Immunomodulating therapy has proven efficacy in the treatment of patients with multiple sclerosis (MS), which indicates that the disease has an autoimmune genesis. However, a passionate debate over the pathophysiological contribution of ‘chronic cerebrospinal venous insufficiency’(CCSVI), an as yet unproven hypothesis of cerebrovenous congestion, has arisen, and endovascular surgical intervention of the putatively pathogenic venous stenoses has been suggested as an appropriate treatment for such a condition. In a pioneering interventional study, Zamboni et al. interpreted MS to be a consequence of intracerebral erythrocyte extravasation caused by elevated transmural venous pressure, followed by erythrocyte degradation and iron-driven phagocytosis [1–3]. Numerous observational trials aimed at proving or disproving the existence of CCSVI by means of duplex sonography, magnetic resonance venography (MRV), or catheter angiography, have yielded inconsistent results. Furthermore, interpretation of these findings is compromised because despite intense research, neither the existence of CCSVI nor its relevance to MS has been proven to date.