This Is MS Multiple Sclerosis Community: Knowledge & Support

I am the only patient that this doctor in NYC has given Rituxan to at this point. I am not part of a formal study, but the doctor treats me like a show dog. HaHa! We are all so happy with my rapid results. Literally, 48 hours after receiving my first infusion of Rituxan, all of a sudden it was like a dam broke in the left side of my face and head. Where I had numbness on the entire left side of my head, nose, mouth and tongue. Within minutes, my numbness disappeared and full/normal sensitivity was restored. It was so dramatic that I said loudly, "How my!" and my son said what's wrong? It was like a miracle.

My situation is rather atypical. I am over 50 years old, extremely healthy, have no banding in spinal fluid; however, my symptoms continued to worsen before treatment as my lesion grew. It was growing rapidly and my health was declining. After the first two infusions of Rituxan, my next MRI showed a somewhat reduced brain stem lesion that was not enhanced. I have not (knock on wood) developed new lesions and it has remained stable for the most part. After one year from the first treatment, there is a little enhancement of the lesion, so we are going to do another MRI and repeat the Rituxan treatment.

The doctor and I are playing it by ear for now. I will take Rituxan this year and keep a watch on things with MRIs. Even if I have to continue on with this drug, I am ok with that. It doesn't impact my daily life and I tolerate the drug well, so far. I have a great life, I exercise daily and very happy and fortunate.

I made the decision to go to NYC to get a second opinion and am really glad I made the move.

I hope this helps someone!

I suggested Potts post this in the CCSVI forum because of this statement. This sounds like the "on the table" improvements experienced during PTA, decompression of cranial nerves and brain stem. One of the effects of rituxan is that it decreases cortisol and aldosterone. I don't know if that is the mechanism by which the sudden improvement occurred but I think there is a good chance it is.

Drug treatment should be considered by those who suffer symptoms related to cranial nerve/brain stem compression and reduced cerebral perfusion. PTA isn't the only option and it may not be the best option in some cases.

CCSVI needs to be renamed and redefined. In MS, it is reduced cerebral perfusion and csf drainage caused by a number of factors. These factors include not only valve malformation and venous stenosis. They include damage caused to blood vessels by the unique endocrine profile associated with MS and the resulting nutrient deficiencies. This should be treated conservatively with drugs and nutritional supplements at first. If the drugs and supplements fail, proceed with PTA. If this statement proves to be true, I think "CCSVI" is much more likely to be accepted by neurologists and mainstream medicine.

Making assumptions regarding Rituxan, CCSVI research and your personal theory may be a bit early, Anonymoose. Especially with regards to recommending medications.

I don't include the following info for Potts, he's doing well on Rituxan and may that continue!
But there are serious FDA enforced black box warnings on this medication for PML, infections, blood and cardiovascular problems which should be considered before beginning treatment.


http://online.wsj.com/article/SB124381351149970563.html


http://dermatology.cdlib.org/121/review ... nfeld.html

Glad you are doing well, eating well and exercising, Potts....stay healthy!
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

With all due respect cheer, ccsvi PTA has been performed to "treat ms" for years without a full understanding as to how or why it causes improvements. They aren't even certain which patients it will help. To dismiss assumptions based on actual evidence of a cause/effect relationship between MS endocrine issues and the impact on cerebral perfusion and csf drainage but to fully embrace ccsvi PTA without such supporting evidence is odd to say the least.

I have not recommended any medications other than clonidine which I have taken myself without adverse side effects (so far). Quite the contrary, I have enjoyed positive side effects. The risk of taking clonidine under doctor's supervision relative to the risk of having PTA is negligible. I've not heard of anyone's jugular collapsing as a result of taking an anti-hypertensive that has been widely used since the 1950s and that is currently used on children with ADHD as well as for a number of other off label conditions.

Also, there are flow issues that cannot successfully be treated by PTA or stent. Compression of the left innominate vein by the aorta and veins compressed by bone or muscle come to mind. Treatment of other "ccsvi" factors might help in these cases.

There are people who still need help with these issues. We should be looking for alternative treatments. CCSVI led us to the realization that perfusion and csf flow are issues in MS. However, PTA is not the end of this path.

Congrats, Potts!
I would've missed this elsewhere. The connection would be the immediate improvements. Immediate improvements are not due to sudden healing of damaged neurons. So in Potts case, what were the immediate improvements due to? Does forty-eight hours later still count as immediate?
Rituxan is a chemotherapy treatment? Is it like tysabri and the blood-brain barrier slams shut and inflammation goes down and that's the cause of the improvements? I wonder if vein and brain inflammation go down quickly after CCSVI treatment. Steroids result in immediate improvements too?

