MSBOB wrote:That is ok because brain cells live for 75 years or more, they don't need to regenerate as often as other less protected cells.
I would like my brain cells to be protected from myelin-sensitized t-cells, inflammation, hypoxia, venous congestion, poor CSF flow, starvation, toxic build-up, whacks to the head, viruses, bacteria, and wallerian degeneration. Not a comprehensive list but if we take care of all these conditions that would be an excellent start.
X-ray Angiography is error-prone when the vessel is noncircular, because it uses a projection view of the geometry.
Experimental studies of stenotic vessels have typically focused
on the flow downstream of the stenosis, particularly on the disturbance
produced by the stenosis and whether the resulting flow is
turbulent, not on the mechanisms of plaque rupture.
Venous Flow Restriction: The Role of Vein Wall Motion in Venous Admixture
S Raju , , G Cruse, M Berry, S Owen, E.F Meydrech, P.N Neglen
River Oaks Hospital and University of Mississippi Medical Center, Jackson, MS, USA
Accepted 21 April 2004. Available online 7 June 2004.
Objectives. There are wide differences in flow between vascular beds at rest, even more during stress. The hydrodynamic energy (Energy grade line or EGL) of venous outflows must also vary considerably between vascular beds. We explored the mechanism of venous admixture of differing energy flows using a mechanical model.
Materials and methods. The model simulated two venous flows coalescing at a venous junction and then flowing through collapsible venous pumps. Flow rates and pressures were monitored when the venous pumps were full (steady state) and when they were compressed and allowed to refill inducing wall motion (pump flow).
Results. With increasing EGL differences between two coalescing venous flows, reduction or cessation (venous flow restriction) of the weaker flow occurred during steady state; higher base EGL of both flows ameliorated venous flow restriction and lower base EGL the opposite. Outflow obstruction favoured venous flow restriction. Pump action in the vicinity of the venous junction abolished venous flow restriction and maximized both venous flows.
Conclusion. The model suggests a pivotal role for vein wall motion in venous admixture and regional perfusion. Observations in the model are explained on the basis of network flow principles and collapsible tube mechanics.
Morphological details of diseased vessels, such as surface irregularity and stenosis curvature, have been shown to have important effects on the blood flow.
Both pressure and velocity distributions are similar for all three
Reynolds numbers, with magnitudes of both pressure and velocity
increasing with Re. Figure 5 shows the contours of total pressure
~static plus dynamic pressure! for this range of Reynolds numbers.
A large pressure force acts on the wall just upstream of the stenosis
throat in the internal carotid artery.
At diastole, vortex shedding
is observed from the shoulder of the carotid sinus, far upstream of
the most severe occlusion. The vortex that has formed at t50.230
seconds has detached by t50.290 seconds. This shed vortex is
carried into the sinus, where it dissipates. Another vortex has
formed at the shoulder by t50.50 seconds. This would indicate a
shedding frequency of 3.7 Hz, or a Strouhal number of 0.84 to
The assumption of Newtonian
behavior may break down when the shear rate is low
(;0.1 s21!, for example in small arteries and downstream of
stenoses. In some diseased conditions, including atherosclerosis,
blood exhibits some non-Newtonian behavior @38,39#. The effects
of non-Newtonian behavior on flows in stenotic vessels are first
considered for axisymmetric 50 percent stenoses
The advanced lesion experiences a dramatically different flow
field from that of a healthy artery or one in the early stages of
atherogenesis. Fluid shear stress in undiseased arteries ~comparable
in size to the common carotid artery! is on the order of
1–2 N/m2, while endothelial cells in the throat of a tight stenosis
may experience shear stresses greater than 30 N/m2. As
Fry observed, shear stresses in this range may severely damage
endothelial cells, or even strip them from the vessel wall.
Tensile wall stresses, distributed evenly around the circumference
of a healthy vessel, are likely to be focused at the most vulnerable
shoulder regions of a diseased vessel @43#. ~The ‘‘shoulder regions’’
contain transitions from normal to diseased artery wall.!
A k-v model such as that of
Wilcox, also given high marks by Patel et al., may be more
suitable than k-e models for flows in stenotic vessels.
Parenchymal abnormalities associated with developmental venous anomalies.
Diego San Millán Ruíz, Jacqueline Delavelle, Hasan Yilmaz, Philippe Gailloud, Enrico Piovan, Alberto Bertramello, Francesca Pizzini, Daniel Rüfenacht
INTRODUCTION: To report a retrospective series of 84 cerebral developmental venous anomalies (DVAs), focusing on associated parenchymal abnormalities within the drainage territory of the DVA. METHODS: DVAs were identified during routine diagnostic radiological work-up based on magnetic resonance imaging (MRI)(60 cases), computed tomography (CT)(62 cases) or both (36 cases). Regional parenchymal modifications within the drainage territory of the DVA, such as cortical or subcortical atrophy, white matter density or signal alterations, dystrophic calcifications, presence of haemorrhage or a cavernous-like vascular malformation (CVM), were noted. A stenosis of the collecting vein of the DVA was also sought for. RESULTS: Brain abnormalities within the drainage territory of a DVA were encountered in 65.4% of the cases. Locoregional brain atrophy occurred in 29.7% of the cases, followed by white matter lesions in 28.3% of MRI investigations and 19.3% of CT investigations, CVMs in 13.3% of MRI investigations and dystrophic calcification in 9.6% of CT investigations. An intracranial haemorrhage possibly related to a DVA occurred in 2.4% cases, and a stenosis on the collecting vein was documented in 13.1% of cases. Parenchymal abnormalities were identified for all DVA sizes. CONCLUSION: Brain parenchymal abnormalities were associated with DVAs in close to two thirds of the cases evaluated. These abnormalities are thought to occur secondarily, likely during post-natal life, as a result of chronic venous hypertension. Outflow obstruction, progressive thickening of the walls of the DVA and their morphological organization into a venous convergence zone are thought to contribute to the development of venous hypertension in DVA.
cheerleader wrote:Cece wrote:The argument that MS might cause CCSVI tends to be made by those who consider CCSVI to be a stricture of the vein itself and not as intraluminal abnormalities.
Is this suggesting that the CCSVI is causing the reduced metabolism and morphological changes in the brain?
I have the full paper, and the posits are that the MS disease creates hypometabolism of brain tissue and this leads to less blood flow and CCSVI, or CCSVI strictures create hypoperfusion and reduced visability of vasculature....
but Cece makes a GREAT point.
In studies, like the one from the Cleveland Clinic, announced today---intraluminal defects are found in the veins of pwMS at much higher rates than normals. These are not "strictures" or "stenosis" created by hypovolemia or inflammation---these intraluminal defects are truncular venous malformations, as we see in other congenital venous disease.
1eye wrote:How many dots do we have to connect? The theory of CCSVI is not just a theory any more. It is supported by multiple independent and otherwise unrelated statements about both "MS" and CCSVI.
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