Venöse Multiple Sklerose Hypothese | CCSVI

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Spezielle MS publication

1. [gallup10a] Gallup AC, Gallup GG, and Feo C: Yawning, sleep, and symptom relief in patients with multiple sclerosis. Sleep Med. 2010 Mar;11(3):329-30. Epub 2010 Feb 16. PMID 20163983, doi:10.1016/j.sleep.2009.12.007.
   Department of Biological Sciences, Binghamton University, Binghamton, NY 13902, USA.
   Abstract

   BACKGROUND: Patients with multiple sclerosis (MS) suffer from thermoregulatory dysfunction, and repetitive yawning and sleep problems are symptoms of MS. Because yawning and sleep are involved in thermoregulation, we investigated the association between yawning, sleep, and symptom relief in patients with MS. METHODS: Sixty patients filled out a questionnaire about how often they yawned, whether yawning provided relief of MS symptoms, and how sleep affected these symptoms. RESULTS: Results showed that over one in three patients reported that their MS symptoms improved following a yawn, and of those experiencing relief, nearly half reported that it lasted for several minutes or longer. Not getting a good night's sleep often made MS symptoms worse, while napping during the day provided symptom relief. CONCLUSION: This is the first study showing that yawning provides symptom relief in patients with multiple sclerosis.
   Extract

   Recent research has provided additional evidence of an association between MS and cerebral thermoregulatory dysfunction, showing a strong connection between MS and chronic cerebrospinal ven...ous insufficiency [Zamboni et al.]. Thus, we propose that enhanced facial and cerebral blood flow resulting from a yawn may act to overcome the altered modality of venous return in MS patients, providing temporary circulation of cooler blood to the brain and ultimately providing short-term remission of MS symptoms.
   Source: CCSVI at UBC MS Clinic, 15.03.2010
2. [prineas09] Henderson AP, Barnett MH, Parratt JD, and Prineas JW: Multiple sclerosis: distribution of inflammatory cells in newly forming lesions. Ann Neurol. 2009 Dec;66(6):739-53. PMID 20035511, doi:10.1002/ana.21800. Abstract, PDF$.
   Institute of Clinical Neuroscience, Department of Medicine, University of Sydney, Sydney, Australia.
   Comment

   Die Resultate weisen darauf hin, dass Plaquebildung einen anderen Ursprung als destruktive Immunzellenangriffe gegen Myelin oder Oligodendrozyten Antigene haben könnte. Die gängige Autoimmunhypothese wird in Zweifel gezogen.

   See [prineas04]
   Abstract

   OBJECTIVE: CD4 T-cell-dependent macrophage activation directed against a myelin or oligodendrocyte antigen is generally thought to be the mechanism causing myelin destruction in multiple sclerosis (MS). However, areas within expanding MS lesions may exhibit prominent oligodendrocyte loss and apoptosis in the absence of infiltrating lymphocytes. The present study was designed to further investigate the inflammatory profile of different regions within rapidly expanding MS lesions. METHODS: Twenty-six active lesions from 11 patients with early MS were serially sectioned and immunostained for T and B cells, plasma cells, ramified microglia, macrophages, monocytes, and CD209-positive dendritic cells. Cell counts were compared in prephagocytic, phagocytic, and immediately postphagocytic areas. RESULTS: Parenchymal T and B cells were largely absent in areas of initial oligodendrocyte loss and in areas of degenerate and dead myelin infiltrated by myelin phagocytes. In contrast, trailing areas of complete demyelination packed with lipid macrophages, and, in some lesions, regenerating oligodendrocytes, showed large numbers of T cells, B cells, and immunoglobulin G (IgG)-positive plasma cells. Lesions in 2 exceptionally early cases contained relatively few T and B cells, and no IgG-positive plasma cells. INTERPRETATION: Early loss of oligodendrocytes is a prominent feature in tissue bordering rapidly expanding MS lesions. Macrophage activity is largely an innate scavenging response to the presence of degenerate and dead myelin. Adaptive immune activity involving T and B cells is conspicuous chiefly in recently demyelinated tissue, which may show signs of oligodendrocyte regeneration. The findings suggest that plaque formation has some basis other than destructive cell-mediated immunity directed against a myelin or oligodendrocyte antigen.
3. [bartholomaeus09] Bartholomäus I, Kawakami N, Odoardi F, Schläger C, Miljkovic D, Ellwart JW, Klinkert WE, Flügel-Koch C, Issekutz TB, Wekerle H, and Flügel A: Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions. Nature. 2009 Nov;462(7269):94-8. Epub 2009 Oct 14. PMID 19829296, doi:10.1038/nature08478. Abstract (Full$), Nature News (Full$)
   Max Planck Institute for Neurobiology, 82152 Martinsried, Germany.
   Abstract

   The tissues of the central nervous system are effectively shielded from the blood circulation by specialized vessels that are impermeable not only to cells, but also to most macromolecules circulating in the blood. Despite this seemingly absolute seclusion, central nervous system tissues are subject to immune surveillance and are vulnerable to autoimmune attacks. Using intravital two-photon imaging in a Lewis rat model of experimental autoimmune encephalomyelitis, here we present in real-time the interactive processes between effector T cells and cerebral structures from their first arrival to manifest autoimmune disease. We observed that incoming effector T cells successively scanned three planes. The T cells got arrested to leptomeningeal vessels and immediately monitored the luminal surface, crawling preferentially against the blood flow. After diapedesis, the cells continued their scan on the abluminal vascular surface and the underlying leptomeningeal (pial) membrane. There, the T cells encountered phagocytes that effectively present antigens, foreign as well as myelin proteins. These contacts stimulated the effector T cells to produce pro-inflammatory mediators, and provided a trigger to tissue invasion and the formation of inflammatory infiltrations.
4. [prineas04] Barnett MH, and Prineas JW: Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion. Ann Neurol. 2004 Apr;55(4):458-68. Type: Case Reports. PMID 15048884, doi:10.1002/ana.20016. Article$, PDF.
   Institute of Clinical Neurosciences, Department of Medicine, University of Sydney, Australia.
   See [prineas09]
   Abstract

   The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis, who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases, namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.
5. [lassmann03a] Lassmann H: Hypoxia-like tissue injury as a component of multiple sclerosis lesions. J Neurol Sci. 2003 Feb;206(2):187-91. Type: Review. PMID 12559509.
   Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria. hans.lassman@univie.ac.at
   Abstract

   Recent data suggest that the mechanisms of demyelination and tissue damage in multiple sclerosis (MS) are heterogenous. In this review, evidence is discussed, which show that in a subset of multiple sclerosis patients the central nervous system (CNS) lesions show profound similarities to tissue alterations found in acute white matter stroke, thus suggesting that a hypoxia-like metabolic injury is a pathogenetic component in a subset of inflammatory brain lesions. Both, vascular pathology as well as metabolic disturbances induced by toxins of activated macrophages and microglia may be responsible for such lesions in multiple sclerosis.

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