Open letter to Fred D. Lublin and co-workers re the article “Defining the clinical cours of multiple sclerosis. The 2013 revisions“ (Neurology 2014; 83: 278-86)
PDF: https://dl.dropboxusercontent.com/u/66292082/Schelling%20-%20MS%20Definitions%20-%20Lublin%20phenotypes.pdf


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Dr. Franz Schelling did it again!:) - Open letter to Fred D. Lublin and co-workers re the article “Defining the clinical course of multiple sclerosis. The 2013 revisions“

(Neurology 2014; 83: 278-86) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4117366/

"Ladies and gentlemen,

In 1965 ten neurologists convened to arbitrarily define multiple sclerosis (MS) via its clinical course: Two (or more) cryptogenic central nervous dysfunctions of separate origin, distinctively specified, as it were, by their having persisted for at least a day and manifested at least a month apart - or, instead, evolved over a period of no less than six months - came to be instituted as proof for the presence of MS.

The reasons for choosing exactly 24 hours, less precise 28 to 31 days, and sometimes hard to verify half of an year as cut-off points were not divulged/told.

Defining the time course of what is defined by its time course amounts to circular reasoning.

As a whole, your paper only slightly modifies some of the 1996 notions of what should be used to ensure a clinical standard categorization of the course of MS.

What nonetheless evokes acute interest is the recent characterization of the 1996 drafts of the ways in which MS clinically manifests over time as THE ORIGINAL MS PHENOTYPE DESCRIPTIONS.

Good phenotypes ultimately make a concrete thing what it is, or disclose its most striking or peculiar traits.

Increased understanding of MS and its pathology is noted to have ‘prompted a re-examination of MS disease phenotypes’ (of not disclosed nature).

However instead of looking more closely into the ‘pathologic differences’ underlying more conspicuous clinical and MRI events, you declare you ’have intentionally avoided drawing pathologic conclusions’ (regarding the nature of MS?) ‘until more data become available’.

Why? MS is already drowned in a swirl of ill-considered pathological findings claiming to be peculiar to MS. Waiting ‘until more data becomes available’ is accordingly an exercise in futility.

Some pertinent ‘MRI findings may be non-specific’. Indeed. But why ignore the specific or pathognomonic ones? Having met to determine whether the MS-phenotypes could be better characterized by including MRI and other imaging techniques:

1 did no one realise that serial MRIs at short intervals depict the patterns of recurring inroads of the process of MS on the brain? (1)

2 did anyone notice that these inroads advance, against the direction of normal blood flow, splashing off Dawson’s fingers or ovoid plaques from well-defined lengths or sectors of a definite group of veins leading out of the brain? (2,3)

3 is it really so hard to see that focusing on these points might prove the ideal research strategy for identifying and discriminating actual original MS phenotypes?

Evaluating serial MRIs by simply counting UBOs (unidentified bright objects) and trying to tally them with clinical course descriptions puts the cart of the clinical sequelae before the horse of the preceding injury.

Are you surprised attempts to trace distinctive relationships between changes in biological body fluid markers and the various clinical course(s) of MS have failed? An MS course description is only a crude sketch as it is impossible to continuously monitor all of a patient’s nervous dysfunctions or even all the divergences in their course.

Monitoring the temporal relationships between cerebral tissue destructions (release of myelin, neuron, astroglia bio-markers) seen on MRI and the inflammatory or immunological events in the body fluids would in fact demonstrate that MS is primarily neurodegenerative. Inflammatory responses are a secondary reaction to tissue injury and no different from those seen in stroke or traumatic brain injury.

Recognition of the true MS phenotype is the conditio sine qua non for any success in MS research. Only a perceptive, perspicacious and objective review of the autoptic and imaging evidence on MS, starting with Carswell’s MS observation of 1831, will achieve this goal. (4)

The claim MS is an inflammatory demyelinating process of an autoimmune origin reflects nothing but a stagnant interpretation of neurological ward and consulting room observations.

Pharmaceutical industry partners may prefer keeping up appearances of an MS definition based on an artifact of circumstantial suppositions. But patients desperately require a dependable MS phenotype, based on concrete pathological, MRI and vascular FACTS to be brought to their care.

No wonder Dr Kurtze once warned that prescribing MS drugs is like shooting arrows into a dense fog.

Sincerely,

Franz Schelling, M.D."

1 http://www.med.harvard.edu/AANLIB/cases/case5/mr2/020.html.

2 http://www.ajnr.org/content/21/6/1039.full.pdf

3 https://docs.google.com/file/d/0B_Ed_wxZvab3clRhVEsybFRLRzQ/edit?pli=1

4 http://www.ms-info.net/evo/msmanu/839.htm