White matter lesions are found in stroke and neurodegenerative disease. Myelin basic protein is attacked in the same way in MS as it is in other ischemic events. The t-cell reactivity is not unique in MS.
Myelin antigen reactive T cells in cerebrovascular diseaseshttp://www.ncbi.nlm.nih.gov/pmc/article ... 8-0161.pdf
Department of Neurology, Karolinska Institutet, Huddinge Hospital, Stockholm, Sweden
INTRODUCTION In acute ischaemic cerebrovascular diseases (CVD), mononuclear cells appear in the brain parenchyma within 1-2 days and increase in number over the ensuing 5-30 days.Also in cerebrospinal fluid (CSF), elevated numbers of mononuclear cells may be detected. These cells are considered to mainly represent monocytes-macrophages, but there are no detailed studies on their lineage with,e.g.,antibodies to different cell surface markers. Oligoclonal IgG bands are present in the CSF while missing in corresponding serum, in about 10% of patients with CVD [2,3].A local B cell response directed to neurotropic viruses,as in patients with multiple sclerosis, has been reported in those patients with CVD who displayed oligoclonal IgG bands in CSF .Taken together,these observations indicate that patients with acute CVD may display an intrathecal immune response......
The strong increases in numbers of MBP, MBP peptide and PLP reactive T cells in blood, and of MBP reactive T cells in CSF, which we here report in our patients with Cerebro Vascular Disease, are in the same range as we have previously observed in MS [10,11].Thus, both diseases are accompanied by an expanded pool of myelin autoreactive T cells and they may well be secondary to damage to the central nervous system.
T-cells react the same way in stroke....
"To date, there has been little interest in exploring the possibility that autoimmune responses to brain antigens might affect outcome from stroke. There are, however, studies that document the fact immune responses to brain antigens do occur following stroke.http://stroke.ahajournals.org/cgi/conte ... uppl_1/S75
For instance, lymphocytes from stroke survivors show more activity against MBP than the lymphocytes from patients with multiple sclerosis.18,19
In addition, myelin-reactive T cells are found in higher numbers among patients with cerebrovascular disease.20 These data thus provide evidence that a cellular immune response to brain antigens occurs following stroke.
Furthermore, there are increased titers of antibodies to brain antigens, including neurofilaments and portions of N-methyl-<span>D</span>-aspartate receptor, following stroke, indicating that there is also the development of a humoral response to these antigens.21,22 The immune response to CNS antigens after stroke is likely just an epiphenomena of stroke given that cerebral ischemic injury to the blood–brain barrier allows for the systemic immune system to come into contact with the antigens that are normally sequestered from it. Nonetheless, it is possible that this response leads to "collateral damage"; whether these immune responses affect outcome from stroke is largely an unanswered question."
More evidence of hypoxia in MS--
Divergent role for MMP-2 in myelin breakdown and oligodendrocyte death following transient global ischemia.
Walker EJ, Rosenberg GA.
Departments of Neurology, Neurosciences, and Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA.
Transient global ischemia causes delayed white matter injury to the brain with oligodendrocyte (OLG) death and myelin breakdown. There is increasing evidence that hypoxia may be involved in several diseases of the white matter, including multiple sclerosis, vascular dementia, and ischemia.
Matrix metalloproteinases (MMPs) are increased in rat and mouse models of hypoxic hypoperfusion and have been associated with OLG death. However, whether the MMPs act on myelin or OLGs remains unresolved. We hypothesized that delayed expression of MMPs caused OLG death and myelin breakdown. To test the hypothesis, adult mice underwent hypoxic hypoperfusion with transient bilateral occlusion of the carotid arteries. After 3 days of reperfusion, ischemic white matter had increased reactivity of astrocytes and microglia, MMP-2 localization in astrocytes, and increased protein expression and activity of MMP-2. In addition, there was a significant loss of myelin basic protein (MBP) by Western blot and caspase-3- mediated OLG death. Treatment with the broad-spectrum MMP inhibitor, BB-94, significantly decreased astrocyte reactivity and MMP-2 activity. More importantly, it reduced MBP breakdown. However, MMP inhibition had no effect on OLG loss. Our results implicate MMPs released by reactive astrocytes in delayed myelin degradation, while OLG death occurs by an MMP-independent mechanism. We propose that MMP-mediated myelin loss is important in hypoxic injury to the white matter.
My husband's myelin did not regrow after his jugular veins and stenotic dural sinus were repaired. NO ONE IS CLAIMING IMMEDIATE REMYELINATION. We are discussing enhanced cerebral oxygenation, as shown by fMRI. My husband's fatigue and sleep apnea disappeared. He no longer woke up, gasping for air in the night. His spasms remitted. He no longer needs baclofen. He has no new lesions on MRI--(his 20 prior lesions are shrinking, but still visible) His cerebral atrophy has reversed as shown on MRI.
Dr. Hubbard and Dr. Haacke are showing increased perfusion and O2 after angioplasty with fMRI and BOLD technology. That is what is creating the symptom relief in many.
Oh, and Cece understands the basic physiology. Collateral circulation is not the same as primary circulation.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS