désolé, vous devrez traduire et mettre en forme le tout... Mais voici ce que m'a communiqué Nineeleven... Je pense que tout y est! Bonne lecture! La source est fiable et expérimentée (plus de 20 ans de recherches dans le domaine!) Ceci devrait vous interesser ;-)
CCSVI: How to diagnose and treat nervous affections attributable to
a recurrence of violent venous flow inversions
Conventional understanding of chronic cerebrospinal venous insufficiency
In principle, the term chronic cerebrospinal venous insufficiency (CCSVI) simply points to
the presence of critically narrowed passages in internal jugular veins and azygos vein, main
channels of cranial and vertebral venous drainage. Immediate effect of any such hindrance to
venous outflow is a damming up of blood in the venous periphery, engorging tributary vessels
and flooding collateral veins. This venous congestion may be aggravated by a slowing down
of the blood stream, referred to as stasis: lacking in nutrients and gorged with metabolic waste
products, the venous periphery exudes liquids and even tiny spots of blood.
Less obvious consequences of CCSVI
A damming up of blood in jugular and azygos veins may yet also predispose to a another kind
of deleterious events: Prevented from escaping toward the heart fast enough, the engorged
veins’ content may be driven back in direction of brain or spinal canal during any form of
jugular and azygos vein compression.
Such events appear the rather hazardous:
(1) The larger blood volumes are to be displaced in direction of the venous periphery;
(2) The higher the local rises in venous pressure;
(3) The longer blood is being driven back
(a) from neck veins into some part of the brain, or
(b) the more vehement larger volumes of it are being displaced from abdomen into
especially lumbar spinal canal;
(4) The more the involved veins are already filled;
(5) The more, with right or left internal jugular vein, a separate cerebral drainage system, or
also the spinal drainage system of the lumbar veins with or without azygos vein is exclusively
being involved;
(6) The more strictly limited the involved cerebral venous drainage system’s peripheral
territory’s, and
(7) The more easily walls and surroundings of veins of brain and spinal canal momentarily
yield to a column of regurgitant blood.
As for factor (1) not just momentary or lasting hindrances of ordinary venous outflow from
internal jugular and azygos veins come into play. At times enormous widening of especially
lower parts of internal jugular veins may also unfavourably modify the course of events.
Regarding factor (2), we can note but the following:
During muscular exertion pressures attaining heights of 500 mm Hg are known to impact
upon veins of the trunk – a value which may be far surpassed in all sorts of accidents.
The point, however, how far jugular or sub-occipital venous pressure can rise during moves or
exertion of, and, in particular, external impacts upon the neck seems never to have been
investigated into.
Not much more can be said in view of factor (3):
(a) The time span available for venous reflux into the skull - depending on the ongoing
balancing of, on the one hand, differing venous pressures without and related venous and
arterial pressures within not only the brain but the entire cranio-vertebral space is of crucial
importance for the depth to which venous flow inversions may penetrate into a distinct venous
territory of the brain.
(b) As for the duration of venous reflux into the spine, there exists merely anecdotal evidence
from fluoroscopic observations of massive respiratory displacements of cerebrospinal fluid
from lower into upper parts of the cranio-vertebral space within very short periods of time.
Regarding point (4) we must be aware of the fact that a substantial engorgement of internal
jugular veins does by no means only occur with enduring organic obstructions. The extremely
changeable positioning, extreme rotation, flexion or extension, of the head as against the chest
has long been known to be able to dam up jugular veins as well.
In obstructions of the upper end of internal jugular veins it has to be kept in mind that large
volumes of blood may be driven back, in direction of the brain, also from massively engorged
collateral veins, i.e. in particular from suboccipital vein plexuses, via posterior or lateral
condylar veins.
Remarkably little concern aroused point (5) (a), i.e. the fact that blood being driven back from
(or via) either right or left internal jugular vein can selectively burden either the cortical or the
inner venous drainage of the cerebrum. This despite the fact that anatomical variations of the
confluence of sinuses predisposing to insufficient or missing levelling out of pressure
gradients between inner and outer cerebral venous drainage system have often been described
already in the 19th century AD. With completely split straight sinus, it is even possible that
only left or right inner cerebral veins may be overburdened by flow inversions in the jugular
vein of the same side.
(b) Enormous pressure gradients may be briefly built up between veins in the trunk, especially
in the abdomen, and epidural veins of the lower end of the spinal canal. Here obstructions of
the azygos vein may predispose to more massive venous shifts from outer lumbar veins into
veins of the epidural space of the lumbar canal. Such a venous reflux can obviously be the
more violent, the more external, and the less internal veins of the spinal canal are filled, the
wider their connections between the former and the latter veins are, and the weaker a counter
pressure against upward displacements of spinal subarachnoid fluid is being exerted in
cranium and uppermost part of the spinal canal.
