Plasmapheresis & Rituxan Treatment

[KMBludworth]

Has anybody heard of this treatment? It has been around and offers much success. If so, was it successful for you? I did not get approval for stem cell overseas (PPMS) and I'm looking for different options. Any insight would be appreciated.

Thanks, Karen

[1eye]

Mitochondria are thought to have been messed up somehow, possibly by clonal expansion of mutated ones, possibly clonal expansion of ones damaged by infection, say, by EBV. That would cause inability to absorb oxygen (termed 'virtual hypoxia').

I have thought that, since B cells are suspected of harboring latent Epstein-Barr virus, perhaps complete blood replacement might help, and I would follow that with the CCSVI procedure, since cerebral blood transit time in MS is twice as slow as normals, and with hyperbaric oxygen to help healing.

I have since read, in the same paper that investigates cerebral blood transit time, as well as others which use different means to get the same result, that this slowed cerebral transit time phenomenon is unrelated to CCSVI. The therapy you referred to sounds like it would clean out the rogue B cells, and perhaps make you have cleaner mitochondria.

CCSVI therapy operates on jugulars and other large veins.

What if the problem with metabolism of O2 were primary, and somehow, that lead to a reaction at the level of control of the speed of blood through the brain; i.e., the reason for the low transition time of blood through the brain was that the brain was reacting to a widespread inability to absorb oxygen by constricting the capillaries and venules and arterioles as much as possible, in order to slow blood's passage through the organs of the brain, and squeeze out what seems to be a small amount of available fuel, to keep the metabolism going? What if a good way to do this on a wide basis was to increase the expression of the hormone endothelin-1? What if the release of a large amount of stored NO was a reaction of extracranial body parts and organs, to the excess of ET-1 in the blood, by expanding the blood vessels outside the brain, to compensate, allowing a higher throughput outside the brain, where fuel being scarce was less important?

pwMS seem to be in a condition where these two powerful agents of blood vessel diameter control, ET1 and NO are both overabundant, in an unusually delicate balance, where small things to normal people, like an increase in temperature, can throw things off balance easily, and the loss of more finely grained control of fuel delivery and availability is swamped by the gross control needed to provide enough brain metabolism going?

This seems to require that we identify two things: 1., the agents of the fine vessel diameter control that operate more locally, and are not dependent on a widespread release of NO or ET-1, and 2., the reason for the widespread loss of ability to consume fuel. the virtual hypoxia that requires the general slowdown of blood transit in the brain, to allow metabolism there to be maintained above the survival level.

Or maybe I am trying to think beyond my depth, and the problem with my brain has resulted in my depth being rather shallow. I do want to find a way to solve the thing, so I can get better.

[1eye]

What do you think, Karen? Did you get the treatment? Were your questions answered? Muddled minds need to know...

[KMBludworth]

No. Not at all. I've already had the procedure for CCSVI with no results. I am looking for any results and knowledge for plasmaphersis and rituxan. Thanks