Venöse Multiple Sklerose Hypothese | CCSVI

Eine Auflistung von Publikationen rund um die Hypothese der venösen Multiple Sklerose. Die Referenzen sind zeitlich geordnet, die neuesten zuerst.

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• ms-mri.com: A brief history of the early venous vascular observations in MS
• msrc.co.uk: The venous connection to MS- a timeline

1. [adams88] Adams CW: Perivascular iron deposition and other vascular damage in multiple sclerosis. J Neurol Neurosurg Psychiatry. 1988 Feb;51(2):260-5. PMID 3346691. Article, PDF
   Division of Histopathology, United Medical School of Guy's Hospital, University of London, UK.
   Abstract

   Evidence of damage to cerebral vein walls was sought in 70 cases of multiple sclerosis. Seventy control cases were also examined. The multiple sclerosis cases showed venous intramural fibrinoid deposition (7%), recent haemorrhages (17%), old haemorrhages revealed by haemosiderin deposition (30%), thrombosis (6%) and thickened veins (19%). In all, 41% of all multiple sclerosis cases showed some evidence of vein damage. Occasional control cases showed haemosiderin deposition in the brain but, unlike the multiple sclerosis cases, these were diffuse and almost entirely related to coexistent cardiovascular or cerebrovascular disease. Haemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis.
2. [nicolson88] Nicolson M, McLaughlin C: Social constructionism and medical sociology: a study of the vascular theory of multiple sclerosis. Sociology of Health & Illness Vol. 10 No. 3, pp. 234–261 1988, published online: 28 Jun 2008. ISSN 0141-9889, doi:10.1111/j.1467-9566.1988.tb00008.x. Article, PDF
3. [adams87] Adams CW, Abdulla YH, Torres EM, and Poston RN: Periventricular lesions in multiple sclerosis: their perivenous origin and relationship to granular ependymitis. Neuropathol Appl Neurobiol. 1987 Mar-Apr ;13(2):141-52. PMID 3614542. PDF
   Abstract

   The periventricular region was studied in the brains of 129 cases of multiple sclerosis, with the purpose of establishing the mechanism and order of events in the development of the periventricular plaque, and deciding whether there is any relationship between granular ependymitis and such plaques. Periventricular plaques were found in 82.2% of cases. Observation and computerized morphology showed that the early stage of the periventricular plaque is the formation of a lesion around a subependymal vein and that adjacent lesions later coalesce. These plaques do not appear to arise from the ependyma, which is against any role for the CSF in their initial development. Chronic or burnt-out periventricular lesions often show overlying granular ependymitis (10.9% of cases) and subependymal gliosis (17.8%), presumably as a result of the long-continued low-grade inflammatory process. This process, which is not specific for multiple sclerosis, is sometimes associated with transfer of IgG and C3, as shown with peroxidase methods, across the subependymal vein wall and the ependymal epithelium. Increased permeability of the inflamed ependyma constitutes a possible abnormal entry route from plaque to CSF or, in reverse, from CSF to brain.
4. [lightman87] Lightman S, McDonald WI, Bird AC, Francis DA, Hoskins A, Batchelor JR, and Halliday AM: Retinal venous sheathing in optic neuritis. Its significance for the pathogenesis of multiple sclerosis. Brain. 1987 Apr;110 (Pt 2):405-14. PMID 3567529. Article$
   Abstract

   A systematic study of the frequency of retinal vascular abnormalities and cells in the media has been made in 50 patients presenting with acute optic neuritis. Abnormalities were found in 14 (fluorescein leakage in 10, perivenous sheathing in 6, cells in the vitreous in 6 and in the anterior chamber in 4; in 2 the cells in the media were seen without vascular changes). After a mean follow up of 3.5 years multiple sclerosis (MS) had developed in 8/14 patients with vascular abnormalities and/or evidence of inflammation and in 5/32 without; the difference is significant (P less than 0.02). The occurrence of perivenular abnormalities in a region free of myelin and oligodendrocytes provides evidence that the vascular changes in MS can occur independently of contiguous demyelination, and may be the primary event in the formation of a new lesion.
5. [schelling86] Schelling F: Damaging venous reflux into the skull or spine: relevance to multiple sclerosis. Med Hypotheses. 1986 Oct;21(2):141-8. PMID 3641027. PDF
   Abstract

