Here's another suggestion that blood vessels have a role to play in MS, this time saying that high blood pressure can cause fistulas, (holes or channels which shouldn't be there and which allow material to flow),
1: Med Hypotheses. 2007 Dec 11 [Epub ahead of print]
Raised venous pressure as a factor in multiple sclerosis.
Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Du Cane Road, London W12 ONN, United Kingdom.
It is hypothesised that the inflammatory condition seen in MS and the progressive myelopathy that is being successfully halted by obliteration of dural arteriovenous fistulas (DAVFs), may actually be two sides of the same coin. Excessive venous hypertension can stretch vein walls sufficiently to separate the tight junctions between endothelial cells forming the blood-brain-barrier (BBB). Colloids, etc., but not necessarily erythrocytes, could then pass through the exposed porous basement membranes. The resulting changes in osmotic pressure, etc. would disrupt the axon and dendrite internal transport systems, leading to their disintegration. The normal inflammatory processes which would follow, might be indistinguishable from those associated with autoimmune disease. Ascending progressive myelopathy and disablement are associated with an intracranial DAVF when its outflow enters the spinal venous system and descends past the cervical region. This can be arrested, and some degree of recovery produced, if the can be successfully eliminated or blocked. However, if the DAVF outflow is entirely into the spine, intracranial venous pressure may be normal and so there is nothing to alert the clinician to the presence of an intracranial DAVF. It is suggested that where spinal MS has been diagnosed from clinical observations, patients should be referred for angiological investigation to search for DAVFs within the head to identify any treatable subjects.
PMID: 18079069 [PubMed - as supplied by publisher]