http://www.expert-reviews.com/doi/pdf/1 ... ern.10.174
Recently, it has been demonstrated that there is reduced perfusion and even loss of small medullary vein visibility in MS . Juurlink discusses the role of hypoperfusion in MS . He comments that the reduced perfusion can be detrimental to oligodendrocytes, preferentially affects white matter, causes demyelination and leads to microglial activity. He notes that these can be most marked in the optic nerve and tract. He then states: “There is now ample evidence that ischemic insults of sufficient severity can cause upregulation of cell adhesion molecules onto the endothelial cells, thus allowing infiltration of leukocytes into the brain parenchyma, resulting in an inflammatory lesion.” He goes on to point out that hypertension of genetically susceptible lesions leads to vascular damage, which in turn leads to ischemia. There is actually a body of evidence suggesting reduced perfusion in MS patients. Back in the 1980s, Swank et al. found that past the age of 40 years, MS patients had markedly reduced blood flow compared with normal individuals . Using MRI, there has been a thrust in the last 10 years to study perfusion in MS. The work of Meng Law  and others [28–32] demonstrates that there is reduced perfusion as a function of severity of disease. Law et al. reported a significant decrease of cerebral blood flow and a prolongation of mean transit time in the normal-appearing white matter (NAWM) at the level of the lateral ventricles in MS patients . These reductions often appear in the basal ganglia and thalamus and have been related to fatigue [30,31,33]. A study of seven patients with relapsing–remit- ting MS revealed decreased relative cerebral blood volume (CBV) in chronic lesions and further reduced relative CBV in one acute lesion in white matter compared with that in gray matter . Haselhorst et al. examined 25 patients with MS and found that acute lesions had significantly higher relative CBV than NAWM and that chronic plaques had significantly lower relative CBV than NAWM . Inflammatory activity can cause compensative vasodilatation and result in increased cerebral blood flow and CBV, which is found in enhancing lesions. On the other hand, any evidence of increased perfusion in some chronic nonenhanc- ing lesions can be explained by lesion reactivity with new vascular inflammatory changes.