   Unequal propagation of central venous excess pressure into the different cerebral and spinal venous drainage systems is the rule rather than the exception. The intensity of the forces thus to be exerted on vulnerable cerebrospinal structures by the resulting pressure-gradients in the craniovertebral space is unknown. There is a need to consider the various conditions which may cause individual proneness to heavier reflux into particular cerebral as well as epi- and subdural spinal venous compartments. An attempt is made to indicate eventual consequences of excessive retrograde dilatation especially of internal cerebral veins. The importance of elucidating the neuropathological and clinical implications of undue reflux into the skull or spine is deduced from the probability of relations between localized backflow into the craniovertebral space and unexplicated cerebrospinal diseases. In this regard the features of multiple sclerosis are discussed.
6. [adams85] Adams CW, Poston RN, Buk SJ, Sidhu YS, and Vipond H: Inflammatory vasculitis in multiple sclerosis. J Neurol Sci. 1985 Jul;69(3):269-83. PMID 4031947. PDF
   Abstract

   Fifty-two plaque or lesion areas were examined from 25 cases of multiple sclerosis. Twenty-four of these showed acute features, whereas the rest were more chronic in nature. The acute lesions showed lymphocytic infiltration (79%), fibrinous exudation (63%), lymphocytic meningitis (50%) and venulitis (58%). Of the chronic lesions, there were only 21% with lymphocytic infiltration, 11% with fibrinous exudates, none with meningitis, 29% with organising endovenulitis, 36% with fibrosed vein walls. The finding of a fibrinous inflammatory exudate in the acute lesion is a new observation in multiple sclerosis. Likewise, the observation of an inflammatory infiltrate confined to the vein wall (and often present at a distance from the plaque) has not been previously recorded in the disease. The chronic lesion, by contrast, showed relatively little fibrin, but there was considerable reparative thickening of the walls of the involved veins. The evidence provides new humoral and cellular evidence of an inflammatory process in multiple sclerosis which precedes or is not directly associated with the demyelinating process.
7. [walton84] Walton JC, and Kaufmann JC: Iron deposits and multiple sclerosis. Arch Pathol Lab Med. 1984 Sep;108(9):755-6. PMID 6547829.
   Abstract

   A recent publication described autopsy samples from five brains in which positive staining for iron was observed as surrounding demyelinated plaques. Because this has not been previously reported, autopsy material from 13 patients who were being followed up at the Multiple Sclerosis (MS) Clinic, University Hospital, The University of Western Ontario, London, Ontario, was reviewed. A total of 32 paraffin-embedded blocks containing demyelinated plaques of varying age were sectioned and stained using a standard acid ferrocyanide technique (Peris' test) for iron. Microscopic examination failed to detect the presence of significant positive staining either within or surrounding the areas of demyelination. Positive histochemical staining for iron identifies hemosiderin, the presence of which suggests either iron overload or remote hemorrhage. Support for these two processes in the pathogenesis of MS could not be provided from our material.
8. [adams75] Adams CW: The onset and progression of the lesion in multiple sclerosis. J Neurol Sci. 1975 Jun;25(2):165-82. PMID 1151432.
   Abstract

