Although CSA is measured in B-mode and a negative ΔCSA is an abnormality, B-mode abnormality has to do with abnormal valves, membranes, septa, etc.Cece wrote:B-mode abnormality is when the CSA of the jugs are bigger when you stand compared to lying down (the opposite of what they should be). ...
drsclafani wrote:why restenosis
Cece wrote:Try this thread, Nigel, it's full of everything I could find by drsclafani on verts:
Thekla wrote:I got the one third numbers from Prof Vogl. He said about one third of patients experienced great results, one third small slow results and about one third nothing. Whether that was his personal experience or from others' talks, I don't know. He said I appeared to be in the second group with small positive results, primarily lack of fatigue.
I do wonder whether standardization of diagnosis and procedure might not eliminate some of the variability in outcomes.
AlmostClever wrote:Dr. Sclafani,
Many PwMS on TiMS have been told they have similar conditions to mine and that there is still adequate blood flow from their legs.
I believe you are very correct in that I do not have "classical" May Thurner. The vein is not cut off or constricted and I have no severe pain or swelling in either leg. (Feet sometimes really hurt!)
I really think Nunzio's interpretation (p. 277) is a great explanation:
The left common iliac is dilated due to a blockage in the IVC, which resulted in a collateral vein formation between the left and right iliac.
That would result in enlargement of the ascending lumbar vein. I didnt think that was the case.The blockage in the IVC is causing overflow into the ascending lumbar.
As a result there is diminshed flow in both legs and therefore diminshed oxygen to leg muscles and nerves. My symptoms could be mainly due to claudication. (cold feet, leg fatigue, numbness, limping - same symptoms!) It's worse on the right due to the reflux created by the collateral coming from the collateral flow from the left iliac.
The lesions in my spine (like Nunzio suggested) are probably from the overflow from the left common ilac vein into the ascending lumbar combined with a faulty lumbar system and/or renal vein which overloads the azygous. (I added the claudication, lumbar system/renal part!)
I know it's like a Perfect Storm but so is getting MS?!?
There are papers where people with similar conditions have had IVC stenting and improved. (Nunzio can provide!)
Would you consider getting treatment of the IVC (stent)?
Thanks so much! We all know how hard you work for us - I don't think words can express it!!!
Cece wrote:drsclafani wrote:Lets not give up hope about neurologist partnerrs. We really do need them
I wonder then what it will take to convince them.
Lena wrote:Dear Dr. Sclafani,
My 15 year old daughter has not been officially diagnosed with MS (about a year ago she was diagnosed with brain lesions after paralysis of her right leg from the knee down which lasted about two weeks). Her only symptoms at this time are fatigue and somewhat foggy thinking. She was also born with one kidney (accidental discovery during a late ultrasound). Fortunately she hasn't had any issues with the kidney, but I'm really worried about repeated exposure to the contrast agent during an MRV and later on during the actual procedure. My question is, do you know of any physicians diagnosing CCSVI solely based on a doppler ultrasound or IVUS?
Thank you so much!
MS_HOPE wrote:Oh dear, Dr. S, now I'm really confused. Thanks so much for your summary of the Belfast debate. One statement you made really got my head spinning: "I made four major points
1. that ccsvi has many causes although ms was the most common cause...."
YIKES. From all I've read, I'm convinced it's the other way around - that MS is probably caused, at least in large part, by CCSVI (and other concurrent, and probably variable factors, depending on the individual pwMS.) I am persuaded by the thinking of Ashton Embry (cited on p. 226 of this thread by NZer1) as to the probable causes of MS.
I won't be surprised to learn, eventually, that other diseases like Parkinson's, Alzheimer's, and normal pressure hydrocephalus (NPH) also have vascular malformation(s) as a component. (Though there's NO other MS in my very large, extended family, my father had Parkinson's, my mother had NPH, and an uncle had Alzheimer's.) I'm intrigued by the quote (provided by NZer1 on p. 227) attributed to Michael Flanagan (uprightdoc.com) that mentions Parkinsons, NPH, and Alzheimers in addition to MS when discussing brain blood flow issues. (I've yet to read up on that.) Apparently Dr. Hubbard has also recently found CCSVI in a Parkinson's patientAny comments or clarification of your thoughts on this would be much appreciated!
spiff1970 wrote:spiff1970 wrote:Dear Dr. Sclafani,
If we assume that the CCSVI theory is right then how can the following have an impact on bloodflow/MS lesions forming issues:
a) Posture and position: is it better/worse to be in the supine or lying down position? Can having a bad posture have an impact?
b) Physical exercise: does physical effort impact on impaired blood flow when we have CCSVI?
c) Diet: are some nutrients worse/better for CCSVI?
d) Climate: does cold/heat affect the impact of CCSVI?
Many thanks for your attention.
Dear Dr. Sclafani,
Can you reply to my queries whenever possible?
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