Medicine: Diagnosing MS:


Understanding MS: A Case of Definition


by Dr. Franz Schelling


Dornbirn, Austria



Wish to understand MS? .... Truly? - which one? Faceless MS? Clinically-defined CDMS?


Nerve dysfunctions, deemed diagnostic, provided they:

• Have no known cause, 

• Persist, in between pause, for set periods of time. 


Devoid of substance, of form, of any physical or organic property, this ward and consulting room diagnosis of multiple sclerosis is ultimately nothing but red flags of what it must not be mistaken for,  a widely adopted smokescreen for diverse changes of an untraced nature. 


Inflammatory demyelinating or 'ADEM-EAE' MS?

Natural acute disseminated encephalomyelitis (ADEM) and its experimental allergic counterpart EA[D]E[M] is millet to pea-sized longish foci, or rather sleeves, formed around blood vessels in the course of inflammatory reactions. These mark the spread of some circulated agent(s). 


A report on such a condition (Rindfleisch 1863) led to confusion in discussing this micro-metastatic form of pathology in a context of not specified observations of an active injurious process of spinal and cerebral sclerosis attributed to Rokitansky.


A MS-specific inflammatory demyelination, agent, or MS case set apart by what marks ADEM and EAE has never been identified. 


To the contrary, a circulated agent is unable to invade the spinal cord and the brain in the ways MS lesions spread, as first noted by Steiner in 1931. 


Another red herring? At any rate there is nobody who ever has shown this CDMS associated 'ADEM-EAE' [MS] to be more than a clinically convenient explanatory construct. 


Distinct MS nature in the brain and spinal cord?

From Carswell (1831) to Oppenheim (1978) autopsies disclosed more and more findings proper to spinal MS. 


In cerebral MS radically different MS specific traits were pictured at post mortem first by Charcot (1866) and since 1981 routinely, serially on MRI. 


Puzzling in themselves, these findings resist being fitted together into a coherent whole unless they are studied separately. 


Thereby emerges a distinct picture as to how cerebral and spinal MS evolve.

Fully appreciating the two natures of MS will require: 

• An acquaintance with some clearly shown and yet widely missed facts:,

• Riddance of misleading doctrines: 

• Facing up to the ways in which brain and cord lesions actually advance:




But how else can we comprehend the fact that:

(A) Venous wetterwinkel/corpus callosum MS lesions mirror those of traumatic brain injury (TBI):

(B) Mooring lesions of traumatic spinal cord injury (TSCI) so closely mimic spinal MS? 

(C) These changes can only be conceived as a concussive injuring of the brain and/or spinal core by sporadic overly intensive expansions of veins in either the brain or spinal canal?


Any MRI time-lapse series of MS patients that shows: 


· A 'cockscomb' (Heckl 1994) lesion growth along and off the outer angle of a lateral ventricle, 

· Splashy (Steiner 1931) single-hit plaques (Raine 1997), hemorrhages spread in the same way

· Engorgement, then shrinking of local veins…

· A sclerosing process invading the spinal cord from insertion zones of mainly the denticulate ligament…

The attribution of multiple sclerosis to a fusion of perivenular lesion sleeves is patently absurd... except if one feels obliged to maintain a vacuous MS. 


Specific form of CCSVI primed MS?

The kind of brain and cord damages that relates to stenoses of internal jugular or prevertebral veins is, quite paradoxically, nowhere discussed. 


The stenoses of these veins further three principally different kinds of injury:

·  A swelling, at times dotted with ring-bleedings, that involves the obstructed vein's entire periphery; usually the result of complete obstructions of intracranial segments of venous pathways of the brain.

· Farther off the skull, hindrances to the cerebral venous flow predispose to a different kind of events, rather known to occur in the legs: Compression of an engorged suprastenotic vein length drives blood back in direction of, and eventually into, especially exposed veins of the brain. The routing of such a flow at the confluence of sinuses attains critical significance.

· The retrograde emptying of blood dammed up in pre- or perivertebral veins hardly ever overburdens spinal cord veins themselves; abrupt engorgements of some part of the wide, dense mesh of epidural veins instead seek to dislocate the dural sac's subjacent contents.  


In obstructions of internal jugular veins it has to be found out whether there is: 

(i) A diffuse stasis that encompasses the obstructed vessel's entire periphery, or 

(ii) A picture of recurrent impacts exerted on the part of first its larger and later smaller collecting veins.  In obstructions of major prevertebral veins (inferior cava, azygos, left renal, or iliac vein) or big deep cervical veins, 

(iii) A progressive damaging of the cord via insertions of its mooring in the spinal dural sac has to be taken into account.  Not granting attention to these circumstances, the interventions for CCSVI cannot be expected to surpass their experimental stage. 


In summation: Treating MS patients not knowing what they are affected by denies them reliable benefits and entails an unwarrantable risk of aggravating their misery.


About the author:

The town of Linz in Austria was being hit by an air raid when Franz Alfons Schelling was born there on March 31, 1945. Early on, the boy was gripped by a passion for pursuing problematic

issues to their concrete sources. Since 1970, the year during which he earned the status of medical doctor, Dr. Schelling has confronted questions concerning the genesis of infantile hydrocephaly.


Soon after that, he took a special interest in clarifying the significance of the differences in the development of the emissary veins, the venous outlets of the human skull. He started this work

in 1973 at the Institute of Anatomy of the University of Innsbruck, and pursued it during his final two years of internship in Linz. Finally, in 1978, during the third year of his surgery practice, he

arrived at a preliminary conclusion in presenting his comprehensive evaluation of the anatomy of emissary veins.


Returning in 1981 to neurosurgical training at the Regional Hospital for Nervous Diseases of Salzburg, Dr. Schelling wanted to clarify to what extent the cranial venous outlets’ global conductivity has an influence upon the individual cerebrospinal fluid pressure. Thus, he found that unusually large cranial venous outlets were to be observed mainly in the radiographies of patients who were thought to be suffering from multiple sclerosis. As the findings seemed to be caused by a continual repetition of massive venous flow reversal, they aroused the suspicion that corresponding back-jets could also be involved in the causation of multiple sclerosis. Unfortunately, his subsequent working periods in the Neurological and Radiological Departments of the Regional Hospital of Voralberg brought no substantial advance beyond that state of affairs. There was no access to post mortem examinations which would have allowed Dr. Schelling to discover the preconditions for the particular back-jets’ recurrence, nor was there any chance to produce a flow-mapping which might have traced the back-jets themselves. In 1985 he therefore returned to his surgery practice, resigning himself, for the next dozen years, to a study of the literature on multiple sclerosis.


To his astonishment, Dr. Schelling discovered that the characteristics which proved peculiar to specific instances of multiple sclerosis could thoroughly, easily and only be explained by considering the effects which recurring venous back-jets into definite venous drainage of the brain’s respective spinal canal were bound to produce. He thus became convinced that multiple sclerosis was to be overcome not by ever more drug trials, but in soberly considering to which interplay of forces and structures the multiple sclerosis-specific lesion developments

were due. Harassed, since 1997, by a state of nervous exhaustion which put an end to his medical practice, Dr. Schelling yet enhanced his effort at pointing a way out of the blind alley into which multiple sclerosis research has maneuvered itself. Helped by his two sons Bernhard and Matthias, he was eventually granted, in 2002, relief in the presentation of his e-book Multiple Sclerosis: the Image and 1st Message at




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