Biomedical subjects

R U Schwyzer

Publications and source records attributed to R U Schwyzer.

3 recordsLinked to original sources

PubMed1992

Multiple sclerosis: prevention of serious illness--vision of a desired future for newly ascertained patients.

The increased prevalence of MS worldwide and the resultant high frequency of serious illness among young adults urges that the developed methods of prophylaxis are fully tested. Reference is made to the hypothesis of a circulating toxin playing a role in disease development. Insights from basic research now in progress may expand or amend the scenario. This discussion pertains to biological reasoning and a prophylactic treatment which is able to postpone or avoid disability in MS.

Adult↗

PubMed1988

Reflections on the pathogenesis of optic (retrobulbar) neuritis in multiple sclerosis.

The conditions which lead to a plaque of demyelination in the retrobulbar optic nerve are discussed. Growth of the plaque occurs along venules as small fingerlike sleeves which develop outwards from the contour of the plaque. This occurs slowly and at intervals; the very gradually expanding lesion remain for a long time clinically silent. It is here postulated that the change to clinical disease is induced if cells digesting myelin debris settle in a more distal part of the perivascular space of a vein, than during the subclinical phase. In sufficient numbers these cells will impede the movement of molecules from extra-cellular fluid surrounding nodes of Ranvier into cerebrospinal fluid. A restriction in this vital drainage pathway results in oedema causing disturbed signal transmission in neurons passing through the veins drainage territory. Depending on intensity this can induce the characteristics symptom of blurred vision. These concepts have been used to speculate on sequential changes in neurons and to relate them to various phases of the disease. This seems to be justified as the pattern evolved corresponds well with the clinical symptomatology.

Central Nervous System↗

PubMed1983

Multiple sclerosis: plaques caused by 2-step demyelination?

Selected studies concerning events at the contour of a progressive plaque are reviewed and an explanation of the subtle changes in periplaque white matter which various investigators have observed on autopsy or biopsy is presented. Recurrent exposure to toxic small molecular weight substances carried by arterial blood and capable of diffusing through the walls of blood vessels cause modification of protein or glycoprotein in the myelin sheath. These then act as allergens (modified native tissue considered as 'nonself' tissue by the immune system) which induce antibody formation (termed allo-auto-allergy). Phagocytosis of altered myelin, debris removal and cellular action to maintain homeostasis in the fluid surrounding neurons characterize the premorbid phase of multiple sclerosis. We suggest that the accumulation in the perivascular space of macrophages with large lysosomes digesting myelin debris (visible in electron micrographs) causes bottlenecks in the lymphatic channels serving the extracellular space near nodes of Ranvier. This changes the chemical microclimate and leads to the second step of demyelination and degeneration of the oligodendrocytes, i.e. plaque formation. Reference is made to outstanding problems. Research into the diffusion of small molecular weight substances into the extracellular spaces of white matter would aid in evaluating the hypothesis.

Astrocytes↗