DrSclafani answers some questions

[drsclafani]

Does this mean we will be addressing Sal as Mr President from now on?

Finally after three weeks a question!
The answer is i hope you do not. Only my mother is allowed to call me president

Any other questions?

[Robnl]

President Elect: Dr. Salvatore Sclafani??

Who is he??

Congrats doc, go for it!

[NHE]

Any other questions?

Last summer I had a standard MS MRI which included a transverse section of my cervical spine. While I realize that it's far from ideal for CCSVI imaging, looking through the images I can clearly observe my veins and arteries. Is it possible to use these images to get an overall sense of the condition of my jugular veins, i.e., large blockages, collaterals, etc? Thanks.

[drsclafani]

Any other questions?

Last summer I had a standard MS MRI which included a transverse section of my cervical spine. While I realize that it's far from ideal for CCSVI imaging, looking through the images I can clearly observe my veins and arteries. Is it possible to use these images to get an overall sense of the condition of my jugular veins, i.e., large blockages, collaterals, etc? Thanks.

I do not think that MRI is particularly helpful for CCSVI. Many of the abnormalities of CCSVI are intraluminal and not seen at all by MRI.

If you have MS, you have statistically have abnormalities of the cerebrospinal venous circulation until proven otherwise. Therefore venography is reallly what is necessary. MRI is in my opinion inadequate to exclude ccsvi in a patient with MS

If you do not have a diagnosis of MS, you need to have a screening test that shows some abnormality since the prevalence of ccsvi in patients who do not have a diagnosis of MS is not common. Screening duplex ultrasound is non-invasive and is a reasonable first step before venography.

[pelopidas]

ok, i have a question
what are the conditions that you think it's possible to provoke a relapse?
could be some kind of threshold, some flow change in time?

Pelopidas,
that is way over my head. I have no idea about that.

hi Mr President
i have some idea now after all these years
i think that a relapse could be an acute compartment syndrome of the brain
the flow worsens suddenly, the possible reasons are to be discussed
but the clinical appearance seems to be an acute compartment syndrome.
what do you think?

[Matthewa100]

Dear Dr Sclafani,

Firstly thanks for taking time to answer all these questions its really appreciated. Secondly I apologise as I am MS Free and am only suffering from Dysautonomia (or== autonomic dysfunction, autonomic neuropathy). I have read how tough the MS condition is and I am truly sorry for what others are suffering.

Dr Sclafani, I have had Dysautonomia for over 4 months now and my conditions are worsening. I fear if I don't nip it in the bud now then I will develop secondary stages to this illness. I have researched at great length and believe surgery either conducted by yourself or Dr Arata's 'ballooning' techniques is my solution. What is the primary differences between your technique and Dr Arata's? As you actually remove obstacles in the pathway rather then 'ballooning' would this seem to have more longevity? I know this isn't very technically medical but I am not sure how long the balloon will stay static in the neck if that makes sense. Also do you see Dysautonomia only patients or gernally MS with Dysautonomia?

Thanks in advance.

Matthew

[Cece]

Dear Dr Sclafani,

Firstly thanks for taking time to answer all these questions its really appreciated. Secondly I apologise as I am MS Free and am only suffering from Dysautonomia (or== autonomic dysfunction, autonomic neuropathy). I have read how tough the MS condition is and I am truly sorry for what others are suffering.

Dr Sclafani, I have had Dysautonomia for over 4 months now and my conditions are worsening. I fear if I don't nip it in the bud now then I will develop secondary stages to this illness. I have researched at great length and believe surgery either conducted by yourself or Dr Arata's 'ballooning' techniques is my solution. What is the primary differences between your technique and Dr Arata's? As you actually remove obstacles in the pathway rather then 'ballooning' would this seem to have more longevity? I know this isn't very technically medical but I am not sure how long the balloon will stay static in the neck if that makes sense. Also do you see Dysautonomia only patients or gernally MS with Dysautonomia?

Thanks in advance.

Matthew

That's a great question. Welcome to the site & I am sorry to hear about your dysautonomia.

[NZer1]

Hi Dr S, long time since the last time.
Had an abstract thought, lol

Is the thrombosis that occurs after PTA in any way related to the type or number of lesions?

