« An MD Dr. Farough Owiesy in southern California specializing in migraine headaches began treating CCSVI – MS as a dysfunction of the autonomic nervous system as it impacts the veins of the central nervous system. It is clear to me that he has found the missing link to the Multiple Sclerosis mystery and a plausible, inexpensive treatment. »
It appears that the well known Interventional Radiologist Dr. Arata arrived at much the same conclusion in treating CCSVI. See the June 12, 2014 article by Charles Moore in Multiple Sclerosis News. « Researchers Report Alternate Explanation Discovery Of How And Why CCSVI Treatment Works In MS Patients »
https://multiplesclerosisnewstoday.com/ ... -patients/
« However, while the debate over CCSVI and MS continues, new data suggests that Dr. Zamboni may have gotten it right in looking at the veins for treatment, but it might not be venous abnormalities that are the real problem, with a team of California-based researchers contending that it is the nerves surrounding the veins not the veins themselves that are being treated by ballooning, with expansion of the jugular vein leading to stimulation of the autonomic nerve fibers, which run alongside the jugular and are responsible for communication between the brain and the central nervous system… »
There it is, the dysfunction in the autonomic nervous system. And to my mind it is precisely this dysfunction which drives MS Progression. More quotes :
They say that ongoing research and a growing body of clinical data strongly indicate that Dr. Zamboni’s CCSVI procedure may be the first viable treatment for an even more pervasive problem — dysautonomia — which is seen not only in almost all MS patients but also in patients diagnosed with a long list of other diseases and conditions. As a result, they believe the CCSVI procedure is better described by the term TVAM (Transvascular Autonomic Modulation)… The new study, published in the June, 2014 edition of the Journal of Endovascular sheds light on the positive effect of CCSVI on the sympathetic nervous system, explaining how researchers were able to pinpoint how the procedure improved abnormal sympathetic function found in patients with many chronic conditions including Multiple Sclerosis.
Titled “Transvascular Autonomic Modulation: A Modified Balloon Angioplasty Technique for the Treatment of Autonomic Dysfunction in Multiple Sclerosis Patients” (Journal of Endovascular Therapy: June 2014, Vol. 21, No. 3, pp. 417-428), the study coauthored by Newport Beach, California based Interventional Radiologist, Michael Arata, MD, and his research associate, Zohara Sternberg, PhD, compares the efficacy of the TVAM procedure vs. traditional balloon angioplasty in improving cardiovascular autonomic nervous system (ANS) dysfunction in Multiple Sclerosis (MS) patients. Drs. Arata and Sternberg report that they found using an angioplasty balloon to stimulate vein-associated nerves increased sympathetic activity shows promise for patients who suffer from MS…
The coauthors observe that in this instance, TVAM involved the coupling of balloon angioplasty of the internal jugular veins with application of external manual compression and dilation of the azygos and renal veins; unlike traditional angioplasty for CCSVI, which treats only abnormal veins (50% stenosis or static valve), all targeted vessels were treated with TVAM regardless of the presence of an abnormality…
Drs. Arata and Sternberg conclude that the combination of balloon angioplasty of anatomically normal veins coupled with external compression during dilation of these veins can improve indicators of ANS dysfunction, reporting that the safety and efficacy of TVAM in MS patients observed in this pilot study is encouraging, paving the way for the treatment of dysautonomia in pathological states other than MS…“The current study demonstrates the procedure’s effect on autonomic function, offering an explanation for why patients may see symptom improvement with venous ballooning even though separate studies have failed to show a relationship between venous obstruction and Multiple Sclerosis. The mechanism of symptom improvement is improved autonomic tone rather than relief of flow obstruction,” says Dr. Arata.
There it is. Improved autonomic tone rather than relief of flow obstruction. Note that the treatment includes « external manual compression. » Akin to Shiatsu Massage, for example? (Though my first major « attack » ceased subsequent to a Shiatsu Massage, no one apparently wants to believe it or act upon it.) In Dr. Arata’s treatment, no doubt specific veins are targeted. I simply wish to point out that my massage solution to getting the fluids flowing, and now, the autonomic nervous system stimulated, may be as good as any. This means help is immediately available even if one can’t access a specialized treatment center.
The following quote is from my site :
« Dr. Owiesy has observed that when the middle layer of the vein composed of smooth muscles go into spasms, blood flow is obstructed. Again the problem resides “exterior” to the vein, not “interior”. The veins may be weak or somehow defective, but the mechanism which shuts off the blood flow isn’t “intima”. This corresponds completely to my experience. The treatment? Dr. Owiesy administers a mixture of dexamethasone/lidocaine/thiamine in the area around the Internal Jugular Vein. Outcomes have been impressive, risks and expense minimal. »
I confess I have been a bit cavalier about the potential risks of dexamethasone which is a corticosteroid – an anti-inflammatory and immunosuppressant. It can weaken the immune system and should not be used if one has a fungal infection etc. Lidocaine is used to numb tissue. Thiamine is Vitamin B1. All are inexpensive.
