Vascular aspects of multiple sclerosis
June 21, 2011 at 1:35pm
I have the complete review paper from Lancet Neurology. It is a review of recent research in MS and is a compilation of the many studies we've linked on this page. The endothelium, hypoperfusion, ischemia , CCSVI and the many terms we've learned over the past two years are all mentioned. I do not want to violate copyright laws, and can't copy and paste the full paper, but I'll give a brief breakdown. You'll see text from the paper in italics, and then my comments.
Note the word "might" is used extensively. They review the research connecting the vascular system to MS. While this is not earth-shattering to those of us who know CCSVI, up close and personal--it is encouraging to see this review in a neurological journal.
Vascular aspects of multiple sclerosis
Miguel D’haeseleer, Melissa Cambron, Ludo Vanopdenbosch, Jacques De Keyser
Three types of vascular dysfunction have been described in multiple sclerosis (MS). First, findings from epidemiological studies suggest that patients with MS have a higher risk for ischaemic stroke than people who do not have MS. The underlying mechanism is unknown, but might involve endothelial dysfunction secondary to inflammatory disease activity and increased plasma homocysteine concentrations. Second, patients with MS have global cerebral hypoperfusion, which might predispose them to the development of ischaemic stroke. The widespread decrease in perfusion in normal-appearing white matter and grey matter in MS seems not to be secondary to axonal degeneration, but might be a result of reduced axonal activity, reduced astrocyte energy metabolism, and perhaps increased blood concentrations of endothelin-1. Data suggest that a subtype of focal MS lesions might have an ischaemic origin, and there seems to be a link between reduced white matter perfusion and cognitive dysfunction in MS. Third, the pathology of MS might be the consequence of a chronic state of impaired venous drainage from the CNS, for which the term chronic cerebrospinal venous insufficiency (CCSVI) has been coined. A number of recent vascular studies do not support the CCSVI theory, but some elements of CCSVI might be explained by slower cerebral venous blood flow secondary to the reduced cerebral perfusion in patients with MS compared with healthy individuals.
#1 People with MS have ischemic stroke more often than healthy people.
Inflammation is widely accepted to play an integral part in the pathogenesis of atherosclerosis.18,19 Endothelial dysfunction is an early step towards overt atherosclerosis and the immune system seems to be highly involved in both processes.20 Endothelial dysfunction has been described in the very early stage of rheumatoid arthritis, probably as a result of inflammatory disease activity.21 Rheumatoid arthritis is an autoimmune disease22 in which increased cardiovascular morbidity and mortality has been noted.23 Alterations in endothelial function, as well as platelet activation and thrombophilia, have been reported in MS.24–26 Moreover, oxidative stress contributes to the development of endothelial dysfunction.27 Higher amounts of systemic and CNS oxidative stress have been reported in patients with MS than in healthy controls.28–30
The concentration of plasma homocysteine, which is believed to be an independent cardiovascular risk factor,31 is also raised in patients with MS.32,33 The cause of the increase in homocysteine concentration is unknown, but it occurs independently of serum concentrations of vitamin B12, vitamin B6, or folate.34 There is evidence that hyperhomocysteinaemia can cause endothelial dysfunction, even at moderately increased concentrations of homocysteine.35,36
The above evidence suggests that the increased frequency of ischaemic stroke in MS might be mediated through converging inflammatory pathways, oxidative stress, and raised homocysteine concentrations leading to endothelial dysfunction.
What this section is saying is that oxidative stress, endothelial dysfunction, endothelin-1 levels and homocysteine levels are higher in pwMS, and may contribute to higher stroke levels. (We've talked about this on here for awhile, it's why I created the endothelial health program for Jeff--I noted this connection in his serum numbers, and tried to help him thru diet, supplements, exercise and lifestyle.)
The researchers are positing that this is all due to inflammation and the immune system in MS. They believe it all begins there. But they have no proof of this. It's just their theory--their way of looking at the evidence thru their prism of MS as immune. But what we've discussed on here is that all of these factors are also found in diffuse cerebral hypoxia, or low levels of O2 in the brain. We don't need to involve the immune system in this theory if we look at it thru the prism of reduced oxygenation in the brain due to slowed blood flow.