Member- Aug 27, 2016
- 928
- Tinnitus Since
- 06/2016
- Cause of Tinnitus
- Unidentified
Auditory Brainstem Implant for the Treatment of Tinnitus — Clinical Trial
- Thread starter Candy
- Start date
The Red Viper
Member
- May 11, 2016
- 384
- Tinnitus Since
- March 15, 2016
- Cause of Tinnitus
- Current Theory: Neck injury (Tendonitis @ trap/SCM junction)
If I were to have an implant in my brain stem, it better give me superhuman mental abilities, cognition, and memory.
Well it is not the results of the clinical trial, but it is a related case study.
Neural Substrates of Tinnitus in an Auditory Brainstem Implant Patient
Introduction: It was previously demonstrated that tinnitus due to profound unilateral hearing loss can be treated by the use of electrical stimulation via a cochlear implant (CI) with long-lasting positive effects. In cases where patients are not suitable for cochlear implantation due to aplasia/hypoplasia, cochlear malformations etc., an auditory brainstem implant (ABI) may be a solution. While auditory performance with ABI is well investigated, it is currently unknown whether stimulation through ABI also renders tinnitus reduction in patients with incapacitating tinnitus. The current case study reports on the subjective tinnitus perception during a 5-year follow-up period. In addition, a first H215O PET imaging study in an ABI patient is carried out revealing underlying neural substrates of tinnitus.
Methods: A 56-year-old male single-sided deaf patient with incapacitating tinnitus received an ABI after insufficient auditory performances and only minor tinnitus reduction with CI. Audiological follow-up was carried out during a 5-year follow-up period comprising pure-tone audiometry, speech-in-quiet testing, speech-in-noise testing, tinnitus questionnaires (tinnitus questionnaire and numeric rating scale) and the HISQUI19 questionnaire. To investigate the neural substrates of tinnitus in this subject, H215O PET tomography scans were acquired in three different conditions: 1) ABI switched off which was considered as the resting-state measurement rendering the loudest possible tinnitus for the patient (ABI OFF); 2) ABI switched on causing a small suppression of tinnitus due to electrical stimulation (ABI ON); 3) ABI switched on and 70 dB SPL white noise presented directly to the external audio processor through a direct audio cable providing the maximum tinnitus suppression for the patient (NOISE).
Results: Subjectively the patient reported a significant tinnitus reduction after implantation which remained stable over time with a decrease in tinnitus questionnaire from grade 4 to grade 2 and a 50% reduction in the numeric rating scale (from 8 to 4) during the 5-year period. Comparing the ABI OFF and ABI ON conditions, significant increase in regional cerebral blood flow (rCBF) was observed in brain areas involved in the salience network showing already suppression of tinnitus only by electrical stimulation in the absence of auditory stimuli. The NOISE condition showed relatively decreased rCBF in the insula (as well as in the orbitofrontal cortex) as compared with the ABI OFF condition. Abnormally activated areas comprising the salience network may have been significantly suppressed by the NOISE condition both by acoustic and electrical stimulations of the auditory pathway. Moreover, the NOISE condition showed significantly decreased rCBF in the parahippocampus as compared with the ABI OFF condition. This finding supports the idea of distinct tinnitus generators depending on the amount of hearing loss.
Conclusion: The reduction of tinnitus in the current ABI subject may be attributable to partial peripheral reafferentation-induced deactivation of the parahippocampus-based tinnitus generator as well as the salience network. Further validation is required by the use of a follow-up study with a larger number of subjects.
Source: https://journals.lww.com/otology-ne..._Substrates_of_Tinnitus_in_an_Auditory.5.aspx
Neural Substrates of Tinnitus in an Auditory Brainstem Implant Patient
Introduction: It was previously demonstrated that tinnitus due to profound unilateral hearing loss can be treated by the use of electrical stimulation via a cochlear implant (CI) with long-lasting positive effects. In cases where patients are not suitable for cochlear implantation due to aplasia/hypoplasia, cochlear malformations etc., an auditory brainstem implant (ABI) may be a solution. While auditory performance with ABI is well investigated, it is currently unknown whether stimulation through ABI also renders tinnitus reduction in patients with incapacitating tinnitus. The current case study reports on the subjective tinnitus perception during a 5-year follow-up period. In addition, a first H215O PET imaging study in an ABI patient is carried out revealing underlying neural substrates of tinnitus.
