Finally after three weeks a question!AMcG wrote:Does this mean we will be addressing Sal as Mr President from now on?
The answer is i hope you do not. Only my mother is allowed to call me president
Any other questions?
Finally after three weeks a question!AMcG wrote:Does this mean we will be addressing Sal as Mr President from now on?
Who is he??President Elect: Dr. Salvatore Sclafani??
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 wrote:Any other questions?
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.NHE wrote: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 wrote:Any other questions?
pelopidas wrote:
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?
hi Mr Presidentdrsclafani wrote: Pelopidas,
that is way over my head. I have no idea about that.
That's a great question. Welcome to the site & I am sorry to hear about your dysautonomia.Matthewa100 wrote: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
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.NZer1 wrote: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 will answer you soonpelopidas wrote:pelopidas wrote:
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?hi Mr Presidentdrsclafani wrote: Pelopidas,
that is way over my head. I have no idea about that.
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?
A "case-based interactive format" sounds like exactly what has been shared here over the last several years. We have had front row seats.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