What appear of decisive importance is factor (6): The strictness of the limitation of the
involved cerebral venous drainage system’s peripheral territory. If venous flow inversions in
one internal jugular vein tend to exclusively or primarily overburden either superior sagittal
sinus or straight sinus, veins of the latter obviously far more at risk: Individual tributary veins
of the straight sinus tend to be directly and selectively burdened according to momentary
pressure resistance of their vascular periphery while the often narrowed orifices of the cortical
veins, in pointing to the superior sagittal sinus’ usually blind anterior end, tend to be burdened
as a whole; apart from this, the cortical veins are rather interconnected in the form of a mesh,
whose main channels often have access to extracranial veins at the base of the skull not being
burdened by venous reflux.
The direct invasion of the straight sinus’ affluent veins underlines the significance of factor
(7): The transmural pressures exerted along each venous affluent depend not only on
configuration and distribution pattern of each of them; they are also greatly modified by
venous and arterial counter pressures exerted on the part of the cortical vessels invading the
local venous periphery – the perfusion of the latter being continually altered according to the
activation of separate functional units of the brain. The lower the momentary local tissue
pressure, the rather walls and surroundings of some branch of the Galenic vein will be unable
to resist the impact of a column of regurgitant blood.
Thereby falling cerebral perfusion pressure, inspiratory, position or motion dependent
emptying of even widely distant cerebral or epidural spinal veins may greatly enhance the risk
for venous reflux to injurious degrees of venous reflux.
Brain and spinal cord damages to be effected in CCSVI
A superabundance of venous collateral channels usually ensures that even complete
obliteration of both internal jugular veins does, of and by itself, not cause any lasting damage.
In a stark contrast to this, obstructions of superior sagittal sinus (1) or straight sinus (2)
typically result in pools of edema, dotted with hemorrhages, marking out the stasis-affected
tissue domains. In the latter, histopathologically, potentially reversible demyelination prevails.
As for CCSVI, no systematic investigation into the way it affects brain and spinal cord has
still been carried out. Venous obstructions as observed in CCSVI yet appear hardly ever
capable of producing peripheral circulatory stasis. In keeping with this, the nervous affections
seen in patients with CCSVI do not show the clinical pictures previously observed in severe
cervical venous obstruction of any cause.
The most striking observation made in severe instances of CCSVI was in fact this one:
Forced expiration alone did suffice for inverting the direction of flow in inner cerebral
veins pertaining to the straight sinus’ vascular territory (3). Lesions emerging in comparable
distribution patterns could thus be expected to give evidence of comparable venous activities.
Under certain circumstances, any kind of muscular or outside compression of extracranial
veins being engorged on account of obstructions in internal jugular veins can be expected to
preferentially overburden veins in the straight sinus’ small, strictly confined venous domain:
This in particular with a straight sinus being directly, just primarily or even exclusively,
related to an obstructed internal jugular vein. More generally, however, the straight sinus’
tributary vessels are at a greater risk simply on account of their branching along, and radiating
off into pulpy tissues bordering considerable volumes of, at times, most easily yielding
cerebrospinal fluid where they are but confronted with a last ebbing out of any competing
arterial pulsation.
Considering all this, it seems quite obvious that CCSVI-lesions cannot but first emerge about
large subependymal veins next to spread along their most readily accessible affluent veins.
Farther out, the neighbourhood of vascular bends and ramifications might be primarily at risk.
In this way, compact, well delineated lesion cones and waves can be expected to arise from
inner surfaces into the substance of the cerebral hemispheres, lying in line with later emerging
peripheral plaques. All in all, this kind of CCSVI lesion spread ought to simply mark out
where blood being driven back into the straight sinus’ vascular territory unduly burdened the
involved veins’ walls and periphery.
Involved tissues would thus from time to time fall prey to fleeting concussions or blunt
contusions exceeding from their veins’ content. Clinically, corresponding affections might be
manifest but for seconds (concussion with slight intracellular disorganisation) or last up to
months (traumatic demyelination). Incapacitations produced by severe contusions, ending up
in neuronal or complete tissue destruction, however, were lasting for life.
Sheathed in a tough dural sac being encircled by a mesh of broadly interconnected veins, the
spinal cord can hardly be invaded by a spread of venous excess pressures into its veins.
Venous blood being driven back into especially the lower spinal canal may yet momentarily
displace the mantle of cerebrospinal fluid embedding the cord, thereby taxing both the spinal
cord’s surfaces and even more points and lines of insertion of the ligaments by which it is
fixed to its sheaths.
Regarding the risk of venous flow inversions reaching injurious intensities, brain and spine
may further be expected to differ in the following: The impact of a venous reflux invading the
brain can be expected to increase with the degree of the involved venous pathways’
engorgement along especially also their intracranial course. Venous reflux into the spinal
canal, on the other hand, will be the more vehement, the more copiously the veins outside and
the poorer those inside the spinal canal have come to be filled.
