Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 MY SOS is minimal. But after being desensitized in April 2008 everything else is so much better. Polyps are present and small thus not much of a problem. I can breathe through both nostrils. I have actually gone a whole year without prednisone. Although I have a supply ready to go if necessary. Sometimes I want to take prednisone just so I can smell coffee again! I take 650 Mg of aspirin once a day. Re: Re: Loss of Sense of Smell Do all of you lose all sense of smell? Or just partial? Loss of Sense of Smell > > > > > > & g t; > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > > > > ----------- > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > > Lane AP, J, May L, R. > > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 I lost all SOS. Haven't smelled anything for at least a year now. Was on Pulmicort for a while. Initially it worked but then it didn't. Am reluctant to have surgery again (had 2). The desense idea makes me nervous. The thought of taking that much aspirin seems like a bad idea to me.... samters From: tami1961@...Date: Tue, 16 Feb 2010 09:56:31 -0600Subject: Re: Re: Loss of Sense of Smell Do all of you lose all sense of smell? Or just partial? Loss of Sense of Smell> > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed.> > > > > > -----------> > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9.> > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization.> > Lane AP, J, May L, R.> > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287.> > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions.> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 Of course its a matter of choice, but usually the doctor is able to adjust the aspirin dose so that it works for the patient. Some as low as 325mg a day, some even lower, though the effectiveness then often diminishes. It is so far the only thing that has been proven to help the majority of people with Samter's. For me, in addition to having a SOS, one of the main benefits of desensitization is that I can eat everything again, whereas before I was sensitive to salicylates, and couldn't have wine, tea, most fruits, etc. If aspirin sensitivity doesn't affect your diet it might not seem as compelling to be desensitized, though for me living w/o a sense of smell felt like a real deprivation. On Feb 16, 2010, at 11:32 AM, D Preis wrote: I lost all SOS. Haven't smelled anything for at least a year now. Was on Pulmicort for a while. Initially it worked but then it didn't. Am reluctant to have surgery again (had 2). The desense idea makes me nervous. The thought of taking that much aspirin seems like a bad idea to me.... samters From: tami1961verizon (DOT) netDate: Tue, 16 Feb 2010 09:56:31 -0600Subject: Re: Re: Loss of Sense of Smell Do all of you lose all sense of smell? Or just partial? Loss of Sense of Smell> > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed.> > > > > > -----------> > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9.> > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization.> > Lane AP, J, May L, R.> > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287.> > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions.> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 Burke, are you desensitized? I had similar success with using pulmicort that way, which is recommended by Scripps, but the folks at National Jewish think that it's better to use the pulmicort in your nasal rinse because the dose isn't as high. It's hard to not do something that you know works, unless it's as nasty as prednisone. > > > > > > What causes partial loss do you think? I can smell some things and not others all in the same day. > > > Tami > > > > > > Loss of Sense of Smell > > > > > > > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > > > > > > > ----------- > > > > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > > > Lane AP, J, May L, R. > > > > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > > > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 Been reading this thread... compels me to ask this question. IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so " light " that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo .... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen. Maybe turn the question around... how " light " would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery? Thanks Mike Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 Mike, I would say if you are comfortable with the way things are, you don't need to rush out and get surgery. It really depends on what your goals are for your personal health and well being. For me, it was important to reach the following goals (not in order of importance, but with the biggest factors for me starred): 1. well controlled asthma, preferably without need for daily medication 2. ability to eat a regular diet 3. reduction or discontinuation of facial pain and the ability to treat myself with pain medication when needed ***THIS WAS A BIG ONE 4. no more chronic infection ***ANOTHER BIG ONE 5. Feel better every day. It is one thing to get sick sometimes, another to be sick all the time, and I couldn't be a good mom doing the latter.