MemberI don't know do you feel unbalanced (Like you're about to fall down) for exemple when you get up or in the dark or do you fell like you're drunk...
Steroid nasal spray is like Prednisone instead it is more local instead of being the whole body.
Sudden Low Frequency Hearing Loss??
- Thread starter SilverSpiral
- Start date
I don't know do you feel unbalanced (Like you're about to fall down) for exemple when you get up or in the dark or do you fell like you're drunk...
Steroid nasal spray is like Prednisone instead it is more local instead of being the whole body.
Because if it is a viral infection in the inner ear I wouldn't use the spray. But since you used it for three days already you would have felt a big worsening in your T and balance.
Might be a leftover from the accoustic trauma...
Might be a leftover from the accoustic trauma...
I think the frequencies of noise induced hearing loss probably reflect the frequencies you are most exposed to.
- Aug 21, 2014
- 5,049
- Tinnitus Since
- 1999
- Cause of Tinnitus
- karma
My understanding is that this is generally true, with the caveat that high frequency hair cells are the outermost, which is why general degenerative hearing loss tends to start there.
Saw the ENT, he said to continue with prednisone, see him in 10 days, told me about intratympanic steroid injection but didn't offer, got the impression he might next time. Mentioned HBOT but costs thousands, and each session would require a full day of travel and over 100 dollars travel expenses. He also mentioned he doesn't know anybody who has had overwhelming success with the HBOT. Discussed possibility that this is SGN related, as blood work shows nothing, still waiting MRI. I'm going to inquire about getting the steroid shot.
Maybe it could be delayed endolymphatic hydrops caused by the acoustic trauma you had? Did your symptoms lessen, or are they still the same? Do you feel dizzy?
Edit: Or maybe some kind of TTTS causing the weird distortions and autophony?
Edit: Or maybe some kind of TTTS causing the weird distortions and autophony?
I have not had dizziness or vertigo. After 5 doses of prednisone, the new loud broad low hum tinnitus that came in the ear with the sudden slope below 1k does seem a bit quieter compared to when it developed or days 1/2 of prednisone, i think the fullness sensation may be a bit less, but still nowhere near what it was before the increase (and i had fullness since initial acoustic trauma) and i haven't been woken up the past couple nights by loud T. Unsure if it is the prednisone, but i'm glad I let my doctor do the ear syringing just so that he could rule out infection and prescribe me it.
@SilverSpiral how are you doing? I have had a similar thing happen to me recently. I'm SURE it's due to the acoustic trauma I suffered a year ago. I think if we have areas of hair cells that have been damaged but are not completely dead, they are super fragile to future noise (even low level noise). I also have had the fullness in my ears since the trauma, I'm sure this has something to do with this. My theory is that it's maybe some form of cochlear hydrops which has been brought on by the trauma. If you google it there are studies that confirm a link between acoustic trauma and cochlear hydrops. You don't need to have vertigo as a symptom...fullness, tinnitus, hyperacusis, hearing loss are sufficient. Please let me know how things go. I'd be extremely careful to protect your ears if you get an MRI.
I think this is probably correct, and it implies that those hair cells could be recovered if the right medical protocols existed. It may be that those who report initial improvement with steroids are seeing some penetration of the drug into this region and maybe anti-inflammatory dosing in many cases is too low a dose and too short a duration for the effect to be sustained. It seems kind of obvious, and yet I've never seen any studies done along this line.
hey guys
im hanging in there, I decided to distance myself from this site as well as anything and anybody else as I became more acutely suicidal, and began planning. I neither wanted my death to cause any grief, nor satisfaction.
But My SSNHL actually responded quite well to the prednisone, my thresholds returned to normal on a standard audiogram, and I had over -25db loss across 3 bands and the lowest was the most severe it was like -40 at the lowest and thats where the audiogram cuts off so who knows how low it had gone in the lower frequencies, my ENT said this was not uncommon to see such recoveries, but my audiologist said it was among one of the best recoveries he has seen (he seemed perhaps a bit new to his job though?). He said "prednisone is a hell of a drug wish I had gotten it". As he also has tinnitus. Well I do too wish I had gotten prednisone, for the initial acoustic trauma, then the ssnhl probably wouldn't have happened. Seeing this improvement made me feel like if I had gotten prednisone from my GP from the initial acoustic trauma, I may have recovered, or atleast the ssnhl wouldnt have happened. After the treatment, the distortions are now more asymmetrical (whereas before they were fairly symetrical, my constant tones were just way louder in the bad ear and it always had this heavy feeling) and I notice my hyperacusis is much worse in general. Only the one ear had the SSNHL so visibly severe on the audiogram, so I'm not sure why the hyperacusis in both ears would get worse after the prednisone treatment. Maybe both ears simply worsened, just the most affected one most severely.
