Cece wrote:Does anyone know, what does it mean for perfusion to be 'pressure dependent' when it's below 60 mm?
What are the figures for what the cerebral perfusion in MS patients is? This has been studied, perfusion is lowered in MS patients, although the cause is/was not known.
Compared to controls, CBF and CBV were significantly lower in all NAWM regions in both PP-MS patients (p values from <0.0001 to 0.001) and RR-MS (p values from <0.0001 to 0.020).
Compared to RR-MS, PP-MS patients showed significantly lower CBF in the periventricular NAWM (p=0.002) and lower CBV in the periventricular and frontal NAWM (p values: 0.0029 and 0.022).
EDSS was significantly correlated with the periventricular CBF (r=-0.48, p=0.0016) and with the periventricular and frontal CBV (r=-0.42, p=0.015; r=-0.35, p=0.038, respectively).
This study suggests that the hemodynamic abnormalities of NAWM have clinical relevance in patients with MS. DSC perfusion MRI might provide a relevant objective measure of disease activity and treatment efficacy.
MR perfusion imaging is useful not only in the assessment of stroke, but also in the assessment of stroke risk. Under normal circumstances, the brain has an autoregulatory mechanism for maintaining adequate cerebral oxygenation in the face of decreasing cerebral perfusion pressure, which allows normal blood flow despite fluctuations in systemic pressure. This mechanism may be impeded in patients with hemodynamically significant carotid artery stenosis who are at high risk for stroke. The ability to maintain an autoregulatory response to hemodynamic stress has been termed "cerebrovascular reserve capacity." Areas of the brain supplied by a markedly stenotic or occluded artery, in which vasodilatation has already occurred to maintain adequate flow, lack cerebrovascular reserve capacity. ....In addition to a poor response to a vasodilatory challenge, perfusion imaging may show other abnormalities in the cerebral hemisphere ipsilateral to a severe carotid stenosis or occlusion, such as delayed bolus arrival time and prolonged mean transit time [42, 43] (Fig. 6A,6B,6C,6D).
I certainly do not state that I understand the theory when well respected vascular specialists whom I talked to do not undesrtand it. The coin has two sides. What kind of info could I collect before my procedure? There were the Dr Z's stamenets that operation has no risk and many people had improvements (only anecdotical reports), mainly those who are in an early stage. The other side said what I just posted. So, I deciced I have nothing to lose and I got the operation. It was done by small balloon, just as Dr Z did originally. My vascular specialist said that he finds it risky to use large balloon or to destroy valves (so he just dilated the valves). Life justified him as now even most of the IRs refrain from large balloons. No, improvement, only deterioration. So, I started talking to specialists here in Europe who are independent. They are nice guys not influenced by any money group. Most of them studied CCSVI, but they are still not convinced. So, this is why I think it is quite condescending when I hear someone talking about CCSVI or CCSVI and MS link as a fact.You seem ( and I don't want to sound condescending) that you are just starting to understand the theory, not someone post-procedure. Forgive me but that is the impression I got from your posts.
Believe me, I am very happy to hear that. On the other hand I am just wondering what her symptoms were before the operation. Does she have RRMS, I guess? I have to admit that I have also symptoms that go away sometimes for a few months, but the only hard issue I think is mobility. I have RRMS patients friends who do nothing, no medications, no operation, etc., but even a few years after their diagnosis, they live as normal people. They dance, sport, etc.My daughter was treated for her CCSVI 1 month after her MS diagnosis and she had relief of many (12) symptoms. But not before she ( and I ) had a solid understanding of the theory and the risks of treatment, weighed against the risks of MS progression and/or the risks of DMDs ( which she doesn't take)
She works full time, dances, works out, bikes, hikes, kayaks, and is a great mom (without her 12 symptoms).
I am in an early stage, but mobility problems did not change just got worse after the operation. As I said the specialists (not neuros) whom I talked to and who examined reports of CCSVI clinics in Europe told me that they did not find any scientifically documented improvements of patients, only anecdotal stories. So, I am just wondering the validity of those numbers. An IR can validate the condition of a vein but he has no idea about neurological conditions.The research showed us that:
Each patient must know that 30% see marked improvement, 30% see minimal improvement and 30% see no change.
It also showed the earlier you get treated the better the outcome.
It's too late to call it "SURREAL" for anecdotal reports might not count for research but those anecdotal patients ( like my daughter) are very REAL pwMS.
Here is another peer-reviewed research paper ... http://www.ajronline.org/cgi/content/full/175/1/207
Stenotic vessels affect perfusion time. They change the autoregulation function you refer to. The brain lacks a cerebrovascular reserve capacity when stenotic vessels slow CBF.
cheerleader wrote:HP--I'm sorry about the insurance issue--but I have no jurisdiction over private insurance companies. Neither does a group of volunteers with MS who pay for their own travel. Jeff and I have donated thousands to CCSVI Alliance, and continue to raise funds and host a website with all of the research. www.ccsvi.org We're doing the best we can by convening doctors and hosting informational events, but this is an up hill battle....and I completely understand the frustration and we'll be talking about this issue next phone board meeting.
I'm talking about trying to save people from great harm when they restenose and can't get coverage for another procedure.
colros wrote:How do you define "restenosis" and what is the "great harm" someone with it faces. The insurance companies will ask will ask for scientific proof of these allegations. If symptoms keep recurring throughout the life of an MS patient whose disease is presumed to be caused by "CCSVI" is the number of "liberations" on one patient and their cost unlimited?
colros wrote:As a doctor, I know that even total occlusion of both internal jugular veins causes no harm. The paraspinal veins are quite capable of handling the venous outflow via the emissary veins. So, again, what do you mean by "restenosis" causing "great harm"? re "the paraspinal veins are quite capable of handling the venous outflow via the emissary veins." there is absolutely no evidence if that is true in me, in someone with CCSVI, in someone with MS, or even in someone with both CCSVI and MS. Those veins may be compromised in ways that have not even been studied yet.
Insurance companies pay for those drugs because there are randomized controlled trials showing acceptable risk/benefit with proven slowing of disease progression. insurers had to be dragged into covering the DMDs just like they might have to be again for CCSVI. There is zero scientific evidence for the benefit of "liberation" in slowing disease progression. There is zero scientific evidence for the benefits of "DMDs" in slowing disease progression, too (let alone in helping disease symptoms!) Anecdotes of subjective improvement don't count as scientific evidence. Who said anecdotal evidence is the same as scientific evidence? They're not the same, but anecdotal evidence is often the genesis for scientific evidence to be accumulated (as we're now witnessing). So even if the risk of "liberation" is small I agree with this! there is no reason to take it without any scientifically proven benefit on disease progression. There most definitely can be reasons to have the procedure done when all other treatments have failed and one's neurological condition is rapidly worsening.
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