Welcome to This is MS, the leading forum for Multiple Sclerosis research and support. Join our friendly community of patients, caregivers, and researchers celebrating over 20 years of delivering hope through knowledge.
https://www.thisisms.com/forum/
Please refer back to my original post because I never referred to CCSVI as a dead end(amazing how quickly things get blown out of proportion on the CCSVI forum).sou wrote:If we called this venous stuff "dead end", how should the autoimmune path be called after all these years (and dollars) of "success"?
Please, help me. I am not a native English speaker and I can't find a "heavier" word than dead. The question is literal.
. I was just responding to the inaccurate statement that for 20 years no one has looked into any other causes other then autoimmune which is not true. Trust me I never would or I have ever claimed that something is absolutley not true only that some seem to be more valid than others. By the way Zamboni and most of the other "leading" CCSVI researchers encourage people to stay on their current meds. so I would suggest to people that they take the comments about injectables not working with a grain of salt. They certainly are not a cure but at this point they are the best we have.Of course, the treatment is a patient's choice after having taken the doctor's advice. No doctor can force a patient take anything. Curing CCSVI and taking MS drugs are not mutually exclusive conditions. Should anybody undergo vascular treatment, it would be best if he/she behaved to MS just like he/she did before treatment.Doodles wrote:As to Dr. Zamboni and others encouraging patients to continue taking medication, what is the point to be made here? Perhaps they are being cautious, maybe they don't think they know it all and, dare I say it, perhaps they are being open-minded enough to think that while they may have found a part of the answer to the MS dilemma, there may be more to come.
I am torn between agreeing with this and agreeing with what MegansMom has said, about the CRABs having only been tested on pwMS who have not had their CCSVI treated and so we do not entirely know the safety profile or effectiveness of the CRABs in the pwMS who have been treated for CCSVI.sou wrote:Should anybody undergo vascular treatment, it would be best if he/she behaved to MS just like he/she did before treatment.
This statement was qualified by Dr. Zamboni...if the patient is RRMS, and has been doing well on their dmd (no relapses, no progression, no adverse affects) they should remain on their protocol. Which is why his wife and my husband remain on their injectables. But copaxone was not the "best" Jeff had, by any stretch of the imaginantion. Jeff was not having relapses, but he was also not able to stay awake for more than 3 hours at a time. He couldn't sleep thru the night, he had terrible spasms. All of this reversed after angioplasty. His gray matter atrophy reversed after angioplsty. Copaxone didn't touch those issues---and he had been on it for 2 years prior to angio. Copaxone was not the "best" he could receive...scorpion wrote:By the way Zamboni and most of the other "leading" CCSVI researchers encourage people to stay on their current meds. so I would suggest to people that they take the comments about injectables not working with a grain of salt. They certainly are not a cure but at this point they are the best we have.
The best we have seem not to address at all the >50% of pw'MS' who have progressive disease. Are we to be shuffled off to an early grave? No, I think there is evidence that CCSVI procedures save lives, and should be standard life-saving therapy for the more than 0.5 percent who die every year from CCSVI/'MS'. They should be standard for all of us whose lives are in no immediate danger, too.They certainly are not a cure but at this point they are the best we have.
cheerleader wrote:His gray matter atrophy reversed after angioplsty.
Dr. Dake and his neuro have compared MRIs. Jeff was beginning to show slight gray matter atrophy in '09, prior to angio. No signs of it on recent MRI 12/10. Shrinking lesions, and a plumper brain. Too bad there can't be a paper written, since there was no IRB...but hopefully future studies will show the same.patientx wrote:cheerleader wrote:His gray matter atrophy reversed after angioplsty.
I'm curious how you know this.
