Open letter to Dennis Bourdette & Jeffrey Cohen re the editorial Venous angioplasty for “CCSVI“ in multiple sclerosis. Ending a therapeutic misadventure. Neurology 2014 (July 29); 83:1-2 of Franz Schelling
The intention of your editorial is, to all appearances, to sound the death knell for further research into a vascular syndrome unpredictably related to multiple sclerosis (MS). But there is no mournful undertone for ruining the prospects of many an MS patient desperate for a cure.
Esteemed, T & B cell rather than being vein-interested colleagues, aren’t you aware of this fact? The result of an investigation into the CCSVI/MS relationship depends on whether the patients examined display brain and cord damages of a specifically venous origin, or whether they do not.
Clinically defined/definite = CDMS was introduced in 1965 to prepare the recruiting of comparable patient populations for the testing of MS drugs. It appeared convenient to diagnose CDMS in the presence of unexplained neurological anomalies showing definite patterns of a progression in time.
Over and over again, quite embarrassingly, autopsies, new tests for cerebrospinal infections, advanced vascular and MR imaging have since then come to reveal, under diagnoses of CDMS, a lumping together of a variety of pathological processes which differ in nature and cause. No wonder, defined just via numbers and times, CDMS has no substance, no form, no concrete let alone specific physical property.
The bed-side identification of CDMS with an (again cryptogenic) inflammatory/degenerative demyelination attributable to a no less cryptogenic autoimmune aggression, discussed in context with a bewildering range of commonplace and speculative notions, must no prevent us from perceiving this deficiency.
Given this fact, the expectation that there will ever be some biomarker or immunological parameter that sets CDMS reliably apart does not make sense.
For the same reasons the (e-)valuations of CCSVI on the basis of CDMS will never produce consistent or conclusive results. Heaping up statistical data on the relationship may satisfy the human craze for taming the unpredictable. It is, however, no substitute for the sober deductive reasoning.
Quibbling over statistical minutiae, the scientific community virtually forgot about the first, telltale CCSVI criterion, the finding of expiratory flow reversals in inner cerebral veins. Severe instances of MS were, however, repeatedly shown to have this CCSVI criterion alone. And the only re-evaluation of the topic stresses the urgency of focusing on this point (Tromba L ea. Prevalence of CCSVI in MS: a blinded sonographic evaluation. Phlebology 2013, Nov 15; epub ahead of print).
The sporadic venous flow reversals deep in the brain tell of pressure surges that can only be due to compressions of extracranial parts of the venous pathways involved. Their coming about and efficacy depends on the presence of some hindrance to the normal venting of the momentarily pressurized blood volume in direction of the heart and its insufficient venting via immediately sub-, trans- and intracranial venous collaterals.
Chemistry, immunology, and zoology cannot be expected to reveal anything about occurrence, causes and consequences of the given events or to further the acquaintance with as well as understanding of the anatomical, histological and hemodynamic aspects of an MS patient’s vein-dependent lesion developments.
Two texts of 2002 and 2012 were actually intended to pave the way for the outstanding investigations: (1) www.ms-info.net (for telltale pictorial evidence > table of contents > overview of plates); (2) Schelling F. CCSVI in MS: Weighing the findings. Sang, thrombose, vaisseaux 2012; 24: 394-404.
In order to achieve predictable cures of “CCSVI-MS“ and related MS pathologies, the conditions and events underlying its venous pathology have to be understood.
Franz Schelling, M.D.
Honorary President "CCSVI nella Sclerosi Multipla – Onlus"
July 11th 2014
Rev. 3.3 of July 12th 2014