is the buzzing or ringing sound inside one or both the ears.

It may come and go or may be continuous.

People suffering from tinnitus hear wide range of noises inside their ears.

Tinnitus is basically of two types’ objective and subjective tinnitus.

In the case of objective tinnitus the patient as well as the people around him can hear the buzzing sound inside his ears.

And in subjective tinnitus only the patient hears the buzzing sound inside his ears.

There are many causes for tinnitus such as allergy, aging, exposure to the loud noises, blood circulation problems and head or neck injury resulting in the damage of hearing nerve in inner ear.

Home remedies for tinnitus come in various forms and one can always choose the best suited home remedy.

Use of apple cider vinegar is one of the most common home remedies for tinnitus. All you have to do is drink a solution of water (eight ounces) and apple cider vinegar (two tablespoons).

It will give you relief from ringing and is most effective in allergy related tinnitus.

Eating pineapple most often helps in curing tinnitus related to inflammation.

You can even try spraying into the throat and nose a mixture of glycerin (one teaspoon) and salt (one teaspoon) three times a day.

This will treat problems related to sinus as well as ringing in the ears.

Consume raw garlic daily in order to get relief from tinnitus problem.

Ginkgo biloba helps in improving blood circulation to the neck and head region, which will provide relief to tinnitus sufferers.

Chewing dry fruits also help in improving blood circulation and is considered beneficial in treating tinnitus related problems.

One of the effective home remedies for tinnitus is to put 20 to 40 milligrams of Maidenhair tree extract inside your ears.

Because of the loud noise many people suffer tinnitus.

It is recommended to wear ear plugs in such cases.

You can even try aromatherapy. Rose, rosemary, cypress or lemon oils can be used to treat tinnitus related to circulation problems.

Put any of these oils in a vaporizer which will put the scent into the air surrounding you.

You should avoid tea, chocolate or coffee which is rich in caffeine.

Avoid soft drinks, alcohol and smoking.

Stay away from foods like dairy products, saturated fats, salt, sugar and processed foods.

Eat a protein rich diet along with vegetables and fresh fruits.

Also try to have a diet rich in zinc, chlorine, vitamin E, Vitamin B and Vitamin A.

These home remedies for tinnitus as mentioned above are simple, easy and safe to use.

Fuente:
http://enbusca.com/home-remedies-tinnitus-easy-simple-natural-cure/

11.24.2011

Them Crooked Vultures y el tinnitus

RyR Escrito por: RyR, el 23 de November de 2011 | 3:30 pm




No vuelvas a salir sin tus tapones de oídos, especialmente si vas a un concierto de Them Crooked Vultures, la banda conformada por Josh Homme de Queens of the Stone Age, Dave Grohl de los Foo Fighters y John Paul Johnes de Led Zeppelin.

Robert McIndoe, un hombre inglés de 52 años, lo hizo y lo lamentó hasta el momento en que, supuestamente, se suicidó por no soportar el tinnitus (ese beeeeeeep sostenido que generalmente desaparece unas horas después de escuchar sonidos muy altos) que le provocó el concierto y que le impidió dormir durante tres meses hasta que finalmente se inflingió una puñalada mortal el 31 de octubre pasado (después de intentar suicidarse con somníferos 15 días antes).

Su esposa declaró a que “Cuando comenzó no le importó mucho porque creía que pasaría (el tinnitus), el amigo que lo acompañó al concierto también lo tuvo.

Pero para Robert era una molestia constante.

No logró dormir ni una noche después de eso”.

Fuente: http://www.rockandroll.com.mx/blog/2011/11/them-crooked-vultures-y-el-tinnitus/

NOTA DE LA REDACCIÓN:
Un tratamiento médico apropiado seguramente habría ayudado al oyente y paciente Robert Mc Indoe a superar sus acúfenos agudos, una proteccion auditiva con protectores de oido adecuados habría evitado que los acufenos aparecieran, estos casos extremos son exactamente eso, casos excepcionales y extremadamente infrecuentes de evolucion de pacientes con acúfenos.

Dysfunction of fronto-limbic brain circuitry in depression

Authors:
C. Liaoa, Z. Fenga, Corresponding Author Contact Information, E-mail The Corresponding Author, D. Zhoub, Q. Daia, B. Xieb, B. Jib, X. Wangb, X. Wangc
Purchase
a Educational Center of Mental Health, Third Military Medical University, Chongqing 400038, China
b Radiology Department, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
c Xuanwu Hospital, Beijing 100053, China

.
Abstract

Background: depression is characterized by a stable negative bias toward emotional stimuli.

This bias is associated with abnormal activities in emotion-processing regions (such as the amygdala) and cognitive-control regions (such as the dorsolateral prefrontal cortex [DLPFC]).

However, it remains unclear whether the emotion-processing and cognitive-control regions affect negative cognitive bias independently or reciprocally.

Experimental procedure: a functional magnetic resonance imaging (fMRI) study of 16 depressed patients and 16 matched control subjects was conducted during an emotion-interference task.

Results: the accuracies were significantly lower in the depressed group than in the control group when subjects attended to the happy and the neutral faces.