Should one focus on the smooth muscle layer of the veins or the autonomic nerve fibers themselves which apparently run alongside the jugular ? I don’t know. I am neither a scientist nor an M.D. I’m simply trying to understand how to find the best treatments for myself, based in large part on my experience. All of the above makes sense in light of that experience.
Now check this out.
https://jneuroinflammation.biomedcentra ... 017-0900-z
Journal of Neuroinflammation“Identification of the flotillin-1/2 heterocomplex as a target of autoantibodies in bona fide multiple sclerosis”
So what exactly is “bona fide multiple sclerosis”?
Currently the 2010 McDonald criteria are considered the gold standard method in determining true Multiple Sclerosis. See Quotes from Wikipedia.
« Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing.[.. The McDonald criteria, which focus on clinical, laboratory, and radiologic evidence of lesions at different times and in different areas, is the most commonly used method of diagnosis[..4]
Clinical data alone may be sufficient for a diagnosis of MS if an individual has had separate episodes of neurologic symptoms… In those who seek medical attention after only one attack, other testing is needed for the diagnosis. The most commonly used diagnostic tools are neuroimaging, analysis of cerebrospinal fluid and evoked potentials. Magnetic resonance imaging of the brain and spine may show areas of demyelination (lesions or plaques). Gadolinium can be administered intravenously as a contrast agent… Testing of cerebrospinal fluid obtained from a lumbar puncture can provide evidence of chronic inflammation in the central nervous system…. The nervous system in MS may respond less actively to stimulation of the optic nerve and sensory nerves due to demyelination of such pathways. These brain responses can be examined using visual- and sensory-evoked potentials. »
In my experience Neurologists are excessively obsessed with working up a diagnosis dossier. First thing they requests the MRI, Spinal Tap and visual and sensory evoked potentials. If the neurologist is competent she will consider other disorders which mimic MS such as Vitamin B12 deficiency and Lyme disease. But after all that is done what have they to offer? Very slim pickings. A plethora of “disease modifying drugs”, but do they “work”? Will they make you sicker than you already are? Will they kill you?For one thing, it has become increasingly clear that lesions don’t correspond to handicap. See the work of well known MS researcher Professor George Ebers, Oxford University who wrote on March 12, 2012 that there are (my emphasis)
www.mscureenigmas.net/after-diagnosis-ebers-drug-research.html“ major doubts about the outcomes used in MS trials. This is not a matter of opinion really since they have been subjected to careful study by the Sylvia Lawry Centre in Munich using results from some 40 trials, and have also been carefully evaluated in our studies on the natural history of MS where approx. 1000 patients were followed untreated for nearly 30 years on average. This population evaded so-called disease-modifying drugs as accrual ended in 1984 and by the time they were being promoted they were either too disabled to be considered or had done too well to want them.
In the first instance relapses were unrelated to long term outcome and surely no study should now be published with this as the outcome nor should studies be done in which patients are subjected to risk where this is the primary outcome. It is clearly unethical by consensus criteria, which reasonably insist that the outcomes have to be meaningful for risk to be taken on, otherwise no result of value to patients can come out of such trials. This result is supported by there being little from long term followup of the original treatment trials to indicate that relapses are a meaningful indicator of treatment effect when long term disability is considered. After all Long Term disability is the overwhelming medical social and economic impact of MS.
(Note – (When the Sylvia Lawry results became apparent the response of the International Federation of MS Societies was to withdraw their funding…)
« rather than saying the outcomes are worthless it seems more appropriate to say they have not been validated. Frankly this is damning enough and if patients have been promised benefit in the long term, this is overstating the evidence… »
Prof GC Ebers
Quotes taken from Lesions and Relapses--Part One - Facebook
Marie A. Rhodes, author of CCSVI as the Cause of Multiple Sclerosis
(Part Two of Lesions and Relapses is worth reading as well.)
On March 21, 2013 it was announced that Dr. Ebers had been chosen to receive the National MS Society/American Academy of Neurology’s 2013 John Dystel Prize for Multiple Sclerosis. This freed him to give a lecture titled “Critical Review of outcomes used in MS clinical trials” which was posted on You Tube November 4, 2013 by the European Medicines Agency. www.youtube.com/watch?v=OqY-_K1fYJY
(see my blog entry for May 23, 2014 Vitamin D, Veins and Epstein Barr Virus)
His heresy was thus twofold.