I wondered if there is a similar happening at the lesion sites and their attempts at healing because the visual lesion of MRI are assumed to be the cause of symptoms. My reason for saying that the symptoms are assumed to be caused at the lesions is because of my research into Neuroplasticity. It appears there is strong possibility that the brain can change itself in regard to the regions for functions to occur if damage to grey matter occurs.

If the same inflammation is occurring in the brain as what is occurring after PTA and by that I mean that the PTA is damaging the endothelial layer which has to heal and the BBB breaches that occur in MS brains has to heal, then is the inflammation and immune system the problem rather than the leaking endothelial as the first step/stage in MS?

If the immune system was fully functional then the action of a breach of BBB/endothelial would heal in good time?

Is the problem with malformed valves in the veins also a a problem of cellular mutation that has occurred, which has 'caused' the deformed leaflets?

Could cellular mutation occur in the endothelial layer or in the immune system?

Ed and I have been gas bagging about inflammation, genetic mutations and the commonalities of many symptoms in many diseases. Seems that the finding of CCSVI is showing a deeper issue and that finding it is creating deeper thought!

;)
Nigel

[drsclafani]

Hi Dr S, long time since the last time.
Had an abstract thought, lol

Is the thrombosis that occurs after PTA in any way related to the type or number of lesions?

I wondered if there is a similar happening at the lesion sites and their attempts at healing because the visual lesion of MRI are assumed to be the cause of symptoms. My reason for saying that the symptoms are assumed to be caused at the lesions is because of my research into Neuroplasticity. It appears there is strong possibility that the brain can change itself in regard to the regions for functions to occur if damage to grey matter occurs.

If the same inflammation is occurring in the brain as what is occurring after PTA and by that I mean that the PTA is damaging the endothelial layer which has to heal and the BBB breaches that occur in MS brains has to heal, then is the inflammation and immune system the problem rather than the leaking endothelial as the first step/stage in MS?

If the immune system was fully functional then the action of a breach of BBB/endothelial would heal in good time?

Is the problem with malformed valves in the veins also a a problem of cellular mutation that has occurred, which has 'caused' the deformed leaflets?

Could cellular mutation occur in the endothelial layer or in the immune system?

Ed and I have been gas bagging about inflammation, genetic mutations and the commonalities of many symptoms in many diseases. Seems that the finding of CCSVI is showing a deeper issue and that finding it is creating deeper thought!

;)
Nigel

I think that the thrombosis that occurs after PTA is related to the degree of injury caused by angioplasty, the rate of flow in the jugular vein after angioplasty and the thrombogenic propensity of the patient.

If balloon size is too great the vein wall is stretched too much and may tear totally or significantly tear the wall,exposing the muscle layer to the blood. This causes 1. stickiness and adhesion of platelets to the vein wall and to themselves, 2. turbulent flow and 3. increased activation of clotting factors. All of these can result in thrombosis of the vein.

If flow rate of the vein is slow, then this also leads to higher risk of thrombosis. Slow flow can result from vessel distortion from the angioplasty, from associated muscle compressions in J2 and J3 and from large collaterals that have developed from long standing stenosis.

Hypercoagulability can be congenital, associated with birth control pills, smoking and other environmental influences, and the vascular injury of angioplasty.

I think that the visual lesions, presumably on MRI, are expressions of the pathology. they do not cause the inflammation, they are the inflammation. The symptoms are not necessarily related to the MRI lesions activity. Neuronal death, ischemia and degeneration may be present in areas that are not visible on MRI, or in the spine rather than the brain. Finally symptomss may be the result of the process of ccsvi, namely retarded perfusion, increased intracranial pressure, arterial pulsatility, etc.

THere is suggestion that the abnormalities of the valves are congenital associated with maldevelopment during fetal growth. The valves thicken, there appear to be tissue bands in some that fix the valve in a closed position. However this can be associated with chronic thickening of the valve that can be exacerbated by inflammatory, thrombosis and/ or infection

[drsclafani]

ok, i have a question
what are the conditions that you think it's possible to provoke a relapse?
could be some kind of threshold, some flow change in time?

Pelopidas,
that is way over my head. I have no idea about that.

hi Mr President
i have some idea now after all these years
i think that a relapse could be an acute compartment syndrome of the brain
the flow worsens suddenly, the possible reasons are to be discussed
but the clinical appearance seems to be an acute compartment syndrome.
what do you think?

i will answer you soon

[vesta]

Hello Dr. Sclafani:

I want to apologize for having offended you. I hope you can forgive me.