Compared with control participants, depressed patients showed abnormal activity in bilateral amygdala and the right DLPFC.


In addition, a significant correlation was found between the right amygdala and the right DLPFC when subjects observed happy faces.

Conclusions: the results suggest that the dysfunctions in positive emotion-processing and cognitive-control regions may reciprocally affect negative cognitive bias.

Additionally, altered positive emotional interference processing in the fronto-limbic brain circuitry might be another cause of negative cognitive bias that finally leads to depression.

Highlights

▶Emotion-processing and cognitive-control regions affect negative cognitive bias. ▶Depressed patients showed dysfunctions in the right amygdala and the right dorsolateral prefrontal cortex. ▶A significant correlation was found between the two regions.

Key words: depression; emotional processing; cognitive control; brain circuitry; fMRI

Abbreviations: ACC, anterior cingulate cortex; BDI, Beck Depression Inventory; CCMD-3, Chinese Classification of Mental Disorders; DLPFC, dorsolateral prefrontal cortex; fMRI, functional magnetic resonance imaging; FOV, field of view; MDD, major depressive disorder; ROI, regions of interest; RT, reaction time; SDS, Self-rating Depression Scale; TE, time-to-echo; TR, repetition time

Fuente: Neuroscience
doi:10.1016/j.neuroscience.2011.10.053
Available online 22 November 2011

Tinnitus: zumbido que no cesa

Esos zumbidos frecuentes en el oído no son normales. El tinnitus se define como un ruido similar a un campaneo, zumbido, o silbido. Es una sensación percibida individualmente, que puede ser continua o intermitente. El atinnitus o acúfenos puede ser definido como el ruido que la persona oye y percibe como si proviniera de su oído, cabeza, o ambos, cuando no existe en el exterior.

El Dr. Jorge Francisco Moisés Hernández, Otorrinolaringólogo, Jefe del Área de Cirugía Endoscópica del Hospital General de México, lo define como la percepción de algún sonido que no existe, pero que el paciente refiere.

El tinnitus es común en personas mayores de 40 años, pero cada vez es más frecuente en jóvenes, debido al aumento de los niveles de ruido cotidianos, incluyendo los causados por el uso incontrolado de aparatos portátiles de música. Aunque el tinnitus es más común entre las personas que sufren pérdida de audición, cualquier persona puede sufrirlo.

No es una enfermedad, sino un síntoma que ocurre con frecuencia; afecta al 17% de la población mundial. En casos muy severos altera la calidad de vida, en circunstancias como concentración y sueño. Se reporta que el tinnitus se asocia a Hiperacusia (es la disminución en la tolerancia al sonido) en aproximadamente 40% de los casos.

“Se calcula que 6 de cada 10 personas han presentado en algún momento de su vida algún acufeno, un zumbidito en el oído. Las probabilidades de presentar un acufeno pasando los 40 años, se incrementa hasta un 12%”, señala el Dr. Moisés Hernández.

Algunos consejos que pueden ayudarte son : evitar la ansiedad o el estrés, tener un descanso adecuado y evitar la fatiga, evitar el uso de estimulantes, incluyendo el café, el alcohol y el tabaco, evitar las situaciones que más pueden dañar la audición (ruido excesivo), y proteger las orejas de lesiones y riesgos laborales. Use ropa protectora para los oídos cuando sea apropiado.

En la actualidad gracias al avance médico y tecnológico, ya existe un tratamiento que quita o disminuye significativamente la presencia del molesto acúfeno.

El Dr. Jorge Francisco Moisés Hernández asegura que el Gingko Biloba tiene la ventaja de mejorar el aporte sanguíneo, la circulación y la oxigenación y eso hace que las células sean más resistentes a las agresiones, a los traumas, a la exposición al ruido, o a situaciones como colesterol alto que también puede ir tapando vasos, e ir generando un daño mayor.

Los usos terapéuticos del extracto especial de Ginkgo Biloba EGB 761® comprobados clínicamente, incluyen la mejoría sintomática de mareos, tinnitus y cefaleas así como para el déficit de memoria y de atención; depresiones. Este fitofármaco tiene la ventaja de que en su composición ubica varios elementos, como ginkólidos los cuales tienen un efecto antiinflamatorio muy parecido a los esteroides. También tiene efecto a nivel de la agregación plaquetaria, la responsable de formar trombos, cabe destacar que además posee una reacción positiva a nivel de metabolismo celular. Dependiendo de los síntomas y del tratamiento será la dosis que se recomienda.

Existe una gran variedad de condiciones o enfermedades que eventualmente podrían desencadenar tinnitus. Algunos ejemplos son un tapón de cerumen, infección en oído, y con menor frecuencia un tumor en el nervio auditivo. Pero aun así, no se cuenta con una causa precisa que explique en su totalidad la presentación del tinnitus.

Otras condiciones médicas relacionadas son: Hipertensión arterial, Enfermedades cardiovasculares, anemia, e hipotiroidismo. La causa más común relacionada con el tinnitus es la exposición a sonidos o ruidos de alta tonalidad, se tienen en cuenta otros factores como el alcohol, tabaquismo, bebidas oscuras con cafeína, la ansiedad, estrés y preocupaciones.

