religiousnessa wrote:
Not trying to answer a specific question.  I'm just trying to make sense of why some people might improve or get worse, and also to give us a better sense of what we can expect about the likely progression of the disease based on our individual case.  

Yes, I agree that it makes sense to research as much as possible to try to understand how all these things fit together. We get help from some members of the medical community but to a certain extent the responsibility is on us to look out for our own best interests.
religiousnessa wrote:
I disagree with your distinction between "pure atrophic rhinitis" and "secondary atrophic rhinitis."  I think the right distinction is between "primary atrophic rhinitis" (which is indeed rare) and "secondary atrophic rhinitis."
Yes, I am not trying to make a distinction between "pure" and "primary" AR. To be more clear, I should have used the term "primary" as you did.
religiousnessa wrote:
The key thing to realize is that, according to the largest review of atrophic rhinitis cases (Kern and Moore), the only real distinction between primary and secondary AR is *cause.*  In the former, it's usually an unknown cause, although it seems to have something to do with growing up in a really unhygenic environment (e.g., bathing on a daily basis in a dirty river), whereas in latter it usually has a very specific cause (surgery, granulotomous disease, etc.)  But other than cause, primary and secondary AR are very very similar: similar symptoms (obstruction, crusting, bleeding, lost sense of smell), similar objective findings (ct scans and histological findings are usually indistinguishable), and similar course of the disease.  Now even if there are some other small differences between primary and secondary AR (e.g., it's more likely that there's something bacterial going on with primary AR), you still get the sense from the literature that primary and secondary AR are 90% the same.
I definitely agree that in some of the literature they make very little distinction between primary and secondary AR. But I would say that the literature provides a variety of explanations and causes. Much of the literature refers to primary AR as from unknown etiology. Some literature refers to K. ozenae as a cause of AR and some literature speculates that the appearance of K. ozenae  is a result of AR. As you say, there is no real agreement yet as to the specific cause of primary AR. Obviously and sadly we know that surgery is the cause for most secondary AR. Overall, I agree with your assertion that from a symptom perspective, primary and secondary AR have a lot in common. It seems to me that a big distinction between primary and secondary AR is that with primary AR, ozena (a distinct strong odor) is much more common.  I would say that there is still a significant and important difference between the underlying issue. A simplified analogy is that two people with a hurt leg may have very similar symptoms (for example walking with a limp) but the underlying cause could be quite different. A person with a broken bone would need to be treated differently than someone with a sprained muscle. So an example that I can think of is that with primary AR, the underlying submucosa is rarely damaged. With many people with secondary AR, there can be a significant amount of missing submucosa (submucosal resection) or scarred submucosa (like from cauterization). This could suggest that the treatment of the underlying symptoms may need to be different for primary and secondary AR. For example, Young's Procedure is discussed as a possible cure for Primary AR but is not something we often hear about in connection with secondary AR. 

I also think that this may lead to a different long term expectation. There is evidence that with primary AR that the symptoms can reduce over time as the sufferer ages. It seems to me that this is more associated with the underlying disease resolving to some extent. Since secondary AR has a typically surgical cause, there would not be the same resolution as with primary AR. That said, I acknowledge that in some way I am contradicting myself as there is somewhat of a discrepancy with how we commonly see someone with ENS versus ENS-type healing (as I said above). I could see that someone with secondary AR (dryness and crusting) but not with all the ENS symptoms (ie suffocation) could very well expect things to improve overtime as with Primary AR.  Likewise as it seems that there are reports of ENS-type symptoms reducing over time, so then someone with ENS-type could reasonably have hope to get improvement over time but I think I would make a distinction that it is unlikely to be to the same extent as someone with primary AR.
religiousnessa wrote:
I think the confusion is probably more over the first category (pure ENS) than the third category (mixed ENS and AR).  I think the third category is by far the largest category of ENS suffers, and it's the one that most of us think of when we think of ENS.  But I think there are also a few pure ENS people out there: they only had a small amount of their turbinates removed (e.g., maybe 10 percent) and don't have a lot of crusting, bleeding, etc., but they do expierience breathing problems and pain because of the nerve damage.

I totally agree with your point about the amount of turbinates remaining being pretty important to prognosis.  Your body is going to do a much better job of regenerating an organ if it has something to work with.  That actually brings up a good point about the "pure ENS" group:  if there are people who just have nerve damage because they didn't have much turbinate removed, they might be likely to recover somewhat as their remaining turbinates help them to regenerate.


I think that I understand what you are trying to get at here. I think that when you say "pure ENS" you are referring to someone that has ENS or ENS-type but does not necessarily have all the symptoms of AR. There are probably some people that fit into this category. I speculate that still most of these people still have dryness to some degree but maybe not as severe as others that have symptoms such as bleeding. I probably cannot point to specific proof, but I think that dry mucosa is most often associated with pain and sensation issues. From my perspective, when nerve damage is discussed it is issues with the many tiny nerve endings in the mucosa that cause the sensation issues versus a problem with a specific issue with a larger nerve.  

I hope that you understand that I do not claim to have all the answers and that I am not trying to be argumentative. I appreciate that you are trying to work out how all this works and I am trying to constructively exchange some ideas with you to further develop both of our understandings. Thanks