--at the same time the spinal/brain MRI's were ordered, but that is because at the time the Staten Island neuros were loking for MS or another central nervous system demyelinating disease--neuropathy had not occurred to them, as my symptoms were acute, body-wide, and entirely sensory.

Apparently, no one there had heard of acute sensory neuropathy as a variant of Gullain Barre syndrome, or of acute gangliopathy; I found out about these entities later as a result of Internet research. 43-year old presents with acute body-wide neural pain, without a single abnormal inflammatory or autoimmune blood marker (including an immunofixation electrophoresis)--what do you look for? Central nervous system demyelination. But---and this is where I fault many doctors--the other entites are certainly possible, and should have been known about, and considered, especially by neurologists (who are supposed to specialize in these areas, right?). I had to go to Cornell Weill to access doctors who were familiar with these entities and who were aware of autimmune reactions that involved specific antibodies to components of peripheral nerve, and who could run those tests.

The interesting thing was, all the assays for known antibodies to peripheral nerve came up negative for me. But when Cornell Weill ran their own ganglioside agglutinin assay--a "gross" measure designed to just check for demonstrable nerve autoantibody activity across the spectrum--that was a slight positive, implying that I had autoantibody activity, but it was not identifiable as part of a presently known category. Dr. Chin and I both speculated that this might have indicated autoantibody activity unique to my own small-fiber nerve structure. He and Dr. Latov and their colleagues believe, and have written, that many "idiopathic" neuropathies, especially of the small fibers, are immune mediated by autoantibodies that we have just not as of yet isolated/identified; after all, even the "known" antinerve antibodies have only been identified in the last 25 years or so.

The Cornell Weill group is well known as a strong advocate of IVIg; in fact Dr. Latov has argued that even if one has no specific "identifiable" autoantibodies, the result on the ganglioside agglutinin test, or a result of protein in the cerebrospinal fluid from lumbar puncture (and lumbar puncture is on the Cornell protocol as part of secondary neruopathy investigation), is enough to argue for a trial of IVIg. This is considered a fairly radical stance in immunity circles at this point.

I was not offered IVIg, as my neuropathy was acute and apparently monophasic, slowly improving over time, but if my symptoms had assumed a more CIDP-like relapsing-remitting pattern, the staff said they would have recommended it. I do know there are some people getting IVIg infusions at Cornell-Weill based on what other researchers would consider less than slam-dunk evidence of autoimmune factors. (I've had some interesting conversations in the waiting rooms, as well as with Drs. Chin and Latov.)