De acuerdo a lo anterior el tinnitus no se asocia a alteraciones serias; sin embargo, se recomienda consultar para intentar detectar su causa de origen por la valoración y examen físico realizados por un otorrinolaringólogo.

Autor Bertha Sola | Bienestar
2011-11-24
Fuente: http://www.cronica.com.mx/nota.php?id_nota=618909
Mexico

«El médico debería estar obligado a una evaluación continua»

GENERACIÓN XXI: FÉLIX DÍAZ CAPARRÓS




El otorrinolaringólogo cartagenero, pionero en novísimos implantes auditivos, sugiere reformas en la sanidad pública para facilitar la formación de profesionales
26.11.11 - 00:38 -
GINÉS CONESA |


QUIÉN ES
Nombre: Félix Díaz Caparrós.
Lugar y año de nacimiento: Cartagena, 1967.
Profesión: Médico otorrinolaringólogo.
Estado civil: Casado con Ana Laura Trasante. Cuatro hijos.
Aspiraciones: «Ser una persona completa».
Aficiones: Viajar, Naturaleza y deporte.
Le agrada: La sinceridad. «Las personas con la cabeza llena, que tienen empatía y que saben comunicar».
Le disgusta: La incompetencia y la vanidad. «Me molestan la mentira y la gente que se disfraza todos los días».
Idiomas: Inglés.
Creencias: Agnóstico. «Sé que existe algo que no somos capaces de entender. Tengo un gran respeto por las religiones, pero no por la ignorancia tan supina que nos desborda».
Breve historial: .Hijo de militar, durante todo el Bachiller tenía asumido que seguiría los pasos de su padre. Pero fue su propio progenitor quien le liberó del compromiso. Se decidió por la Medicina, aprobó el MIR a la primera y no ha parado de asistir a cursos, congresos, conferencias e investigar (se doctoró 'cum laude' con una tesis sobre el buceo), dar docencia (profesor asociado de la Universidad de Murcia, y en el Centro de Buceo de la Armada) y trabaja en tres hospitales (Santa Lucía, La Vega Y Mesa del Castillo) y en su clínica, que es su mayor ilusión ya que nació de la nada y ahora es un referente en muchos campos como los implantes de oído, la coblación, la patología del buceo, vértigo y equilibrio, trastornos de la voz, del ronquido, problemas estéticos de nariz y oído y hasta tratamientos para dar a la piel un aspecto más joven. Por todo ello se considera una persona con mucha suerte: «Tengo una familia maravillosa, empezando por mi mujer, que es el pilar de mi vida, mis hijos, mis hermanos, mis padres, a los que les debo todo, mis suegros y, además, no me caben los amigos». Cree que en la sociedad española hay una falta de valores enorme. «Todo el mundo quiere conseguir objetivos materiales, pensando que les van a proporcionar la felicidad. No hay respeto por el prójimo. Quieren derechos sin obligaciones. El esfuerzo murió».
«Hoy no hay excusa para decirle a un paciente que no podrá oír nunca»
Pionero en la Región de Murcia en modernos implantes para recuperar el oído y reconocido como médico de referencia para aplicar la tecnología de coblación (una técnica que combina energía de alta frecuencia y soluciones salinas para remover tejidos blandos de forma mínimamente invasiva, que él emplea para operar de anginas) la trayectoria vital del otorrinolaringólogo Félix Díaz Caparrós no se ha caracterizado por ser súbdito de la sociedad del consumo y del entretenimiento que sigue engulléndonos, a pesar de la crisis económica. Muy al contrario, en vez de mirar hacia fuera escuchó sus voces internas, desoyó las que le hablaban de comodidad o de miedo, es decir ordenó su interior, y se puso a la tarea. El resultado es la personificación de un profesional inquieto, que no se conforma con ser testigo pasivo. Adjunto al área de Otorrinolaringología en el Hospital Universitario de Santa Lucía, Félix Díaz desea que la Sanidad Pública también se ocupe de la formación de sus facultativos.
-¿Mediante ayuda económica?
-No tiene porqué ser económica, pero sí en días que permitieran estudiar e investigar. Mi actividad en el hospital casi se ha convertido solo en consulta y quirófano. No tienes tiempo para dedicarlo a la formación.
-No parece ser su caso, pionero en implantes de avanzadas técnicas.
-El médico que tiene inquietud casi tiene que costearse su formación, aprovechando vacaciones y pagándose los cursos que merecen la pena. La Sanidad Pública -a la cual yo defiendo rotundamente- tiene que cambiar en varios aspectos y uno de ellos es la evaluación de sus profesionales. Es importantísimo: el médico que tiene una plaza en propiedad tiene que ser evaluado. Ya se hace en muchos países.
-¿Una especie de evaluación continua?
-Continua, sí. ¿Para qué? Para saber en qué se forma, qué investiga, cuáles son los resultados que obtiene. No sería lógico que estuviera operando siempre de la misma manera sin evolucionar en técnicas.
-Tal vez la estructura sanitaria pública sea demasiado funcionarial.
-El concepto de Medicina actual, desde mi punto de vista, está completamente equivocado. La Medicina se ha convertido en la superespecialización del médico y en tratar al paciente por partes. El futuro de la Medicina será la prevención, sin lugar a dudas. Pero al paciente hay que tratarlo de forma globalizada. No puede ser que tengas un problema de retina, por ejemplo, te den cita para no sé cuándo (las listas de espera son enormes) y a lo mejor el problema de la retina es diabético. Hay que ver el conjunto de su patología.
-El que hace esa función es el médico de cabecera ¿no?
-El médico de cabecera y el de Medicina Interna a nivel de hospital son, digamos, los encargados de ver un poquito global al paciente, pero el resto se ha perdido. Está muy compartimentada la asistencia médica.
-¿Y qué solución le ve?
-Soy partidario de la evaluación continua y de la motivación económica del profesional.
-¿Más gasto ahora que están recortando?
-Habría que hacer ajustes. En vez de que la Medicina pública sea siempre deficitaria, se podía utilizar sus recursos, como se hace en Francia, para tratar pacientes de compañías privadas y con ese dinero hacer más rentable, pero tiene que cambiar el concepto de asistencia. De hecho una de las cosas más bonitas que hay en la Medicina y que hoy día se ha perdido era que los médicos de 50, el ojo clínico. Muchísimas enfermedades se diagnosticaban sin necesidad de ninguna prueba, viendo solo al paciente, la piel, el oído, la vista&hellip.. Ahora van directamente a la prueba. Un escáner, una analítica, una resonancia y nadie te pregunta si los escáner que has pedido están justificados o no.
[Habla de forma pausada y con cierta entonación docente. Todo parece tenerlo planificado, pero no por motivos que tengan que ver con la seguridad de la rutina, sino por método y, en cuanto a su permanente objetivo de 'estar al día' no le importa convivir con la incertidumbre: entrena los músculos de la confianza y de la decisión para acometer nuevas metas. Fue precisamente el músculo del coraje el que le condujo a entrar en contacto con las firmas especializadas en novísimos implantes auditivos que él fue el primero en aplicar en la Región de Murcia.]
-¿Qué investiga en la actualidad?
-Estoy dirigiendo un máster a una fisioterapeuta alemana que está haciendo un estudio del ruido del oído (acufenos) relacionado con la osteopatía craneal, estudiamos también las causas de las hipoacusias bruscas, las personas que de golpe dejan de oír por un oído.
-¿Ya tienen algún resultado?
-De momento el estudio aporta que el estrés es un factor fundamental para estas hipoacusias bruscas, que ahora mismo es una incidencia muy grande en la sociedad.
[Lleva otra línea de estudio: un tratamiento muy novedoso, surgido en Alemania, aplicable a los pacientes que tienen problemas de ventilación del oído. «Hasta ahora no se podía mucho más que abrir el tímpano y colocar un tubito, ahora ha tenemos el balón Bielefeld». Es un tratamiento de dolencias auditivas mediante ventilación y el doctor Díaz es uno de los otorrinos españoles y el único de la Región de Murcia que lo está aplicando.]
-¿Qué le motiva?
-El paciente. No conformarse con que llegue un paciente que diga que tiene ruidos en el oído y responderle que eso es para toda la vida y enviarlo a que se compre un audífono. El médico debe ser honrado con el enfermo y estar formado para poder darle esperanza de que se cure, sin engañarlo, claro. De cara al futuro los implantes son una solución pasajera y sé que dentro de equis años todo se curará con terapia genética, con células madre. Pero mientras eso llega, también es verdad que hoy ya no hay excusa para decirle a una persona que no puede oír nunca.

