It was recently published on Canadian Medical Association Journal (CMAJ) the study" Validity of the diagnostic criteria for chronic cerebrospinal venous insufficiency and association with multiple sclerosis." Authors point out major methodological questions relating to the proposed diagnostic criteria for CCSVI. Nowadays we respond to Canadians with a comment of our honorary president, Dr. Franz Shelling, one of the first researchers to have correlated Multiple sclerosis and vascular disease
Comment on the article
by Franz Schelling, M.D., Honorary President of "Associazione CCSVI nella Sclerosi Multipla – Onlus"
The paper’s mystifying title announces an evaluation of the criteria for making a diagnosis of chronic cerebrospinal venous insufficiency (CCSVI) and (of its, their, some other?) association with multiple sclerosis (MS).
The introductory paragraph of the article yet addresses the question of whether altered cerebrospinal venous hemodynamics might play a role in the pathophysiology of multiple sclerosis (MS) or, to be more precise – as soon becomes evident, of clinically defined/definite or CDMS proven by McDonald and Poser criteria.
A comparison of the prevalence of the second through fifth CCSVI criterion in patients with a diagnosis of MS and healthy controls is supposed to clarify this point.
According to the given statistical evaluations, the two study populations showed no difference regarding their venous patency.
From this, the authors conclude “We detected no link between chronic cerebrospinal venous insufficiency (CCSVI) and multiple sclerosis“, and end their paper with the statement “We … dispute the authenticity of this diagnosis“.
The reader is left to decide whether ‘this diagnosis' applies to the way in which CCSVI or instead MS have been identified.
A CDMS proven by McDonald and Poser criteria is but a dysfunctional syndrome of unknown origin that progresses according to one or the other 0f two arbitrarily chosen time schemes.
CDMS has no distinctive finding, no concrete substance of its own. It cannot accordingly be said to work or not to work in a specific way. There is no way of physically examining CDMS itself, no chance of determining its own, or relationship to a different pathomechanism.
Derived from no more than pragmatic clinical deliberations, CDMS admits only to be associated with such anavailingly broad terms as a (genetically and/or environmentally conditioned) inflammatory demyelination respectively cerebrospinal degeneration/atrophy.
Is there, ultimately, a more general and less committal way of speaking of a pathological process than as a condition scattered in time and space?
As for their methods, the authors mention in passing that they did no research on the first CCSVI criterion, i.e. the finding of exspiratory venous flow reversals deep in the cerebral hemispheres. Recent data (Tromba L ea. Prevalence of CCSVI in MS: a blinded sonographic evaluation. Phlebology 2013 Nov 15 [epub ahead of print] show the importance of focusing on this point.
Having ‘observed no evidence of large-volume reflux that would have approached the intracranial veins’ by no means excludes the sporadic occurrence of displacements of blood from extracranial into cerebral veins.
Much store is laid instead by reductions in the venous cross-sectional area.
Focusing considerations on the dynamics of the cerebral bloodflow on this detail bespeaks a disquieting lack of awareness of the overriding significance of the individual variations in the intracranial intra- and transcranial venous collateralization.
How often and how well especially the one-sided, but also the bilateral ligature of the internal jugular veins, and even the sporadic or continual reflux via one of these veins tends to be generally tolerated, and this particularly in the long run, seems widely unknown.
A recurrence of vein-related lesion developments extending from the lateral cerebral ventricles in particular along Steiner’s wetterwinkel and into the undersurface of the corpus callosum has, on the other hand, been characterized as specific and pathognomonic of of MS (Heckl RW. MS. Thieme, Stuttgart 1994; Gean-Marton AD ea. Abnormal corpus callosum: a sensitive and specific indicator of MS. Radiology 1991; 180:215-21). Such damages are physically to be accounted for exclusively by the impacts of a recurrent venous reflux. Identical brain lesions found after traffic accidents leaving the cranium intact reflect the work of a single corresponding episode (literature on request).
In realizing the momentary nature of such events, the senselessness of recording a reflux only if it has a >0.88 second’s duration is obvious.
The alterations in cerebral venous hemodynamics with explain these MS specific lesions’ vein-dependent development await their being physically explained. Here it has to be kept in mind: In contrast to venous stasis, venous reflux becomes injurious by the immediate transmission of the pressure surge of an extracranial venous compression onto particular cerebral veins. The outcome varies with the pressure relieving venous collaterals’ natural variance.
Due acquaintance with the given pathomechanism alone enables to a solid weighing of the pathogenic significance of the different findings which form part of a diagnosis of CCSVI.
For to make advances in CCSVI and MS research we must know, and understand, what we are talking about.
Franz Schelling, M.D., Honorary President of "Associazione CCSVI nella Sclerosi Multipla – Onlus"