Meng Law, MD, Amit M. Saindane, MD, Yulin Ge, MD, James S. Babb, PhD, Glyn Johnson, PhD, Lois J. Mannon, RT, Joseph Herbert, MD and Robert I. Grossman, MD
- Author Affiliations
1From the Departments of Radiology (M.L., A.M.S., Y.G., J.S.B., G.J., L.J.M., R.I.G.) and Neurology (J.H.), New York University Medical Center, MRI Department, Schwartz Building, Basement HCC, 530 First Ave, New York, NY 10016. Received June 24, 2003; revision requested September 3; revision received October 16; accepted November 12. Supported by National Institutes of Health grants RO1CA093992, NS29029, NCRR M01 RR00096 GCRC, and R37 NS 29029–11. Address correspondence to M.L. (e-mail: email@example.com).
We interpret our findings of diminished perfusion in NAWM as evidence that MS has a primary vascular pathogenesis, and there is histopathologic evidence to support this hypothesis: Adams et al (9) described frequent edematous onion-skin changes and lymphocytic infiltration of vein walls in NAWM without adjacent parenchymal inflammation; this suggests that MS represents a form of subacute or chronic vasculitis that could precede lesion development. Allen and McKeown (46) have also observed perivascular inflammation in areas of macroscopic NAWM.
Nonetheless, the vascular or ischemic basis for demyelination is intriguing. Provocation of symptoms in response to a hot bath, exercise, and food and alcohol intake are features of MS (56); similarly, experimental neural ischemia produces both conduction block and focal demyelination (57). All of these provocative stimuli share a common denominator—namely, vasodilatation of the extraneural vascular bed. Hence, despite autoregulation in regions of impaired perfusion, shunting of vascular reserve away from critically perfused regions in the central nervous system may trigger an acute deterioration. Although it has long been noted that there are vascular occlusive changes in MS (19), attention has been drawn to evidence in recent histopathologic studies of MS of hypoxia-like tissue injury (58)."
So do MSers have their symptoms provoked after a hot bath, exercise, food or alcohol intake because these are all things that vasodilate the extraneural vascular bed (?) and shunt vascular reserve away from the already underserved brain? I don't think so, I've understood vasodilation to be good for us, but I dunno?
I did a search for this article here and it does look like it was discussed in cheerleader's original long sticky, but I was not able to find where.
My other reason for posting this is that: these guys at New York University Medical Center should have been all over CCSVI, has anyone contacted them?