1eye wrote:Maybe some things affected by autonomic nerve pathology get more automatic, and some less. Then wouldn't it depend on individual physiological differences, and how they affect specific nerves? And be predictable, but only in a particular individual?
Not only genetic makeup, but life history as well?
That's a big clue...the differences in the disease in all of us. It doesn't mean MS is caused by something different in different people. It means what causes MS is variable in everyone depending on genetics, diet, physiology, stress, etc.
1eye wrote:Does the vagus predominate in the symptoms? Is it involved in intention tremor, which was among my earliest symptoms? Where do eyeballs fit in? Vision is pretty voluntary, so not placebo. In fact, aren't most eyesight improvements very testable, outside of placebo concerns? You can't turn it off without blinking.
The only way to really find out is to organize a study of VNS in PwMS. Anyone know how to throw that together? I'd volunteer for that before I would CCSVI angioplasty. (Unfortunately or fortunately my symptoms probably aren't strong enough to be impressive in a study) Incidentally, I don't think the vagus nerve necessarily has to be directly responsible for tremors, vision, etc issues. Stimulation of the nerve could result in a chain reaction that causes improvement in those issues.
I was reading through CCSVI treatment improvement stories yesterday and saw one instance in which a man went in for his followup checkup and thought he would be given the thumbs up since all of his improvements from treatment were still there. He had restenosed and had to be re-ballooned. To me, this suggests that improvements aren't necessarily dependent upon the ballooning/stenting. What if stimulation of the vagus nerve does correct the hpa axis dysregulation and it is that correction that causes improvements? Aldo has a 35 minute lifespan in our bodies. All that excess aldo could be gone within 35 minutes of VNS and if hyper-response was corrected, it wouldn't build back up. If my theory is correct, this would lead to instant improvement from the reduction of vasoconstrictor aldo and continued improvement as the veins are allowed to heal from all of the damage excess aldo does to them.
Also, as MS progresses, hpa axis dysregulation increases. It seems that the people who opt to have CCSVI have progressed far enough in their disease to take the risk of angioplasty. The correction of a great dysregulation would probably produce startling results.