Latest "Tinnitus Today" Article about Tinnitus Cancellation

Good info Karl. I am still skeptical on these therapies but I hope this one is successful. It seems Dr Dalton has put all his eggs into this basket so that is a good sign. I am hoping someone will one day develop a more affordable treatment plan since all these treatments include Dichonics, Neuromonics, Soundcure, etc all cost thousands of dollars.

 

Karl, thanks for this post and I agree Dr Dalton is on the right path. -- Dr Dalton, keep it up!

Clonazepam/klonopin does help a majority of people with T but I don't think it really lowers the volume, I think it just improves a persons negative reaction or anxiety toward the sound which can make it seem lower (and if that does the trick -great). I am not sure if mine is any lower than 2 months ago, it seems so, but I am much better at dealing with it now and I don't have nearly the same negative anxiety toward it so in my mind it is better. The same can be said using Clonazepam, Ativan, Xanax or any of the other related benzos. The main problem with these is they are addictive and hard to get off if you have been on them long term. OHSU uses a plan to administer Xanax for 6-8 weeks and they claim almost 80% improvement in all areas of T that you mention above. They have been doing this protocol for over 20 years.

 

I agree, calm down the nervous system and that affects both psychological and physical components. I am just wondering if it just gives you the break you need so you can better habituate in the long run because once you stop taking them you would think the noise level would increase and you would be right back where you started. For me I didn't take anything (prescriptions) when I got T. I was given my script after I already dealt with T for 3 months and by that time it was already getting easier for me. I just keep them on hand because it is nice to know that I do have something should I need it. I have only taken it once in past month and that was 1/2 dose.

Just got email from Dr Dalton's group---GULP!:

Hello everyone,

Patient scheduling is on hold until late fall. However, I am here to answer any questions you have and will do anything I can to help while fall creeps up.

For anybody who would like an in-depth analysis of their tinnitus and what the therapy does to the tinnitus, we are encouraging you to participate in our Magnetoencephalography (MEG) studies. Grant money is non-existant, so each patient would have to pay out-of-pocket for the MEG. This is about $2000 dollars per MEG. Dr. Dalton will not make any profit from this; it would go completely to the cost of the MEG scan.

If you are interested or have any questions, please contact me VIA e-mail.

 

I agree $2K per scan is out of the questions for of most T sufferers. Not sure how many scans you would need as part of this study but I would think it would be tough to conduct a study that requires so much out of pocket costs for its participants.

 

If this isn't receiving any grant money, then what to really even think of that.

How many viable studies that could really matter are going to the bin because of no money?

I hope they are getting enough participants even with that cost...

Sigh

 

Karl, I was under the impression there would be more than one MEG scan for the study needed but I could be wrong. I too think it is a brain condition, after all your brain is what interprets and creates the sounds you hear not your ear. We just got some wires crossed.....

We can all agree that T research is severely underfunded for T. I think the ATA does the best it can with what little it gets. $5 million donated to research in 30 years is not going to find a cure that's for sure. They have funded some decent studies recently though....here's a recap:

