Bedankt TvG, dat zijn inderdaad 3 vragen die om antwoord schreeuwen.
Maar WIE kan me die geven?? Huisarts --> vaatchirurg? Ik moet ergens beginnen...
CCSVI - 9
-
TvG
[URL="http://www.hindawi.com/journals/msi/2013/598093/"][U]The Evidence for Hypoperfusion as a Factor in Multiple Sclerosis Lesion Development[/U][/URL]
[QUOTE]As outlined in this paper, there is an abundance of evidence that hypoxia is associated with pattern III lesions. Whether hypoxia is a consequence of the disease process or plays a causal role is yet to be determined, but it is conceivable that hypoxia may play a causal role. A reasonable interpretation of pattern III lesions is that they are early lesions. Hypoxia can account for BBB breakdown and initial oligodendrocyte/myelin damage. NAWM of MS patients experiences greatly lowered blood flow and, thus, must experience a degree of hypoxia as is also suggested by increased expression of hypoxia-inducible genes. That pattern III lesions are not perivenous while well-established lesions are perivenous is likely explained by the fact that immune cells migrate from the blood to the parenchyma via postcapillary venules where they then, encountering damaged myelin, mount an immune attack resulting in the establishment frank demyelinating perivenous lesions. The evidence is sufficient to seriously consider the possibility that hypoperfusion is a precipitating factor in MS lesions and to examine whether improvements in white matter perfusion correlates with improvements of functional outcomes.[/QUOTE]
[QUOTE]As outlined in this paper, there is an abundance of evidence that hypoxia is associated with pattern III lesions. Whether hypoxia is a consequence of the disease process or plays a causal role is yet to be determined, but it is conceivable that hypoxia may play a causal role. A reasonable interpretation of pattern III lesions is that they are early lesions. Hypoxia can account for BBB breakdown and initial oligodendrocyte/myelin damage. NAWM of MS patients experiences greatly lowered blood flow and, thus, must experience a degree of hypoxia as is also suggested by increased expression of hypoxia-inducible genes. That pattern III lesions are not perivenous while well-established lesions are perivenous is likely explained by the fact that immune cells migrate from the blood to the parenchyma via postcapillary venules where they then, encountering damaged myelin, mount an immune attack resulting in the establishment frank demyelinating perivenous lesions. The evidence is sufficient to seriously consider the possibility that hypoperfusion is a precipitating factor in MS lesions and to examine whether improvements in white matter perfusion correlates with improvements of functional outcomes.[/QUOTE]
-
zeiler
Een vriend van mij (ook ms) heeft zich vorig jaar laten dotteren in Belgie, helaas heeft dit bij hem niets gedaan voor zijn ms (vooral weinig energie) maar er is wel een ander verbluffend effect bij hem geweest; zolang ik hem ken (ongeveer 10 jaar) had hij Al last van een hoge bloeddruk, waar niets goed tegen hielp (het bleef altijd te hoog en dat schijnt vooral voor het hart erg slecht te zijn. Direct vanaf het moment dat hij is gedotterd ging zijn bloeddruk omlaag tot ideale waarden en daarop is het sindsdien gebleven. Hij gebruikt ook helemaal geen medicijnen meer daartegen
-
joge
-
Jolande
-
Jolande
Back on topic, hoge bloeddruk en ccsvi lijkt een plausibele combinatie.
Zodra cellen te weinig zuurstof/voeding krijgen zal als een van de eerste mechanismen de bloeddruk worden verhoogd ter compensatie
Mogelijk zit daar een verklaring voor de hypertensieverlaging na herstel van circulatie.
@achterlijk, is die verlaging tijdelijk of houdt deze langer stand?
Zodra cellen te weinig zuurstof/voeding krijgen zal als een van de eerste mechanismen de bloeddruk worden verhoogd ter compensatie
Mogelijk zit daar een verklaring voor de hypertensieverlaging na herstel van circulatie.
@achterlijk, is die verlaging tijdelijk of houdt deze langer stand?
-
zeiler
-
Marsei
Ashton Embry, Direct MS--PREMiSe trial data different than publicity
Ashton Embry, Direct MS--PREMiSe trial data different than publicity
Van [URL="https://www.facebook.com/notes/ccsvi-in ... 8411637211"][U]FB[/U][/URL]: Ashton Embry, Direct MS--PREMiSe trial data different than publicity
[QUOTE]Ashton Embry has some serious concerns about the recent publicity, video and press related to the PREMiSe poster presented at the AAN conference in San Diego-- mainly, what the researchers publically presented is NOT what the poster shows.