You took the words right out of my mouth...scorpion wrote:It is not dissatisfaction with the autoimmune model that has caused frustration Dr. Embry, BUT the pace of MS research that has caused people to grow frustrated. I am sure that people who have cancer, Parkinson's, and Alzheimer's also hope for quick and easy cures such as opening up a vein or eating the right foods but unfortunately these diseases are very complicated and human beings(MS researchers, doctors, neuros) just can not play "god" and perform miracles. Of course as people we want quick and easy answers/cures for anything that afflicts us but as you know that is not the fate of human kind although what the medical community has given us in the way of cures and symptomatic relief from SOME diseases in the last 100 years is astounding if you think about it. While your article is very pragmatic and well written you make assumptions that have not yet been verified through rigorous scientific testing. CCSVI and diet have NOT been proven to correlate with MS is any way and to say so it is misleading, no matter how how hopeful your article may sound, to make a connection between them.Direct-MS wrote:A New Disease Model for MS
Ashton Embry, January, 2011
A disease model is a hypothesis for what causes a disease and how it progresses. A model is developed using all the available empirical data which have accumulated for the disease and combining that with theoretical knowledge gained from studying many diseases. The key aspects of a viable model are that it explains all important observations, is theoretically reasonable and is as simple as possible.
One of the major contributions of a good model is that it allows new understanding of the disease process and points the way to potentially effective treatments. Given a model’s influence on the research effort and proposed/employed treatments for a given disease, it is important to reappraise the model as new data become available. Such reappraisal can take the form of either a minor modification of the model or possibly a complete overhaul, depending on how well or badly the new data fit with the existing model.
Over the last 160 years, many disease models have been proposed for MS but none have led to development of an effective treatment. This suggests we are still awaiting the development of a reasonably realistic model which incorporates the key factors that are causing and driving MS.
Over the past 50 years, two models have received the lion’s share of attention and research funding - the infection model and the autoimmune model. The infection model proposes that MS is caused by either a bacterial or viral infection in the central nervous system. However, the continued failure to identify a causative infectious agent, despite many detailed studies, has downgraded this model such that it now receives little support.
Currently, the preferred disease model for MS is that it is a cell-mediated, autoimmune disease. This model has the immune system becoming sensitized to parts of myelin due to both genetic susceptibility and a viral infection such as Epstein-Barr (EBV). It is also proposed that a defect in immune regulation is needed to promote the initiation and continuation of autoimmunity and vitamin D deficiency is one of the favoured causes of such decreased immune regulation. Over time, repeated autoimmune attacks on myelin eventually cause clinical symptoms and MS is diagnosed, usually in early adulthood.
This model has been preferred because over the years it has done the best job of explaining the available data for MS, including many diverse, epidemiological, genetic and immunological studies. Also, an experimental animal model, called experimental autoimmune encephalitis (EAE), reproduces many features of MS and thus adds further support to the autoimmune disease model. Using the autoimmune model as a foundation, developed therapies have focused on suppressing or modulating various parts of the immune system.
Over the past 20 years, dissatisfaction with the autoimmune model has grown as new observations, which cannot be easily explained by the model, have accumulated. Some of the important data which have raised doubts about the autoimmune model include:
1) Current immune-based therapies have little, if any, effect on disease progression.
2) Neurodegeneration appears to be an important part of MS throughout disease development, becoming dominant in the latter stages.
3) Detailed pathological studies of newly developed lesions have demonstrated that myelin disintegration precedes the invasion of the immune system indicating immune action is secondary.
4) MS lesions are venocentric and often are associated with iron deposits
5) Immune activity sometimes occurs associated with the optic nerve where no myelin is present.
6) No autoimmune activity occurs in the peripheral nervous system where myelin is also present.
These observations have not led to any serious reappraisal of the autoimmune model mainly because no one has been able to provide a better model which would explain these data as well as all the other data which seem to support the autoimmune model.
Little over a year ago, the important observation that most people with MS have impaired venous drainage from the brain (CCSVI) became widely known. Notably, this finding was not compatible with the autoimmune model, especially given the finding that the venous malformations responsible for CCSVI preceded the MS disease process. These new data, which have now been solidly confirmed by venography on thousands of MS patients, have led to the development of an entirely new model for MS.