   The active established plaque in multiple sclerosis is characterized by hypercellularity at its edge and lipid phagocytosis (gitter cells). The hyperactive early plaque shows cells throughout the lesion. Active plaques seems to extend at their edges; proteolysis of myelin basic protein is perhaps an important factor in the myelin breakdown at the rim of these lesions. The hyperactive early plaque usually shows infiltration with monocytes, lymphocytes and plasma cells around its central vein. The phagocytic element is presumably a response to myelin breakdown but the significance of the lymphocytes in these lesions in uncertain. Perivenular infiltrates that are predominantly composed of lymphocytes are seen around veins and venules in the vicinity of established lesions in some patients who died during an acute episode...
9. [fog65] Fog T: The topography of plaques in multiple sclerosis with special reference to cerebral plaques. Acta Neurol Scand Suppl. 1965 ;15:1-161. Type: Case Reports. PMID 5213727.
10. [fog64a] FOG T: On the Vessel-Plaque Relationships in the Brain in Multiple Sclerosis. Acta Neurol Scand Suppl. 1964 ;40:SUPPL 10:9-15. PMID 14194816.
11. [zimmerman50a] Zimmerman HM, and Netsky MG: The pathology of multiple sclerosis. Res Publ Assoc Res Nerv Ment Dis. 1950 ;28:271-312. PMID 15413018.
12. [dow42a] Dow RS, Berglund G: Vascular pattern of lesions of multiple sclerosis. Arch Neurol Psychiatry. 1942;47(1):1-18. Article$
    Institut Bunge, Antwerp, Belgium, and the Department of Anatomy, University of Oregon Medical School, Portland, Ore.
    Introduction

    The theory of a relation between the cerebrovascular system and the lesions of multiple sclerosis has been advanced by many workers. The first of many to assign a primary role to vascular lesions was Rindfleisch.¹ Ribbert² early maintained that the demyelinated areas were related to a primary disseminated thrombosis. He described a congested central vessel in all the sclerotic patches. In two small patches cut in serial section he found white blood cells in the lumen of the vessel, partly adherent to the vessel wall and partly filling the vessel as an embolus. He stated that these changes in the vessel were multiple thrombi and expressed the belief that they had an important causative role in multiple sclerosis. The most recent adherents to the idea that vascular lesions play a primary role in the pathogenesis of the lesions of multiple sclerosis have been Putnam and his collaborators.³
13. [schlesinger39] Schlesinger B: The venous drainage of the brain, with special reference to the galenic system. Brain, 62:274, 1939. PDF
    Department of Human Anatomy, Oxford.
    Abstract

    On the basis of experiments on dogs, Bedford reported (1937) that a collateral circulation becomes rapidly established after occlusion of the great vein of Galen {Vena magna cerebri). He concluded, therefore, that the hydrocephalus which was occasionally found by Dandy and Blackfan (1914) and by Gulecke (1930), in dogs in which the vein had been blocked experimentally, was not directly due to the occlusion of the vein. In a subsequent series of experiments, Bedford (1934) occluded the great vein of Galen in monkeys. These animals likewise failed to show hydrocephalus after a survival period of six weeks, but no evidence was found of the manner in which the collateral circulation had developed in the choroidal plexus and the basal ganglia. Schwartz and Fink (1925-26), who injected the great vein of Galen in human brains, were unable to reach positive conclusions regarding the collaterals of the vein and the venous drainage of the basal ganglia, and they suggested that these investigations required to be further extended. A study of the venous system is also of importance for the question of the localization and pathogenesis of certain infections and other pathological conditions which have been described in the monkey and in Man, and are known to have a definite topographical relationship to the venous channels of the grey and white matter. The present paper comprises a report of an investigation, based on the examination of normal and experimental material, with the object of elucidating these details of the circulation.
14. [putnam37b] Putnam T: Evidences of vascular occlusion in multiple sclerosis and encephalomyelitis. Arch Neurol Psychiatry 1937;37(6):1298-1321. PDF$
    Neurological Unit, Boston City Hospital, and the Departments of Neuropathology and Surgery, Harvard Medical School.
    Introduction

    Recent experimental work¹ has made it seem probable that the lesions of multiple sclerosis and also those of the forms of "disseminated encephalomyelitis" which seem to represent a more acute stage of the same process² are produced by a local circulatory disturbance, apparently of the nature of an obstruction on the venous side. According to this point of view, there must be a primary change in the contents of the vessels of the central nervous system, or possibly of the intimal lining, which leads to thrombosis of venules. This produces local passive congestion and a mild degenerative process which affects myelin sheaths more than other structures. The myelin degenerates and is phagocytosed. The "inflammatory" phenomena would then be regarded as secondary or symptomatic and the gliosis as reparative or reactive. This hypothesis obviously must remain largely a speculation as long as it rests on the results of experimentation …
15. [putnam37a] Putnam T and Adler A: Vascular architecture of the lesions of multiple sclerosis. Arch Neurol Psychiat, 38:1, 1937. PDF$
    Neurological Unit, Boston City Hospital, and the Departments of Neuropathology and Surgery, Harvard Medical School.
    Introduction