Nah, jump into PTA headfirst. Neckfirst, really.
No amount of drugs or supplements could have fixed my bad valves. My diet improved 10x after the procedure because of how good food tasted. I exercise more and harder now because of the improvements. Etc etc.
It's ok if the neurologists don't accept CCSVI yet. Research is needed (and apparently funding is needed for the research). I'd like to see greater acceptance of CCSVI among the IRs. That's what I look for at these SIR and ISET conferences. The IRs are the ones we need to do the research and offer the procedure and perfect the procedure.

Cece,
On clondine, my stiff neck and shoulders resolved overnight. When my dose wasn't right, I could feel the tension coming back but as it was doing so, I felt strange throbs in what I assume is my brain stem area. My energy/endurance has increased to a point that I am flabbergasted by how much I can do without tiring. My mind is much quicker and clearer. Most of my sensory issues are gone. I am left with only a little insensitivity in my finger tips. I can walk around barefoot without cold feet in the winter. Sounds PTA'ish, no?

Clonidine is a drug that is sometimes effective in relieving iih (poor csf drainage) and it inhibits aldosterone which is known to impair cerebral perfusion. I think it takes some time for the drugs to shut down whatever is interfering with csf flow and perfusion. Unfortunately, I never really had any major issues that could easily be attributed to cranial nerve/brain stem compression or impaired cerebral perfusion so that obvious connection couldn't be made with me.

Potts' did have those symptoms though and an "on the tablish" sudden improvement in symptoms. Rituxan reduces cortisol and aldosterone so it might be the same thing happening via a different avenue. I don't really know much else about rituxan so I have no idea how else it might cause such an improvement. It is impressive though!!

I believe your valves were contributing to your issues and maybe that was your only issue. I really do hope so. I also think it's nice that with PTA there doesn't seem to be a need for long term meds (I still fear damage caused by aldosterone coming back to bite PTAees later on). But I think for at least some people, there are opportunities to correct csf flow and perfusion with drugs. You worry about these people as much as I do. It can't hurt to explore those opportunities...for those that PTA doesn't help and for those who can't afford PTA.

The neurologists do matter. Most MS patients depend upon a neurologist for leadership in their management of MS. Only a fraction of MS patients find themselves on TIMS and other similar boards. The neurologists need to embrace the concept of "CCSVI" in MS in order to help all of us.

I hope you're onto something with the Clonidine. Those both sound like valid possible reasons for why it would work, and your results speak for themselves.
There will be pharmaceutical options once we get that far with the new vascular angle.

I think neurologists are a lost cause until we have hard evidence.

The main action of Rituxan is to eliminate B cells from the body. Interestingly, B cells are the main place that EBV inculcates itself in the human body in its dormant state. By eliminating B cells, Rituxin goes a long way towards eliminating a patient's EBV load. This could be of tremendous significance, as the Epstein-Barr virus is almost certainly integral to the MS disease process (people not infected with EBV don't get MS), and could be a triggering mechanism for human endogenous retroviruses resident in a patient's DNA. These pieces of ancient retroviruses that have become part of the human genome had been assumed to be strictly dormant, but recent studies suggest that in the presence of smoldering infections they can become activated, leading a person's own cells to secrete proteins that would identify those cells as hostile invaders. Thus, a cascade ensues that can cause all kinds of trouble.

There are trials now ongoing using very strong antivirals to try to achieve a similar result, based on many of the above facts and assumptions.

Regarding the risk of Rituxan and PML, the drug has been used on tens of thousands (if not hundreds of thousands) of lymphoma patients, with a very low incidence of PML. The chance of contracting PML on Rituxin is infinitesimally smaller than that of contracting the infection while on Tysabri. The Rituxin safety profile is quite robust, the drug has been on the market for well over a decade and its use is well known and well documented.

How and if this plays into anything vascular is at this point completely a matter of conjecture. The elimination of B cells, which are increasingly being understood to be one of the major players in MS disease etiology, would seem to be the most likely mechanism of action, but the concurrent elimination of EBV, and the possible benefits of such, hints at another paradigm shifting development in our understanding of the MS disease process.

Full disclosure: I underwent Rituxan therapy several years ago, to no apparent benefit. But, as always, I am a bad patient by which to measure the efficacy of any treatment, as my disease may or may not be MS, and continues to stump the best minds in the business.

_________________
Marc
www.wheelchairkamikaze.com