In this CCSVI model, extra-cranial, venous blockages cause altered blood flow in the brain which in turn results in myelin breakdown in various ways including oxygen deprivation (hypoperfusion). It is also hypothesized that the altered flow leads to iron deposition in the walls of veins, consequent breakdown of the blood-brain barrier, the introduction of noxious elements into the CNS, and consequent neurodegeneration. Immune involvement is seen as part of the clean up process by a normal immune system.
Presently, a war of words is going on between the supporters of the conventional, autoimmune model and those that favour the upstart CCSVI model. Notably both sides use observations which are not compatible with their opponents’ model to argue against it. For example, the autoimmune model supporters use the common presence of a specific immune gene, immune dysregularities, and the requirement of an EBV infection, to discredit the CCSVI model. They also make the valid argument that some cases of CCSVI do not result in MS. The CCSVI model supporters use the established presence of venous blockages and altered blood flow, as well as the six points which had previous raised doubts about the autoimmune model, to disparage it.
Given a valid model has to incorporate all the important data, both the autoimmune and CCSVI models are not valid because they both fail to include critical data. Clearly, a new disease model for MS is required. It must honour the data which had formed the basis of the autoimmune model but must also include the key observations related to CCSVI. The key aspect of this model is that two independent conditions - CCSVI and immune dysregulation - must occur for MS to develop. Notably both of these pathologies depend on both genetic and environmental factors for their manifestation.
In this “two to tango” model, CCSVI gradually erodes the integrity of the blood-brain barrier which contributes to neurodegeneration and also allows the dysregulated immune system access to the CNS. This results in an abnormal immune reaction to disintegrating myelin and eventual permanent damage to the nerve axons themselves. The strength of both CCSVI and the immune dysregulation will vary greatly between individuals and hence very different presentations of MS would be expected. For example, those with lesser immune dysregulation may not experience an immune-related, relapsing and remitting phase and may be diagnosed with a progressive course driven mainly by CCSVI-related neurodegeneration.
Given this new, improved model, the best way to treat MS is to:
1) Upon diagnosis, be tested and treated for CCSVI
2) Use nutritional strategies to counter any immune dysregularity and to promote vascular health
3) Consider using an MS drug to help counter immune activity only if the actions of points one and two fail to halt disease progression.
We have to hope the scientists and clinicians who deal with MS will put aside their prejudices and allegiances to the drug companies and acknowledge the autoimmune model is no longer valid. Only then will they realize that their current research and treatment strategies for MS need to be completely rethought and changed.
There are too many other drugs that have not been tested for pwMS specifically. Even the use of antibiotics for an infection. Personally, the choice was easy. I took nothing before, I am taking nothing after. However, the participants in the Zamboni's pilot study kept taking the CRABs so there does not seem to be a specific problem about that.Cece wrote:I am torn between agreeing with this and agreeing with what MegansMom has said, about the CRABs having only been tested on pwMS who have not had their CCSVI treated and so we do not entirely know the safety profile or effectiveness of the CRABs in the pwMS who have been treated for CCSVI.sou wrote:Should anybody undergo vascular treatment, it would be best if he/she behaved to MS just like he/she did before treatment.
So it sounds like this is based on a longitudinal study. Could you be more specific on the methods used? Is this based on hypointense lesion volume on T1-weighted images? T2 hypointensities? Parenchymal fraction? Gray matter fraction? Voxel-based morphometric analysis?cheerleader wrote:Dr. Dake and his neuro have compared MRIs. Jeff was beginning to show slight gray matter atrophy in '09, prior to angio. No signs of it on recent MRI 12/10. Shrinking lesions, and a plumper brain. Too bad there can't be a paper written, since there was no IRB...but hopefully future studies will show the same.patientx wrote:cheerleader wrote:His gray matter atrophy reversed after angioplsty.
I'm curious how you know this.
cheer