Direct-MS wrote: It is important to be able to evaluate the data and interpretations of all research efforts done on CCSVI..
Direct-MS wrote:It would be very helpful if we could get a translation of this paper. It is important to be able to evaluate the data and interpretations of all research efforts done on CCSVI.
To ignore such work brings us down to the bottom-feeding level of the neurological community which patently ignored Dr Zamboni's work for 3 years until the CTV documentary forced them to have to deal with it in a scientific fashion. Of course now that the neurological community can no longer ignore it, they are trying hard to discredit it.
I am curious to see the scientific level of this latest effort to dismiss CCSVI and to prevent testing and treatment.
, only in that we do not yet know the exact causation of vascular stenosis in CCSVI. It has been posited, and indeed, agreed upon by phlebologist society that the strictures are congenital, and in fact are initiated in the 3d month of gestation. This does not account for all of the different presentations of CCSVI, or MS. Dr. Sclafani has suggested that what he saw in my MRV pics, could be caused by pathology lower down - like brachio-cephalic plexus, or such. Then there is Vena Cava Syndrome, azygos involvement, that spirochetes (Lyme disease, syphilis) have an affinity for the endothelium. Could it be that spirochetes attack the venoules in the brain, that later trigger jugular, and other stenoses?The authors conclude that the „chronic cerebrospinal venous insufficiency (CCSVI)“ cannot represent the exclusive pathogenetic factor in the pathogenesis of MS.
Johnson wrote:I don't see an outright dismissal, and in fact, sympathise with this statement:The authors conclude that the „chronic cerebrospinal venous insufficiency (CCSVI)“ cannot represent the exclusive pathogenetic factor in the pathogenesis of MS.
Currently, the hypothesis that altered venous hemodynamics might play a causative role in the pathogenesis of multiple sclerosis (MS) is being controversially discussed. This new "venous hypothesis" postulates that obstructions of the cervical venous system cause an increased pressure of the intracranial venous system and that in turn intracranial congestion disintegrates the blood-brain barrier initiating the inflammatory process in MS.The "venous hypothesis" is analyzed and evaluated with regard to the following aspects: first concerning the validity of published data, second with regard to the plausibility in view of the currently approved pathogenetic model of MS, and third with regard to the compatibility with preliminary neurosonological findings in a small but unselected cohort of patients at our department.The authors conclude that the "chronic cerebrospinal venous insufficiency (CCSVI)" cannot represent the exclusive pathogenetic factor in the pathogenesis of MS. In our cohort, only 20% of the patients fulfilled the required neurosonological features of CCSVI. So far, the pathogenetic relevance of these findings remains speculative. Thus, based on the current scientific position we cannot justify invasive "therapeutic" approaches, especially if they are performed outside of clinical trials.
I am curious to read if these researchers followed Dr. Zamboni's doppler and transcranial doppler ultrasound protocol?
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