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Professor P. Zamboni,
From the two articles(“Intracranial Venous Haemodynamics in Multiple Sclerosis” and “Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis”) I found out about the idea that you support concerning multiple sclerosis. With your permission, I would like to lead this discussion on another track.
Very recently, in the summer of 2009,at the Congress in Prague "Controversies in Neurology" 8-11 October 2009, someone comes up with the idea of unifying theories about inflammation in general ( "The 'Continuum' of a unified theory of diseases" - G. Vithoulkas -- University of the Aegean, Mytilene, Greece). It's an observation of great common sense. But the concretization is missing. In this sense comes my attempt to explain this, with direct application of what is happening in the particular case of multiple sclerosis.I had some previous communication attempts on inflammation but received no reply.
You will wonder perhaps when I begin to invoke some strange disease that are not too often recognized by medicine today. The first is Castleman's disease, a pre-lymphoma which has a lot of inflammation and is very heterogeneous in its manifestations, pathological, clinical and evolutionary. In this disease there is the phenomenon of "bulge in the vein" (http://www.castlemans.org/about
) that I cite as the cause of the venous stenosis that you identified. An evolutionary and slow phenomenon, presumably present also at young age, since the literature abounds in communication about Castleman disease, a localized form in children. Maybe the stenosis of large veins (jugular and azygos vein) is one of the unknown localizations of the disease. As for evolution, I do not understand, for example why your case, Augusto Zeppi 40 years from Ferrara, required a second intervention in a year because of the restenosis from one of jugular veins.
Another phenomenon that baffles almost all clinical medicine today is the identification, in the early 90s, of micro-vesicle (MVS), micro-particles (MPs) and exosomes, in almost all diseases (atherosclerosis, cancer, multiple sclerosis, collagenosis etc..). Never was medicine so disconcerted as when faced with this phenomenon. As time passes, these MVS, MPs and exosomes seem to be something alien to the human body. The explanation that they are oxidative modified lipoproteins ( only in case of the atherosclerosis) is clearly false.
A third situation that i bring into discussion is an infectious disease called melioidosis, with its gram negative bacterial agent - Burkholderia pseudomallei, a germ that eschews identification with current bacteriological methods, so that it came to be called also ... "Stealth organism”
Before I carry forth with, in my opinion, demystifying the three cases raised above, two sentences from the DISCUSSION section of your paper "Intracranial venous Haemodynamics in Multiple Sclerosis" namely: "It has been established that steady laminar shear stress promotes the release of factors from endothelial cells that inhibit coagulation and migration of leukocytes, while simultaneously promoting normal endothelial cell function "(Bergan et. al., 2006, Sorescu et. al., 2004) as:" It has been established that chronic venous reflux is MLSP capable to further activated either in the vein wall or in the surrounding tissue (Sansilvestri et. al., 2007, Bergan et. al., 2006), determining an imbalance of extracellular matrix production / degradation " I remember like an echo, all I read about MVS, MPs and exosomes .In this way I found out astounded that endothelial dysfunction is invoked in atherosclerosis,in cancer and in multiple sclerosis with exosomes release and cell apoptosis.
And now the promised demystification (in my opinion).
Castleman's disease (a peculiarity, actually) as it is described up to the present time, is only ... "a tip of the iceberg" of a chronic pre-larval parasitosis with the Corti Mezocestoides Cestoda,a cestoda that does not have the whole biological cycle, fully explained up to this date. All that is strange concerning cellularity in Castleman’s disease is represented by the proligerus capsules of the Cestoda that ... release specific metascolex. In fact, hidatic sand which in the stage of protoscolecx interferes with... MVS, MPs and exosomes. It seems shocking but this situation is suitable, in my opinion, to explain something simple and natural, namely that the pre-larval Cestoda is parasited by the above mentioned bacteria - Burkholderia pseudomallei (B. P.). Based on the evidence of medical literature, B. P. is already proven to do this (intracellular parasite) in amoeba Acanthamoeba and fungus Gigaspora decipiens. From where ... it escapes! It is also very likely to have a transmissibility of a prionic type, a mechanism often invoked in connection with MVS, MPs and exosomes. In the case of multiple sclerosis, in which you have identified vein stenosis, it is likely to escape gradually, in relation to the prolongation of the circulation time of venous flow.
Another feature of B. p. is to cause hemorrhage and necrosis in acute lesions, causing ... "Iron buildup" also described and identified today by Prof. Mark Haacke (Detroit and Hamilton). In multiple sclerosis, this explosion factor that is B. P., explains the high variability of clinical forms, beginning with what is even stranger and more dramatic - fulminating forms, supra-acute (Neuromyelitis optica, acute disseminated encephalomyelitis, acute hemorrhagic leukoencephalitis - A.H.L) in which the feeling of the action of an infectious factor is very strong, yet unproven. Why, for example, in A.H.L. acute vasculitis with unidentified infectious agent interests the walls of capillary veins with necrosis and perivenous demyelinization? In these forms the situation is probably decided by the bacterial virulence and not by other factors. In the same sense, aims the article :” Association of demylinating lesions in the spinal cord and disc disease” (M. Quigg, A. Lugo, B Greenberg - Journal of Neurology volume 255 suplement 2-June 2008) which puts out the customs of classical neurology: „Pathologically, a herniated disc could impair venous outflow, at the level of the epidural venous plexus, thus creating an inviting environment for immune cells to cross the blood brain barrier. Based on this theory, herniated discs do not cause lessions, but rather create appropiate environments for their creation in individuals with autoimmune predispositions”. I don’t think we are speaking about “appropriate environments” but more likely of a bacterial agent which is present medullary and in the cartilaginous structures; melioidosis being by excellence yet another disease with musculoskeletal tropism.
I support the fact that the bacteria B. P. is a candidate and actual factor in explaining inflammation in all medicine today, as the article listed in the beginning tries to achieve with the unification of all the diseases. It is, if you will the middle ground between explaining multiple sclerosis only through inflammation or only through vascular disorder, as you have already demonstrated.
Is the epistemolog, Thomas S. Kuhn, right with the paradigmatic pattern of development in science?
In order not to waken endless discussions about "possible and impossible", I mention that the proximity to the city of Ferrara of the city Bologna, where some of your colleagues operate, raised the question: „Che cosa succede a Bologna?”.„In this context, the recent report on the isolation of B. pseudomallei in 7% of tested water resources in Bologna, northern Italy is a disquieting fact”.
http://www.phidias.us/phinfo/topicSearc ... pathogenID
PS: If you manifest the interest, I could send you my other attempts, in the form of „Letter to the Editor” ,which were turned down by a publication the previous year.
Tudor Mihaita M.D.
Departament of neurology
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