Berthold Langguth, M.D., Ph.D., University of Regensburg
Project: Combined Transcranial Magnetic Stimulation in Treatment of Chronic Tinnitus Using Double Cone Coil
Roadmap to a Cure Paths: C,D
Funded: $50,000, 1-year project*
Type: Human research study
"It is well known that tinnitus is related to increased activity in central auditory pathways. Repetitive transcranial magnetic stimulation (rTMS) is an innovative method for locally modulating brain activity. With the idea to downregulate increased activity in the auditory cortex, rTMS has been introduced as a new treatment for tinnitus. Reduction of tinnitus by rTMS has been demonstrated in many studies, however unfortunately the over-all benefits from this treatment are only relatively small. In the last years additional brain areas have been identified, which are strongly connected with the auditory cortex in tinnitus patients. These neural networks reflect the adverse emotional reaction (i.e. the suffering caused by the sound perception) and the conscious perception of tinnitus. With the aim to attack tinnitus more efficiently we propose a new stimulation protocol using a newly developed TMS coil. The specific form of this coil allows a deeper penetration depth of the magnetic field in the brain and offers the possibility to directly modulate deeper brain structures which are known to be involved in generating feelings of suffering. We expect that this new rTMS procedure will reduce tinnitus better and in more patients than the existing procedure and will thus provide an efficient new treatment option for the many patients suffering from tinnitus.
Transcranial magnetic stimulation (TMS) has been introduced into neuroscience in 1985 by A.T. Barker (1). It consists of a technique providing a strong and focal magnetic field by a coil connected to an electrical power source. The induced magnetic field penetrates the scull easily and painlessly and leads to depolarization of neurons in mostly superficial cortical regions. It constitutes a non-invasive and well-tolerated (2) neuromodulatory approach which is known to modulate neural activity not only in directly stimulated but also functionally connected brain areas (3, 4). By repetitive TMS (rTMS) application over auditory brain areas a persisting modulation of neural activity and an alleviation of tinnitus complaints can be achieved in a subgroup of tinnitus patients (5-7). Treatment effects could be enhanced by high-frequency stimulation of the left prefrontal cortex before lowfrequency stimulation of temporo-parietal locations (8). Recent imaging studies indicate the critical involvement of the dorsal anterior cingulate cortex (dACC) in tinnitus pathophysiology. The dACC can be reached by a newly developed stimulation coil, the so-called double cone coil (DCC) (9). The angulated geometry of the double cone coil enables a deeper penetration depth of the magnetic impulse. Thus, mediofrontal stimulation with the double cone coil results in a direct influence of the dACC (9).
In the proposed study this new stimulation procedure (high frequency mediofrontal stimulation with the DCC followed by low-frequency temporoparietal stimulation targeting auditory cortical areas) will be investigated. For the assessment of the treatment effects patients will be asked to fill out a compilation of standardized and validated questionnaires. In addition, before and after the treatment consisting of 10 rTMS sessions electroencephalographic (EEG) examinations will take place. Clinical data will be stored and analyzed using the TRI Database (http://database.tinnitusresearch.org/). Data storage will be effected in a pseudonymized way, data handling and its statistical analysis will be performed according to high quality standards following a pre-defined statistical analysis plan (SAP). Additionally, clinical data will be correlated with EEG power spectra and
connectivity."

Jennifer Melcher, Ph.D., Massachusetts Eye & Ear, Harvard Medical School
Project: Brain Function and Attention in Tinnitus
Roadmap to a Cure Paths: A,B
Funded: $49,983 1st year of 2-year project
Type: Human research study
"The project will examine brain function during selective and involuntary attention in people with tinnitus using fMRI and a classic dichotic listening task with two novel elements:
(1) Tinnitus and non-tinnitus subjects will be matched for performance on the listening task in order to specifically image processes recruited when tinnitus subjects work to maintain normal performance. It has been hypothesized that daily “management” of tinnitus engages extra cognitive, and hence neural, resources. A first aim of this project is to identify areas of the brain that are engaged.
(2) A potent auditory distracter (the subject’s name) will be used to engage involuntary attention mechanisms. This aspect of the experimental design is motivated by a common report of tinnitus patients: that they are easily distracted or have difficulty concentrating. While it is possible that these symptoms result from the distracting tinnitus percept itself, it is equally possible that hypervigilance to the auditory domain causes people with tinnitus to be more vulnerable to hijacking of attention by any potentially salient auditory stimulus. A second aim is to examine the brain processes behind auditory distraction in tinnitus in a controlled way. We expect this project will shed light, at a physiological level, on the role of attention in tinnitus and suggest ways to inform and improve emerging attention-based tinnitus therapies
There are multiple aspects of attention controlled by different parts of the brain. For instance, we sometimes pay “selective” attention to a particular thing – someone’s voice, for instance - or ones tinnitus. The focus of attention can sometimes be controlled voluntarily or, it can be involuntarily captured, for instance by someone calling your name or, again, by tinnitus. This project begins to examine whether the brain processes of selective and involuntary attention are different in people with tinnitus and if so how. There are already researchers working on tinnitus therapies that involve attention training exercises. Our hope is that this project shows ways to improve on these therapies, perhaps by showing which aspects of attention need shoring up.
The research seeks to understand brain processes underlying the condition of tinnitus and thus intersects paths A and B in the ATA Roadmap. By working directly in people with tinnitus and on an aspect of tinnitus that is being targeted by therapies, this project also has a clear eye toward path C."


