The benefit to this is to placebo control for the very strong effect surgery has on people in terms of placebo effect.
Surgeries are strong placebos, actually the strongest they've tested in allopathic medicine which is why someone in the audience in Bologna said it was not "fair" that this was a surgery. If you didn't know if you got a stent or not then they would control for this strong placebo and neuro's "could" accept the data as meaningful supposedly if treated people did a lot better afterwards. Potentially the patient and the neuro who follows up would not know which patient had the procedure so it could be double blind. Neurologists will only feel confident that they need to step aside for the vascular doctor after such has been done they seem to be saying. I do not agree with this idea of faking stent placement however.
I refer you to these facts that do not seem to bother any neurologists at all:
1. Stem cell transplants with chemo are not blinded. As far as I know it is not even true that a blinded neurologist even did the evaluations later, which would be weak blinding but at least an attempt at some objectivity. I have never heard of a neuro holding forth to a patient about how these trials were not blinded so steer clear of this "pseudo science". I suspect that if you were progressing rapidly and had run out of options, your doctor would entertain the idea--without disrespecting the fact your suggested it at all and likely without any lectures on the lack of evidence.
2. ASCT trials are not only done on really tiny numbers of patients (I have not personally seen a trial with a number over 30---and this matters because 30 is the minimum for any kind of validity at all) but they are uncontrolled as well.
Furthermore there is work that suggests these approaches which actually kill the pateint 5-8% of the time, do not work.
REFERENCE: ASCT Fails to stop demyelination and neurodegeneration in MS
Please note that while many studies look at how the pateints seem to be doing after the ASCT, in this case they looked directly at tissue and saw direct evidence of ongoing disease activity even after ASCT.
And from here ASCT REVIEW
Haematopoietic stem cell transplantation (HSCT) appears to represent yet a further escalation. Autologous HSCT encompasses mobilization and preservation of autologous haematopoietic stem cells (HSCs); subsequently, in most cases, myeloablative immunosuppression by a combination of chemotherapeutic drugs and often total body irradiation (TBI); and later the reinfusion of HSCs (Tyndall et al., 1999). Small treatment series with autologous HSCT during the last decade have shown remarkable suppression of inflammatory activity in most patients, but nevertheless—not rarely—at least some progression of disease.
Metz and colleagues (2007) now present interesting data and raise new questions that challenge the mechanistic concept as to how HSCT might work. Their histopathological findings from five MS patients who died after HSCT show that there remains at least some smouldering inflammatory activity, mainly consisting of CD8+ lymphocytes and activated macrophages and microglia, and that active demyelination and axonal damage continue after the profound immunosuppression and autologous HSCT (Metz et al., 2007). This information seems to discourage the further exploration of HSCT as a treatment for aggressive forms of MS.
apparently short of killing the person you can't stop all inflammation and even if you have seeming profound inflammation control (MRI proven) you still get degeneration anyway that you can't see. It is hard to see how you cold knock out the immune system any harder, yet the failure of this logical terminal end version of inflammation control is not apparently bothersome. If this doesn't work, why would weaker versions of suppression be effective?
There are other papers that suggest that ASCT works well for "long periods of time" like, gee, 1-2 years in a stunning 3 people.
This procedure succeeded in halting the rapidly worsening course of disease. The effect was long lasting, as demonstrated by a sustained efficacy over a two-year period in two subjects and 12 months in the third case. In addition, a striking effect on inflammation-related MRI findings was obtained. These results support a role for intense immunosuppression
Huh. REALLY?. This is a good idea because ti worked so well in 3 people over 1-2 years?
Hicy suffers a similar fate in that it, too, has all been trial numbers under 30, as well as unblinded and uncontrolled work. Yet if someone wanted to discuss this with their neuro the chance is good they would be encouraged to go ahead if the regular regimens were not working.
I sincerely doubt eyes would be closed, head shaking "No, no no".
It is not about the quality of the science it is about the hypothesis they all believe is accurate: inflammation causes the lesions, the lesions cause the degeneration after the fact, and if the inflammation can only be controlled adequately then the disease can be managed. Never mind that there is ample evidence this is not accurate.
Because they believe this to be true, weak work, such as the 3 person study, that is based on that theory is treated as if it is automatically "good science" while good work coming from the new model is prejudiced as being bad even before it is read and fairly evaluated.
The thing that is making me crazy is the consistent characterization of Dr Zamboni's work as far less well done that it is, for example not mentioning the fact that it is blinded and rigorously controlled, or mentioning only the one study instead of all 3, or not making a point about the absolutely HUGE study sizes compared to other more typical early work, ignoring the concordance in the face of blinding or pretending that this is a single tiny insignificant study that is very VERY preliminary. There is very little excitement or real interest expressed in this work at all, yet in reality it should be incredibly exciting. Where is a single positive statement about how thrilling it is to have a new avenue of understanding showing such concordance.?
And in the end I keep wondering--
Exactly how much and what evidence does it take an entire field of medicine to convince themselves that, in fact, the seminal event of this disease is not IN their field at all and an entirely new group of doctors is going to be the main physician?
The fact is the neurologists want to only accept CCSVI on neurological terms, they want to define it, find its limits and determine mechanics of the lesion all through the neurological lens as if the vascular lens does not matter and is completely irrelevant.
The oft repeated comment that "I don't see how lesions occur this way" is direct evidence of that.
Yet if this is a vascular disease the only lens that matters is vascular in the same way the only thing that matters in a stroke is the clot or bloodflow, only once that is restored can the neurological clean up begin
Seen through that light the stenosis is important on its own merit, the sluggish blood flow matters because it is there, reflux is a significant sign and the neurological event, even though it exists and is the main way a patient experiences CCSVI, is a side event.
Naturally this is just my opinion and this is op-ed.