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PostPosted: Fri Feb 01, 2013 1:53 am 
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drsclafani wrote:
Cece wrote:
That was one of the best case studies we've been shown. Multiple images from multiple procedures.
drsclafani wrote:
In Spring 2010 she became the second patient of an early adopter of interventional treatment of ccssvi

It doesn't seem good to be among a doctor's first patients. Learning curve.


actually it is not good. My first case took four procedures and three locations to finally identify the lesions.

i am afraid to look back to the beginning of this thread. I fear what i have said. Thankfully, most patients have been supportive of the work in progress that this has been. I continue to lose sleep over my early problems and failures. There are many times i wish for a do-over


The burden of each exploring human?

What if you did not start with the knowledge you had a few years ago??
You did the right thing....no doubt about that. as a patient you have a choice...i also was treated early 2010 when no many patients were treated at Euromedic (dr Simka)
Yes, treatment is much better now...but if i had not done it, would I be here???

Keep up the good work, you got the best treatment at this moment (and i got experience with 4 pta's in 4 different clinics :mrgreen: )

Rgds,

Robert


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PostPosted: Fri Feb 01, 2013 9:49 am 
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Cece wrote:
drsclafani wrote:
my first suggestion would be to review my Downstate lectures by Dr Beggs on Youtube. he speaks well on this issue

Clive Beggs, MD [CCSVI and Fluid Dynamics of CSF
http://www.youtube.com/watch?v=QcT4CyJOckY
Clive Beggs, MD [Venous Hemodynamics in CCSVI and MS
http://www.youtube.com/watch?v=37hFWVFFgXs


Thanks for posting these cece, they go some way towards explaining some of this but I couldn't possibly grasp all of it.

What is interesting is that something as fundamental as the flow of CSF is still not completely understood.

As one of the jobs of CSF is "waste removal" and if we assume that the CSF flow is effected in pwMS, would it be a logical thought that lesions may be a result of CSF not clearing away the waste, leaving deposits that should have been tidied up and triggering the immune response?

I'd always understood something like this had been attributed to bloodflow rather than CSF flow?


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PostPosted: Fri Feb 01, 2013 11:32 am 
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just in case this were to get missed, it's a patient's response and more questions to Dr. Sclafani in a different thread:
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic11857.html#p204206


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PostPosted: Fri Feb 01, 2013 1:31 pm 
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drsclafani wrote:
Cece wrote:
That was one of the best case studies we've been shown. Multiple images from multiple procedures.
drsclafani wrote:
In Spring 2010 she became the second patient of an early adopter of interventional treatment of ccssvi

It doesn't seem good to be among a doctor's first patients. Learning curve.


actually it is not good. My first case took four procedures and three locations to finally identify the lesions.

i am afraid to look back to the beginning of this thread. I fear what i have said. Thankfully, most patients have been supportive of the work in progress that this has been. I continue to lose sleep over my early problems and failures. There are many times i wish for a do-over


Don't be so hard on yourself, Dr. S. You were navigating virtually uncharted waters. We all knew that going in. You did your best and it was pretty damn good. It still is.
Your second patient was a success. Don’t forget that. I'm going on three years now and due for an annual follow-up ultrasound. You may wish you’d done some things differently or knew more in the beginning, but it took guts to be an early adopter, to step out way in front of the curve to help people when no one else would. You did, and you're still here and still helping us.
It also takes guts to be an early patient -- it may not be good but there are no early adopters without early patients. As with the doctors, and especially your first patient, they all have my thanks for braving the unknown.
I also wish all your patients had success. They deserve it; we all deserve it. I can only say you help all of us by continuing to learn and share your knowledge with others.


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PostPosted: Sat Feb 02, 2013 1:46 pm 
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Thank you Dr. Sclafani for your pioneering and courageous angioplasty work. Also for assuming the role of Professor.


Cece wrote:

http://www.ncbi.nlm.nih.gov/pubmed/6460930

Quote:

Morphol Embryol (Bucur). 1981 Jul-Sep;27(3):195-214.
Data regarding the typology and functional significance of the venous valves.
Maros T.

Certain findings suggested a reorganization after birth of the venous valves which are frequently met in fetus. The close relation between hemodynamic mechanisms and the blood guiding structures may explain the changes (disappearance or persistence) of venous valves in some areas after birth.

