Why quick recovery? –

November 10, 2007 at 6:15 pm


You know that immunology book you have? I bet the section on inflammation is similar in length to the section in the one I have: 21 pages. And my book assumes that I have understood the preceding 330 pages, which I don’t yet. My guess is that the inflammation caused by the demyelination affects the other tissues in the nerve, leading to the clinical presentation.

When I first started thinking about this problem, I thought of the nerve as a simple cell, with a central body, an axon, and dendrons, wrapped with a myelin sheath. It is actually more complicated than that. First, what I have described as the nerve is actually a nerve fiber. In what doctors call a nerve, there are lots of nerve fibers, most of which are wrapped in myelin (but not all are). Many nerve fibers are bunched into a nerve bundle, which is embedded in endoneurium. Several nerve bundles are then contained in epineurium. Finally, the epineurium is contained within a perineurium sheath, which also contains lymph. See [I]Grey’s Anatomy[/I], 15th ed., page 47, for a good drawing. My guess is that the demyelination not only inflames the axon (without necessarily causing permanent damage) and the Schwann cell, but also the endoneurium and epineurium.

I think it is like MS patients and heat. I have a friend with MS who can walk, albeit with a cane, for about a quarter-mile without undue exhaustion. On a very hot day, though, walking 100 feet completely exhausts her. Heat slows down nerve conduction in all of us. In her case, though, it is like tipping a scale. The normal slowing caused by heat is just enough to dramatically increase her clinical weakness. Another way to think about it is the pressure paresthesia we all have experienced when we have sat cross-legged too long. This process is, I think, due to an inflammatory response due to a loss of blood supply. Restore the blood, the inflammation goes away, and the paresthesia goes away.

I will also try to discuss this topic with my neurologist on Friday. We have discussed this topic before, but he admits that he doesn’t really know. This time, we will try to spend some time thinking about it. The inflammatory process is complicated, the anatomy of the nerves is complicated, and the interaction of all the components is almost impossibly complicated. The scientists will figure it out one day, but I bet the inflammation section goes from 21 pages to a book all to itself.


I am sure that if the NCV tests show demyelination, then Kevin has demyelination. I think though, like I said to Norbert, is that the inflammation caused by the demyelination tips the balance towards weakness.

Don’t forget that in a normal person, myelin is being replaced continually, just like your hair and nails grow continuously. So in someone with CIDP, there is a continual process of myelination/demyelination. If IVIg is able to suppress the antibody against the myelin, then the myelination should win out. At the end of IVIg’s effectiveness, the antibody production probably ramps up and the demyelination would win out.

I don’t understand why Kevin is getting the protocol he is getting, and I have forgotten what all you have tried. A common protocol seems to be a loading dose like what he is doing now, followed by one or two days every two weeks for a couple of months, then one or two days every month for a few months, followed by one day every 4 or longer weeks, depending on symptoms. That should be less time overall out of his life, and lower costs to your family, within a few months.

I do hope things work out well for Kevin. Why on earth could they not access his port, even with some swelling? Seems ridiculous to me.


We know that what we call CIDP has primarily motor effects in some people, primarily sensory effects in others, and the more usual mix in most. Are they really variants, or just the normal range of variation in response to the same disease? Who knows? As for the enhancement in the MRI, I think just says that there is an inflammation of the nerves near the spine. I think it is a typical process in people with CIDP. In Europe, they typically call CIDP “chronic inflammatory demyelinating poly(radiculo)neuropathy”, where “radiculo” means the nerve roots at the base of the spine. That is, the disease is likely to affect the nerves from the spine out. I would talk to the neurologist about this, but I don’t think the finding is unusual.

I hope my speculations and guesses are helpful and make sense. Please bear in mind that they could be wildly off the mark, as I am not a medical doctor. If so, it would be good if some doctor would jump in here and correct me.