Still stumps me why my low frequency hearing gave out with the ssnhl instead of the high, my ENT had no answer for this, besides saying "it's not uncommon in his experience".
Still waiting on the MRI, I rescheduled it because the MRI techs gave me the standard (yeah 33db foam plugs, so its like probably like 80db minus 33db so it'd be less than 50db so you're fine). and would not give me any hard evidence of the peak decibel output of the MRI machine (IE the technical specs. 80db is a very quiet machine, I'm surprised they supply 33db plugs to normal people if this machine is really so quiet). They also clearly had no knowledge of how the NRR for these foam disposable plugs works, let alone the fact that I have very narrow ear canals, so obtaining a proper fit would be difficult.
Suffice to say I'm waiting until I have class A custom molds to get my MRI.
hope everybody is managing as well as they can.
im hanging in there, I decided to distance myself from this site as well as anything and anybody else as I became more acutely suicidal, and began planning. I neither wanted my death to cause any grief, nor satisfaction.
But My SSNHL actually responded quite well to the prednisone, my thresholds returned to normal on a standard audiogram, and I had over -25db loss across 3 bands and the lowest was the most severe it was like -40 at the lowest and thats where the audiogram cuts off so who knows how low it had gone in the lower frequencies, my ENT said this was not uncommon to see such recoveries, but my audiologist said it was among one of the best recoveries he has seen (he seemed perhaps a bit new to his job though?). He said "prednisone is a hell of a drug wish I had gotten it". As he also has tinnitus. Well I do too wish I had gotten prednisone, for the initial acoustic trauma, then the ssnhl probably wouldn't have happened. Seeing this improvement made me feel like if I had gotten prednisone from my GP from the initial acoustic trauma, I may have recovered, or atleast the ssnhl wouldnt have happened. After the treatment, the distortions are now more asymmetrical (whereas before they were fairly symetrical, my constant tones were just way louder in the bad ear and it always had this heavy feeling) and I notice my hyperacusis is much worse in general. Only the one ear had the SSNHL so visibly severe on the audiogram, so I'm not sure why the hyperacusis in both ears would get worse after the prednisone treatment. Maybe both ears simply worsened, just the most affected one most severely.
Still stumps me why my low frequency hearing gave out with the ssnhl instead of the high, my ENT had no answer for this, besides saying "it's not uncommon in his experience".
Still waiting on the MRI, I rescheduled it because the MRI techs gave me the standard (yeah 33db foam plugs, so its like probably like 80db minus 33db so it'd be less than 50db so you're fine). and would not give me any hard evidence of the peak decibel output of the MRI machine (IE the technical specs. 80db is a very quiet machine, I'm surprised they supply 33db plugs to normal people if this machine is really so quiet). They also clearly had no knowledge of how the NRR for these foam disposable plugs works, let alone the fact that I have very narrow ear canals, so obtaining a proper fit would be difficult.
Suffice to say I'm waiting until I have class A custom molds to get my MRI.
hope everybody is managing as well as they can.
but to clarify, the low pitched rumbling terrifying low frequency T that came with the SSNHL went away. I am thankful for that. I'm telling you that kind of T I don't think anybody could last long with. I'm basically back to how I was before the SSNHL now, except the distortions or whatever it's called is worse in the bad ear, and my hyperacusis in general is worse.
I'm less acutely suicidal right now hence I feel comfortable posting. Right now I am back to hoping someway somehow medical science will advance and I will enjoy sound again rather than be tortured by it.
Again I hope everybody is improving or managing as best as they can.
I'm less acutely suicidal right now hence I feel comfortable posting. Right now I am back to hoping someway somehow medical science will advance and I will enjoy sound again rather than be tortured by it.
Again I hope everybody is improving or managing as best as they can.
- Feb 5, 2017
- 787
- Tinnitus Since
- 2016
- Cause of Tinnitus
- Fluconazole
You know, now that you mention it, it's very possible that my H either appeared or became dramatically severe right after my intratympanic steroid injection. It could be a coincidence of course, but still an interesting coincidence.
It is interesting, but given the severity of the SSNHL symptoms, I'd say it's more probable that whatever was going on may have lead to the increased hyperacusis. I guess it's a "chicken or egg" sort of thing, but in any case that extreme low pitch roaring tinnitus that came along with the ssnhl... if the prednisone is what made that go away, than it was worth it. My goodness I don't think one could bear a week of such noise/sensation. It most closely resembled what this member describes. https://www.tinnitustalk.com/members/snow86.9064/
It was terrifying to experience just how bad this can get, but I'm gonna stop myself from thinking down that path right now. I can live with this how it is today. I don't know why it's worth it, but I must hope for a better life one day.