"I thought this was interesting. We've talked about the malformation of internal jugular vein valves as happening during embryological development. I had never heard about changes in the valves occurring after birth. What sort of changes? "Disappearance or persistence"? How could a valve disappear?"


NZer1 “Maybe there this a connection, CPn/Valve dysfunction?

The diseased cells, dysfunctional cells, hardened valves may have been scared by the infection/inflammation process over time? Pre-birth and Post birth!”

Dr Sclafani Jan 31, 2013
“if the valve is obstructed, generally what happens is that the vein above the stenosis starts to dilate or enlarge. Slow flow or stasis (absence of outflow) occurs. This leads to reduced arterial inflow, poorer perfusion with oxygenated blood into the brain and reduction in cerebrospinal fluid drainage and possibly hydrocephalus. Additionally, when the muscles of the neck contract, they MAY cause the pressurization of the blood within the vein. In the presence of obstruction toward flow into the heart, this blood may jet into the skull and injure deep cerebral veins.”

It is gratifying to see some of my observations confirmed by the professionals. 1) Phlebologists long have believed vascular disorders are congenital in origin. Now it appears valve problems can develop after birth, in other words, they may be developmental in origin. (See Cece) 2) I believe my entry of December 16, 2012 changed the discussion, opening the possibility that blood flow problems may be a consequence of cerebrospinal fluid pressure ON the vein rather than a defect IN the vein, a type of MS I defined as Skeletal. 3) Muscle tension may impede blood flow leading to the blood reflux, a condition which may fall under the rubric of Toxic MS. 4) I’ve decided to split up Toxic MS into 2 types, Infectious and Toxic, both of which may be factors in Developmental vein damage and/or muscle tension.
Thus I define 6 MS types as follows/
1) Congenital
2) Developmental
3) Infectious
4) Toxic
5) Aging
6) Skeletal

I have discussed Developmental MS in detail in my main paper in the site MS Cure Enigmas.net. Chinese Medical theory and practice provided some answers to the epidemiological factors defining MS incidence. Western medicine will have to catch up. But for now this ancient practice based on thousands of years of observation can point to effective treatment.
Both Infectious and Toxic MS may be factors in childhood Developmental MS. Chlamydia Pneumoniae (Cpn) is an example of Infectious MS which may have damaged the vascular system during childhood development, and/or may still be active. This is apparently an issue with NZer1 (Nigel) on Thisisms.com. Other illnesses often associated with MS are Epstein Barr, Mononucleosis and perhaps Lyme disease? Earlier I had included these infections under Toxic MS since they doubtless stress and tense up the organism, but they may well directly damage the veins themselves adding to the severity of the disease (and perhaps further complicating the treatment.)
I believe the toxins in Toxic MS tense up the muscles as they stress the organism. Once the toxins are identified and eliminated, this form of MS is the easiest to cure. Toxins may include mercury in amalgam fillings (see want2bike), aspartame, and food intolerances such as glutens.
Aging MS speaks for itself.
SKELETAL MS: A misaligned skeletal, bone or dental structure can actually restrict the free flow of cerebrospinal fluid which in turn can compress or impede venous blood circulation. Structural problems can be either congenital or developmental in origin (e.g. accidents.) Recent scientific studies have focused on the interdependent dynamic of brain "fluids", the blood and the cerebrospinal fluid (CBF) which bathes the Central Nervous System. Excess cerebrospinal fluid can actually "compress" or limit blood circulation, hence the interest of Chiropractors in adjusting the Atlas bone to assure proper CBF circulation. If the problem is SKELETAL, angioplasty would not be appropriate. In this case it is not a problem INSIDE the vein but OUTSIDE. Chiropractic, Osteopathic or Dental adjustment may suffice to release the brain fluids flow

I do not oppose Angioplasty as some might think. I believe however that all these factors should be considered before intervention.

The main problem now is political, that is to say the power of the big pharma and neurology lobby to block CCSVI and other treatments for MS patients. Dr. Sclafani, you have pioneered the skills and techniques necessary to maximize positive angioplasty outcomes. But you can’t treat everybody for everything. Maybe Angioplasty isn’t the answer for someone who needs spinal/dental adjustments or someone who needs to remove toxins from his body. Or someone like me whose nerve damage is too established to heal.

My purpose here is to help people think things through and to suggest alternative therapies which I’ve found effective.

MS Cure Enigmas.net


Last edited by vesta on Tue Feb 05, 2013 3:26 pm, edited 1 time in total.

