I translated the recent statement of the German MS society (DMSG) concerning CCSVI. I did this very quickly and roughly, so please don't mind some quirky word orders or single words. I will not comment this yet, having no words for this bullshit. Here it is:
New vascular hypothesis of Multiple Sclerosis?
08.12.2009 - up-to-date response of the medical advisory board of the DMSG [german multiple sclerosis society], federal association, about the hypothesis of a venous induced cause of multiple sclerosis.
The hypothesis of "chronically cerebrospinal venous insufficiency (CCSVI)" as cause of multiple sclerosis is recently discussed in many places and also internet-forums (see www.dmsg.de
Thereby it is assumed that a blockage of venous flow leads to a venous obstruction resp. to an increase of venous blood pressure in the brain, which then could lead to perivenous iron accumulation with subsequent inflammatory reaction. (Zamboni 2006, Zamboni 2009).
These predominantly sonographically, i.e. with ultrasound, raised findings, as well as the recently depicted possible prognostic correlation of with transcranial ultrasound detected hyperechogenities in the brain tissue (Walter 2009), indicate that the value of ultrasonic diagnostics within the diagnostic state investigation of MS-patients is widely unknown.
In the discussion of CCSVI or "venous MS" it should not be overlooked that cerebral venous insufficiencies already were discussed as causal in the past, also for other neurological deseases. The ultrasonic findings made in the process aren't in fact identical with the described findings in the "venous MS", however showed comparable indication for the existence of a migraine and a condition with temporary memory loss (transient global amnesia = TGA), (Sander 2000, Chung 2009).
In 86% of the patients with TGA a venous valve insufficiency of the jugular veins was found (Schreiber 2005). Thus, a venous insufficiency of the jugular vein is not exclusive or typical to MS, thus is not pathognomonic at all, which is wrongly stated often. In the described TGA-study, a venous valve insufficiency could be found even in 33% of the controls. So it is to put into question how specific these findings are for the condition. In our own studies, showed only in poster form until now, we could not prove this. (Krogias 2003).
These facts should be considered in the discussion of a possible venous genesis of MS. The doubtlessly very interesting findings of Zamboni and associates should be traced in a rational and serious scientific work and initially be proved or disproved in other workgroups. Zamboni himself dubbed his hypothesis "the big idea" and thus reveals an irrationality hindering in this process (Zamboni 2006). His promoted implantation of venous stents as a treatment to MS he calls "liberation procedure" and thus raises supposably not accomplishable expectations among MS patients.
In a recent study published in the "Journal of vascular surgery" (December 2009, 6:1348-1358.e3) Zamboni and his staff has performed a treatment with balloon dilalation on 35 RRMS, 20 SPMS and 10 PPMS patients. The authors claim that this procedure has led to an improvement of the clinical outcome in the RRMS patients. There are no controls. If the patients got drugs and if so what drugs the paper doesn't say.
The described improvement initially reflects the natural outcome, as attacks in RRMS regress regularly. In SPMS and particularly PPMS this is not the case, consequently the "liberation procedure" has had no influence.
To our scientific judgement, the published studies of Zamboni et al. lack a solid scientific methodology and thus are valueless and even ethically questionable.
For the scientific advisory board of the DMSG, federal association:
Prof. Dr. med. R. Gold (Vorstandsmitglied)
Direktor der Neurologischen Klinik am St. Josef-Hospital,
Klinikum der Ruhr-Universität Bochum
Gemeinsam federführend mit Dr. med. Christos Krogias
Neurologische Klinik am St. Josef-Hospital,
Klinikum der Ruhr-Universität Bochum
Prof. Dr. med. H.-P. Hartung (stellv. Vorsitzender),
Direktor der Neurologischen Klinik, Heinrich-Heine-Universität Düsseldorf
Prof. Dr. med. H. Wiendl (Vorstandsmitglied)
Leiter der Klinischen Forschungsgruppe für Multiple Sklerose und Neuroimmunologie, Neurologische Klinik, Julius-Maximilians-Universität Würzburg
Prof. Dr. med. K.V. Toyka (Vorsitzender)
Direktor der Neurologischen Klinik, Julius-Maximilians-Universität Würzburg
Prof. Dr. med. R. Hohlfeld (stellv. Vorsitzender),
Direktor des Institutes für Klinische Neuroimmunologie der Ludwig-Maximilians-Universität, München
Prof. Dr. med. Peter Rieckmann (Mitglied des AEB)
Chefarzt Neurologische Klinik Bamberg