Fuente: http://www.laverdad.es/murcia/v/20111126/region/medico-deberia-estar-obligado-20111126.html

Evaluation of the efficacy of caffeine cessation, nortriptyline, and topiramate therapy in vestibular migraine and complex dizziness of unknown etiology☆

Evaluation of the efficacy of caffeine cessation, nortriptyline, and topiramate therapy in vestibular migraine and complex dizziness of unknown etiology☆

Anthony A. Mikulec MDa, b, Corresponding Author Contact Information, E-mail The Corresponding Author, Farhoud Faraji BAa, Laurence J. Kinsella MDa, c
a Saint Louis University School of Medicine, St. Louis, MO, USA
b Department of Otolaryngology, Saint Louis University School of Medicine, St. Louis, MO, USA
c Department of Neurology, Saint Louis University School of Medicine, St. Louis, MO, USA

Received 31 January 2011; Available online 24 June 2011.
Abstract
Objective

The aim of this study was to evaluate the efficacy of a therapeutic pathway for vestibular migraine (VM) and complex dizziness of undetermined etiology (CDUE) with caffeine cessation and pharmacotherapy.
Study Design

This study is a retrospective chart review.
Intervention(s)

Patients were recommended to stop intake of caffeine and other putative migraine-triggering agents. Pharmacotherapy was initiated with nortriptyline or topiramate if symptoms persisted despite diet modification.
Main Outcome Measure