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PostPosted: Sat Feb 02, 2013 6:25 pm 
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Needled, glad to hear you are doing well! Three years!


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PostPosted: Sat Feb 02, 2013 6:34 pm 
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EJC wrote:
Thanks for posting these cece, they go some way towards explaining some of this but I couldn't possibly grasp all of it.

What is interesting is that something as fundamental as the flow of CSF is still not completely understood.

As one of the jobs of CSF is "waste removal" and if we assume that the CSF flow is effected in pwMS, would it be a logical thought that lesions may be a result of CSF not clearing away the waste, leaving deposits that should have been tidied up and triggering the immune response?

I'd always understood something like this had been attributed to bloodflow rather than CSF flow?

I suppose the effect of impaired cerebrospinal fluid flow on neurons would fall in the neurologists' domain. And this is not a question they're interested in?
I have to watch the Beggs' videos.


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PostPosted: Mon Feb 04, 2013 11:29 am 
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Cece wrote:
just in case this were to get missed, it's a patient's response and more questions to Dr. Sclafani in a different thread:
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic11857.html#p204206


Quote:
ljelome wrote:
Dear dr. Sclafani,

Thank you for your explanation...i have to read it many times in order to understand what you're saying. Pardon me, my english is not so good.

So you said that maybe my valve is there but it just can't be seen because maybe my valve is just very thin and move so quickly. If it is the case then does it mean that my valve is okay? Coz during my examination, as a comparison, my doctor had my healthy husband to be checked by the same Doppler USG, and we can see the valve very clearly in his IJV.

From my CT Venogram and Doppler USG result, my doctor said that there is no stenosis, no reflux, no absence flow in both IJV . But you said that "if the valve is obstructed, generally what happens is that the vein above the stenosis starts to dilate or enlarge. Slow flow or stasis (absence of outflow) occurs". Yes, in my right IJV my doctor noticed a slow flow in all part of the right IJV (from prox, mid to distal area). Could this slow flow happened because my doctor pressed my neck to hard during the examination?

And you said "This leads to reduced arterial inflow, poorer perfusion with oxygenated blood into the brain and reduction in cerebrospinal fluid drainage and possibly hydrocephalus." But my doctor said there is a hyperacceleration in my arterial flow? Does it mean an increased in arterial inflow?

You said "Additionally, when the muscles of the neck contract, they MAY cause the pressurization of the blood within the vein. In the presence of obstruction toward flow into the heart, this blood may jet into the skull and injure deep cerebral veins." I wonder what activities that can make my neck contract?

And if the obstruction in my IJV's valves is an absence of those valves, then what would happen to the blood flow or what is the impact then?

Oh dr. Sclafani, i'm sorry to ask u so many questions. I wish u could be my doctor:-)

Or maybe, i just have to see another sonographer then? Do you happen, by any chance, to know some one who can do this procedure accurately in Asia? Coz i live in Indonesia and there's never any CCSVI examination done here before, if it wasn't for me. There's so little case of MS here compare to the other countries in America or Europe or Australia.

Please dr. Sclafani, tell me what to do?

Thank you for your time and thank you for your quick reply.

Warm regards,
Linda


Dear Linda
i am so sorry that i cannot convey clearly enough what i said to you. First you must understand that I was speaking in a general way. I cannot speak directly about your personal condition because I have not met you, have not examined you and have neither performed nor interpreted your imaging.

I do not know anyone in indonesia who is familiar or expert in CCSVI screening, diagnosis or treatment

DrS

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Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com

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Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com


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PostPosted: Tue Feb 05, 2013 9:38 am 
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Hi Dr Sclafani I'm one of your patients that recently moved to Fl and the my nuero had me try an IV regiment for three days. I noticed when they were putting a mid line iv with ultrasound they could not push through a needle through the arm vein; in fact it pretty mangled when they removed it and had to go a second vein. It appeared they were unable to pass a valve. I guess in my case there would be many more veins could have poor distribution when you get CCSVI than those checked.


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PostPosted: Tue Feb 05, 2013 6:22 pm 
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milesap wrote:
Hi Dr Sclafani I'm one of your patients that recently moved to Fl and the my nuero had me try an IV regiment for three days. I noticed when they were putting a mid line iv with ultrasound they could not push through a needle through the arm vein; in fact it pretty mangled when they removed it and had to go a second vein. It appeared they were unable to pass a valve. I guess in my case there would be many more veins could have poor distribution when you get CCSVI than those checked.

there are many valves in the many veins of the arms. I think that the large amount of veins in the upper and lower extremities has led doctors to think of veins as expendable sources to the circulation

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Patient contact: ccsviliberation@gmail.com


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PostPosted: Wed Feb 06, 2013 1:35 pm 
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Dr. Sclafani,

Could/does PTA of IJVs lower pressure in the venous sinuses?