***HUGE ONE 6. Smell/taste again For me, surgery was necessary to change my sinus structure (which was undraining) and fix the ossification from chronic infection. My first surgery was 'conservative' and addressed only my maxillary sinus and septum. The second surgery addressed damage from infection and my ethmoid sinus. I wish the first surgery had not been so conservative, perhaps I could have avoided the 2nd if so. Desense was necessary because it allowed me to eat normally, reduce inflammation, treat sinus and other pain effectively. All in all, surgery + desense was the winning combo for me. My asthma is not an issue unless I get sick, so no regular medication, I don't have polyps any more, I only have sinus pain when the weather changes, I FEEL GOOD, the infections I do get seem to resolve with a single course of antibiotics, and I've been able to smell since a few weeks post op. I take 1350mg of aspirin a day (soon to drop to half), and rinse with pulmicort once a day. These are my only regular medications. Good luck figuring out your treatment plan! Jennie > > > Been reading this thread... compels me to ask this question. > > IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. > > I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so " light " that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo .... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen. > > Maybe turn the question around... how " light " would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery? > > Thanks > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 16, 2010 Report Share Posted February 16, 2010 Thanks for posting this. I had always assumed that swelling and inflamation in my ethmoid sinuses pressing on the olfactory nerves was why I had lost my sense of smell. I started losing my SoS in the 90s but would usually get it back after a burst of prednisone for a few weeks. I've had 4 endoscopic surgeries to remove polypps (last in year 2000) and was desensed at Scripps by Dr. son in Oct 2002. I can't really say that being desensed has brought back my sense of smell but my asthma seems to be under very goood control. I take 650mg of aspirin in the morning and am doing the Flovent with baby bottle nipple. In the fall I noticed when I took ibuprofen for muscle aches that my sinuses were less inflamed. So, after talking withe allergist, I added a 600mg ibuprofen in the evening. My last couple of appointments with the ENT have shown much less inflamation than in the past. > > It may not sound new to everybody to write that inflammation causes SoS > loss, but this abstract really is about an important step in discovering > how SoS is lost and, much more important, how it could (conditional) be > regained after the inflammation stops. Obviously, more work in this > direction is needed. > ----------- >snip Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 17, 2010 Report Share Posted February 17, 2010 I'm wondering if there is a connection between aspirin desensitization failure (i.e. no effect on symptoms) and lack of sensitivity to dietary salicylates. I do not appear to be sensitive to salicylates, although I cannot drink red wine or eat wheat. Any thoughts? > > > > > > > > What causes partial loss do you think? I can smell some things and not others all in the same day. > > > > Tami > > > > > > > > Loss of Sense of Smell > > > > > > > > > > > > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > > > > > > > > > > ----------- > > > > > > > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > > > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > > > > Lane AP, J, May L, R. > > > > > > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > > > > > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 17, 2010 Report Share Posted February 17, 2010 Hi , Thanks for the thorough reply! It seems I may have been complaining that the " perfect is the enemy of the good " . Everything you have starred I agree with, and those issues are completely under control. (I've only suffered the facial pain issue just a handful of times.) Two items from my case worth noting... Your item #5 in my case better translates to " a good night sleep every night " . Mouth-breathing does not yield a restful night sleep for me and multi-nights of mouth breathing had taken its told on my mental clarity and etc. Glad to see that's gone. The " perfect " would be to also get the sense of smell back. But more than being a feature of life, it seems a requirement and I was essentially wondering if SOS was the primary reason for others. In my case shortly after I realized I had lost my SOS my car developed a fuel leak that I could not smell. This was on a weekend I got a few miles from home before I realized I needed to go back and get something, when I got there my wife was outside and mentioned the smell and that it was a pretty powerful smell. I wonder (in an abstract way, I'm not emotional about it) what would have happened if I kept on driving that car. It was a high mileage car and the fix was expensive, so we opted to not fix it, but I can't recall what the exact issue was. Anyway, the perspective I got from your list was most helpful. Thanks! Mike > > 1. well controlled asthma, preferably without need for daily medication > 2. ability to eat a regular diet > 3. reduction or discontinuation of facial pain and the ability to treat myself with pain medication when needed ***THIS WAS A BIG ONE > 4. no more chronic infection ***ANOTHER BIG ONE > 5. Feel better every day. It is one thing to get sick sometimes, another to be sick all the time, and I couldn't be a good mom doing the latter.