I am interested in your opinion concerning the following ideas about MS Progression which imply that the earlier one treats CCSVI with angioplasty, the better. Thank you. Vesta

QUOTE

"The French Neurologist Jean-Martin Charcot, practicing at the Parisian la Pitié-Salpetrière hospital, first described Multiple Sclerosis (Sclérose en Plaques) in 1868. Among other things, he defined MS as a “rigidity disorder”. He thus set the tone in the Neurology profession of an unfortunate prejudice towards MS patients by claiming their “rigidity” symptoms were psychological in origin - signs of neurotic (usually female) hysteria. I now believe it is just this rigidity which is at the root of MS progression, but its origin is physiological, NOT psychological. Damaged nerves send “misfired” signals to the muscles which cramp and/or go into spasms. As the nervous system degenerates, the body becomes increasingly rigid, compressed as it is by muscles in spasm. And it is just this rigidity which triggers the process damaging to the central nervous system.

Let’s backtrack a bit.

As early as 1863 the Swiss pathologist George Edward Rindfleisch observed that MS lesions clustered around the brain’s draining veins. Disparate testimonies of this phenomena continued to surface thereafter but it was only in 2008 that the idea “went viral” when Italian Professor Paolo Zamboni published a paper on the Internet offering a medical explanation. He described a condition he has named CCSVI in which venous blood “refluxes” into the Central Nervous System (CNS) owing to stenosed or damaged veins. These blood “refluxes” injure the tissue which leads to inflammation of the myelin sheath and an immune system response. These early “attacks” describe relapse/remission MS (RRMS). Dr. Zamboni has thus discovered the origin of the “wound” which triggers the immune response.

Progressive MS presents the exception. My brief synopsis derived from MS UK’s site reads

“Primary Progressive MS (PPMS) concerns about 10 to 15% of MS cases. In contrast to RRMS (Relapse Remission) cases, the disease progresses continually without respite after striking an older population (age 40’ and 50’s). Unlike RRMS, there is little to no inflammation, there are fewer brain lesions, the lesions which do exist present fewer inflammatory cells, and more are found on the spinal cord than in the brain which leads to mobility problems. While PPMS cases exhibit less inflammation, there appears to be greater damage to the axons.”

PPMS patients are not included in MS drug research and treatment because both target the myelin damaging inflammation of RRMS. Now, if an entire subset of patients is excluded from research because they do not conform to the auto-immune theory of MS, maybe the theory itself is suspect.

Eventually RRMS may evolve into Secondary Progressive MS, meaning it resembles the primary form. I repeat. “there is little to no inflammation, there are fewer brain lesions, the lesions which do exist present fewer inflammatory cells, and more are found on the spinal cord than in the brain which leads to mobility problems. While PPMS cases exhibit less inflammation, there appears to be greater damage to the axons.”

What does this imply to me? It implies that the driving factor in progressive MS is no longer centered in obstructed venous blood flow but in a damaged spine and obstructed cerebro-spinal fluid circulation.

And here we can understand the MS positive feedback loop.

MS venous blood circulation is deficient for any number of reasons. A stress attack can trigger the blood “reflux” into the central nervous system (brain/spine) which inevitably damages the nerves. When the nerves are damaged, muscles cramp up, perhaps go into spasms. As the body freezes up, fluid circulation (blood/cerebrospinal fluid) slows setting the stage for the slightest stress event to trigger another “attack”. Thus each “attack” triggers muscle cramps and body rigidity which in turn sets the stage for more attacks. (I include ANY illness and/or toxicity as stress events. Also, poor blood circulation in the brain persists apart from occasional relapses so constant effort must be made to release body tension and blood/cerebrospinal fluid circulation.)

Eventually the body rigidity/muscle spasms deform and damage the spine. As muscles weaken and atrophy the entire body structure is compromised leading to obstructed cerebrospinal circulation and direct pressure on the spinal cord. At this point it is no longer the blood reflux inflammation which “wound” the nerves so much as lesions and cerebrospinal fluid obstructions which impact the spine. We now have SPMS and increasing issues with mobility. Ideally MSers should turn to functional healers – Osteopaths and Chiropractors - who can manipulate the head/cervicals/full length of the spine to relieve pressure on the spinal cord and free the cerebro-spinal fluid. Physical Therapists and Massage Therapists can provide fluidity and movement so vital to overcoming the natural tendency to rigidity.