Josef Rauschecker, Ph.D., Georgetown University Medical Center
Project: Tonotopic Map Reorganization and the Effects of Frequency Discrimination Treatment in Tinnitus
Roadmap to a Cure Paths: A,C,D
Funded: $50,000 1st year of 2-year project
Type: Human research study

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"Tinnitus research has shown that tinnitus is associated with changes in central auditory as well as limbic structures. However, it is unclear which of these changes, if any, cause tinnitus and which are simply byproducts of the disorder. This project tackles this problem in two ways. First, it assesses whether auditory tonotopic map distortions, thought by some to underlie the tinnitus sensation, occur only in tinnitus patients or in all cases of hearing loss. The latter finding would rule out tonotopic distortion as the ultimate cause of tinnitus. Second, the project investigates a low-cost, non-invasive web-based treatment for tinnitus and identifies areas of the brain responsible for the effectiveness of this treatment. Identifying the brain-bases of symptom improvement would reveal crucial targets for future treatments, and could be used to refine existing treatments.
Tinnitus is a common auditory disorder with largely unknown pathophysiology and no cure. It has been proposed that tinnitus results from loss of peripheral sensory input (usually due to hearing damage) and subsequent distortion of central tonotopic maps. While such distortions have been measured in animals with tinnitus and hearing loss, comparable evidence from human tinnitus patients is lacking. Moreover, none of these studies controlled for hearing loss, leaving open the question whether the observed distortions reflect a normal response to peripheral damage or a pathological process generating tinnitus. Nevertheless, the tonotopic reorganization hypothesis persists and is the theoretical basis for various “sound therapies” of tinnitus. The studies will address these issues by critically examining the relationship between tonotopic map reorganization and tinnitus, and by determining the neural sites of action for sound therapies. Aim 1 of this project uses high-resolution functional magnetic resonance imaging (fMRI) to compare tonotopic maps of tinnitus patients with those of controls matched for hearing loss. Aim 2 is to identify the neural sites of action for sound therapies of tinnitus. Frequency discrimination training is known to increase the cortical representation of trained frequencies in healthy subjects, and is thought to attenuate tinnitus by reversing tonotopic map distortions. However, while such training seems to alleviate tinnitus to some extent, its effects on tonotopic maps has not been demonstrated directly. The studies will use high-resolution fMRI to compare tonotopic maps of tinnitus patients before and after 30 days of a web-based frequency discrimination training to investigate 1) how training affects tonotopic maps, and 2) whether symptom improvement is tied to specific tonotopic map changes or to changes in limbic areas known to be altered in tinnitus. These results will help determine which changes are crucial for alleviating tinnitus, so that future treatments can be focused accordingly.
The research project overlaps with Paths A, C, and D of the Roadmap. It addresses the question of whether tonotopic map distortions occur in all cases of hearing loss, or only in tinnitus patients. While tonotopic map distortions are a proposed source of the tinnitus signal, to date there is no direct evidence that such distortions occur exclusively in tinnitus (Path A: Identification of Generators). Second, the project investigates the efficacy and neural sites of action for acoustic-behavioral therapy, which has shown some success in alleviating tinnitus. Our proposed treatment variation (specifically targeting low frequencies) has never been tested and can therefore be considered “Development of Therapy” (Path C). Finally, the combination of pre/post-treatment fMRI and treatment success measures will identify the neural sites of successful treatment, and will thus serve as a guide for further refinement of the treatment (Path D)."


Sarah Hayes, State University of New York at Buffalo
Student Research Project: Contribution of Stress to Tinnitus Generation: Role of GABAergic Inhibition
Roadmap to a Cure Path: B
Funded: 1-year student grant, $10,000
Type: Animal research study