Methods: A 56-year-old male single-sided deaf patient with incapacitating tinnitus received an ABI after insufficient auditory performances and only minor tinnitus reduction with CI. Audiological follow-up was carried out during a 5-year follow-up period comprising pure-tone audiometry, speech-in-quiet testing, speech-in-noise testing, tinnitus questionnaires (tinnitus questionnaire and numeric rating scale) and the HISQUI19 questionnaire. To investigate the neural substrates of tinnitus in this subject, H215O PET tomography scans were acquired in three different conditions: 1) ABI switched off which was considered as the resting-state measurement rendering the loudest possible tinnitus for the patient (ABI OFF); 2) ABI switched on causing a small suppression of tinnitus due to electrical stimulation (ABI ON); 3) ABI switched on and 70 dB SPL white noise presented directly to the external audio processor through a direct audio cable providing the maximum tinnitus suppression for the patient (NOISE).
Results: Subjectively the patient reported a significant tinnitus reduction after implantation which remained stable over time with a decrease in tinnitus questionnaire from grade 4 to grade 2 and a 50% reduction in the numeric rating scale (from 8 to 4) during the 5-year period. Comparing the ABI OFF and ABI ON conditions, significant increase in regional cerebral blood flow (rCBF) was observed in brain areas involved in the salience network showing already suppression of tinnitus only by electrical stimulation in the absence of auditory stimuli. The NOISE condition showed relatively decreased rCBF in the insula (as well as in the orbitofrontal cortex) as compared with the ABI OFF condition. Abnormally activated areas comprising the salience network may have been significantly suppressed by the NOISE condition both by acoustic and electrical stimulations of the auditory pathway. Moreover, the NOISE condition showed significantly decreased rCBF in the parahippocampus as compared with the ABI OFF condition. This finding supports the idea of distinct tinnitus generators depending on the amount of hearing loss.
Conclusion: The reduction of tinnitus in the current ABI subject may be attributable to partial peripheral reafferentation-induced deactivation of the parahippocampus-based tinnitus generator as well as the salience network. Further validation is required by the use of a follow-up study with a larger number of subjects.
Source: https://journals.lww.com/otology-ne..._Substrates_of_Tinnitus_in_an_Auditory.5.aspx
Preliminary test results for the treatment of tinnitus with an ABI implant are positive.
Complete research paper in English can be found here:
https://www.kno-leden.nl/leden/document/view/id/6260
Short summary:
Complete research paper in English can be found here:
https://www.kno-leden.nl/leden/document/view/id/6260
Short summary:
Thuan
Member
- Jul 5, 2020
- 221
- Tinnitus Since
- 05/2018
- Cause of Tinnitus
- Ear infection right ear 2018. Sound trauma left ear 2020.
Me neither but if it truly eliminates tinnitus... and FX-322 doesn't work... this is the only route left. Then again, I don't think it's worth if it only reduces tinnitus. It would be similar to just masking devices for many but would be a life saver for unmaskable tinnitus.
Too bad severing the cochlear nerve doesn't work.
You probably realized this but the man in this study was completely deaf in one ear and could not mask his tinnitus so this was huge for him.
Auditory Brainstem Implants are not yet used for those with virtually any residual hearing and if you go on YouTube you can hear just how low fidelity the sound transmission is. I think that is part of why they had to pump.in white noise to stimulate the implant more fully but the fact that a dramatic reduction occurred is further evidence tinnitus is not "stuck in the brain." It doesn't seem that it was solely a masking effect in this case.
Cochlear implants produce way better sound than ABI (and often reduce tinnitus even without outside noise/masking) but some people are not CI candidates for a few rare reasons (as I assume the person in the study).
Companies are working on way better implants, however, and Utah Array is even working on one that implants directly into the cochlear nerve instead (with apparently much better quality sound, and likely better tinnitus reduction too).
- Dec 18, 2015
- 618
- 45
- Tinnitus Since
- 03/2015
- Cause of Tinnitus
- Noise induced, loud rock concert
Email reply I got from Minke van den Berge from University of Groningen:
Indeed we have a trial studying the auditory brainstorm implant (stimulating the dorsal cochleae nucleus) for tinnitus. Very interesting! We have now implanted 2 patients. We are enrolling patients with unilateral tinnitus, and hearing loss on this side. We have to enroll more patients before we can publish the results. I expect a definite paper in the next 2-3 years. It will be published in international journals.
Interesting. More researchers aside from Susan Shore exploring Dorsal Cochlear Nucleus stimulation. Long time to wait though.
@Christiaan did you consider to get enrolled?
Indeed we have a trial studying the auditory brainstorm implant (stimulating the dorsal cochleae nucleus) for tinnitus. Very interesting! We have now implanted 2 patients. We are enrolling patients with unilateral tinnitus, and hearing loss on this side. We have to enroll more patients before we can publish the results. I expect a definite paper in the next 2-3 years. It will be published in international journals.
Interesting. More researchers aside from Susan Shore exploring Dorsal Cochlear Nucleus stimulation. Long time to wait though.
@Christiaan did you consider to get enrolled?