***HUGE ONE > 6. Smell/taste again > > Good luck figuring out your treatment plan! > > Jennie > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Tami, That is an excellent question ; no one really knows beyond what is obvious : partial SoS means the olfactory area is inflamed, but not all of it or not yet to the point that SoS is totally gone. > > What causes partial loss do you think? I can smell some things and not others all in the same day. > Tami > > Loss of Sense of Smell > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > ----------- > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > Lane AP, J, May L, R. > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 , it is more likely a problem of inflammation coming back in the olfactory area ; the fact that the SOS came back is consistent with the abstract I posted the other day : when inflammation is reduced, which is likely what happened after the surgery that got rid of the infected tissue there, SOS comes back ; however, inflammation apparently found a way back in. Now, it is difficult to tell if it is inflammation due to Samter's, to allergy, to germs, etc.> >> > What causes partial loss do you think? I can smell some things and not others all in the same day.> > Tami> > > > Loss of Sense of Smell> > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed.> > > > > > -----------> > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9.> > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization.> > Lane AP, J, May L, R.> > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287.> > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions.> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Ernie, Sorry for your SoS. It means inflammation is back, even though it may not be obvious yet. One possibility (without any guarantee) : what about switching the Nasonex for Rhinocort (which is Pulmicort without the benzalkonium chloride they put in Nasonex as a preserver) ? > > > > > > > > What causes partial loss do you think? I can smell some things and not others all in the same day. > > > > Tami > > > > > > > > Loss of Sense of Smell > > > > > > > > > > > > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > > > > > > > > > > ----------- > > > > > > > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > > > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > > > > Lane AP, J, May L, R. > > > > > > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > > > > > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Mike, If your only inconvenience is SOS loss, and if you do not have endless, recurring, medically resistant sinus infections, nor polyp invasion, then it is advisable not to undertake any surgery at this point. Surgery is not a benign act and should be carried out only for a good reason. If the reasoning is that it may give you back some SOS, it could, but it is not certain at all. It may also aggravate your inflammation if it was very low initially. In your case, trigger avoidance plus whatever medication your allergist would feel appropriate should be sufficient. You will always have time to think about it again if the situation seriously aggravates. > > > Been reading this thread... compels me to ask this question. > > IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. > > I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so " light " that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo .... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen. > > Maybe turn the question around... how " light " would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery? > > Thanks > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Thanks for the suggestion, asfy. I'm planning to schedule a checkup soon with my ENT doctor and going armed with some alternatives to Nasonex is one of my goals since he tends to fall back on it without much thought. I suspect inflammation is indeed the culprit. Though I'm mostly noticing it via my lack of SOS now, that's precisely the time to fight it back before it gets the upper hand. Regards, Ernie > > > > > > > > > > What causes partial loss do you think? I can smell some things and not others all in the same day. > > > > > Tami > > > > > > > > > > Loss of Sense of Smell > > > > > > > > > > > > > > > > > > > > > > > > > It may not sound new to everybody to write that inflammation causes SoS loss, but this abstract really is about an important step in discovering how SoS is lost and, much more important, how it could (conditional) be regained after the inflammation stops. Obviously, more work in this direction is needed. > > > > > > > > > > > > > > > ----------- > > > > > > > > > > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > > > > > > > A genetic model of chronic rhinosinusitis-associated olfactory inflammation reveals reversible functional impairment and dramatic neuroepithelial reorganization. > > > > > Lane AP, J, May L, R. > > > > > > > > > > Department of Otolaryngology-Head and Neck Surgery, Center for Sensory Biology, and Department of Molecular Biology and Genetics, The s Hopkins University School of Medicine, Baltimore, land 21287. > > > > > > > > > > Inflammatory sinus and nasal disease is a common cause of human olfactory loss. To explore the mechanisms underlying rhinosinusitis-associated olfactory loss, we have generated a transgenic mouse model of olfactory inflammation, in which tumor necrosis factor alpha (TNF-alpha) expression