sooooo, back to the blood brain barrier, and the model proposed by Dr. Simka, Dake, Zamboni and others-
When Dr. Dake and I were first discussing Dr. Zamboni's research back a year ago, he mentioned that this model of CCSVI in MS looked a lot like congestive venous myelopathy. We already have a medical model for how venous congestion can create demyelinating lesions.
This is venous congestion created by DAVFs or AVMs. The demyelination in venous congestion is well documented. BTW, vascular steal is when there is a reduction of blood flow thru the arteries, due to venous blockage. This creates ischemic injury.
OBJECTIVE: Although venous congestion is considered to be a major cause of progressive myelopathy in patients with spinal dural arteriovenous fistulae (DAVFs), the neurological deterioration in patients with spinal intradural arteriovenous malformations (AVMs) has been attributed to hemorrhage or to vascular steal. To reexamine this theory, we analyzed our own cases of spinal vascular diseases. METHODS: In 24 patients with spinal vascular diseases, those who demonstrated progressive myelopathy with T2 hyperintensity in the spinal cord on magnetic resonance imaging (MRI) were diagnosed as patients with congestive myelopathy. We further examined the clinical courses, MRI findings, and reversibility of these cases. RESULTS: Venous congestion was judged to be a cause of neurological deterioration in 13 patients (7 DAVFs, 6 intradural AVMs). The T2 signals on these patients' MRI scans were located in the center and extended over several levels not corresponding to distribution of ischemia due to arterial steal. Of the patients who were diagnosed with congestive myelopathy, no differences between those with DAVFs and those with intradural AVMs were apparent in terms of clinical manifestations and reversibility. Eight (four DAVFs, four intradural AVMs) of 13 patients experienced neurological improvement after treatment. All patients with poor outcomes had intervals from onset of more than 3 years and showed contrast enhancement of the spinal cord on MRI studies. CONCLUSION: Spinal intradural AVMs as well as spinal DAVFs can be a cause of venous congestive myelopathy. Regardless of its etiology, congestive myelopathy is potentially reversible if properly diagnosed and treated.
an aside....this study states congestive venous myelopathy is potentially reversible if caught early...it seems 3 years after injury had poorer outcomes. This is why Dr. Zamboni urges studies now.http://www.ncbi.nlm.nih.gov/pubmed/11383723
http://www3.interscience.wiley.com/jour ... 1&SRETRY=0
We describe three patients with progressive myelopathy, in whom autopsy revealed spinal cord pathology compatible with that of venous congestive myelopathy (VCM) associated with dural arteriovenous fistula (AVF), formerly known as angiodysgenetic necrotizing myelopathy (Foix–Alajournine syndrome). In these three patients, common symptoms were gait disturbance and sensory disturbance of the extremities, and these symptoms slowly worsened. The clinical diagnoses varied and included spinal cord intramedullary tumor, cervical spondylosis and multiple sclerosis. At autopsy, all the patients showed enlarged, tortuous venous vessels on the dorsal surfaces of the spinal cord at the affected levels. In the affected spinal cord parenchyma, necrotic lesions manifested by various degrees of neuronal loss and gliosis, with increased numbers of hyalinized vessels, were evident. The presence or absence of associated spinal dural AVF could not be identified histopathologically. Even with the help of modern neurological examination methods, early and accurate clinical diagnosis of VCM is sometimes difficult. When encountering patients with progressive myelopathy, VCM, although recognized as rare, should be considered as an important differential diagnosis.
So, here is someone diagnosed with MS who had tortous veins upon autopsy....creating progressive myelopathy.
I know, I know...this isn't exactly
what Dr. Zamboni....this is DAVFs or AVMs in the spinal veins creating venous congestion, rather than stenotic lesions in the jugular and azygos veins creating venous congestion. But as Dr. Dake told me, we have a medical model for how venous congestion creates neurodegeneration and demyelination in the body. And it was a better explanation than the unknown mystery antigen the autoimmune proponents hypothesize. That was enough for me and Jeff.