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Tinnitus is the perception of sound within the human ear in the absence of corresponding external sound.
Tinnitus is not itself a disease but a symptom resulting from a range of underlying causes. Featured TestimonialI have struggled with hearing loss for many years, and bought hearing aids elsewhere before I went to HearFlorida. Severe disabling tinnitus (SDT) refers to a symptom severe enough to disrupt affected patients' routine and keep them from performing their daily activities. In 2000, using single-photon emission computed tomography (SPECT) and the benzodiazepine radioligand 123I lomazenil, Shulman et al. In a 2002 retrospective study, Gananca [7] found that clonazepam was very effective and safe in the treatment of SDT. Generally accepted today is that SDT of cochlear origin always has a central component that keeps the symptom active, even after deafferentation [9].
We used the VAS to measure the degrees of intensity and annoyance before and after the drug treatment. After 6 weeks of treatment, the degrees of intensity and annoyance of tinnitus were again measured via the VAS. SDT intensity and annoyance were significantly decreased in groups 1 and 3 as compared to group 1, but no statistically significant difference was detected between groups 2 and 3 (Tables 4-12). Four patients in group 2 experienced drowsiness and nausea, and two patients had sexual dysfunction (clonazepam). Tables 7-12 show the statistical analyses of the results using the SSPS version 13 software (SPSS Inc.), and Figure 1 summarizes the results in the three groups.
The discrepancy between Shulman's results and ours may be due to the different patient populations but, to be sure about that, it is necessary to study patients with SDT of a predominantly central origin, comparing the results of placebo, benzodiazepines alone, and benzodiazepines combined with GABAergic drugs. The addition of GABAergic drugs to benzodiazepines does not modify the results of the treatment of SDT of predominantly cochlear origin.
This study was performed with help from Fundacao de Empreendimentos Cientificos e Tecnologicos (FINATEC), Brasilia-DF, Brazil.
Presented at the Twenty-Fifth Meeting of the Politzer Society, Seoul, Korea, October 5-9, 2005.
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Symptoms such as tinnitus can be caused by ­damage and diseases that affect the conductive apparatus of the ear, its receptor organs, the auditory nerve, and nerve cells in the nuclei of the auditory system, including the cerebral auditory cortex.
Tinnitus can also be caused by activation of neural plasticity (causing plasticity diseases), which can cause altered function at the cellular level in the brain and re-routing of information. The brain is not a fixed system but it is continuously shaped and re-shaped by signals it receives from the outside world.
Neural plasticity is a property of the nervous ­system that becomes apparent only when turned on. Activation of beneficial neural plasticity facilitates recovery from damage to the nervous system (such as from strokes).
Activation of harmful neural plasticity is involved in creation of symptoms of disease (plasticity ­disorders) such as some forms of tinnitus, central neuropathic pain, and some forms of muscle spasm.


