colros wrote:Changes in refraction over time are universal, have nothing to due with the retina and nothing to do with MS. That "colors brightened immediately" is highly subjective. What was the evidence that you brain blood flow was so reduced as to cause cerebral hypoxia? If blood flow was that reduced you would have lost consciousness long before color perception changed.
With all due respect to Dr Sclafani, the ONLY way venous occlusion can potentially cause brain damage is by an increase in intracranial pressure which could secondarily reduce blood flow. No study has ever shown a primary reduction in cerebral flow causing MS. Cerebral flow will be reduced secondarily in long-standing MS secondary to loss of active brain tissue. Indeed, we do not know what breaks the BBB and leads to infiltration of inflammatory cells, but it has nothing to do with blood flow or pressure.
We all care very much about MS. Unfortunately, "CCSVI" and its surgical treatment, as superficially attractive as it is, is not the answer.
Dr. Rose, just wanted to bring this study to your attention.
Correlation of Diffusion Tensor and Dynamic Perfusion MR Imaging Metrics in Normal-Appearing Corpus Callosum: Support for Primary Hypoperfusion in Multiple Sclerosis
A.M. Saindanea, M. Lawa, Y. Gea, G. Johnsona, J.S. Babba and R.I. Grossman
From the Department of Radiology, New York University Medical Center, New York, NY
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Fundamentally, there are 2 possible causes for NAWM hypoperfusion, which can be categorized as primary or secondary. In the first scenario, a primary vascular pathologic lesion results in decreased perfusion in the NAWM with consequent ischemic parenchymal injury. In the second scenario, axonal damage in MS lesions leads to WD of axons traversing distant areas of white matter, resulting in decreased axonal attenuation, regional hypometabolism, and secondary hypoperfusion of the NAWM. The distinction between these mechanisms has potentially important implications, because ischemia may be an early and potentially reversible finding, whereas hypometabolism from axonal degeneration would represent advanced and irreversible disease.
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We interpret these findings as support for primary hypoperfusion (ischemia) in MS.
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This study does not refute the presence or importance of WD in MS; however, it suggests that hypoperfusion is due to alternative (primary vascular) pathologic conditions.
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Considerable histopathologic evidence supports a primary vascular pathologic lesion in MS. Studies have described perivascular inflammatory changes such as lymphocytic infiltration and edematous onion-skin changes of vein walls in NAWM lacking adjacent parenchymal inflammation, suggesting that MS could represent a form of subacute or chronic vasculitis.31,42 Vascular occlusion in MS was described on histopathologic examination by Putnam43,44 in the 1930s and later by Wakefield et al,45 who demonstrated fibrin deposition and thrombosis of vessels in the absence of cellular infiltration, suggesting that thrombosis of small veins and capillaries could represent an ischemic basis for disease. More recent studies have demonstrated the presence of extensive oligodendrocyte apoptosis46 and preferential loss of myelin-associated glycoprotein,47 which is suggestive of hypoxic-ischemic-type tissue injury.
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The results of this study correlating DTI and perfusion changes are more consistent with what would be expected in primary ischemia than in secondary hypoperfusion from WD. Further investigation, including larger and longitudinal studies are warranted to additionally support the concept of ischemic injury in MS. A better understanding of the role of ischemia could aid in predicting clinical course, monitoring response to therapy, and designing novel targets for therapeutic intervention for MS.