Obviously this implies that at the onset of RRMS one should make every effort to enhance blood/cerebrospinal fluid circulation through the brain/spinal cord in order to stop the blood “reflux” and the attendant muscle spasms/rigidity. I can see that had I known about CCSVI and followed the advice on this site 25 years ago, I wouldn’t need a cane today and needn’t worry now about the increasing rigidity in my spine.

I can also understand why “liberation therapy” (angioplasty) works best in the early RRMS phase when stenosed veins are the primary problem and treatment “liberates” the blood flow. One has thus prevented the wound. Once Progression sets in, there is little to no inflammation which implies that the veins are no longer the primary issue. In that case, while angioplasty might be of help in relieving some symptoms, attention should focus on treating lesions on the spine.

It really won't be that difficult to treat MS once the process is understood as functional rather than biochemical.

Previously published on my site MS Cure Enigmas.net
www.mscureenigmas.net/ "END QUOTE

[Cece]

There's a CCSVI workshop at SIR this weekend? Ah! There it is! http://www.sirmeeting.org/index.cfm?do= ... 03&cb=5003
Best wishes for high turnout and high engagement with the concepts.

Neurointerventions II: Chronic Cerebrospinal Venous Insufficiency (CCSVI)

Sun, 3/1: 1:00 PM - 2:30 PM
In-The-Clinic Workshop
ITC18
GWCC
Room: 314
CME Tech: 1.5
CME Credits: 1.5
This workshop will use a case-based interactive format to expose participants to Chronic Cerebrospinal Venous Insufficiency. CCSVI is a clinical syndrome resulting from outflow resistance of the veins that drain the brain and the spine, presenting clinically with chronic fatigue, short term memory loss, problems of concentration and complex thinking, headaches, spasticity and vision deficiencies and treated with some success by venoplasty and valvuloplasty. The workshop speakers will describe clinical presentations, explain their pre-procedural evaluations and preparations and elaborate on the criteria they use to decide which patients might benefit from the procedure. Each presenter will illustrate and explain the techniques that they use to image and treat obstructions and define the end points of their treatments. Finally they will discuss follow-up schema. The types of cases discussed will include the following: Routine uncomplicated cases that illustrate the key components of each speaker's techniques; cases that reveal nuances in technique of each speaker; misdiagnoses, technical errors and complications; "re-do" and "bailout" procedures.
Objective
At the end of the session, the learner should be able to:
1.Describe the pathology and pathophysiology, and clinical presentation of CCSVI
2.List the various screening, diagnostic and surveillance approaches to CCSVI
3.Identify the venographic appearances of CCSVI and formulate a strategy for their detection
4.Discuss the variety of neurodegenerative processes that may be associated with abnormalities in venous drainage
5.Recognize, reduce and treat complications of treatment

Coordinator
Bulent Arslan, MD, Rush University Medical Center - View Disclosure - Contact Me
Speaker
Salvatore Sclafani, MD, FSIR, SUNY Health Science At Brooklyn - View Disclosure - Contact Me
Educational Pathways
Neurovascular and Carotid Interventions

A "case-based interactive format" sounds like exactly what has been shared here over the last several years. We have had front row seats.
"CCSVI is a clinical syndrome resulting from outflow resistance of the veins that drain the brain and the spine" -- no mention of MS in that definition or in the presenting symptoms.
My questions would be how CCSVI is perceived and generally received by this year's SIR attendees.
Also, with all the Mr. President talk, there was never any discussion of what goals you might have as president of ISNVD.

[Sharon]

Dr. Sclafani .. I look forward to seeing you on Sunday at the CCSVI workshop

https://www.facebook.com/pages/CCSVI-Al ... 2427429118

Sharon

[Cece]

No updates yet! Where is the real-time internet immediate-info revolution when it's really needed!

[Sharon]

Drs Arslan and Sclafani presented a few of their case studies - talked about the importance of balloon size, reasons for non-response (Dr Sclafani has addressed these issues on this thread). We were unable to do a video interview, but did get a short audio with the two doctors. Will get it posted on CCSVI Alliance FB. I enjoyed talking with some of the "pioneer" CCSVI doctors outside of the classroom.
Sharon