Moose :)


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PostPosted: Wed Feb 06, 2013 2:09 pm 
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Anonymoose wrote:
Dr. Sclafani,

Could/does PTA of IJVs lower pressure in the venous sinuses?

Moose :)


firstly, the pressures are low in the veins and sinuses in general, in healthy patients and in PwMS
secondly small changes in pressure may be difficult to accurately assess given standard measuring techniques
However reducing outflow obstructions may improve pressure increases if they occur.

but the bottom line is that relieving the outflow obstructions by
PTA allows improvement in flow by relieving resistance, not by lowering pressure and improvement in flow probably improves perfusion of the brain and drainage of CSF

_________________
Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com


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PostPosted: Wed Feb 06, 2013 2:26 pm 
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drsclafani wrote:
Anonymoose wrote:
Dr. Sclafani,

Could/does PTA of IJVs lower pressure in the venous sinuses?

Moose :)


firstly, the pressures are low in the veins and sinuses in general, in healthy patients and in PwMS
secondly small changes in pressure may be difficult to accurately assess given standard measuring techniques
However reducing outflow obstructions may improve pressure increases if they occur.

but the bottom line is that relieving the outflow obstructions by
PTA allows improvement in flow by relieving resistance, not by lowering pressure and improvement in flow probably improves perfusion of the brain and drainage of CSF


Hi Dr S is there any updates on Dr Zamboni's collar? It would be good to know.

;)
Nigel


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PostPosted: Wed Feb 06, 2013 3:02 pm 
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drsclafani wrote:
Anonymoose wrote:
Dr. Sclafani,

Could/does PTA of IJVs lower pressure in the venous sinuses?

Moose :)


firstly, the pressures are low in the veins and sinuses in general, in healthy patients and in PwMS
secondly small changes in pressure may be difficult to accurately assess given standard measuring techniques
However reducing outflow obstructions may improve pressure increases if they occur.

but the bottom line is that relieving the outflow obstructions by
PTA allows improvement in flow by relieving resistance, not by lowering pressure and improvement in flow probably improves perfusion of the brain and drainage of CSF


Thanks Dr. Sclafani. Another of my ill-born theories bites the dust. :) I think that leaves only really complicated explanations. I give!

Edit: Thanks to Cece's etiology of ccsvi thread, I read that Csf drainage is dependent upon relative pressure of the venous sinuses and csf. When pressure in the sinus is less than that of the csf, the arachnoid villi open like valves to drain csf. It also drains around the cranial and spinal nerve roots. Is there some other way it drains?


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PostPosted: Thu Feb 07, 2013 8:38 am 
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Anonymoose wrote:
drsclafani wrote:
Anonymoose wrote:
Dr. Sclafani,

Could/does PTA of IJVs lower pressure in the venous sinuses?

Moose :)


firstly, the pressures are low in the veins and sinuses in general, in healthy patients and in PwMS
secondly small changes in pressure may be difficult to accurately assess given standard measuring techniques
However reducing outflow obstructions may improve pressure increases if they occur.

but the bottom line is that relieving the outflow obstructions by
PTA allows improvement in flow by relieving resistance, not by lowering pressure and improvement in flow probably improves perfusion of the brain and drainage of CSF


Thanks Dr. Sclafani. Another of my ill-born theories bites the dust. :) I think that leaves only really complicated explanations. I give!

Edit: Thanks to Cece's etiology of ccsvi thread, I read that Csf drainage is dependent upon relative pressure of the venous sinuses and csf. When pressure in the sinus is less than that of the csf, the arachnoid villi open like valves to drain csf. It also drains around the cranial and spinal nerve roots. Is there some other way it drains?

Dr. Sclafani,

It seems I am repeating history. There isn't another way it drains (thanks, Cece). So, since CSF drainage is a passive system, slowed blood flow causes slow CSF drainage (??).

You must be the most patient person on the planet.

Edit: That doesn't work either. It isn't completely passive it's pressure driven. How could csf drainage increase without reduced sinus pressure? I've got to give up before I drive us both bonkers.

Many thanks for your help.


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