Self-reported dizziness is the main outcome measure.
Results

Vestibular migraine and CDUE were considered contributing factors to dizziness in 34 and 10, respectively, of 156 patients. Fourteen percent of patients reported improvement in symptoms upon caffeine cessation, whereas 46% of patients reported a reduction in dizziness after nortriptyline therapy (P = .007). Topiramate reduced symptoms in 25% of patients. In total, 75% of VM patients and 56% of patients with CDUE received sufficient benefit from this therapeutic pathway to not progress to other treatments.
Conclusions

Vestibular migraine and CDUE can be treated effectively with a therapeutic pathway consisting of caffeine cessation followed by pharmacotherapy.
Article Outline

1. Introduction
2. Materials and methods
3. Results and analysis
4. Discussion
5. Conclusion
References

1. Introduction

A portion of patients presenting to dizziness clinics have symptoms that may be attributed to vestibular migraine (VM). Vestibular migraine, also known as migrainous vertigo and migraine-associated dizziness, is a migraine variant for which specific diagnostic criteria have been proposed [1]. However, VM has not been officially recognized by the International Headache Society as a migraine variant [2]. As a result, this lack of recognition may act as a contributing factor to a subset of patients with dizziness escaping categorization despite a thorough evaluation. In our practice, we describe another subset of patients as having “complex dizziness of unknown etiology” (CDUE)—those patients who do not have an underlying cause for their dizziness identified despite evaluation by both a neuro-otologist and neurologist specializing in dizziness. We have chosen to initially treat patients with CDUE equivalently to those with VM under the rationale that, because migraine is relatively common and VM is ill defined, it is possible that patients with CDUE may have a migraine variant as a cause of their dizziness.

Various treatments, including diet therapy, have been reported for VM [3]. Some patients with migraine, be it VM or other variants, appear to have dietary or environmental triggers, and avoiding such triggers can result in relief of symptoms. Both the use of caffeine and caffeine withdrawal have been suggested to be triggers of migraine for some patients, yet caffeine is a component of over-the-counter migraine medications and has also been used in clinical trials as a therapy against migraines [4], [5], [6], [7], [8] and [9]. In an effort to resolve the ambiguity currently in the literature regarding the role of caffeine in migraine and to identify an effective method to treat patients with VM and CDUE, the authors retrospectively reviewed the records of patients presenting to the clinic with the primary complaint of dizziness to evaluate the efficacy of a therapeutic pathway to VM and CDUE with long-term caffeine cessation as a first step and pharmacotherapy with nortriptyline or topiramate as the second step.
2. Materials and methods

In this retrospective study, the records of 156 consecutive patients seen at a tertiary combined dizziness clinic by a neurologist and a neurotologist from 2005 to 2009 were reviewed. The records of patients who had reported caffeine intake and caffeine cessation, had undergone treatment with topiramate or nortriptyline, or had been diagnosed with VM or CDUE were selected and examined in detail. All patients diagnosed with CDUE had undergone thorough evaluation, including assessment for vestibular, neurologic, autonomic, and cardiac dysfunction as an underlying cause of dizziness.

This study was initiated with the purpose of assessing the prevalence of VM and the average quantity of caffeine consumption in our combined dizziness clinic, as well as to evaluate the efficacy of caffeine cessation, treatment with nortriptyline, and treatment with topiramate in patients with VM and CDUE. The caffeine concentrations used in this study were acquired either from company Web sites or by direct inquiry from the company and rounded to the nearest multiple of 5. The values for these calculations are listed in Table 1.
Table 1. Caffeine standards
Beverage Volume (oz) Caffeine (mg)
Generic brewed coffee 12 200
Decaffeinated generic coffee 12 15
Diet Coca Cola 12 50
Coca Cola Classic 12 35
Pepsi and Diet Pepsi 12 40
Dr Pepper and Diet Dr Pepper 12 40
Mountain Dew 12 55
Tea, brewed 12 75
Decaffeinated tea Negligible
Summary of the standard concentrations used to calculate patient daily caffeine intake.

Pharmacotherapy was initiated if patients continued to complain of dizziness symptoms after 4 to 6 weeks of caffeine cessation and diet modification. Nortriptyline was prescribed in an escalating fashion, starting with a dose of 25 mg nightly for 2 weeks, then escalating to 50 mg nightly for 2 weeks, and then finally escalating to 75 mg nightly. Patients were recommended to maintain the lower dose of 25 or 50 mg if they received sufficient benefit at that dose. Topiramate therapy was initiated at 25 mg twice daily and occasionally increased to 50 mg twice daily based on patient tolerance and preference. Drug selection was based on cost, side-effect profile, interactions with other patient medications, and familiarity of the prescribing physician with the medication. The Saint Louis University Institutional Review Board approved this study.

Statistical analysis was conducted using a 2-tailed Fisher exact test with the GraphPad QuickCalc online statistical tool: http://www.graphpad.com/quickcalcs/contingency1.cfm (accessed November 2010).
3. Results and analysis

Of the 156 charts reviewed, a total of 57 patients were suspected of VM, had reported caffeine intake and cessation results, or had been treated with topiramate or nortriptyline. This group ranged in age from 22 to 85 years, with a median age of 45 years, and was composed of 23% men and 77% women. For further analysis, the group was divided into patients with definite or probable VM and those with complex dizziness of unclear etiology (CDUE).

