There exists the possibility, however, that diminished venous vasculature on SWI in MS represents altered venous hemodynamics or venous vascular occlusions (15). A previous study of ours in MS patients found significantly reduced cerebral blood flow in normal appearing white matter using perfusion MRI (16).
cheerleader wrote:http://www.direct-ms.org/sites/default/ ... S%2009.pdf
The chicken and egg debate will continue....which comes first? Brain damage due to MS disease process creating CCSVI or reduced perfusion due to CCSVI creating MS? If we look at perfusion studies in early MS, we find that hypoperfusion occurs early on in the disease process----before the blood brain barrier breakdown and immune activation.
Squeakycat wrote:But if you look more directly at the nature of the problems being found in CCSVI, it is pretty hard to figure out how MS inflammation could cause a valve malformation or a septum to form. It just doesn't seem possible that these congenital problems could be caused by an inflammatory disease process unless I'm missing something. The cart has gotten in front of the horse.
MS patients with higher number of venous stenoses, indicative of CCSVI severity, showed significantly decreased venous vasculature in the brain parenchyma. The pathogenesis of these findings has to be further investigated, but they suggest that reduced metabolism and morphological changes of venous vasculature may be taking place in patients with MS.
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?
cheerleader wrote: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....
CureOrBust wrote:Although its really off-topic, I think we have to be careful of not acting like those that you are deriding. People are quick to point fingers at neuro's for dismissing CCSVI to quickly, and just because we do not see it now how MS could possibly cause CCSVI, I think we can not presume that it is not at all possible; but I do think the ball is in their court.
I have not read the book, but a lot of people quote him in situations other than actual war.Sun Tzu wrote:Never underestimate your enemy
Background: The venous vasculature of the brain parenchyma is significantly less visible on susceptibility-weighted imaging (SWI) in patients with multiple sclerosis (MS) compared to healthy controls (HC), as previously described.
Objective: To investigate the relation between the altered venous vasculature visibility in the brain parenchyma and Cine Cerebrospinal Fluid (CSF) Imaging and Perfusion Weighted Imaging (PWI) MRI metrics in patients with relapsing-remitting (RR) and secondary-progressive (SP) MS disease course, and HC.
Methods: Fifty nine (59) MS patients [41 RR and 18 SP] and thirty three (33) age- and sex-matched HC were scanned on a 3T GE scanner using CSF imaging, PWI and SWI. Mean age at scan was 44.3 yrs, mean disease duration 13.2 yrs and median EDSS 2.5. CSF flow rates (positive, negative and net), Mean Transit Time (MTT), Cerebral Blood Flow (CBF) maps and Cerebral Blood Volume (CBV) maps were calculated. 3D multi-scale line filter was used to extract the venous vasculature from SWI images. Absolute venous volume (AVV) was estimated in milliliters (ml); relative venous intracranial fraction (VIF) was calculated to correct for head size and amount of brain atrophy. Vein volumes were classified by vein radius: <0.3mm, 0.3-0.6mm, 0.6-0.9mm and >0.9 mm. Voxel brain average distance-from-vein (DFV) maps were calculated.
Results: MS patients showed reduced AVV, volume of veins with diameter <0.3mm and VIF (p< .05) and increased DFV (all p< .001) with respect to HC. In MS patients lower AVV, volume of veins with diameter <0.3mm and VIF, and higher DVF were strongly related to lower net negative flow (Spearman r = .48 to .61, p< .001) and higher net positive flow (r = .53 to .64, p< .001). A similar relation was found with an increased MTT (gray matter: r = .36 to .43, p< .01; white matter: r = .40 to .46, p< .001) and a decreased CBF (gray matter: r = .38 to .45, p< .01; white matter: r = .37 to .49, p< .001). The relationships were consistently stronger in RR than SP MS patients. No significances where found for HC.
Conclusions: This study showed that lower brain parenchyma venous vasculature visibility on SWI is related to altered hemodynamic CSF flow and hypoperfusion in patients with MS. The events contributing to these findings are probably occurring early in the disease process. Further studies are needed to elucidate relationship between reduction of venous vasculature and the hemodynamic MRI parameters in MS patients.
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