alexa Chronic Cerebrospinal Venous Insufficiency in Multiple Sclerosis: The Hydrostatic-Immune Paradigm and the Flow Cytometry as a Diagnostic Tool
ISSN: 2376-0389

Journal of Multiple Sclerosis
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Research Article

Chronic Cerebrospinal Venous Insufficiency in Multiple Sclerosis: The Hydrostatic-Immune Paradigm and the Flow Cytometry as a Diagnostic Tool

Tsamopoulos NG1*, Kalodimou VE2, and Vlachos S3

1 Mediterraneo Hospital, Department of Interventional Neuroradiology, Athens, Greece

2 IASO Maternity & Research Hospital, Department of Flow Cytometry-Research & Regenerative Medicine, Athens, Greece

3 Department of Anesthesiology, Naval and Veterans’ Hospital of Athens, Greece

Corresponding Author:
N.G. Tsamopoulos, MD, PhD
Mediterraneo Hospital - Department of Interventional Neuroradiology
8-12 Ilias str. Glyfada, 166 75 Greece
Tel: +302109117010
E-mail: [email protected]

Received date: March 21, 2014; Accepted date: April 22, 2014; Published date: April 26, 2014

Citation: Tsamopoulos NG, Kalodimou VE, and Vlachos S (2014) Chronic Cerebrospinal Venous Insufficiency in Multiple Sclerosis: The Hydrostatic-Immune Paradigm and the Flow Cytometry as a Diagnostic Tool. J Mult Scler 1:103. doi:10.4172/2376-0389.1000103

Copyright: © 2014 Tsamopoulos NG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

In recent years, chronic cerebro-spinal venous insufficiency (CCSVI) has been associated with multiple sclerosis
(MS). Balloon angioplasty of the affected veins (internal jugulars, azygos) has been proposed as a treatment
method, with controversial results. The conflict is based on how a primarily immune disease can be affected by a
primarily hydrostatic condition and its reversal. In our paper we briefly review novel paradigms in multiple sclerosis
pathogenesis and propose a mechanism by which CCSVI could theoretically lead to blood brain barrier disruption,
altered neuronal microenvironment, astrocyte and oligodendrocyte loss and demyelination. Altered antigen transfer
to regional lymph nodes, affecting antigen presentation and processing could also contribute, affecting the sensitive
balance between tolerance and immunity. Thus, a combined hydrostatic-immune paradigm of MS emerges, which
may explain the potential role of CCSVI in MS pathogenesis and provide a theoretical framework for future research.

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