Today while looking through the thread "Stem Cells" I looked into a link dignan had provided and I find that a researcher evidently makes the same assumption regarding what is responsible for the relapsing/remitting phase
I'm beginning to believe that the commonly held assumption of what is going on "behind the scenes" in the relapsing/remitting phase isn't in alignment with my assumption which, until tonight, I thought would have been the obvious assumption most anyone would make.Spontaneous repair of brain damage also occurs and is the reason that many
patients recover partially or completely from their first MS attacks. On the long run however,
spontaneous recovery and pharmacological treatment cannot prevent the disease from progressing.
This "other" assumption seems obviously faulty because it relies on every relapse doing enough damage to the myelin to impair function of the axon, yet we are to believe that the body repairs that myelin in what sometimes is a very short timespan between relapse and remission and repairs it so completely that sometimes what had seemed to be severe damage sometimes returns to normal function? It does NOTHING to console the fact that steroid administration during relapse can quickly provide positive results by doing nothing more than reducing inflammation. It's illogical and beyond the realm of possibility.
My belief? Remember the comparison the researchers long ago provided as a simple way to make us ignorant laypeople understand a complex situation? You know, the axon is the electric wire and the myelin is the insulating sheath? I'm convinced that we need to take that comparison absolutely literally. ABSOLUTELY LITERALLY.
Anyone familiar with electricity knows that you avoid sharp corners and bends when running electrical wiring. Sharp corners and bends create resistance which impedes function, despite the fact that the insulation is present.
Now imagine on a tiny scale what is going on inside the brain during a relapse. Those long strands of myelin wrapped axons find themselves running through a twisting inflamed, irritated and swollen pathway. At this point we need to remember that we aren't really considering metal wiring and insulation and instead are talking about biological wiring in which the extra moisture involved in swelling and the inflammation itself has additional negative effect on transferring impulses.
This very handily explains how damage can seem so severe during relapse and dissapear to such a great extent during relief of inflammation, irritation and swelling...otherwise known as remission.
Even with my theory some damage to the myelin is done during a relapse which of course is dependant on the severity of the attack. Sometimes nothing more than some minor cracking (for lack of a better term) which the body is capable of repairing and no damage to the axon. Sometimes in a severe relapse the damage is so bad that enough axons are beyond recovery as to show remaining disability even after the relapse ends.
As with any blatant speculation not supported by fact, there are different directions this theory could have headed which are too numerous to mention. Even stating it as simply as I have I think it is hands-down more believable than relapse=damage...remission=the body healed itself.
As I mentioned earlier, otherwise how can it be explained that steroid treatment quickly provides relief? Steroids speed up the body's myelin repair process? I don't think so.
OK, it's your turn. Shred my theory.