is induced in a temporally controlled manner specifically within the olfactory epithelium (OE). Like the human disease, TNF-alpha expression leads to a progressive infiltration of inflammatory cells into the OE. Using this model, we have defined specific phases of the pathologic process. An initial loss of sensation without significant disruption is observed, followed by a striking reorganization of the sensory neuroepithelium. An inflamed and disrupted state is sustained chronically by continued induction of cytokine expression. After prolonged maintenance in a deficient state, there is a dramatic recovery of function and a normal histologic appearance when TNF-alpha expression is extinguished. Although obstruction of airflow is also a contributing factor in human rhinosinusitis, this in vivo model demonstrates for the first time that direct effects of inflammation on OE structure and function are important mechanisms of olfactory dysfunction. These features mimic essential aspects of chronic rhinosinusitis-associated olfactory loss, and illuminate underlying cellular and molecular aspects of the disease. This manipulable model also serves as a platform for developing novel therapeutic interventions. > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Mike, please try drinking 2 tsp apple cider vinegar mixed with water a few times a day for a week. I noticed a difference with inflamation and smell after a week. My issue is I don't remember to do it often enough as my sos falls secondary to my headaches. Tell yourself it's wine...it may help it go down easier. I personally like it and anything acidic like that. Nani juice is also a great wine substitute...too expensive to drink like wine thought! Tami Re: Loss of Sense of Smell Mike,If your only inconvenience is SOS loss, and if you do not have endless, recurring, medically resistant sinus infections, nor polyp invasion, then it is advisable not to undertake any surgery at this point. Surgery is not a benign act and should be carried out only for a good reason. If the reasoning is that it may give you back some SOS, it could, but it is not certain at all. It may also aggravate your inflammation if it was very low initially. In your case, trigger avoidance plus whatever medication your allergist would feel appropriate should be sufficient. You will always have time to think about it again if the situation seriously aggravates.>> > Been reading this thread... compels me to ask this question.> > IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. > > I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so "light" that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo ... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen.> > Maybe turn the question around... how "light" would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery?> > Thanks> > Mike> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Bragg apple cider vinegar is the best. From: samters [mailto:samters ] On Behalf Of Tami Klumpyan Sent: Saturday, February 20, 2010 10:26 AM samters Subject: Re: Re: Loss of Sense of Smell Mike, please try drinking 2 tsp apple cider vinegar mixed with water a few times a day for a week. I noticed a difference with inflamation and smell after a week. My issue is I don't remember to do it often enough as my sos falls secondary to my headaches. Tell yourself it's wine...it may help it go down easier. I personally like it and anything acidic like that. Nani juice is also a great wine substitute...too expensive to drink like wine thought! Tami Re: Loss of Sense of Smell Mike, If your only inconvenience is SOS loss, and if you do not have endless, recurring, medically resistant sinus infections, nor polyp invasion, then it is advisable not to undertake any surgery at this point. Surgery is not a benign act and should be carried out only for a good reason. If the reasoning is that it may give you back some SOS, it could, but it is not certain at all. It may also aggravate your inflammation if it was very low initially. In your case, trigger avoidance plus whatever medication your allergist would feel appropriate should be sufficient. You will always have time to think about it again if the situation seriously aggravates. > > > Been reading this thread... compels me to ask this question. > > IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. > > I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so " light " that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo ... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen. > > Maybe turn the question around... how " light " would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery? > > Thanks > > Mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 20, 2010 Report Share Posted February 20, 2010 Apple Cider Vinegar....that's really interesting for me. I have some anectdotal evidence that I inherited this condition. I believe, although I can't prove it, that my maternal grandfather had it. I know he got sick with asthma when he was in his 40's. At that point in his life he turned to 'health foods'---lots of raw vegetables and fruits etc... He drank APPLE CIDER VINEGAR w honey every day. Lived til he was 91. samters From: sjpeterman@...Date: Sat, 20 Feb 2010 11:34:55 -0800Subject: RE: Re: Loss of Sense of Smell Bragg apple cider vinegar is the best. From: samters [mailto:samters ] On Behalf Of Tami KlumpyanSent: Saturday, February 20, 2010 10:26 