Based on vestibular testing and patient history, VM was considered a contributing factor to dizziness in 41 patients. The median age of the VM group was 44 years, ranged from 22 to 68 years, and was composed of 22% men and 78% women. These patients met the Neuhauser criteria for probable VM as described in Table 2[1]. Thus, probable VM had a prevalence of 26% at our tertiary dizziness clinic. The retrospective nature of this study precluded the authors to diagnose definite VM with certainty.
Table 2. Diagnostic criteria for definite and probable VM
Definite VM
• Episodic vestibular symptoms of at least moderate severity
• Current or previous history of migraine according to the 2004 criteria of the International Headache Society (IHS)
• One of the following migrainous symptoms during 2 or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual aura, or other aura
• Other causes ruled out by appropriate investigations
Probable VM
• Episodic vestibular symptoms of at least moderate severity
• One of the following:
(1) current or previous history of migraine according to the 2004 criteria of the HIS;
(2) migrainous symptoms during vestibular symptoms;
(3) migraine precipitants of vertigo in more than 50% of attacks: food triggers, sleep irregularities, or hormonal change; or
(4) response to migraine medications in more than 50% of attacks
• Other causes ruled out by appropriate investigations
Comment: Vestibular symptoms are rotational vertigo or another illusory self- or object motion. They may be spontaneous or positional. Vestibular symptoms are “moderate” if they interfere with but do not prohibit daily activities and “severe” if patients cannot continue daily activities.Adapted from Neuhauser and Lempert [1].

Sixteen patients were diagnosed with CDUE. Patients included in the CDUE group presented with an amalgamation of poorly defined symptoms defying easy categorization. Some patients reported symptoms consistent with episodic vertigo, some reported symptoms of disequilibrium without vertigo, others reported more vague sensations such fogginess or instability, and yet others reported a combination of the aforementioned symptoms. The age range in this group was 25 to 85 years, with median age of 58 years. The CDUE group was composed of 31% men and 69% women. Fig. 1 and Fig. 2 outline the therapeutic pathway used to treat patients with VM and CDUE, respectively.

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Fig. 1.

This decision tree illustrates the therapeutic pathway for patients in the vestibular migraine group.


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Fig. 2.

This decision tree illustrates the therapeutic pathway for patients in the complex dizziness of unclear etiology group.

Of the 57 patients, 34 in the VM group and 10 in the CDUE group had caffeine intake records specific enough to quantify by estimation. The mean caffeine intake for all patients was 320 ± 270 mg/day and ranged from 40 to 1200 mg/day. Caffeine intake in the VM group ranged from 50 to 850 mg/day, with a mean intake of 275 ± 215 mg/day. The CDUE group had caffeine intake in the range of 40 to 1200 mg/day, with a mean intake of 440 ± 360 mg/day. Vestibular migraine and CDUE groups did not differ significantly in caffeine intake. Data on patient age, sex, and caffeine intake are stratified into VM and CDUE groups and summarized in Table 3.
Table 3. Summary of patient age, sex, and caffeine intake
Age (y), median (range) Sex (M:F) Caffeine intake (mg/d), mean (range)
Overall 45 (22–85) 23:77 320 (40–1200)
VM 44 (22–68) 22:78 275 (50–850)
CDUE 58 (25–85) 31:69 440 (40–1200)

Cessation effective 40 (33–68) 17:83 200 (50–300)
The row entitled “Cessation effective” specifies the characteristics of patients who reported at least a partial reduction in dizziness symptoms after caffeine cessation and diet modification.

All patients who reported caffeine intake and consumption of other putative migraine precipitants—including aged cheeses and monosodium glutamate—were recommended to completely discontinue all intake of migraine precipitants, especially caffeine. Overall, 14% of patients reported any reduction in symptoms of dizziness or headache upon caffeine cessation. In the VM group, 5 (15%) of the 34 patients who had caffeine intake on record reported any benefit from caffeine cessation. In the CDUE group, 1 patient (10%) reported a reduction in symptoms upon caffeine cessation (Table 4). No significant difference was noted between the efficacy of caffeine cessation between VM and CDUE groups. The caffeine intake in the 6 patients who improved upon caffeine cessation ranged from 50 to 300 mg/day, with an average of 200 ± 85 mg/day. It should be noted that most patients who reported a benefit from caffeine cessation did not find caffeine cessation alone as sufficient relief from dizziness symptoms. In fact, only 1 patient received sufficient relief from caffeine cessation and diet modification to decline pharmacologic intervention. Because this patient was part of the CDUE group, the progression-free benefit rate of caffeine cessation is 10% in the CDUE group and 2.3% overall in this study. Most patients who attempted caffeine cessation and dietary modification went on to be prescribed either nortriptyline or topiramate. Dosage regimens for both drugs are detailed in “Materials and methods.”
Table 4. Efficacy of caffeine cessation, nortriptyline therapy, and topiramate therapy
Caffeine cessation Total (n = 44) VM (n = 32) CDUE (n = 10)
Effective 6 (14%) 5 (15%) 1 (10%)
Not effective 38 (86%) 29 (85%) 9 (90%)

