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What goes on during a relapse?

Posted: Wed Mar 24, 2010 9:51 am
by JennP
Hi, if anyone could answer my question I would really appreciate it.
CCSVI makes a lot of sense to me, the only thing I really don't get is what is going on with the veins during a relapse. Is the stenosis, or valve problem (or whatever your venous problem is) worse during a relapse. I just want to have all the information clear in my head before going to my doctor with my request to see a local interventional radiologist.
Thanks

Posted: Wed Mar 24, 2010 10:17 am
by Apuman
I don't think anyone really knows the answer to that yet. There's been some suggestion that stenosis can come and go, possibly playing into the relapsing-remitting pattern that we see, but franky, it's still way to early in the game to know these sorts of things.

Posted: Wed Mar 24, 2010 10:42 am
by Cece
It could be that the brain gets along at a suboptimal level until some oxygen deprivation event (hiking at altitude, bad illness, childbirth) pushes things over the edge.

My first optic neuritis attack was after hiking on Mt. Haleakala on Maui, so I am partial to this as explanation.

Posted: Thu Mar 25, 2010 4:39 pm
by tipsyturtle
Interesting thought Cece,
I've had 2 major attacks in the past few years- one started during or right after a flight, and one after a major bout of throwing up due most likely to food poisoning.
Both fit into this idea of oxygen deprivation.

Posted: Thu Mar 25, 2010 4:55 pm
by astro
These are all good ideas, but I'll throw in another possibility...

The immune system is still a supporting actor in this play, if only in that it is crossing the BBB to try and fix damage caused by iron/reflux. So it makes sense to me that a relapse could be triggered by any other event which might put our immune system on overtime.

I know I've sometimes found symptoms to get worse following a cold, infection, etc.

Posted: Thu Mar 25, 2010 5:47 pm
by North52
I have often wondered if exacerbations are caused by some underlying reversible worsening of obstruction, such as temporarily enlarged lymph nodes, which are around the jugulars. It might be an interesting study to scan patients to quantify flow, both during a stable period and during an exacerbation. A documented reduction in flow during an exacerbation (if this is what actually happens) would provide good support for the CCSVI theory.

North

Posted: Thu Mar 25, 2010 11:59 pm
by costumenastional
Just my 2 cents and feel free to correct me. After all i want to learn from fellow patients who know a lot more than i do.

Here goes:
Relapses have nothing to do with veins apparently.
It is the reaction of the immune system in already "infected" sites, where microbleeding, excess of iron and other toxic deposits takes place due to BBB breach.
Relapse is actually an inflamatory process and this is why active lesions may be found during or shortly after one when t cells are performing their catastrophic job leading to tissue scarring (lesion formation).

The cns is an uncharted teritory and noone really knows why when a relapse happens there are more than one sites that go frenzy. For instance along with my optic neuritis everything else went wrong. It was the time i knew what exactly is the damage in my cns. If i had to guess (like neurologists do) i d say a relapse is actually when the immune system go to work and sends its troops to every single affected site. In my case most of them chose to fight at my optic nerve and the rest in my cervical spine lesions. So along with blindness i experienced leg and arm spasms, numbness bla blah... My MRI showed that my CS lesions where not active but i would bet my life that if it was a 7 tesla magnet instead of a 1,5 one a "few" shity t cells would have been seen messing with my already demyelinated nerves.

All the other time (between relapses for rrmsers or the whole time for ppmsers) there is simply no immune response. Just pure death for axons due to lack of oxygen most probably says Zamboni (does this makes sense for once or not?) shrinkage of the brain and spinal cord volume etc etc...

A relapse is when MS is working out in public.

The hypothesis is that once normal blood flow has been restored no more accumulation of toxic substances will take place leading to immune response halting. According to CCSVI theory the sooner you stop the whole "abnormal flow" thing the better since there will be no new sites for the immune system to "clean up". And most important, our brains will have the oxygen they need to survive. Our spinal cords will remain lesion free.

It is the first time in history there are clear answers to why we keep going down the slope (like Joan's husband says) all the time. Neurologists prescribe drugs for stopping relapse (if only they could manage) but they admit that they do not know jackshit for the obvious death and loss of brain volume.

Hope i make sense.

Re: What goes on during a relapse?

Posted: Fri Mar 26, 2010 3:43 am
by sbr487
JennP wrote:Hi, if anyone could answer my question I would really appreciate it.
CCSVI makes a lot of sense to me, the only thing I really don't get is what is going on with the veins during a relapse. Is the stenosis, or valve problem (or whatever your venous problem is) worse during a relapse. I just want to have all the information clear in my head before going to my doctor with my request to see a local interventional radiologist.
Thanks
Our immunity is always active and going in rounds throughout the body looking for suspicious activities (bacteria etc.). But unless a certain threshold is reached, the immunity will not activate. When you have an infection and fever, it is a sign of our body fighting the infection. But the infection would have set in before the fever came. Similarly, immune system cleaning up the dead cells is no different. Once it kills, it waits until enough accumulation has happened before it attacks again.

In the context of CCSVI, more severe the reflux is, more the dead cells in the brain and more frequent the attack is.

The only contribution of veins in all this is that they do a bad job of draining the blood. Thats all is there as far as veins go.

This is the perspective from a non specialist like me ...

Posted: Fri Mar 26, 2010 5:47 am
by bluesky63
Just throwing this out there . . . someone else can make something of it :-)

When I went to see Dr. Dake in December I was actively having a flare-up. He ordered bloodwork including a d-dimer. My d-dimer was quite high, indicating a possible blood clot or embolism, and I had to go to the ER and get screened. Thorough screening showed no clots or embolism. Repeated d-dimers (over weeks) in which the flare continued showed the elevated d-dimer. When the flare resolved the d-dimer resolved.

Dr. Dake said he was tracking the d-dimer because he had seen an elevated d-dimer in other people as well without clots or embolisms. Now, this is me, not a doctor: I wondered if that could interact with narrowed veins during times of relapse and decrease blood flow to produce the MS symptoms.

So one question might be, if some people have narrowed or flattened veins, what happens periodically in a subset of people to trigger the thicker or maybe hypercoaguable blood that interacts with the problematic veins and causes a flare-up of symptoms? In some people. If you will. :-)

Edited to add this little gem featuring diseased mice with high d-dimers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1603566/

I picture tiny hypo's and miniature alcohol wipes. The detail on the scoring of their little spastic backends almost made it worth squinting through this thing. Where is Tim Burton to animate this nightmare when we need him? Actually, what I want to know is, where is my spastic little tail? :-)