AMsamters Subject: Re: Re: Loss of Sense of Smell Mike, please try drinking 2 tsp apple cider vinegar mixed with water a few times a day for a week. I noticed a difference with inflamation and smell after a week. My issue is I don't remember to do it often enough as my sos falls secondary to my headaches. Tell yourself it's wine...it may help it go down easier. I personally like it and anything acidic like that. Nani juice is also a great wine substitute...too expensive to drink like wine thought! Tami Re: Loss of Sense of Smell Mike,If your only inconvenience is SOS loss, and if you do not have endless, recurring, medically resistant sinus infections, nor polyp invasion, then it is advisable not to undertake any surgery at this point. Surgery is not a benign act and should be carried out only for a good reason. If the reasoning is that it may give you back some SOS, it could, but it is not certain at all. It may also aggravate your inflammation if it was very low initially. In your case, trigger avoidance plus whatever medication your allergist would feel appropriate should be sufficient. You will always have time to think about it again if the situation seriously aggravates.>> > Been reading this thread... compels me to ask this question.> > IMHO my samters is now at a relatively benign stage. I can not smell, but with daily nasal rinses, winter-time vitamin D supplements and alcohol avoidance I can breathe through my nostrils with little difficulty. If I take a short Prednisone dose I can regain my sense of smell or ... if I go completely alcohol free for about a month I may spontaneously regain my sense of smell. Thing is in either of those 2 cases the SOS is short lived... days. Finally, my aspirin sensitivity seems to be fairly low (reaction to aspirin is not very strong). My doctor/allergist noticed it before I did. > > I've been like this for the past year or more. Have had samters for the past 8 years or so. My question to those who have had the surgery is ... are my symptoms so "light" that surgery isn't worth it? I'm depressed that the return of SOS is relatively short lived with the surgery. It does sound like the combo ... surgery/desen seems to work for a lot of folks, but I'm not ready yet to try the desen.> > Maybe turn the question around... how "light" would your samters have to be so that you WOULDN'T have had the surgery? How bad does it have to get before you DEMAND the surgery?> > Thanks> > Mike> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 21, 2010 Report Share Posted February 21, 2010 Thanks, asfy! This is what my ENT said after looking up my nose; that I can't breathe or smell because I am so inflamed. I'm much better as I type this, the meds she gave me must really work. > > > > > > What causes partial loss do you think? I can smell some things and > not others all in the same day. > > > Tami > > > > > > Loss of Sense of Smell > > > > > > > > > > > > > > > It may not sound new to everybody to write that inflammation > causes SoS loss, but this abstract really is about an important step in > discovering how SoS is lost and, much more important, how it could > (conditional) be regained after the inflammation stops. Obviously, more > work in this direction is needed. > > > > > > > > > ----------- > > > > > > > > > J Neurosci. 2010 Feb 10;30(6):2324-9. > > > > > > A genetic model of chronic rhinosinusitis-associated olfactory > inflammation reveals reversible functional impairment and dramatic > neuroepithelial reorganization. > > > Lane AP, J, May L, R. > > > > > > Department of Otolaryngology-Head and Neck Surgery, Center for > Sensory Biology, and Department of Molecular Biology and Genetics, The > s Hopkins University School of Medicine, Baltimore, land 21287. > > > > > > Inflammatory sinus and nasal disease is a common cause of human > olfactory loss. To explore the mechanisms underlying > rhinosinusitis-associated olfactory loss, we have generated a transgenic > mouse model of olfactory inflammation, in which tumor necrosis factor > alpha (TNF-alpha) expression is induced in a temporally controlled > manner specifically within the olfactory epithelium (OE). Like the human > disease, TNF-alpha expression leads to a progressive infiltration of > inflammatory cells into the OE. Using this model, we have defined > specific phases of the pathologic process. An initial loss of sensation > without significant disruption is observed, followed by a striking > reorganization of the sensory neuroepithelium. An inflamed and disrupted > state is sustained chronically by continued induction of cytokine > expression. After prolonged maintenance in a deficient state, there is a > dramatic recovery of function and a normal histologic appearance when > TNF-alpha expression is extinguished. Although obstruction of airflow is > also a contributing factor in human rhinosinusitis, this in vivo model > demonstrates for the first time that direct effects of inflammation on > OE structure and function are important mechanisms of olfactory > dysfunction. These features mimic essential aspects of chronic > rhinosinusitis-associated olfactory loss, and illuminate underlying > cellular and molecular aspects of the disease. This manipulable model > also serves as a platform for developing novel therapeutic > interventions. > > > > > > Quote Link to comment Share on other sites More sharing options...
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