I've been researching for Sjogrens and stumbled into this article today:

http://appneurology.com/showArticle....leId=188500771

If it works on Impaired Glucose Tolerance Neuropathy, maybe it will help other neuropathies.

Billye

Silverlady,
Let me add a recent article from A. Gordon Smith's group in Utah which has been a leader in the arena of diet & exercise and the affect on small fiber neuropathies, IGT and prediabetes. They, and others now claim that up to
~40% of all idiopathic PN's are characterized by impaired FG and/or OGT results. I've been following this work for a while and trying to incorpoarate the recommendations into my own lifestyle since my last OGT was 139 which a local neurologist declared was normal (technically, she is absolutely correct) but my repsonse was that if it had been 140 you would tell me that I'm prediabetic.

http://care.diabetesjournals.org/cgi...ract/29/6/1294

alkymst

Good article Alkymst! This is a good thread. Maybe it will help some people.

Billye

Thanks Billye. That is a great article. It's a review of several clinical studies using patients with either prediabetes or diabetes and PN. The studies explore the effects of glucose control alone compared with glucose control with diet changes and exercise in reducing pain and reducing or reversing peripheral nerve damage.

There was no improvement in reported pain relief and nerve density as determined by punch skin biopsy in the groups that had placebo only, or glucose control with Metformin as compared to groups that also had diet control and exercise. The diet control and exercise groups had reduced pain, reenervation, and improved glucose tolerance.

This is highly significant because the neurological community generally believes that PN is progressive and irreversable. We are ahead of that curve, because we know from peoples' experience in this forum that that isn't necessarily true.

We need a separate thread in the stickies containing research reports or summaries and links to them of factors that stop the progression of PN damage, or that promote healing and reenervation.

These are extremely important studies. Many medical folks working with neuropathic disorders think that many diagnosed as "idiopathic" have IGT. It is vital that anybody not yet diagnosed accurately have proper testing for IGT, ideally a five hour GT test with both glucose and insulin measured.

I am so glad to see some research that does not try to explain a disease by using genes. Turning all illness into a hunt for the "responsible" genes threatens to undermine progress in health care.

It took an awful long time to finally overthrow the idea that the brain and nervous system were not immutable and in fact have great plasticity. Hopefully there will be a renewed trend towards taking charge of our own health. Science and scientific research can help but not if it slants perspective by giving too much control to genes and such.

rafi

Silverlady,
I hope this may be of some interest so I thought I would follow-up my earlier post w/ a complementary and recent paper (2006) again from Smith and Singleton re: idiopathic neuropathy, prediabetes, and metabolic syndrome.
http://www.sciencedirect.com/science...d469fd5964375c

I think the article is worth reading and I’ll try for a capsule synopsis:
The authors have a nice overview of the epidemiology of PN and cite some remarkable statistics about PN research, e.g. <100 research papers have been published re: PN which they estimate may afflict 15-20 million Americans of which ~1/3 are idiopathic whereas there are >4000 papers concerning Guillain-Barré Syndrome, which presents clinically in a more distinct manner but is much less prevalent.
The authors continue w/ a brief historical perspective of idiopathic PN beginning in 1981 and acknowledge the difficulties to recognize new causes of predominately sensory-dependent neuropathies. This gives them an intro to their own work which now focuses on “the Metabolic Syndrome”, the combo of obesity, hypertension, hyperlipidemia, and insulin resistance. They propose that many cases of idiopathic neuropathy result from insulin resistance and are frequently tied to prediabetes and Metabolic Syndrome.
As in their other work, they showed that in a small patient population that DIET and EXERCISE not only improved glucose control and reduced weight, LDL cholesterol and triglyceride levels but that it improved small fiber function, increased intraepidermal nerve fiber density and improved neuropathic pain severity.
It seems that much of the very valuable and useful treatments described here by PN sufferers are now being “proven” clinically. One can hope this will stimulate significant research, future advances and pain relief for us all!
Alkymst

I think my neuro said it all on my last visit to him with these few words " nerves will not repair in the wrong inviroment ",

I don't know how many times i have read on the old BT that doc's haven't a clue whats causing the members PN, because all normal tests have showed nothing, but when asking if their had a 3 -5 hour glucose tolerance test, there has been a few no's, but they say " the doc has checked for diabetes so it can't be anything to do with diabetes ". yeah right.

