To those doctors who insist the venous
connection to MS
is an unproven theory, I offer a timeline of doctors who might beg to
differ.
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.
1930s 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)
1960s Dr. Torben 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
1980s 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. And in putting together, bit by bit, 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.
Here is Dr. Schelling's website for more information. His book (available for free on his site) outlines the history of the connection of MS to the venous system.
http://www.ms-info.net/evo/msmanu/984.htm
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.
1930s 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)
1960s Dr. Torben 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
1980s 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. And in putting together, bit by bit, 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.
Here is Dr. Schelling's website for more information. His book (available for free on his site) outlines the history of the connection of MS to the venous system.
http://www.ms-info.net/evo/msmanu/984.htm