Notes on the CCSVI vs autoimmune theories

With thanks to Joan Beal, here's an extract from her site:

Please read this note I posted last January about hypoperfusion (slow blood flow) and the MS brain.  Many researchers had noted this phenomena before Dr. Zamboni came forward with his discovery of CCSVI.  Slow blood can create an hypoxic (low oxygen) situation in the brain, and this in itself can damage brain tissue, causing axonal death and activating the immune system.  Here is the note:
http://www.facebook.com/note.php?note_id=229656952210

Remember, the autoimmune theory of MS is still just a theory.  Doctors have never proven that MS is started by the immune system.
Here is a wonderful editorial on this topic by Dr. Peter  Behan, called
"The Futility of the autoimmune orthodoxy in multiple sclerosis research"
"...a false orthodoxy claiming that multiple sclerosis is an autoimmune disorder has developed and formed the present basis of treatment, drug trials and research. The outcome of this misplaced creed has been truly catastrophic.”
http://www.expert-reviews.com/doi/pdf/10.1586/ern.10.69

If you are curious as to how CCSVI could cause lesions and brain and spinal damage in MS, please, read this note and the paper I have linked.  Yes, it is very technical, but I break it down into chunks, and explain what the researchers found.

Again, Here's the Note
http://www.facebook.com/note.php?note_id=229656952210

No matter what neurologists may claim, they have never proven that MS is a purely autoimmune driven disease.  Researchers have noted that in the beginning the lesions look like ischemic (low oxygen) events, even before the immune system is activated.   Here is a link to Lassmann's paper on this:  http://www.ncbi.nlm.nih.gov/pubmed/12559509

Here is a paper by Prineas and Barnett--where they study fresh lesions upon autopsy, and discover that there is axonal death without ANY immune activation:  This discovery makes them question EAE as a model for MS.
Relapsing and Remitting Multiple Sclerosis: Pathology of the Newly Forming Lesion
Michael H. Barnett, MBBS and John W. Prineas, MBBS
The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis,
who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases, namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.
http://www.cpnhelp.org/files/Ref1_Annals04.pdf

It is vitally important that we understand the science behind Dr. Zamboni's discovery, in order to be informed patients and caregivers.  Slowed venous drainage can create slowed perfusion....just like all those researchers noted in MS brains.  There will continue to be much push  back from the status quo.   They need to maintain the current dogma on MS, in order to keep their jobs and pharmaceutical ties.   But we need to ask, How do you KNOW MS is initiated by the immune system?  Have you read the other research??

Be informed.  Read the research.  It's not snake oil.  It's scientific fact.

Zamboni believes that the high association of MS and thyroid disorders is due to slowed venous flow. The thyroid veins connect directly into the jugulars.

http://www.bentham.org/cnr/openaccessarticles/cnr6-3/Paolo%20ZamboniII.pdf

 And here is the link in Pub-Med for your doctors:

http://www.ncbi.nlm.nih.gov/pubmed/19534716

The newest, freshest lesions--found upon autopsy, have the ischemic injury before immune activation. The only way to study lesions is in autopsy brain tissue, after the patients have passed and time has passed. But here is a study on fresh lesions in accident victims and newly deceased by Prineas and Barnett
http://www.cpnhelp.org/files/Ref1_Annals04.pdf

Back to work Part 1

I went back to work this afternoon for a half day. It felt good to be able to walk in, no stick, not needing dark glasses to cope with the fluorescent light, not needing to sit in a quiet space to allow me to think.

But the biggest plus was being able to think like a pharmacist again; to able to draw all the different threads of knowledge and experience together and apply them to whatever was in front of me. I didn't realise how much it was an essential part of my psyche and how much I had missed it, until the ability came back.

The nearest and simplest analogy that I can come up with is typing something on a keyboard. You can use one finger to hack and peck or touch type away freely. You  get to the same point eventually, but the latter is much less drawn out and satisfying. Or learning to play the piano. The novice hovers over each key nervously, whilst the expert's hands cause the music to flow seemingly effortlessly.

I have myself back.

Saw my Neuro today

Still feeling good. Robin says my walking is getting faster all the time.

It was time for my routine appointment with my neurologist today, and Robin came along with me. I told him about my operation in Poland and showed him details of what I had done. After the initial shock, he was quite open to discuss the procedure.