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"Although the majority of tinnitus patients suffer from hearing loss, not all individuals with hearing loss develop tinnitus. This discrepancy emphasizes the need to better understand factors that may increase the susceptibility of individuals to tinnitus generation. One such factor may be chronic stress and its effects on GABAergic inhibition. Although clinical observations and subjective reports from tinnitus patients suggest a link between stress and tinnitus, they provide only anecdotal evidence that stress may contribute to tinnitus susceptibility. Elucidation of a cause and effect relationship between stress and tinnitus generation requires a study in which both hearing loss and the level of stress are tightly controlled for; something that can only be done in an animal model. By screening for behavioral evidence of tinnitus in noise-exposed rats with or without prior exposure to chronic restraint stress, this study will determine whether stress increases the incidence of noiseinduced tinnitus. Additionally, given the known ability of chronic stress to reduce GABAergic inhibition in a number of brain regions, this proposal will be the first to investigate whether chronic stress can alter GABAerigic inhibition in the auditory pathway by quantifying protein levels of the GABAergic markers GAD65/67 and the GABAA receptor α1 subunit. Given that a loss of inhibition in the auditory pathway is believed to play a significant role in tinnitus generation, stress-induced changes in inhibition may underlie a potential mechanism in which stress can contribute to the development of tinnitus. Understanding the contribution of stress to noise-induced tinnitus may help identify individuals at increased risk for developing tinnitus and may lead to novel preventative and treatment strategies.
This proposal addresses Path B of ATA’s Roadmap to a Cure (Elucidation of Mechanisms of Tinnitus Generation). The goal of the experiments is to better understand how factors such as stress contribute to tinnitus generation by altering GABAergic inhibition along the auditory pathway. A better understanding of how stress-induced changes in GABAergic inhibition can contribute to tinnitus generation, can lead to future development of therapies to prevent and treat tinnitus (Path C, Development of Therapy)."

 

Chicken,

You're right, there are many factors to T and strong evidence that it is more than just hairs and hearing loss. Somatic sensory neurons can certainly play a part in tinnitus since the nervous system is part of all of this and very connected to the auditory brain system. Since I have no hearing loss and can modulate my tinnitus with head, neck and jaw movements, I believe this to be what I have.....


Here is a great write up on
Neural mechanisms underlying somatic tinnitus

Somatic tinnitus is clinically observed modulation of the pitch and loudness of tinnitus by somatic stimulation. This phenomenon and the association of tinnitus with somatic neural disorders indicate that neural connections between the somatosensory and auditory systems may play a role in tinnitus. Anatomical and physiological evidence supports these observations. The trigeminal and dorsal root ganglia relay afferent somatosensory information from the periphery to secondary sensory neurons in the brainstem, specifically, the spinal trigeminal nucleus and dorsal column nuclei, respectively. Each of these structures has been shown to send excitatory projections to the cochlear nucleus. Mossy fibers from the spinal trigeminal and dorsal column nuclei terminate in the granule cell domain while en passant boutons from the ganglia terminate in the granule cell domain and core region of the cochlear nucleus. Sources of these somatosensory–auditory projections are associated with proprioceptive and cutaneous, but not nociceptive, sensation. Single unit and evoked potential recordings in the dorsal cochlear nucleus indicate that these pathways are physiologically active. Stimulation of the dorsal column and the cervical dorsal root ganglia elicits short- and long-latency inhibition separated by a transient excitatory peak in DCN single units. Similarly, activation of the trigeminal ganglion elicits excitation in some DCN units and inhibition in others. Bimodal integration in the DCN is demonstrated by comparing responses to somatosensory and auditory stimulation alone with responses to paired somatosensory and auditory stimulation. The modulation of firing rate and synchrony in DCN neurons by somatatosensory input is physiological correlate of somatic tinnitus.

There has long been evidence that connections exist between higher-order neurons subserving different senses (e.g., some neurons serve both the auditory and entorhinal cortices). But only in recent years has it become apparent that these connections exist even in first and second order neurons of the brainstem — and, further, that the connections are functional even in normal animals. How might these connections manifest clinically?

FOR More In Depth Reading on this click on
Neural mechanisms underlying somatic tinnitus

 

Hi Chicken, wikipedia has a good explanation of Somatic Tinnitus. Even though it may be caused by outside factors or a combination of hearing and muscle stress, it still regarded as a brain issue just like other tinnitus - somatic tinnitus, caused by disorders outside the ear and nerve, but still within the head or neck. It is further hypothesized somatic tinnitus may be due to "central crosstalk" within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.

As for a cure, I don't know. Some say suppressing GabaA/GabaB receptors will help reduce excitability in the DCN, others state treating muscle jaw and neck tension over time helps to eleviate tinnitus somewhat but I have read everything I can on Somatic tinnitus and not once come across anything that promises a cure...yet. I an currently visiting a chiropractor who specializes in these areas but not sure after 2 months if it is really helping or not. Not sure if below works or not either.