I believe that it is very possible for a person that has PN and is prediabetic can reverse the damage that has been done to their nerves, by eating & drinking properly with high fibre low GI foods, plenty of water which i think is extreemly important to our health, a sensible amount of exercise, and plenty of vitamin B & B12, & any other supplements that haved proved to be helpfull, repairing time would have to vary depending on the amount of damage that has been done.
It makes me wonder how many people out there that are suffering purely because they just haven't been tested properly, early in my PN days i had a neuro that done a NC Test wrote a letter back to my GP which said " your patient shows no signs of Peripheral Neuropathy as we conducted a Nerve Conduction Test and nothing showed up ", even though i kept on telling him that i felt that my feet were on fire, also i was sent to a rheumo' that didn't send me for any tests at all, and also wrote back saying " i can't find anything wrong with your patient ", i asked him at the time that i would like to be sent to a neuro, " he said no way what for ? you don't show any sign of nerve damage" as he looked at the Nerve conduction test that idiot neuro done , these so called specialists actually get paid for this, what a joke.

I never in a million years would have thought i had anything to do with Diabetes, i had no [known] family history of diabetes on both sides and thats going back 3 generations, but the gene factor is present with me as my Aunt suffered many years with Neuritis in her face.

Silverlady and Wings42,
Although I am very new to this site I completely agree w/ Dave that a separate thread in the stickies devoted the latest info re factors that "stop the progression of PN damage, or that promote healing and reenervation" could be invaluable to all PN sufferers. I'd certainly contribute anything that I have and that I find to such a thread or continue with this one, whatever works best. I've followed this area for sometime and continue to do so.

Just an unsolicited offer.

Alkymst

I may have missed it, but are any of these studies saying anything about the large nerves can also heal in the right environment ?
The reason i ask is, that i had also some large nerve involvement as well small nerve, but both have healed.

Brian,
I know that NCS’s are not good measures of small-fiber function whereas comparisons of distal/proximal IENFD’s by 3mm skin punch biopsies are accurate and reliable ways to assess small-fiber function. In the paper in my 1st post the authors noted that “only measures of small-fiber function improved in the 1st year of follow-up of IGTN” and concluded that the small fibers were particularly able to regenerate.

The authors noted that typical NCV studies of large myelinated fiber function were not reliable markers for IGTN (impaired glucose tolerance neuropathy). For example, the sural sensory response for sensory axonal function varied widely in their patient population and can have test reliability issues. Similarly, the peroneal motor conduction velocity for large myelinated motor fibers, while reproducible, is known to be relatively insensitive to reflect the small-fiber neuropathy characteristics of IGTN. Overall, the authors’ study did not show any statistically significant improvement in any NCS or QST test parameters for large-fiber function.

The authors also stated that their study was limited by the small number of patients and the lack of a placebo comparator group since all 40 patients were treated similarly but they were confident that their results were not due to a placebo affect since IENFD is a quantitative histologic measurement not subject to placebo – same rationale for their QSART results.

My own take on all this is that while after 1 year they couldn’t demonstrate a meaningful and measurable improvement in large fiber function, they could demonstrate meaningful and measurable improvements in small-fiber function and reinnervation including a reduction in pain.

Maybe future work w/ larger and more diverse patient populations together w/ placebo and blinded studies will demonstrate improvements in both large and small fiber function. In the interim your own regimen seems to have greatly improved all aspects of your PN which suggests to me that both small and large fibers could be affected in some way.

Hope this long post helps.

Alkymst