I have it all day every day and I'm deaf in the other ear too. I'm surviving it and you could too.
Well, thank you for that. My point is that you could get through it if it got that bad again and even if it was worse than that. There are lots of things that you can try to improve things. Recently, I got a hearing aid that takes sound from my deaf side and brings it to my good ear. I didn't think it would do much without amplification but it makes a world of difference. The biggest thing you can do is to stop worrying about it. My life got a lot better when I stopped obsessing over it. It takes a while, but you'll get there.
My ENT did mention in his experience recurrence is common... suggested I get regular hearing tests, but I'm hoping it doesn't happen again. If it does I'll be getting intratympanic injections I guess... you list your cause of tinnitus as unknown. What was weird with mine is that I had an acoustic trauma, and the most affected ear always had this heavy sensation, when the SSNHL happened, that heavy sensation increased exponentially, and my low frequency hearing went away, and got replaced by loud roaring. This stuff is weird. Thanks for your words, I really admire your strength.
Is hyperacusis an issue for you? If so how does the hearing aid interact with that?
I would just take the Prednisone orally since it worked so well for you. Sometimes the injections cause problems for people. Hopefully, you won't have to worry about it.
I don't have hyperacusis which is strange considering most people here seem to and I wouldn't consider my T mild. I don't wear ear protection unless I am somewhere really loud. Maybe that has something to do with it. Idk. If you do have it, from what I have read TRT seems to be pretty helpful in getting rid of it.
Well, tinnitus pitch is not assessed (low tone?), and I don't get their therapy + therapeutic effectiveness, and immunopathological mechanisms of anti-endothelial cell autoantibodies (AECEs) on tinnitus is not assessed.
The Role of Anti-Endothelial Cell Autoantibodies and Immune Response in Acute Low-Tone Hearing Loss
Objective: Immunity is associated with acute low tone hearing loss. However, the exact pathophysiology of immunity-mediated acute low tone hearing loss remains unknown. In this study, we evaluated the presence, therapeutic effectiveness, and immunopathological mechanisms of anti-endothelial cell autoantibodies (AECEs) in patients with acute low-frequency hearing loss.
Material and Methods: Forty-nine patients who were treated as inpatients having acute low-frequency hearing loss and additional symptoms, such as ear fullness, tinnitus, dizziness, or hyperacusis, were enrolled in this study. Serum samples from these patients were collected for laboratory serum autoimmunity detection, including AECAs, antinuclear antibodies, immunoglobulin, and circular immune complex. Therapeutic responses to combination therapy in short-term outcome and serum cytokine levels were compared between AECA-positive and AECA-negative patients.
Results: Anti-endothelial cell autoantibodies–positive patients tended to show significantly less response to standard therapy compared with AECAs controls (P < .05). Moreover, some serum cytokine levels elevated in both AECAs and AECAsþ groups. Positive ratio of interleukin-8 and concentrations of macrophage inflammatory protein-1a were found higher in AECAsþ groups (P < .05).
Conclusion: The results supported that AECAs might wield influence on the short-term outcome of acute low-tone hearing loss (ALHL) treatment. Furthermore, AECA-mediated acute low-frequency hearing loss possibly involved dysregulation of inflammation process and release of cytokines.
The Role of Anti-Endothelial Cell Autoantibodies and Immune Response in Acute Low-Tone Hearing Loss
Objective: Immunity is associated with acute low tone hearing loss. However, the exact pathophysiology of immunity-mediated acute low tone hearing loss remains unknown. In this study, we evaluated the presence, therapeutic effectiveness, and immunopathological mechanisms of anti-endothelial cell autoantibodies (AECEs) in patients with acute low-frequency hearing loss.
Material and Methods: Forty-nine patients who were treated as inpatients having acute low-frequency hearing loss and additional symptoms, such as ear fullness, tinnitus, dizziness, or hyperacusis, were enrolled in this study. Serum samples from these patients were collected for laboratory serum autoimmunity detection, including AECAs, antinuclear antibodies, immunoglobulin, and circular immune complex. Therapeutic responses to combination therapy in short-term outcome and serum cytokine levels were compared between AECA-positive and AECA-negative patients.
Results: Anti-endothelial cell autoantibodies–positive patients tended to show significantly less response to standard therapy compared with AECAs controls (P < .05). Moreover, some serum cytokine levels elevated in both AECAs and AECAsþ groups. Positive ratio of interleukin-8 and concentrations of macrophage inflammatory protein-1a were found higher in AECAsþ groups (P < .05).
Conclusion: The results supported that AECAs might wield influence on the short-term outcome of acute low-tone hearing loss (ALHL) treatment. Furthermore, AECA-mediated acute low-frequency hearing loss possibly involved dysregulation of inflammation process and release of cytokines.
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