To see this for yourself, here is the press:
[URL="http://medicine.buffalo.edu/news_and_ev ... etail.html"][U]link[/U][/URL]
here is the poster: (link klopt niet)
Here is the complete summary from Ashton Embry.
[URL="http://www.direct-ms.org/sites/default/ ... 202013.pdf"][U]link[/U][/URL]
And here is a summary from Ashton Embry. Please read this, it is very concerning.
++++++++++++++++++++++++++++++
The Actual Data from PREMiSe Do Not Support the Highly Publicized, Anti-CCSVI Claims and Warnings of the University of Buffalo Researchers
Ashton Embry, DIRECT-MS, April, 2013
[B]Quick Summary[/B]
The actual data from the PREMiSe Trial do not support the highlypublicized claim that CCSVI correction by angioplasty is not of valuefor MS and may worsen disease activity. In sharp contrast, the datasuggest that CCSVI correction may well be of substantial value forMS. The misleading claims made by University of Buffalo researchersare based on irrelevant data from the failed Phase 2 portion of thetrial in which no one had their CCSVI corrected. The anti-CCSVI biasand baseless claims may be explained by the conflicts of interest.
[B]Executive Summary[/B]
University of Buffalo (UB) MS researchers put out a press releaseand Youtube video with claims that the Phase 2 portion (controlled,randomized and double blind) of their PREMiSe clinical trialdemonstrated that CCSVI correction (restoration of >75% venousblood flow from the brain) by means of venous angioplasty, was notof value for MS and was possibly harmful.
An inspection of the PREMiSe data on the poster presented by UBresearchers at the recent AAN convention in San Diego reveals thefollowing
1) All the subjects in the open label, Phase 1 portion of thePREMiSe trial had their CCSVI was corrected (>75% blood flowrestored by venous angioplasty). They had very good clinicalresults over the 6 months with no relapses and only 2 newlesions among the ten subjects
2) The controlled and blinded Phase 2 portion of the PREMiSetrial was a failure because those receiving angioplasty did nothave their CCSVI corrected (i.e. they did not have their bloodflow restored to >75%).
3) Among the nineteen, Phase 2 subjects, all of whom did nothave their CCSVI corrected, there were a total of 4 relapsesand 20 new lesions.
4) The reason for the failure of the angioplasty procedure tocorrect CCSVI in any of the Phase 2 subjects is unknown and isof concern because there was 100% success in Phase 1.
5) The failure of angioplasty to correct CCSVI in the Phase 2patients means any comparison between the clinical outcomesof the angioplasty patients and sham ones has no scientificsignificance. Any detected differences between the clinicaloutcomes of the two groups are purely random and aconsequence of the very small trial size and the acceptance ofonly persons with active MS into the trial.
6) The excellent clinical results of Phase 1 subjects, all of whomexperienced CCSVI correction, compared to the adverseclinical results of Phase 2 subjects, none of whom experiencedCCSVI correction, suggest CCSVI treatment may be ofsubstantial value for MS.
An added complicating factor is that some of the researchers involvedwith PREMiSe are in a major conflict of interest in that they receivelarge sums of money from MS drug companies. Because CCSVItreatment has the potential to replace drug therapy in some cases,the compromised researchers and their drug company benefactorswould potentially financially gain from a bogus claim that CCSVItreatment was of no value and might even be harmful.
The PREMiSe researchers launched a major media campaign a) toclaim their data showed that CCSVI treatment was of no value andmay be of harm, b) to dissuade persons with MS from getting CCSVItreatment outside of trials, and c) to dissuade practitioners from doingCCSVI treatment. These claims and warnings are entirely baselessbecause of the lack of significance of the results from Phase 2 inwhich no one had their CCSVI corrected. They may have beenmotivated by the major conflicts of interest referred to above.
The University of Buffalo should retract the currently available pressrelease and Youtube video and replace them with ones that containthe real story told by the data of the PREMiSe trial.
+++++++++++++++++++++++++++++++++++
Because Direct MS has supported BNAC CCSVI research financially, raising a hundred thousand dollars-- Dr. Embry has every right to point out the problems associated with this study's presentation.
Please share your thoughts, and share this information with the press, your MS community, politicians and other interested parties.
We need independent research----this is too important.
