Amir wrote:marcstck wrote:
Just playing devils advocate here, as you know that I'm a believer (I should be, with a big muscle bundle pinching my jugular closed), but I also believe in healthy skepticism. In a nutshell, shouldn't signs of CCSVI not require the arcane methods invented by Zamboni to detect them?
I found this posting by Marcstck (Wheelchair Kamikaze) posted during August 2010 on Dr Sclafani's thread. Perhaps Marc can elaborate about "the muscle bundle pinching his jugular closed".
coming to this thread really, really late, but I'll throw my two cents in as well as explain the above quote.
Back in March, 2010, I was one of Dr. Sclafani's first batch of patients treated for CCSVI. During my venoplasty, he discovered a very large, very significant impingement in my right jugular that did not respond to ballooning. At the time, he didn't know what to make of this, but Dr. Sclafani investigated further, consulting with other physicians (including Dr. Zamboni) and determined that the impingement was a muscle external to the vein. Strangely, a CT scan of my jugulars done a few months earlier did not show this anomaly. It's quite likely that this impingement is positional; that is, depending on the angle of my head and neck, the degree of impingement can change. Dr. Zamboni noted that the impingement did not significantly disrupt blood flow, and therefore was not truly problematic. It's important to remember that we're talking about the deleterious effect of venous problems on blood flow, and not all areas of stenosis create significant blood flow disturbance.
As to the question of cause/effect, as I haven't read through this entire thread I may be going over old ground here, and if I am please forgive me, but the argument doesn't simply boil down to whether or not the venous anomalies now called CCSVI are congenital. Certainly, fused valves and anomalous membranes are in all likelihood congenital. However, this by no means indicates that they are THE cause of MS. It's much more likely that they play a role in a multifactorial disease etiology that includes genetic predisposition and exposure to environmental factors.
The ongoing BNAC studies, as well as the recent cadaver study conducted by the Cleveland Clinic, strongly indicate that there are folks with MS who do not have CCSVI, as well as folks with CCSVI who do not have MS. Having congenitally malformed CNS venous structures may predispose a person towards susceptibility to MS (and, perhaps, other neurologic diseases), but does not mean they are assured of developing the affliction.
Certainly, all of us are born with congenital abnormalities throughout our body systems (some within normal variance, some not). A person may be born with congenitally weak or short ligaments in their knees, but this does not guarantee that they will necessarily develop knee problems. If they live their life without encountering environmental conditions that would bring their congenitally abnormal ligaments into play (for example, an impact to the knees), these abnormalities may very likely never be discovered or cause detriment. If they do encounter such environmental factors, the subject's likelihood of sustaining significant damage, or damage more severe than a person without congenitally compromised ligaments, might be quite high.
Likewise, we've all heard the tragic stories of world-class athletes suddenly dying of congenital heart problems either during or immediately following heavy workouts. The irony behind the stories is that if these people had not been world-class athletes, subjecting their hearts to extremes of physical exertion, they very well may have lived long lives without their cardiac abnormalities ever coming into play.
Of course, there are some congenital abnormalities that create problems without outside influences. However, the presence of MS clusters, patterns of MS prevalence among migratory populations, the near universal infection of MS patients with EBV (usually two strains of the bug), the increasingly clear role of specific genotypes, and the heterogeneity of disease presentation from patient to patient, along with other factors, strongly point to MS being a multifactorial disease that requires an unfortunate confluence of physical predisposition and environmental factors to set off the disease process.
I'm quite sure that CCSVI does play a role in the development and/or the severity of MS in most but not all patients, but to my mind it's becoming increasingly clear it's not the whole enchilada. I think this is further borne out by the wide variance in effectiveness of CCSVI treatment.
Again, if this has been a rehash of discussions conducted previously in this thread, my apologies…