Nortriptyline Total (n = 24) VM (n = 17) CDUE (n = 7)
Effective 11 (46%) 8 (47%) 3 (43%)
Not effective 13 (54%) 9 (53%) 4 (57%)

Nortriptyline in caffeine cessation nonresponders Total (n = 21) VM (n = 14) CDUE (n = 7)
Effective 11 (52%) 8 (57%) 3 (43%)
Not effective 10 (48%) 6 (43%) 4 (57%)

Topiramate VM (n = 16)
Effective 4 (25%)
Not effective 12 (75%)

Topiramate in caffeine cessation nonresponders VM (n = 6)
Effective 1 (17%)
Not effective 5 (83%)
Summary of patients who reported results of caffeine cessation, nortriptyline, and/or topiramate therapy. Results have been reported for all patients (total), the VM group (VM), and the complex dizziness of unclear etiology group (CDUE). For patients who underwent pharmacotherapy with either agent, results of the efficacy of pharmacotherapy are reported for all patients and for those who reported no benefit from caffeine cessation. Only patients in the VM group were treated with topiramate.

Nortriptyline was prescribed to a total of 30 VM and CDUE patients with the primary intention of alleviating dizziness symptoms. The patients whose response to treatment could not be found in their records are summarized as “Unknown Result” and are not included in the efficacy analysis. Six such patients were treated with nortriptyline; thus, only 24 patients were included in the analysis. Eleven (46%) patients reported a reduction in dizziness after therapy with nortriptyline, which was a statistically significant difference relative to caffeine cessation and diet modification (P = .007). Fig. 3 compares the efficacy of caffeine cessation, nortriptyline therapy, and pharmacotherapy with either nortriptyline or topiramate. Nortriptyline improved the symptoms of 8 (47%) patients in the VM group and 3 (43%) patients in the CDUE group (Table 4).

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Fig. 3.

The efficacy of caffeine cessation vs pharmacotherapy. The pharmacotherapy columns represent combined nortriptyline or topiramate efficacy results. Combined data from VM and CDUE groups are shown.

Included in the 13 (54%) patients who received no benefit from nortriptyline therapy are 2 patients who were unable to tolerate the adverse effects and thus discontinued nortriptyline (Table 5). One patient showed a temporary reduction of symptoms but subsequently developed refractoriness to the drug. Nortriptyline worsened the symptoms of 1 patient, was not tolerated by 2 patients, and became refractory in 1 patient. For the purposes of the analysis, nortriptyline was deemed not effective in all of these patients.
Table 5. Comparison of tolerability and the development of refractoriness of nortriptyline and topiramate
Unable to tolerate Developed refractoriness to effects
Nortriptyline 2/24 (8%) 1/24 (4%)
Topiramate 1/16 (6%) 3/16 (19%)

Nortriptyline was administered to 21 patients who did not respond to caffeine cessation. It reduced dizziness in 11 (52%) of these patients (Table 4).

Topiramate was administered to 16 patients, all of whom were diagnosed with probable VM. It proved effective in reducing dizziness and headache in 4 (25%) patients (Table 4). One (6%) patient discontinued topiramate due to the adverse effects, 3 (19%) patients developed refractoriness to the drug, and 1 patient whose symptoms were improved by discontinuing topiramate were all included in the not effective group. Table 5 depicts a comparison of the tolerability and development of refractoriness of nortriptyline and topiramate. Because patients only in the VM group were treated with topiramate, Fig. 4 compares the efficacy of topiramate, nortriptyline, and caffeine cessation therapy in VM patients. The difference between the efficacy of topiramate and that of caffeine cessation was not statistically significant.

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Fig. 4.

Caffeine cessation vs topiramate vs nortriptyline in patients with VM.

Six patients who did not respond to caffeine cessation were administered topiramate. Topiramate was effective in 1 (17%) patient. Topiramate was ineffective in 1 patient and was refractory in 2 patients, and 2 patients discontinued use because of their inability to tolerate the adverse effects, all of whom were counted in the not effective group (Table 4). As shown in Fig. 5, the difference between the efficacies of nortriptyline therapy vs topiramate therapy in caffeine cessation nonresponders was not statistically significant.

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Fig. 5.

Topiramate vs nortriptyline in caffeine cessation nonresponders.

Overall, 75% (12/16) of the patients with VM and 56% (5/9) of the patients with CDUE who completed the therapeutic pathway received sufficient benefit from it to not progress on to other treatments.
4. Discussion

Various treatments for VM have been described including physical therapy [10], diet therapy [3] and [11], and prophylactic pharmacologic therapies [12] and [13]. The drug of choice for VM has not been standardized, with selection of medication, as in this study, often determined by physician familiarity and preference. Generally, the pharmacologic treatment of VM involves trial and error of various medications. In this retrospective study, we evaluated the efficacy of a therapeutic pathway for the treatment of VM and CDUE wherein the first step for patients who reported caffeine intake, as assessed by questionnaire, was discontinuation of caffeine. Patients without a significant caffeine intake and those who failed caffeine cessation were then treated with prophylactic pharmacologic therapy with either nortriptyline or topiramate. The choice between the 2 drugs was not based on the patient's symptom complex, but rather on ancillary characteristics such as cost, side-effect profile, interactions with other patient medications, and familiarity of the prescribing physician with the medication (A.A.M. being more familiar with nortriptyline and L.J.K. being more familiar with topiramate). Overall, 75% (12/16) of the patients with VM and 56% (5/9) of the patients with CDUE who completed the pathway received sufficient benefit from it to not progress on to other treatments.

