Fundamental Problems in the Pathology of Multiple Sclerosis and Allied Demyelinating Diseases

The relationship between enzyme activity and neuroglia in plaques of multiple sclerosis

“…At the centre of the latter type of plaque there is a reduction in the number of oligodendrocytes but this loss is far from complete. These observations accord neither with those of Lumsden (Lumsden, 1951;McAlpine, Compston, and Lumsden, 1955), who regarded the disappearance of the oligodendrocyte as an essential histological and pathogenic feature of the plaque in multiple sclerosis, nor with those of Friede (1961a) who recorded the absence of oligodendrocytes from the centre of both active and quiescent plaques.…”

“…It has been suggested by Lumsden (Lumsden, 1951;McAlpine, Compston, and Lumsden, 1955) that the oligodendrocyte is selectively damaged in multiple sclerosis. 'A complete loss of this cell' was observed 'from the plaques of demyelination both in the acute and chronic lesions of multiple sclerosis.…”

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy

“…Further epidemiological studies failed to confirm an increased diagnosis of autoimmune diseases in families with MS (Langer-Gould et al 2010). Lumsden (1955) in a careful post-mortem study of a very large number of patients with MS was unable to show any evidence or stigmata of autoimmune disease. Broadley et al (2000) found the highest association in first-degree relatives with thyroid disease, but this is a difficult and misleading condition to use as a prime example of an autoimmune disease.…”

“…The inflammatory cerebral lymphocytic infiltrates that occur in most cases of MS are usually weak, scant, lack aggressiveness (Dawson 1916;Lumsden 1955;Adams 1977) and, as pointed out by Lumsden, cannot be compared to those of ADEM (Lumsden 1955). Mild inflammatory haematogenous infiltrates and oedema which are not consistent pathological findings in MS have been deemed by Lumsden (1955) not to be essential morphological criteria for the diagnosis. He drew attention to the self-propagative character of the MS lesion which showed variable discontinuous sleeves of demyelination surrounding blood vessels which he regards as the essential distinction between the more regular and uniform perivenular lesions of ADEM and EAE (Lumsden 1955).…”

“…Mild inflammatory haematogenous infiltrates and oedema which are not consistent pathological findings in MS have been deemed by Lumsden (1955) not to be essential morphological criteria for the diagnosis. He drew attention to the self-propagative character of the MS lesion which showed variable discontinuous sleeves of demyelination surrounding blood vessels which he regards as the essential distinction between the more regular and uniform perivenular lesions of ADEM and EAE (Lumsden 1955).…”