TREATMENT OF SOMATIC TINNITUS
A Bjorne,
Vertigo, Tinnitus and Pain Unit, Ystad Hospital, SE-271 82 Sweden.
E-mail: assar.bjorne@telia2.se

Introduction
Since 1988, I have been interested in tinnitus and vertigo related to muscular tension in the jaw and neck. I made my first observations on tinnitus; the lateral pterygoid muscle was more tender on the ipsilateral side where single sited tinnitus was experienced. I also found that intramuscular injection (Lidocaine) in the lateral pterygoid muscle on the tinnitus side reduced tinnitus in a consecutively sampled group of 38 tinnitus patients with 63 % according to VAS. When the anaesthetics were off, tinnitus returned as before the injection. From 1993 until today my whole clinical work was devoted to these patients. During this time I have examined/treated about 2000 referred patients with tinnitus as the first complaint, about 1000 with
vertigo as the first complaint, 500 diagnosed with Meniere´s disease and about 300 with Whiplash Associated Disorders. Since 1996 to 2005 I have published 5 articles about tension in jaw and neck in patients diagnosed with Meniere´s disease, and suggested a new treatment concept to reduce tension and sick leave in this group.

Criteria for Somatic Tinnitus
There are 3 criteria for somatic tinnitus, probably the most common type of tinnitus,also including tinnitus in patients diagnosed with Meniere´s disease.
1. The patients are able to alter their tinnitus sound, both sound level and pitch
by performing movements of their jaw, neck and eyes.
2. Many patients are able to alter their tinnitus sound by putting pressure with a
fingertip on the temples, mandible, cheek , tragus, behind the ear and in the
neck.
All these movements increase tension signals from tensed muscles in the
innervation area of the sensory trigeminal nerve linked into the acoustic
pathways.
3. The examination shows a muscular tension in the jaw and neck muscles.
We have also found a subgroup in this field of tinnitus patients. The examination
exposes an often severe muscular tension typical for patients described at above
criteria, but they are not able to manipulate their tinnitus. Despite hearing loss and
hearing damage, their tinnitus benefit much from the treatment.

Examination
The examination includes an assessment of the patients’ self-administered questionnaire and palpation of the jaw and neck muscles. The mobility of the jaw and neck and restrictions in mobility are measured, as well as pain on movement. The examination of the dental occlusion is made with the neck in an upright posture. We consider that the jaw and upper cervical spine constitute an integrated motor system, so the posture is central in both examination and treatment. A forward head/neck posture is mostly a compensation for a disorder in the dental occlusion bringing the mandible and neck forwards in chewing and swallowing reflexes.

Treatment
The aim of the treatment is to reduce the muscle tension in jaw and neck. Many patients have noticed that tinnitus debuted during a life crisis with stress and depression and from which they often still not are cured. These patients consult our stress therapist as a complement to the other treatment. With the neck/jaw in an optimal central posture, the dental occlusion is adjusted by grinding. This may be done several times to reduce the tension. Shining bruxing facets are identified and dulled by a light touch of dental grinding. If they reappear shining at the nextv isit, they are diagnosed as the result of masticatory muscle hyperactivity during the REM sleep. Each time they reappear they are dulled. The patients are carefully trained to feel the new stabile occlusion both when standing, lying and sitting to develop a good posture of the body. The worst posture they have when sitting.

About 25% of the patients receive special bite splints against tooth and tongue clenching. About the same amount are referred to a physiotherapist for further treatment of the tension in the neck and training in relaxing and posture. Patients are also instructed to do a stretching exercise of their suboccipital muscles
which they are asked to do frequently. After the stretching exercise they are also asked to perform rotation movements in the atlanto-occipital joint especially to the restricted side. The homework also includes relaxing exercises involving breathing with the diaphragm.

Results
The treatment of the muscle tension in jaw and neck shows a significant reduction of tinnitus both frequency and severity. The 3-year follow-up period, with half-year controls also shows a significant reduction of other tension related symptoms as vertigo, feeling of fullness in the ear, pain in the jaw and neck and headache.

 

Unfortunately, until someone puts some real money at this, we'll be discussing this same thing in 10 years. The ATA as good intentioned as it is, will not find a cure any time soon unless they get some real funding. $10,000 here, $50,000 there is not going to do much. They need to petition the Dept of defense which as a demonstrated interest in a tinnitus cure for the thousands of returning veterans suffering from T, for funding.