In this study, 14% of patients received at least some reduction in dizziness symptoms with caffeine cessation and diet modification alone. However, many of these patients did not find caffeine cessation and diet modification alone as sufficient relief from their dizziness symptoms. The approximate amount of caffeine present in various beverages is shown in Table 1. It should be noted that those who responded to caffeine cessation tended to have moderate, rather than extreme, caffeine intakes, suggesting that physicians could reasonably recommend caffeine cessation for these patients and not only for those who have very high caffeine intake.

The success of diet therapy for VM has been previously reported [3]. Although we recommended avoidance of many known dietary triggers of migraine, our study focused, in particular, on caffeine cessation under the rationale that expecting Americans to transition abruptly to a completely migraine friendly diet free of MSG, preservatives, and all other migraine triggers was unrealistic. Not all patients were treated with caffeine cessation because they already exhibited little or no caffeine intake. Although only a low percentage of patients responded to caffeine cessation, we feel that caffeine cessation and diet modification should be the first step in treatment of patients with VM or CDUE. It remains unclear what level of caffeine intake, if any, is acceptable for patients with VM. The allowable amount may well be none.

Nortriptyline has been previously described in the treatment of VM [13]. Adverse effects of nortriptyline include somnolence, which is why the medication was prescribed to be taken at night. Care must also be taken when prescribing this medication to women of childbearing age because both nortriptyline and topiramate are listed category C agents in pregnancy [14]. Other common adverse effects included weight gain and sexual dysfunction [15]. In this study, the success rate of treating VM with nortriptyline as initial or secondary pharmacologic management was 46%, a statistically significant improvement in symptoms relative to caffeine cessation and diet modification.

Topiramate has also been used in the treatment of VM alone [11], in children [16] and in combination with amitriptyline, an analog of nortriptyline, in the treatment of migraine in general [17], [18] and [19]. Topiramate has shown to be efficacious for general migraine prophylaxis [19] and [20]. In this study, the success rate of treating patients with VM with topiramate, either as initial pharmacologic therapy or after nortriptyline failure, was 25%.

Few studies of CDUE exist because this is, by definition, a cryptic category. Some patients with CDUE may experience a yet undescribed underlying cause of dizziness. Given the known heterogeneity of migraine presentation and the high prevalence of migraine, it is reasonable to deduce that some patients who do not fit the criteria of probable or definite VM as defined by Lempert and Neuhauser [21] may, in fact, have migraine. The fact that patients with CDUE were less likely than patients with VM to respond to caffeine cessation or treatment with nortriptyline or topiramate suggests that patients with CDUE are either less likely to have migraine as an underlying pathology or have a variant of migraine that is less responsive to these 2 medications than VM. We have included the category of CDUE in this study to demonstrate that it can, in some cases, be successfully treated with antimigraine medications.

Limitations of this study include its retrospective nature, lack of randomization, and relatively small number of patients. Nonetheless, despite the relatively small sample size, statistical significance was achieved in some analyses, and other analyses may approach significance in larger patient populations, supporting the pursuit of larger scale, prospective, controlled, randomized clinical trials to validate this therapeutic pathway. Like all studies regarding VM, ours suffers from the lack of a firm and accepted definition of the entity in question. Because the choice of initial pharmacologic prophylactic therapy is, as in this study, often somewhat arbitrary, and clear data regarding efficacy are lacking, prospective randomized trials comparing various medications would be of great value to the field. We feel that nortriptyline and topiramate represent 2 medications worthy of further analysis in the treatment of VM.
5. Conclusion

Vestibular migraine and CDUE can be treated with a therapeutic pathway, with caffeine cessation being a reasonable first step. The ideal pharmacologic intervention for VM remains to be determined. Patients with dizziness of unknown cause may reasonably be treated with the same medications used for VM.
References

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☆Declarations: 1. Each of the authors has contributed to read and approved this manuscript. 2. None of the authors has any conflict of interest, financial or otherwise. 3. This manuscript, or any part of it, has not been previously published; nor is it under consideration for publication elsewhere. In consideration of the American Journal of Otalaryngology's reviewing and editing my submission, “Evaluation of the Efficacy of Caffeine Cessation, Nortriptyline, and Topiramate in the Treatment of Vestibular Migraine and Complex Dizziness of Unknown Etiology,” the authors undersigned transfers, assigns, and otherwise conveys all copyright ownership to Elsevier Inc. In the event that such work is published in the American Journal of Otolaryngology.


Corresponding Author Contact InformationCorresponding author. 3635 Vista Avenue, 6FDT, St. Louis, MO 63110, USA.

Fuente: American Journal of Otolaryngology
Volume 33, Issue 1, January-February 2012, Pages 121-127