Joan[/QUOTE]
Van [URL="https://www.facebook.com/notes/ccsvi-in ... 8411637211"][U]FB[/U][/URL]: Ashton Embry, Direct MS--PREMiSe trial data different than publicity
[QUOTE]Ashton Embry has some serious concerns about the recent publicity, video and press related to the PREMiSe poster presented at the AAN conference in San Diego-- mainly, what the researchers publically presented is NOT what the poster shows.
To see this for yourself, here is the press:
[URL="http://medicine.buffalo.edu/news_and_ev ... etail.html"][U]link[/U][/URL]
here is the poster: (link klopt niet)
Here is the complete summary from Ashton Embry.
[URL="http://www.direct-ms.org/sites/default/ ... 202013.pdf"][U]link[/U][/URL]
And here is a summary from Ashton Embry. Please read this, it is very concerning.
++++++++++++++++++++++++++++++
The Actual Data from PREMiSe Do Not Support the Highly Publicized, Anti-CCSVI Claims and Warnings of the University of Buffalo Researchers
Ashton Embry, DIRECT-MS, April, 2013
[B]Quick Summary[/B]
The actual data from the PREMiSe Trial do not support the highlypublicized claim that CCSVI correction by angioplasty is not of valuefor MS and may worsen disease activity. In sharp contrast, the datasuggest that CCSVI correction may well be of substantial value forMS. The misleading claims made by University of Buffalo researchersare based on irrelevant data from the failed Phase 2 portion of thetrial in which no one had their CCSVI corrected. The anti-CCSVI biasand baseless claims may be explained by the conflicts of interest.
[B]Executive Summary[/B]
University of Buffalo (UB) MS researchers put out a press releaseand Youtube video with claims that the Phase 2 portion (controlled,randomized and double blind) of their PREMiSe clinical trialdemonstrated that CCSVI correction (restoration of >75% venousblood flow from the brain) by means of venous angioplasty, was notof value for MS and was possibly harmful.
An inspection of the PREMiSe data on the poster presented by UBresearchers at the recent AAN convention in San Diego reveals thefollowing
1) All the subjects in the open label, Phase 1 portion of thePREMiSe trial had their CCSVI was corrected (>75% blood flowrestored by venous angioplasty). They had very good clinicalresults over the 6 months with no relapses and only 2 newlesions among the ten subjects
2) The controlled and blinded Phase 2 portion of the PREMiSetrial was a failure because those receiving angioplasty did nothave their CCSVI corrected (i.e. they did not have their bloodflow restored to >75%).
3) Among the nineteen, Phase 2 subjects, all of whom did nothave their CCSVI corrected, there were a total of 4 relapsesand 20 new lesions.
4) The reason for the failure of the angioplasty procedure tocorrect CCSVI in any of the Phase 2 subjects is unknown and isof concern because there was 100% success in Phase 1.
5) The failure of angioplasty to correct CCSVI in the Phase 2patients means any comparison between the clinical outcomesof the angioplasty patients and sham ones has no scientificsignificance. Any detected differences between the clinicaloutcomes of the two groups are purely random and aconsequence of the very small trial size and the acceptance ofonly persons with active MS into the trial.
6) The excellent clinical results of Phase 1 subjects, all of whomexperienced CCSVI correction, compared to the adverseclinical results of Phase 2 subjects, none of whom experiencedCCSVI correction, suggest CCSVI treatment may be ofsubstantial value for MS.
An added complicating factor is that some of the researchers involvedwith PREMiSe are in a major conflict of interest in that they receivelarge sums of money from MS drug companies. Because CCSVItreatment has the potential to replace drug therapy in some cases,the compromised researchers and their drug company benefactorswould potentially financially gain from a bogus claim that CCSVItreatment was of no value and might even be harmful.
The PREMiSe researchers launched a major media campaign a) toclaim their data showed that CCSVI treatment was of no value andmay be of harm, b) to dissuade persons with MS from getting CCSVItreatment outside of trials, and c) to dissuade practitioners from doingCCSVI treatment. These claims and warnings are entirely baselessbecause of the lack of significance of the results from Phase 2 inwhich no one had their CCSVI corrected. They may have beenmotivated by the major conflicts of interest referred to above.
The University of Buffalo should retract the currently available pressrelease and Youtube video and replace them with ones that containthe real story told by the data of the PREMiSe trial.
+++++++++++++++++++++++++++++++++++
Because Direct MS has supported BNAC CCSVI research financially, raising a hundred thousand dollars-- Dr. Embry has every right to point out the problems associated with this study's presentation.
Please share your thoughts, and share this information with the press, your MS community, politicians and other interested parties.
We need independent research----this is too important.
Joan[/QUOTE]