    A relationship between the location of the lesions of multiple sclerosis and the veins of the nervous system was pointed out by Rindfleisch.¹ The majority of those who have dealt with the subject have agreed that small lesions usually surround small veins and that larger plaques probably arise by coalescence. A similar relationship between lesions and veins in cases of "post-infectious encephalomyelitis" has recently been pointed out by Finley.² In other papers of this series the probable cause for such a relationship has been traced. Veins in the neighborhood of sclerotic plaques are often found to be engorged, tortuous, surrounded by blood pigment, thrombosed or obstructed. Thrombosis of veins in the central nervous system invariably produces lesions of the same general type as those seen in "encephalomyelitis" and multiple sclerosis. Presumably, therefore, the vascular abnormality is primary to the parenchymal lesions.³ It is the purpose of the …
16. [putnam35] Putnam T: "Encephalitis" and sclerotic plaques produced by venular obstruction. Arch Neurol Psychiatry. 1935;33(5):929-940. PDF$, PDF
    Neurological Unit, Boston City Hospital, and the Departments of Neuropathology and Surgery, Harvard Medical School.
    Introduction

    In previous papers it has been shown that a series of histologic pictures resembling those of "postinfectious encephalomyelitis" may be produced in animals by a variety of agents, such as minute doses of tetanus toxin, carbon monoxide poisoning and certain types of embolism.¹ The pathologic alterations ranged, sometimes in a single specimen, from mild perivascular infiltrations with glia and occasional lymphocytic cells through areas of damage to and loss of perivascular myelin to areas of softening and destruction of the axis-cylinders. In one instance, more than a year after the original injection of tetanus toxin, lesions were found which closely simulated those of multiple sclerosis,² with plaques of loss of myelin, but with almost complete preservation of the axiscylinders and with local gliosis. Multiple sclerosis has been observed as a sequel of "postinfectious encephalomyelitis,"³ and the hypothesis that all of these conditions represent variants of the same …
17. [dawson16] Dawson JW: The histology of disseminated sclerosis. Trans Roy Soc Edinb, 50: 517, 1916.
18. [rindfleisch72] Rindfleisch E: A Manual of Pathological Histology. London, New Sydenham Society, 1872, Vol. 2, pp. 344–351.
19. [charcot68] Charcot JM: Histologie de la sclérose en plaque. Gazette Hosp Paris 41:554-566.
20. [rindfleisch63] Rindfleisch E: Histologisches Detail zu der grauen Degeneration von Gehirn und Rückenmark (Zugleich ein Beitrag zu der Lehre von der Entstehung und Verwandlung der Zelle). Arch Path Anat Physiol Klin Med, 26:474,1863.
    Info

    Rindfleisch in Zürich wies 1863 erstmals auf die pathologischen Veränderungen an den Gefässen hin ("ihre Wandung ist durch eine Anhäufung von Kernen und Zellen in der Adventitia enorm verdickt") und nahm ätiologisch "häufig wiederkehrende oder langanhaltende mit Hyperämie verbundene Reizzustände der gesammten Centralorgane" als Primärereignis und die Parenchymveränderungen als Sekundärphänomen an: "Die Neuroglia macht in Fortsetzung der formativen Reizung von den Gefässwänden auf die Nachbarschaft eine Reihe von Metamorphosen durch. Dieser Prozess trägt durchaus den Stempel des Kümmerlichen."

    Zitiert aus Kapitel 1 Historische Übersicht, Seite 17, Jürg Kesselring, Ludwing Kappos et. al, Multiple Sklerose, aus der Reihe Psychiatrie, Neurologie, Klinische Psychologie, Grundlagen - Methoden - Ergebnisse, T. Brandt et al. (Hrsg.), Verlag W. Kohlhammer, 4. Auflage, 2005

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Publikationen (1850 – 1988)