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

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

Thanks for your reply Alkymst, you have certainly done your homework a very detailed answer, and i agree that the skin punch is the most accurate way to test for small fibre damage or comparison.
My large nerve involvement was only picked up by an EMG, my own neuro done it, who is a PN specialist.
Perhaps when the healing process begins the small nerves may heal faster than the larger ones, or there is more to heal in the larger ones,i really don't know, i was lucky in that the cause was picked up very early when my PN started, so there wasn't too much damage to repair, had the cause been found a couple years later, i don't think i would be anywere near were i am now, but the healing process would have been slowly still happening though.
Brian