- The study of 1,000 patients over a 30 year period revealed that relapses are unrelated to long term outcome.
- His 25 year study of Disease Modifying Drugs revealed they don’t stop descent into disability.
A recent study has found that physical disability may have no link to brain lesion volume in some patients with multiple sclerosis (MS)...Read more - http://www.ms-uk.org/physical-disability-may-not-be-directly-linked-brain-lesions-230617-0
Me again : What we can conclude is that current bona fide MS criteria ignores what matters - central nervous system fluid mechanics - and obsesses on what doesn’t matter – lesions, spinal tap results etc, that is to say, the immune system response to what matters, pathological CNS fluid flow.
So now it’s time for those who would treat MS to study fluid flow. Are there obstructions? What is the velocity of blood flow, cerebro-spinal fluid flow? In my opinion The Upright Cine MRI should be an obligatory diagnostic tool to determine the above in studying the spine. (Cine as in Cinema, a film of CSF FLOW.)The CCSVI issue thus becomes one of fluid mechanics. The auto-immune theories are thus largely discredited. I don’t pretend to know the appropriate tools. But the question should be posed.
See Joan Beal’s site The Vascular Connection ccsviinms.blogspot.com/
« There is a new paper recently published in the American Journal of Radiology from Dr. Haacke's superb radiology team at Wayne State University in Detroit, called Jugular Anomalies in Multiple Sclerosis are Associated with Increased Collateral Venous Flow X S.K. Sethi, X A.M. Daugherty, X G. Gadda, X D.T. Utriainen, X J. Jiang, X N. Raz, and X E.M. Haacke
Published May 25, 2017
Jugular Anomalies in Multiple Sclerosis Are Associated with Increased Collateral Venous Flow
The main finding in this study is that in patients with MS com- pared with HCs, venous flow is reduced in the IJV but increased in the paraspinal and other collateral veins. Moreover, in patients with MS, the presence of visible structural abnormalities, such as venous stenosis, is associated with a further decrease in jugular flow and an increase in drainage through the collateral veins…
PC-MR imaging is a viable method for quantifying the extent of compensation in the extracranial venous system in MS and has demonstrated an increase in collateral flow caused by the presence of jugular stenosis. It is possible that this increase in collateral drainage is a compensatory response in the MS-affected brain to reduction of the IJV flow.
As a final observation, It would be useful to see the work of Clive Beggs.
“11 January 2017 - Julia WIlliams
A Leeds Beckett University academic who has pioneered research on fluid mechanics associated with neurological diseases such as Multiple Sclerosis (MS) and Alzheimer’s, has delivered his inaugural lecture as Professor of Applied Physiology.
Clive Beggs, who is also Visiting Professor of Neurology in the medical school at the University of Buffalo, State University of New York, has been able to show through his research that diseases like MS are associated with alterations in the dynamics of the cerebrospinal fluid (CSF) system…
Working with clinical partners who are based overseas, he has gained new insights into the biomechanics of the intracranial space and has been able to show that the dynamics of the CSF system are strongly influenced by the cerebral venous drainage system.
Together with co-workers, Professor Beggs has been able to show that MS is associated with changes in the dynamics of the CSF pulse in the cranium, and that the normal relationship between this and the jugular veins is profoundly altered in MS patients. He has also found that venous drainage anomalies in patients with Alzheimer's disease are associated with blood retention in the cerebral veins, suggesting that constricted venous outflow might be a generic phenomenon implicated in the pathophysiology of other neurological diseases.
Professor Beggs said: “My work suggests that vascular anomalies can profoundly alter the biomechanics of the intracranial space. This is important because there is a growing body of evidence that altered haemodynamics in the cranium are associated with a wide range of neurological conditions.
“In my lecture I discussed the link between altered fluid dynamics in the cranium and neurological disease. Using examples from my own research I showed how cerebral venous outflow plays an influential role in regulating the behaviour of the intracranial CSF system, something that appears to be important in the pathophysiology of several neurological conditions.”…
Back to MSCureEnigmas. I will finish with a great quote made by 1eye on ThisisMS.com.
www.thisisms.com/ Under General Discussion, « Re : new medical entity set apart from MS » June 28, 2017
« Do *you* have "bona fide" MS? How can you tell? Does your MS give you the ability to claim for "disease modifying" therapy? Do you care?
The bottom line on MS is,,. They don't know what causes it. So they can't treat it. And this BUGS THEM.
I am not a doctor. Do not take anything I say as medical advice. »
Tags : Multiple Sclerosis, McDonald Criteria, Professor George Ebers, Disautonomia, TVAM (Transvascular Autonomic Modulation), Dr. Owiesy, Dr. Arata, Clive Beggs, Fluid Mechanics