Deprivation of input, overstimulation, injuries, and unknown intrinsic factors can promote expression of neural plasticity.
Many forms of tinnitus are phantom sensations caused by activation of neural plasticity and similar to phantom sensations in other sensory systems causing central neuropathic pain, paresthesia, and spasm in motor systems. Many forms of tinnitus are associated with changes in processing of information that may involve hyperacusis and distortion of sounds.
Abnormal (pathologic) changes in connectivity may occur because of activation of neural plasticity that opens (unmask) dormant synapses or close (mask) synapses that are conducting normally. Tinnitus is often accompanied by cross-modal interaction, which may be explained by an abnormal activation of non-classical sensory pathways through re-routing of information. Involvement of the non-classical pathways may explain symptoms of mood disorders, phantom sensations, improved perceptual capabilities, or atypical sensory experiences that often accompany severe tinnitus. 12.Sie KCY and EW Rubel (1992) Rapid changes in protein synthesis and cell size in the cochlear nucleus following eighth nerve activity blockade and cochlea ablation. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.
Causes include ear infections, foreign objects or wax in the ear, nose allergies that prevent (or induce) fluid drain and cause wax build-up, and injury from loud noises. But now the Neuromonics Tinnitus Treatment lets you relieve these symptoms and reclaim your life.
I instantly felt comfortable with the staff and audiologist, received more thorough testing than I ever had, am hearing better than I have in years and therefore participating in activities and conversations more. Benzodiazepines and GABAergics in Treating Severe Disabling Tinnitus of Predominantly Cochlear Origin.
SDT of a predominantly central origin has been treated successfully with benzodiazepines and GABAergic drugs. This prompted us to test the treatment with benzodiazepines and GABAergic drugs in SDT of predominantly cochlear origin following a prospective, randomized, singleblind protocol. We defined them as patients who had a 7 or higher score in a visual analog scale (VAS) ranging from 1 (negligible intensity and annoyance) to 10 (unbearable intensity and annoyance). The patients were randomly assigned to three groups: group 1 was treated with placebo, group 2 with clonazepam, and group 3 with clonazepam and GABAergic drugs. Five patients in group 3 reported drowsiness and nausea, and two noticed interference with cognition (clonazepam and gabapentin).
Both annoyance and intensity decreased significantly in groups 2 and 3 as compared to group 1, but no significant difference between groups 2 and 3 was found.
This would be important to clarify the following question: Are we dealing with two different populations of SDT patients or do all SDT patients, regardless of the tinnitus's origin (cochlear or central), have a common central pathophysiology? In sensory systems, it may serve to compensate for loss of function or to adapt the nervous system to change in demand. Tinnitus is also a side-effect of some oral medications, such as aspirin, and may also result from an abnormally low level of serotonin activity. I am so impressed by the knowledge, care, and willingness to help, and cannot be more thankful for this improvement in my life. Our aim was to test the control of SDT of predominantly cochlear origin by benzodiazepines and GABAergic drugs.


This finding was consistent with the implication of GABAergic mechanisms in the genesis of SDT of a predominantly central origin. These patients had tinnitus of the severe disabling type for at least 6 months and, in them, treatment with the usual drugs used for tinnitus control had failed.
Otological diagnosis and hearing status were also very similar in the three groups (see Tables 2, 3). Reduced (3H) flunitrazepam binding in singulate cortex and hippocampus of postmortem schizophrenic brains: Is selective loss of glutamatergic neurons associated with major psychoses? GABA-A-benzodiazepine- chloride receptor-targeted therapy for tinnitus control: Preliminary report. Expression of neural plasticity can make the nervous system adapt to changing demands (prostheses such as cochlear and cochlear nucleus implants). We followed the format of a prospective, randomized, singleblind clinical trial at an academic tertiary-care hospital. A rationale for the treatment of the symptom with benzodiazepines and GABAergic drugs was based on these results.
He treated 30 patients, all having SDT with a predominantly central origin and showing perfusion changes in areas of interest in the brain as documented by SPECT. Patients who had tinnitus as a consequence of otological surgery, who had chronic otitis media, or who had medical contraindications for the use of benzodiazepines and GABAergic drugs were excluded. Our patients had SDT associated with otological diseases that are known to produce tinnitus. Abnormalities of benzodiazepine receptors have been demonstrated in Alzheimer's disease, Huntington's chorea, schizophrenia, and stress [2-6].
Twenty-one patients completed the trial and, of these, 19 had significant improvement of the symptom and increased brain perfusion, documented by SPECT, after the treatment. Therefore, it is reasonable to say that their symptom was of a predominantly cochlear origin.
The VAS alone may not be able to distinguish between sensory (intensity) and affect (annoyance) components of SDT.
We treated 10 patients with placebo (group 1), 10 with benzodiazepine drugs (group 2), and 10 with benzodiazepine and GABAergic drugs (group 3). We recorded a decrease in the annoyance and intensity of SDT as measured by a visual analog scale ranging from 1 (negligible) to 10 (unbearable).
We found statistically significant improvement in comparing groups 2 and 3 with group 1 but found no significant difference when groups 2 and 3 were compared. Addition of GABAergic to benzodiazepine drugs does not modify the treatment results in SDT of a predominantly cochlear origin.



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