Glenntaj:

Thanks for your info. I appreciate it.

I checked my biopsy report. No mention is made of swelling axons, only a length dependent pattern, sweat gland density being low...calf area down to 2 fibers per mm and a -3 in sweat glands....one normal hair follicle was in the sample...one Langerhans cell was located in the thigh sample stained positive with PGP.

Nothing about onion bulbs, or axonal swelling.

I have some horizontal pattern of innervation in the calf.

Nothing seems conclusive........my biopsy was done by a very respected research physician who trained and worked at Mayo....he set up the autonomic testing facility where I go, likely based on his experience at Mayo, so next to Mayo itself, I think it is pretty reliable.

I have never been there, but, I don't hear much mention of Vanderbilt's Autonomic Center, but I read it is quite good and developed from testing astronauts autonomic reaction in space. Of course, not all small fiber neuropathy results in autonomic neuropathy.

Like I said before, I think I have just reached the end of the internet, for now.

I don't think that I can scientifically substantiate a case for molecular mimicry based on B. Burgdorferi, even tho I have the specific bands for Lyme and the clinical diagnosis from EM, and a rising titer, established at that time. Lyme testing is extremely controversial. I did have one lab that tested bands that most labs do not test, (ironically the very same proteins they used for that Lymerix vaccine.) I am positive on all bands for Bb. I am negative on the tests that test IgG, positive on tests of IgM. (Women have different immune systems then men or the fetus would not survive-I have read women have more IgM response) Early antibiotic therapy aborts the immune response to Bb....and all further testing depends on that immune response. I have had negative PCR of spinal fluid, so I do not think there is any active infection. They took 20cc of spinal fluid, so that is a lot to test for Bb proteins.

If axonal degeneration is an outcome of Bb, thru molecular mimicry, it would cost the 'system' quite a bit of money for IVIG. I do not see research proceeding in the direction of proving molecular mimicry causing axonal or neuronal degeneration. The cost of IVIG would bankrupt insurers, and drive up the cost of IVIG due to shortages.

All inflammatory markers, thus far, are negative....which is why I pushed genetic, just to see. Chances of a hereditary cause are likely low, but due to disease progression and my own work on pedigree, my doc agreed.

If I could make a case, I would likely be on IVIG...but my case would be based on Lyme, and Lyme gets a bad rap. Insurers won't buy it.

This biopsy is getting pretty old now, almost 4 years old and symptoms are much worse now then when it was done.

I think confusion comes in with abreviations....CIAP=Chronic Idiopathic Axonal Polyneuropathy, versus, CIDP=Chronic Inflammatory Demyelinating Polyneuropathy....two very distinct types of PN. Even with a medical background, I have to really double check things. I think it would be worth a posting showing all these abreviations and explaining these diseases and how many different types of PN there are.

With idiopathic cases, showing no inflammation, showing disease progression, with negative finds for any of the known disease entities responsible for axonal degeneration, (except for Lyme) I do not think it unreasonable to explore heredity.