--from my body-wide acute onset burning neuropathy has been long, and while there has been considerable improvement over years, as documented by successive skin biopsies and symptomatic impression--I'm now six years out from the "day which shall live in infamy" when this started (4/12/2003)--recovery is not complete, and is unlikely ever to be.

I certainly don't have the constant all-over body burning that I used to, but I'm still subject to flares. These may well be associated with attempts at nerve regrowth--it's common for nerves trying to re-grow and push through other tissue to produce odd sensations before the brain learns to intepret this as apart from damage and things quiet down again. And I'm very prone to any sort of compressive force producing parasthetic or numbness symptoms out of proportiion to the force. A lot of people with conditions that cause small-fiber dysfunction, especially diabetes/impaired glucose tolerance or celiac/gluten sensitivity, have rpeorted this too, even if the condition has been "arrested"--one simply doesn't seem to grow back all the smal lfiber sone has lost, and what fibers do grow back lead to a differenet configuration than that which one started with and which one's brain was used to intepreting.

Non-length dependent sensory neuropathies are relatively rare and very tricky to prognose. I know that some researchers who've studied people with such syndromes, which suggest selective loss of sensory ganglia, wil lnot go beyond saying that most such syndromes are self-limiting, in that one usually suspects an autoimmune molecular mimicry mechanism--the body mounts an immune respons to some pathogen, fights it off, but the now activated immune system goes after any tissue with a similar molecular structure, which varies individual to individual--and the reaction will burn out once most of those structures are destroyed. If these are fibers, some may have, in time, a chance to grow back. If these are ganglia cell bodies, though, they will not return (once you kill a cell it's dead), though if there are any live cells left, they may try to take over some of the function. This is why you often see the rubric "slow, patchy, incomplete recovery" attached to these syndromes. And the ability to actually document gangliar processes awaits better imaging technology, or, as Dr. Abhey Mogehkar, the Hopkins' researcher who has studied these and who I've corresponded with once joked, "your autopsy".

Sorry to be so inspecific here, but the understnading of such syndromes, even by the experts, is not as advanced as is understanding of other neuropathic processes. The key to recovery may be to find out if there is a controllable etiology, such as celiac/diabetes/a known autoimmune process, that may allow whatever recovery is possible if controlled.