- Apr 6, 2020
- 1,031
- Tinnitus Since
- 2016
- Cause of Tinnitus
- 2016: headphones, 2020: worsened thanks to Rammstein
It seems very interesting for those with one sided hearing loss @Mentos.
I have NIHL in both ears. I'm still waiting out for FX-322, RL-81 and an efficient TNF-A blocker (that doesn't diminish the immune system). Last resort is DBS.
I have one sided tinnitus, but mild hearing loss on both sides. I see the inclusion criteria is having tinnitus for longer than a year. The procedure seems quite radical, so I will definitely look forward to seeing the results with those already in the trials before attempting something like this. Good to see serious research going on in the Netherlands and not another CBT waste of time.
- Apr 6, 2020
- 1,031
- Tinnitus Since
- 2016
- Cause of Tinnitus
- 2016: headphones, 2020: worsened thanks to Rammstein
Hey Ela. From what I gather, TNF-a returns to normal serum level after discontinuation of Naltrexone, whether it is used short term or long term. That said, it would be bad news if that wasn't the case, because TNF-a is essential for the regulation of immune cells to protect against infections and it also activates immune responses against tumor formation.
So you would be more prone to forming a tumor? Maybe at least you can take Naltrexone from time to time to take the edge off? My tinnitus is due to brainstem inflammation. My brain scan just confirmed it. Other than DBS, Naltrexone or Potassium channel blockers, I have no options...
- Apr 6, 2020
- 1,031
- Tinnitus Since
- 2016
- Cause of Tinnitus
- 2016: headphones, 2020: worsened thanks to Rammstein
Well, there are a few ifs and buts in that matter. I haven't found a study that exactly quantifies how much a person is more likely to get a disease due to LDN/Naltrexone use, only that there are strong indications & empirical evidence that a compromised immune system makes a person more susceptible in getting an infection / serious affliction.
Here's a systemic review of LDN and Naltrexone concerning cancer proliferation. According to Liubchencko et al. (2022), intermittent use of LDN seems to be considered harmless (perhaps even effective against cancer proliferation) in animal studies. On the other hand, consuming a high dose of Naltrexone for a considerable amount of time seems to have a negative effect.
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Naltrexone's Impact on Cancer Progression and Mortality: A Systematic Review of Studies in Humans, Animal Models, and Cell Cultures (Liubchenko et al., 2022)
Background: Naltrexone (NTX) is an opioid antagonist traditionally used as a treatment for alcohol and opioid use disorders, but various studies have documented its involvement in cancer progression, exploring possible anticancer potential, when administered at high doses or as low dose naltrexone (LDN). Herein we present a systematic review of cancer-related outcomes from case reports, clinical trials, and retrospective and prospective studies conducted using cell cultures, animal models, and human subjects receiving NTX/LDN.
Methods: A systematic search of NTX in cancer therapy was conducted. Outcomes including tumor size and number, latency to tumor development, survival duration, progression of disease, and scan results were assessed in clinical and animal studies, and cell number was used as the outcome measure of culture studies.
Results: Several case reports demonstrate notable survival durations and metastatic resolutions in patients with late stage cancer when administered an average LDN dose of 3-5 mg/day. Animal and cell culture studies suggest an overarching principle of NTX involvement in cancer pharmacophysiology, suggesting that high doses and continuous administration can foster cancer progression, whereas low doses and intermittent treatment may hinder cell proliferation, impede tumorigenesis, and have potential anticancer efficacy.
Conclusion: This review emphasizes the value of potential future research on NTX in cancer therapy, and warrants need for a better understanding of underlying mechanisms. Future controlled studies with more robust sample sizes, particularly in humans, are needed to fully elucidate its potential in cancer therapy.
- Apr 30, 2018
- 2,507
- Tinnitus Since
- 02/2018
- Cause of Tinnitus
- Single 25 mg dose of (anticholinergic) drug Promethazine
Hi @Ela Stefan -- I believe I suffered from brainstem inflammation for most of my life following a severe whiplash injury at age 15. Most of the relief I've experienced has been through using various structural procedures. I think there may be more options for you to consider than you may realize (IMHO of course).
What kind of structural procedures, please?Hi @Ela Stefan -- I believe I suffered from brainstem inflammation for most of my life following a severe whiplash injury at age 15. Most of the relief I've experienced has been through using various structural procedures. I think there may be more options for you to consider than you may realize (IMHO of course).
My clogged inflamed ear made by brain hear less, I think the high frequencies in particular. Plus, the inflammation was on the middle ear muscles, so the trigeminal nerve irritated the somatosensory system in the cochlear nucleus, which is in the brainstem, isn't it?
So in my case everything started in the DCN, not the inner ear.
I went to 20 sessions of mHBOT but maybe it was too late after more than 2 years.
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