CIDP EMG/NCV shows no demylenation

    • Anonymous
      May 13, 2012 at 3:39 am

      I was diagnosed with CIDP in 2007 based on lumbar puncture, EMG/NCV (borderline), and the rest of the standard symptoms. I have been treated with an IVIg loading dose with solumedrol for four consecutive days in every 28 days since then. It has been extremely helpful. Any time we tried to either reduce the dosage or extend the time between treatments I went downhill immediately (numbness, weakness, etc.) I went out to Northwestern the first week in April to be evaluated for the stem cell transplant treatment. However, the EMG/NCV tests that they did there showed no evidence of demylenation (serious axonal damage and other issues were present, and my feet still don’t work). Since the treatment in the Northwestern clinical trial is designed to stop demylenation, I was turned down. I was a bit puzzled, so I went to Mt. Sinai, in NYC, where they were also a bit baffled. They did another EMG/NCV (that’s my fourth) and the results were the same, much to their surprise. Now we are all puzzled, since, except for the anomalous EMG/NCV test results I have a classic case of CIDP and have responded to one of the standard treatments. Has anyone had this experience? Thanks.

    • May 13, 2012 at 1:40 pm

      There are 2 scenarios that I can think of.

      1) The 1st EMG/NCV was botched either by error or environmental factors (I believe being in a cold room can affect the results).

      2) You had very slight demyelination & your treatment regimine allowed the squamous cells to do their job & repair your myelin. It may have been such slight demyelination that it won’t show up on an EMG now.

      My daughter had very slight demyelination on her 1st EMG. It was MUCH better on the 2nd & by the time she had the 3rd it was almost gone. She hasn’t had one in years but I would be willing to bet she no longer has any.


    • May 13, 2012 at 2:33 pm

      my cidp sounds similar to that too fred. Definitely immmune system related, not a lot of demylination, no pain, just distal axonal neuropathy with numbness and weakness in my feet and lower legs. The IVIG is helping some, but not as well as i hoped. prednisone made me worse . Mayo diagnosed it as “atypical cidp” I am getting ready to try an immunosupressant (rituxin) in a few weeks after ruling out any possibility of an underlying tumor which can cause cidp symptoms.
      good to know about your Northwestern experience–i thought about going out there, but just had the feeling i too would be turned down due to the type of cidp I have. I still plan to try if the rituxin doesnt work—trying to buy time until my youngest child is out of high school, and thinking that one day sct might be available everywhere not just northwestern.

    • May 13, 2012 at 6:11 pm

      I just re-read my post. Apparently I should not type before I have my coffee. It’s the schwann cell that remyelinates not squamous cell. Sorry about that. LOL


    • May 13, 2012 at 10:36 pm


      To quote Anne Elk (Monty Python fans unite): I have a theory. Actually, it is a hypothesis, because I have not tested it with experiments. The hypothesis, though, is based on an observation. When I first came down with CIDP, I responded well and immediately to Solumedrol. While not asymptomatic, I was vastly improved by the next day. Clearly, that improvement could not have been the result of remyelination. I heard an explanation later that the Solumedrol, by reducing the inflammation, reduced the edema that was affecting the nerves and thereby resulted in a rapid response.

      My hypothesis is that CIDP has two components, an inflammatory component and a demyelinating component. In most of us, the two are tightly linked. In others of us, though, they are not be so tightly linked. Perhaps, Fred, the reason IVIg/solumedrol works so well is that inflammation is your predominant nerve-damaging mechanism, but it does not result in much demyelination.

      Part of the reason my neurologist does not like to do NCV tests (other than the obvious) is they are not always perceptive low levels of demyelination. He feels that paying attention to clinical symptoms is a better overall indicator.


    • Anonymous
      May 14, 2012 at 2:13 am

      Thank you to everyone for your thoughts on this. Emily’s experience sounds like mine; it is good to know that my experience was not unique. MarkEns’ theory is extremely interesting; it makes a lot of sense to me. Why is it that no doctors have thought of this?


    • May 14, 2012 at 2:56 am

      I have been diagnosed with CIDP as well, but it is atypical. I had three emg’s in four or five months of each other. The first one showed obvious demylenation around my knee (it was my first area I noticed symptoms, but apparently this is a common location for demylenation).. and all my nerves on the ncv were slow (neuro said like a 90 year old and I am31.. however like kelly said- they did not warm up my fingers or toes.
      The 2nd emg they warmed my extremities up in hot hot water (so i wonder if it can effect it the other way)… they didn’t recheck my knee so we don’t know if I had any demylenation on that one, however it was completely normal even in my weakest areas (they were baffled).. The 3rd emg done by the ALS neuro clinic at UTSW was completely normal as well (they warmed up my extremities as well) by this point i was REALLY weak all over (more proximal weakness than distal, however my hands were pretty bad- completely paralyzed “floppy” finger tips of all fingers).. I was admitted into the hospital for a week and given IVIG which has almost completely reversed my symptoms.. (my LP showed upper limit of normal protein first one and elevated 2nd- though I had meningitis from teh IVIG the 2nd one so who knows if that was accurate). Anyhow.. IVIG is working wonders on me.. when I get sick or go 3 weeks in between I can barely walk, swallow hold things at times.. it’s truely amazing!
      Markens- that is a great theory i think! Good luck Fred!

    • May 14, 2012 at 11:39 am

      To add to the stories of atypical tests, my normal nerve conduction studies did not reveal demyelination but when they did nerve root testing, they found the conduction block ( evidence of demylenation) – it was because it was high up in the proximal nerve root that is was missed on testing of the lower part of the nerve. Not all neurologists are able to do this apparently requires special training and it is very painful to have done! Aslo like MarkEns pointed out , inflammation is a huge component and in fact if any of you have had MRI looking at your nerve roots, you can see the swelling and this is used as one of the criteria to support diagnosis. Fred, I am glad to hear you are responding to therapy!

    • GH
      May 14, 2012 at 3:24 pm

      “Atypical” nerve conduction tests are not that unusual. According to Parry and Steinberg: “If multiple nerves and nerve segments are studied, the demyelinating nature of CIDP can be demonstrated in about 90 percent of cases.”