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History                                                                                                                                                                                           

 

1863 Rindfleisch                                                                                                                                                                                         

Dr. E. Rindfleisch noticed that, consistently in all the autopsy specimens of MS brains he viewed with his microscope, a vein engorged with blood was present at the centre of each lesion.

 

Rindfleisch wrote:

"If one looks carefully at freshly altered parts of the white matter ... one perceives already with the naked eye a red point or line in the middle of each individual focus,.. the lumen of a small vessel engorged with blood ... All this leads us to search for the primary cause of the disease in an alteration of individual vessels and their ramifications; All vessels running inside the foci, but also those which traverse the immediately surrounding but still intact parenchyma are in a state characteristic of chronic inflammation."

 

Rindfleisch E. - "Histologisches detail zu der grauen degeneration von gehirn und ruckenmark". Archives of Pathological Anatomy and Physiology. 1863;26:474–483.

 

1930’s Putnam                                                                                                                                                                                             

Dr. T. J. Putnam researched lesions and noted that thrombosis of small veins could be the underlying mechanism of plaque formation

 

Putnam, T.J. (1937) Evidence of vascular occlusion in multiple sclerosis

 

1942 Dow and Berglund                                                                                                                                                                            

Dr. Robert Dow and Dr. George Berglund continue on with Dr. Putnam's research and continue finding venous connections to MS lesions.

 

Vascular pattern of lesions of multiple sclerosis Arch Neurol Psychiatry. 1942;47(1):1-18.

 

1950 Zimmermann and Netsky                                                                                                                                                                   

Dr Zimmerman and Netsky carry on with Dow and Berglund's research, and note that the lesions are indeed venous in nature, but not caused by small thrombosis as Putnam surmised.

 

Zimmerman, H. M., Netsky, M. G.: The pathology of multiple sclerosis. Res. Publ. Ass. Nerv. Ment. Dis. New York 28, 271--312 (1950)

 

1960’s Fog                                                                                                                                                                                                   

Dr. Torben Fog, a Danish professor – noted that MS lesions are predominantly around the small veins. His subsequent study of 51 plaques from two cases of typical MS, making thin sections of the plaques and following their shape and course with direct drawings of each section, showed that most were prolongations of periventricular plaques, and that the plaques did follow the course of the venous system.

 

Fog Torben, The topography of plaques in multiple sclerosis, with special reference to cerebral plaques. Acta Neurol Scand, 41,Suppl. 15:1, 1965)

Fog T. On the vessel-plaque relations in the brain in multiple sclerosis. Acta Psychiat Neurol Scand. 1963; 39, suppl. 4:258

 

1980’s Schelling                                                                                                                                                                                         

The story began in 1973, at the University of Innsbruck, when F. Alfons Schelling, M.D. began investigations into the causes and consequences of the enormous individual differences in the widths of the venous outlets of the human skull. The results of this study appeared, in 1978, in the official organ of the German-speaking Anatomical Societies, the "Anatomischer Anzeiger".

 

F.A. Schelling's 1981 discovery, at the Hospital for Nervous Diseases in Salzburg, of a striking widening of the main venous passageways through the skulls in victims of multiple sclerosis were to occupy the author's thoughts through the following decades of his quite diversified medical career. Gradually piecing together all the observations on the venous involvement in the emergence of the specific, and, in particular, cerebral lesions of multiple sclerosis, he was able to recognize their causes.

 

"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."

 

Damaging venous reflux into the skull or spine: relevance to multiple sclerosis. Schelling F. http://www.ms-info.net/evo/msmanu/984.htm

 

1994 A J Wakefield, L J More, J Difford, J E McLaughlin                                                                                                                     

Immunohistochemical study of vascular injury in acute multiple sclerosis.

AIMS--To examine the vascular changes occurring in three archival cases of acute multiple sclerosis, and to provide immunohistochemical evidence of early endothelial cell activation and vascular occlusion in this condition.

Academic Department of Medicine, Royal Free Hospital, School of Medicine, London. Abstract - J Clin Pathol 1994;47:129-133 doi:10.1136/jcp.47.2.129

 

 

 

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