Evolution in quality of life and epidemiological impact after endovascular treatment of chronic cerebro-spinal venous insufficiency in patients with multiple sclerosis.

BACKGROUND: We report the outcome of 67 patients after endovascular treatment of chronic cerebro-spinal venous insufficiency in patients with multiple sclerosis. Material and methods For evaluating outcome, patients were divided into three groups with respective outcome after three, six and twelve months. Assessment of outcome was done by a disease-specific quality-of-life score that reflects the physical health (physical health composite, PHC) and mental health (mental health composite, MHC) by a score. RESULTS: Improvement in PHC was significant (P < 0.05) in the three- and six-month groups. Improvement in MHC was only significant (P < 0.05) in the three-month group. CONCLUSION: In conclusion, we can state that the result of endovascular treatment seems to decay although the baseline is still higher than preoperative. To confirm this finding, this study needs to be reproduced in a larger patient population.

Multiple sclerosis : is it transplacentally induced?

The aetiology of multiple sclerosis MS is not known. Most research workers believe a viral aetiology. An alternate theory - namely transplacental induction of MS is outlined. Correlative evidence is drawn from epidemiological studies, models of transplacentally induced conditions, metabolic disturbances in utero that can affect myelin development or result in offspring with defective immunological competence and surveillance. The relationship between B group vitamin deficiencies and mineral deficiencies and MS is considered. Primary, secondary and tertiary prevention of MS in view of this theory is outlined.

[Determinant factor and pathogenesis of multiple sclerosis]. / O determiniruiushchem nachale i patogeneze rasseiannogo skleroza.

A clinico-epidemiological and genealogical analysis of 182 patients with disseminated sclerosis, living in climatogeographical conditions of Tadjikistan permits to assume that disseminated sclerosis is an exogenous intrauterine (but not hereditary!), acquired monoetiological disease. At the basis of the pathogenesis lies an ectodermal microdysgenesia with a selective lesion of the embryo oligodendroglia system and an eventual disturbance of postnatal myelinopoesis. This condition is due to an exogenous-mutagen (toxico-allergic) action of the respective climatogeographical regions of "risk" in relation to disseminated sclerosis.