ZekesTraveller
Well-known member
Guys correct me where you feel I am wrong here: There are several known conditions that cause neuromyotonia. These include axonal damage (e.g., from local nerve irradiation or toxins), timber rattle snake envenomation, certain idiopathic or inherited neuropathies and genetic mutations affecting potassium channels. This here is a large factor for this document. That many things can cause this illness and nicely says many are simply not known thus the idiopathic which is doctor talk for we/I don't know. Hell I don't know either. Even if I knew I would still have to come up with a cure. Yeah! Well, I do know of one chemical that can do this across species . These would be neurotoxins like venom or heavy metals. In the remainder, who constitute the majority of patients, the disorder was regarded as idiopathic until studies dating from 1991 showed that many of these patients have strong immunological associations and respond to plasma exchange.[2] guess we have to go through all this data and find what these people have or do not have in common.The neurophysiological abnormalities can be transferred to experimental animals by injection of neuromyotonic IgG,[3] unequivocally pointing to an antibody-mediated disorder and implicating voltage-gated potassium channels (VGKCs) as their target. It was later shown that antibodies to VGKCs could be detected in about 40% of patients by radioimmunoassay using [sup] 125a-dendrotoxin.[4] By down-regulating VGKCs, the antibodies would be expected to interfere with nerve repolarisation and lead to repetitive discharges.This is a tremendous assertion to make on a small population study group of 20 persons. However I am not sure that the entire group of people was actually 20 persons but this document does make it sound like it. It was a preliminary document that was scratching the surface of the illness. But it does make some very stunning and unfounded claims at the time. This of course could have changed and apparently more evidence mounts. Here is were I have a major problem with this document. Since they have isolated the IgG...again this is just doctor speak for an anitbodies. Apparently they knew what causes the problems because they were able to isolate the pathogen as seen by the body of sufferers and inject it into other animals obviously of different species than ourselves. However I would bet this was a shot in the dark because everyone knows this is the most common antibody we have in the human body against almost all invaders. Suddenly there is a jump to VGKC with no apparent explanation on how they arrived at this conclusion. Of course they do not state specifically that they were refering to humans or the animals onto which the isolated human antibody was isolated from. This leaves a lot of questions for me to ask. Further down the line there is a number of 40%. If the serum positive patients numbered 20 then 8 of them must have the antibodies present at very high levels to be deemed anywhere near the culprit. What is very interesting from a research stand-point is that this illness apparently can cross species causing the same effect on the recipient species that it caused in the originating species. I could at this point in time walk into any laboratory and show antibodies to every illness on the planet just like anyone else could do the same thing. In fact I tried it and I am sure everybody on the planet will show some antibody activity to every known illness. That is just the way our bodies work. Of course this would rebound the question back to how many titres were preformed before calling it high. That is how many times was the sample diluted to isolate the antibodies and still call it high. Below is a statement that clarifies how many people actually showed IgG titre levels high enough to this particular antigen. It was 1 out of 20. This equates to 5% of the study group but the test could now be more sensitive than it once was. Neuromyotonia is now increasingly being recognized as a potentially treatable disorder and the study[5] is remarkable for the large number of patients in their series. The disorder was characterised by electromyography in all of them, but measurement of VGKC antibodies was only possible in one patient in whom the titre was markedly elevated. It cannot be assumed that the disorder in all the remaining 19 patients was due to VGKC antibodies. First, VGKC antibodies are only detected in about 40% of patients. Second, neuromyotonia can associate with inflammatory neuropathies presumably as a result of damage to juxta-nodal VGKCs by an unknown disease process that may not involve an autoantibody attack. At this point in time I would have thrown my lot with this camp for several reasons. Largely because BFS/BCFS shares little similaraties with known auto-immune illnesses such as RA, Scleroderma, Lupus etc. BCFS afflicts males as heavily as it does females. All known and verified auto-immune illnesses are by in large diseases that women suffer. Males suffer auto-immunity too but nowhere to the degree that women do. BFS/BCFS then breaks way with this rule of thumb in the field of Rheumatology. I have heard that there are claims that Myasthenia Gravis is the closest relative to our illness. Howeover BFS/BCFS shows absolutly no response to Prednisone the time tested treatment for auto-immune illnesses in just about every documented auto-immune illness known to medical science. If BFS/BCFS shares etiology with Myasthenia then why are we not prescribed Cholinesterase inhibiters but instead are prescribed anticonvusants and anti-anxiety medication. I have not read of a single case on this board where a board member was injected with Tensilon to alleviate the supposedly Myasthenia relative BFS/BCFS. Thirdly and importantly, 11 of the 20 patients had been receiving Ayurvedic medications that, as the authors point out, could have been the incriminating factor in these patients. This important observation needs to be widely known and the authors should be congratulated on bringing this to the attention of neurologists.This here is the meat of this document because nothing else could at the time be taken as fact especially in such a small study group with no controls of any kind. However 11 out of 20 is interesting but I would bet it is nothing more than people seeking alternative treatments for an unkown illness. It was not Ayurvedic that caused the disease in my opinion but simply people looking for treatment wherever they could get it and it just happened that they were on these treatment when they were seen by the research group. This of course was a document that was INITIALLY looking into the illness and no one should fault it for trying. I saw three rheumatologist that ran the entire spectrum of test on me and every single time I came back negative for all auto-immune diseases including Myasthenia but then again i was never given Tensilon. In all fairness to the argument I would not put myself past a subclinical form of Myastheia since I did begin with twitching in my check muscle many years ago and have through the years have the majority of my complaints located in my face. Next time I go see my neurologist I am going to ask for an injection of Tensilon to see what it does. At this point I have passed four of the five criteria to not be diagnosed with Myastheia. 1. neurological exam by three neurologist.......good, does not support Myastheia2. Full anitbody panel by three rheumatologist.....negative for auto-immunity, does not support Myasthenia3. Tension injection.......never had it done4. EMG..........................4 needle EMGs all good, normal, Does not support Myasthenia5. NCV-Test...................4 NCV test all normal, good results, Does not support MyastheniaSo I am back to where I began. Sure there is something wrong with me I just don't know what the hell it is.
) sharon