He gave me a good checkout and saw that I was better than when he last saw me. I still have slight intention tremor in my left hand, my reflexes are "brisk", but my feet responded normally to the touching of my soles. Last time there was no response at all.

We had an interesting discussion about the placebo effect and how technique affects surgical outcomes. This was why I had chosen Poland, because of their vast experience. I am to  see him again in six months,and he is interested in the results of my follow-up examination in Katowice. For the mean-time, I am treating this as a major remission, and intend to keep taking all my medication except the modafinil (Provigil), which I definitely no longer need.

This may be a study of one, but for those of you interested, I intend to keep a record of how I do from here on in, good and bad, so you can use it to make your own judgements about CCSVI.

Second full day at home.

Despite picking up a headcold, I am still feeling much better than before I left. 

I have four days left of heparin injections to ensure I get no post-operative blood clots forming in my newly opened veins. Today I gave myself the injection in my stomach, Robin has done them all so far. It was less difficult than I thought it would be, although diabetics who use insulin daily have my respect. Every instinct cries out against sticking something sharp into yourself, puncturing your skin. I cannot have any alcohol until I've finished the heparin, so the champagne celebrations will have to wait until the weekend.

The staircase is no longer my enemy. Whilst winning no prizes for speed, I can walk upstairs in a fairly normal fashion, one foot per step, and not hanging on to the bannister for grim death. Coming down is a little harder, but still better than before.

There is some criticism of the procedure: that the effects are a results of placebo. If this is placebo, give me more. Seriously though, I have considered this posibility. However, I have had one effect, correcting a problem I didn't know I had.

Robin had said nothing to me, so as not to cause distress, but in recent months the muscles on the right hand side of my face were drooping, making my eyes and mouth lopsided, particularly when I smiled or laughed. I was unaware of this. Since coming back from Poland, that lopsidedness has gone, my face no longer drooping. The first I knew about the whole thing was when Robin told me.

A day in the park.

Each day brings further improvements.

Today we went to Kew Gardens, where I was able to walk around and enjoy the autumn scenery, although with a few rest breaks along the way. A minor victory  included being able to tie my own shoelaces. Doesn't sound much, but a great deal to me.

Although my results have been dramatic enough, I don't want people to think of this operation as the cure for all things MS. If you are truly wheelchair bound, do not expect to get up and walk across the room. It has taken me back to how I was 2-3 years ago. A miracle to someone who hoped for a stop in progression, but the sick man has not picked up his bed and walked away just yet.

We have a long way to go in understanding what the hell is going on here, but I am grateful for the chance to be a lab rat. I will be taking part in the follow-up studies.

Back home.

Despite a very early departure from Katowice airport , the flight home was a very enjoyable experience. As you will remember that I needed special assistance to get through the airports on the way out.

Coming back, I was able to manage on my own, including up and down the steps of the aircraft. Landing at Luton, we joined the queue for passport control as a woman in a wheelchair , helped by special assistance staff, passed by. Robin laughed at me and said he had never seen anyone so happy  to stand in a queue before.

Family and friends who have seen me all remark how well I look. Long may this continue.

Why take the risk?

There has been so much heated debate about the whole issue of CCSVI, and many people, including eminent and well respected physicians, neurologists and patients, advocate waiting  until the whole thing is either proven to be another blind alley or the process becomes well developed and routine.

So why did I go now?

To those outside, it may seem like I made a sudden decision, but this is the culmination of much thought, since I got my official diagnosis in 2006. I have always been very sensitive to heat, particularly the sun on my head. Going out in the sun without a hat is very bad news.

Before my operation, when suffering a bad bout of trigeminal neuralgia sitting upright gave me some relief, relative to lying down. Hyperbaric oxygen does give me temporary improvement - at least 2 bar absolute, and the greater the pressure, the longer the relief.

So long before the advent of CCSVI theory, I felt there was something amiss with with the circulation in my brain.

I also did a lot of reading about MS, from its early days of identification, through to the present day.

Jean-Martin Charcot, professor of Neurology at the University of Paris, was the first to complete a detailed study of multiple sclerosis (MS), an autoimmune disease that affects the central nervous system. In 1868, Charcot analyzed some unusual symptoms in a young female patient—tremor, slurred speech, and abnormal eye movements—comparing them to other patients with similar symptoms. He documented his observations and wrote a clinical-pathological definition of MS that is still accurate today.


Throughout his life, Charcot believed that MS had something to do with the venous circulation of the brain.