What deals the brain such blows, synchronous (at least double) hits — in an exemplary case of multiple sclerosis?

Multiple sclerosis, MS, is viewed as a matter of ongoing random attacks on the central nervous white matter.

Neurologists diagnose a chronic persistence/recurrence of such attacks if they register central nervous dysfunctions which

(1) Can’t be traced back to a disease they know, plus

(2) Point to an affection of at least two distant places of the patient’s brain respectively spinal cord, plus

(3) Manifest in keeping with one of two convened on time-schedules.

But no one has shown how neurological examinations prove the said random attacks as well as their white matter-orientated mode of spread.

The practice conflicts at any rate with what is seen to happen at

http://www.msdiscovery.org/news/news_synthesis/322-more-meets-eye

The restrained caption of the time-lapse video speaks only of spots that form and grow, shrink and disappear — none causing a flaring-up of symptoms.

A closer look at the given sequences discloses mind-boggling sights.

The grandest plaque is seen to pop up alone, backward, deep in one cerebral hemisphere, in projecting an uneven halo that resurges in a second wave (top panels).

Two nearly as extensive plaques erupt simultaneously in the same hemisphere.

The anterolateral one splashes its halo forwards at a remarkable speed (right top panel).

The posterior one explodes a sizeable preexistent plaque.

All recede and leave no residuum.

Cone- and club-shaped, in part old, ventricle-based lesions fluctuate, flicker and ripple along the circumference of the ventricular angle — paradoxically more so in the hemisphere with the less conspicuous outer plaque eruptions.

Seen in context with the alternating mutual displacements taking place between peripheral plaques and ventricle-based lesion cones, this gives the impression of an interplay of in part competing, in part alternating mass effects of larger lesion developments.

Ventricle-based lesions waver up in grey and white matter alike (top left panel) and flare up simultaneously in distant locations — one projecting from a frontal horn while another shines up near the other atrium (top right panel).

A tell-tale, in fact, the most revealing picture emerges last.

A small lesion extended along the posterior ventricular angle abruptly shoots forward and pushes out, at right angles, anteriorly a broad cone and posteriorly, arising from a scarcely perceptible stalk, a slender club.

The given phenomena betray the lesions’ having taken their origin in a curious context with a recently — as repeatedly, new few times before rediscovered vein-relationship.

In the last years a series of papers began focusing on the significance of the “central vein sign,” also trivialized as “central vessel sign.”

It addresses the question of how far a certain percentage of brain lesions that show as their axis or center a vein might contribute to making a diagnosis of MS. https://www.ncbi.nlm.nih.gov/pubmed/?term=(central+vein+sign)+AND+(multiple+sclerosis)

In reviewing these papers the urgency of approaching the topic qualitatively before quantitatively, in perusing all the pertinent pieces of evidence in depth, becomes evident.

The local vascular anatomy leaves no doubt that the changes seen to emerge along the ventricular border (top panels) must stem from veins that join the internal cerebral veins.

To be precise, from the most proximal and downstream located parts of their intraparenchymal course.

This finding indicates the changes’ mechanical, traumatic origin.

The given lesions’ countercurrent propagation, their advancing in the opposite direction to the normal venous flow direction appears self-evident.

This fact can only be accounted for by blood volumes or pressure waves surging up from major neck veins.

It forms an irrefutable argument in support of the changes’ physical and hemodynamic causation, proposed years ago.

https://doi.org/10.24019/jtavr.29

There is a third, widely missed aspect of the central vein sign.

This aspect not only facilitates the recognition of any corresponding condition. It besides again highlights the observed events’ physical causation.

The neglection of this point marks a further blind spot of the prevailing interpretations of multiple sclerosis.

How MS lesions burst forth from their central veins, the pathologist’s parent veins, their veins of origin, seem not to have been monitored in vivo to this very day.

Observations made post-mortem, in studying serially sectioned MS brains, disclose a bizarre detail. It lends itself to exploiting the diagnostic value of the central vein sign to the full.

There is the depiction, of Mark Scheinker, of an MS lesion splashing out just to one side of its vein — see Fig. A at http://www.ms-info.net/evo/msmanu/1029.htm

It is complemented by Torben Fog’s compelling demonstration and documentation of a scarcely known fact: The ways in which cerebral MS lesions spread deviates as a rule from the axis of their veins of origin (references at www.ms-info.net).

Fog’s picture of a grotesquely dilated vein stem transitioning into delicate feeding veins points anew to a primarily proximal affection of the lesions’ veins.

It appears corroborated and extended by the in vivo findings of acute, transient dilations of not only lesion veins but also internal cerebral veins of MS patients (Zeng C ea. Cerebral vein changes in RRMS demonstrated by 3D enhanced T2*-weighted angiography. Eur Radiol 2013; 23(3): 869–78).

The joint and coincident eruptions of both lasting lesions and fleeting concussive effects — irrespective of frequent indications of a competitive lesion-behavior — await equally their being accounted for in physical terms.

Opportunities for watching more than four slices done at the same moment might show there erupt occasionally more than two lesions at once.

A variety of factors comes here into play.

The slower the rise of the blood and pressure waves which burden the cerebral veins from particular neck veins, the more evenly distributed the straining of their tributary veins and these veins’ surroundings will be. The waves producing the cerebral changes emerge in synchrony.

Retrograde venous pressure ascents hit the brain yet the harder, the faster they rise and the higher their peaks. Neither parameter has ever been focused on or monitored.

Any kind of mechanical or biomechanical impact exerted on, in the first instance, extracranial collecting veins relating to separate veins inside the craniovertebral space thereby hinders, respectively shortens the time window available for the intracerebral venous activities under discussion.

The same rule applies, to a minor degree, also to impacts on large arterial vessels which connect to arteries that feed the brain and spinal cord and ultimately even to massive impacts on soft parts of the spine.

What levels out the pressure gradients soaring up due to, and in between competing volume inputs into the craniovertebral space are first displacements of cerebrospinal fluid. Under particularly unfavorable circumstances, such of soft nervous tissues which the intervening space contains.

Synchronous volume inputs into the cranial cavity as well as spinal canal however reduce, and spatially confine, the repercussions of venous blood and pressure waves surging up from large neck veins into the brain.

Course, length and flow resistance of the venous channels which direct the venous pressure rises from the neck up into the brain prime the given activities in critical ways.

The point of what actuates the abrupt surging up of venous excess pressures from the neck into the brain has hardly been considered, let alone been studied with due care.

It is quite a variety of interactions of in part unusual biomechanical factors and structural circumstances which here waits to be taken into account.

The possibility for the patterns and dynamics of the given lesion developments to reflect an unbearable tissue straining on the part of all too high inter-venous respectively inter-vascular pressure gradients seems scarcely have occurred to anybody.

A few disconnected aspects of this problem have as of yet been dealt with in the papers dedicated to the subject of chronic cerebrospinal venous insufficiency (CCSVI).

The individual dispositions to the given hemodynamic events need yet to be systematically evaluated in their natural context.

This as much from a structural as functional viewpoint.

The chapter “Revealing what’s below the tip of the MS-pathology iceberg” of the text attending our video envisages the gray-matter pathology as “the Trojan horse of multiple sclerosis [research].”

Even puzzling together all the pieces of evidence which accrued on this topic during the last hundred-and-fifty years might contribute little to a better understanding of the phenomena indicated above.

Multiple sclerosis research can yet be quite confident to find a way of escape from the intricate maze of its conceptual labyrinth clinging to its red or Ariadne thread: the central vein sign.

It just needs to end its treading out of dead-ending paths and begin with beginning to fathom out how central veins work havoc in many an MS patient’s brain.