Cece--great link. Yes, pressure differences make the difference in O2 utilization. And maybe venous congestion is contributing to that pressure difference in the CCSVI brain. Your link is also right on, it's not about the O2 in the atmosphere--it is the bioavailablity of that O2. The thought is that in CCSVI, the lack of O2 availability and glucose metabolism is due to slowed perfusion. Flying or being at high altitude then becomes the tipping point in an already stressed brain. The Haacke and Hubbard perfusion/BOLD studies will further elucidate this hypoperfusion, hypometabolism and low O2 availabilty.
Mark--it was all this "speculation" (as you call it) that got the doctors to look at hypoperfusion, low O2 and cerebral oxygenation levels in pwCCSVI before and after venoplasty. Researchers are now measuring it and finding a correlation. It is a BIOMARKER and it is important
, even if you do not think it so.
Here is what Yulin Ge (from NYU) says about hypoxia and hypoperfusion in MS. This is his abstract from the ISNVD--
Technology Insights of Oxygen Metabolic Abnormalities in MS (Yulin Ge, USA)
The role of vascular pathology in multiple sclerosis (MS) was suggested long ago by Ribbert (1882) and Putnam (1933). With the invention and advances of imaging technology, now there is accumulating evidence in vivo of primary vascular pathogenesis and hemodynamic impairment in MS. In particular, there is cerebral blood perfusion changes in lesions and normal appearing brain tissues, suggesting there might be an ischemic and/or hypoxic origin of MS disease. In this presentation, I am going to discuss the hemodynamic perfusion changes and vascular abnormalities measured with several advanced MRI techniques and their pathophysiological significance in MS. First, the close perivenous relationship of MS lesions associated with the underlying vascular inflammatory changes can be evaluated with high resolution susceptibility-weighted imaging. Second, cerebral blood perfusion changes including cerebral blood volume (CBV) and flow (CBF) have been evaluated with dynamic susceptibility contrast-enhanced (DSC) and arterial spin labeling (ASL) MRI techniques. The lesions showed different patterns of perfusion change despite that hypoperfusion is a general feature seen in MS tissues. The perfusion changes in MS may provide additional information of microvascular abnormalities. Third, the recent promising vascular ischemic / hypoxic hypothesis can be evaluated in vivo with several techniques including perfusion- and diffusion- weighted imaging during the acute phase and oxygen metabolic measures as well as functional MRI techniques. In summary, there is increased awareness from both histopathologic and imaging studies of the role of microvascular and hemodynamic impairment in tissue injury in MS; therefore, targeting hypoxic injury may be indicated in the new therapeutic strategy.
Here is what Dr. Zivadinov (from BNAC) says about it in his ISNVD abstract-
A hypoxia-like condition has been evidenced in patients with multiple sclerosis (MS). Perfusion MRI is particularly relevant to studying MS pathogenesis because it has been shown that hypoperfusion of the brain parenchyma in MS patients may precede disease onset. MS patients show abnormal blood flow perfusion patterns, such as increased mean transit time (MTT), and decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) within normal appearing white matter (WM) and gray matter (GM). Perfusion MRI abnormalities are present from the earliest stages of the disease in normal appearing WM, while GM perfusion changes were evidenced at later disease stages. In fact progressive MS patients show more severe perfusion changes compared to relapsing MS. Chronic inflammatory events related to local blood congestion and secondary hyperemia of the brain parenchyma are proposed as a cause of these hemodynamic abnormalities detected on perfusion MRI in patients with MS. The hemodynamic abnormalities detected on perfusion MRI in patients with MS are currently interpreted as being a consequence of chronic inflammatory events related to local blood congestion and secondary hyperemia of the brain parenchyma. Furthermore, at this time it is not clear whether reduced perfusion of the brain parenchyma in MS patients is a sign of vascular pathology or decreased metabolic demand. Alternatively, it can be hypothesized as a disorder that involves the major vasoactive substances. Increased perfusion in the area of lesion formation could be a sign of vessel dilation mediated by pro-inflammatory cytokines. Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular condition described in MS patients, characterized by multiple intra- and extra-luminal stenosing malformations of the principal pathways of extra-cranial venous drainage. An altered perfusion pattern may not only be a consequence of local circulatory disturbances due to inflammatory mechanisms in acute or chronic phases, but rather could result from an outflow blockage situated far away from the lesions. CCSVI may impact local hemodynamics at places distant from the location of the mechanical stenosis, as in any condition of venous obstruction of the major trunks. Such a mechanism may lead to capillary hypertension and leakage, consistently contributing to inflammation. Preliminary findings are presented from a pilot study investigating the relationship between the severity of CCSVI and hypoperfusion in the brain parenchyma.
and here's what Dr. Tucker says about it in his abstract---
This increase in blood pressure fluctuation at the venule end of the capillary bed, which would be equivalent to local hypertension, is predicted to reduce the pressure drop across the bed which, in turn, would reduce blood flow through the bed in accordance with Darcy’s Law. Such a reduction in blood flow through the bed would be accompanied by a reduction in the transfer of oxygen, glucose and other nutrients into the brain tissue in accordance with Fick’s Principle. The reduction in oxygen levels in the brain tissue (i.e. hypoxia), would, in turn, be associated with increased fatigue and decreased mental acuity in the subject patient. In addition, cerebral hypoxia may be associated with vasoconstriction of the endothelium and promotion of both leukocyte- endothelial adherence and angiogenesis (ie. growth of collateral veins). The deprivation of oxygen adjacent to the venules may also result in cell death, including endothelial, and oligodendrocyte cells.
This is not "dangerous" or speculative, Mark....it's science, being done by top researchers.