Diagnostics of CCSVI
The process of CCSVI not simply depends upon the degree of stenosis affecting one or both
internal jugular respectively the azygos vein. The ascertainment of individual predispositions
to damaging flow inversions in definite venous pathways of brain and spinal cord accordingly
requires beside a verification of the presence of extracranial to intracerebral or extra- to
intraspinal veno-venous reflux, also a retracing of its individually differing source and course.
The conditions favouring larger volumes, higher pressures, and especially a greater
vehemence and wider reach of venous flow inversions assailing brain and spinal cord thereby
ought to become evident.
A tool being widely available and, as a consequence, preferentially employed for tracing an
occurrence of, and certain preconditions to, flow inversions in veins of the neck is Duplex
sonography. Suited for exploring valvular function and the configuration (stenosis, prestenotic
dilatation) of internal jugular veins, Duplex scans lends themselves for an evaluation of the
risk of venous reflux into and further up along the main extracranial pathways of the brain.
Transcranial colour-coded Doppler sonography, on the other hand, is unsurpassed in its ability
to directly trace venous flow inversions within the skull. Its potential for discriminating
predispositions to venous reflux into, on the one hand, straight sinus and, on the other,
superior sagittal sinus has not been fully exploited as yet.
In the attempt at determining whether it is actually venous reflux that accounts for nervous
and mental incapacitations which otherwise had to remain unexplained, cranial MRI cannot
be done without. Repeated in short intervals, it allows even to monitor the bizarre ways in
which lesions resulting from CCSVI are bound to advance and retreat.
As for the detection of spinal cord lesions attributable to CCSVI, routine MRI has
unfortunately not yet attained the necessary sensitivity and specificity.
MRVs performed according to Haacke protocol are apt to render exact and comprehensive
three-dimensional reconstructions of cervical and intracranial venous anatomy. In doing so,
they may provide evidence of more or less complete separations between right and left-sided
cervical venous drainage of the brain. Here the demonstration of a direct continuation of
straight sinus into one (twice more often the left than right) lateral or also occipito-marginal
sinus attains primary interest.
The most precise means for a sharp, detailed and comprehensive illustration of the route
which such venous flow inversions may take is conventional selective venography.
As for the elucidation of CCSVI processes affecting the brain, expiratory retrograde
jugularography (4) appears to be the most revealing tool.
In the attempt at tracing CCSVI processes affecting the spinal cord, conventional selective
phlebography ought not be limited to the azygos vein. Especially in suspected CCSVI lesions
of the lower spinal cord, the lumbar veins’ connections to both inferior cava vein and the
epidural venous plexuses of the spinal canal need to be studied as well.
Prevention of damages resulting from CCSVI
If the development of lesions appearing characterized and emerging in the ways just described
can be shown to be associated with individual predisposition to massive, intensive as well as
far-reaching flow inversions in definite venous pathways of brain and spinal cord, such events
need to be prevented by appropriate physical means.
This appears all the more urgent as a recurrence of flow inversions in any venous drainage
system tends to stiffen its walls and to dilate the vascular channels being involved. In this way
the process of CCSVI tends to become more and more dangerously intensified.
In severe instances, only well planned surgical interventions can be expected to reliably halt,
or even prevent, otherwise relentlessly progressing neurological and mental incapacitations
due to CCSVI.
Concrete therapeutic suggestions
As yet the treatment of CCSVI has been based upon dilating stenoses of internal jugular and
azygos vein using balloon angioplasty. To counteract the high risk of restenosis, given mainly
in the internal jugular vein owing to its collapse in sitting and standing position, balloon
angioplasty has often been complemented by an implantation of stents. The latter procedure,
nevertheless, has been discredited by the rare occurrence of stent migration. Neither can it
completely eliminate the risk of restenosis, bound to bring in its wake new bouts of nervous
and mental incapacitations attributable to CCSVI.
To more reliably prevent relapses of CCSVI attributable to reflux in or via internal jugular
veins, open surgery, even valve transplants, seem advisable.
Especially in valvular incompetence of a right internal jugular vein bearing, more or less
exclusively, the brunt of venous flow inversions in superior cava vein, valve transplants may
prove the means of choice for preventing cerebral complications of CCSVI.
What might provide no less an effective protection against venous flow inversions pushing
back via straight sinus into its affluent veins is perforating the thin dural septum or bridging a
gap between straight and superior sagittal sinus preventing the levelling out of higher pressure
gradients between the two sinus’ affluent veins.
Owing the greater complexity of the venous systems being involved in the development of
CCSV lesions of the spinal cord, correcting the underlying venous preconditions is
unavoidably more time-consuming and difficult.
Conclusion
Well planned, and carefully performed, surgical interventions intended to correct flow
inversions in internal jugular, azygos, as well as lumbar veins can be expected, without any
particular risks, to put an end to repeated bouts of cerebral and more continuous progression
of spinal incapacitations resulting from veno-venous reflux into the craniovertebral space.
The procedures have accordingly been stated to meet the legal, moral and scientific criteria
specified by concerned organisations, including the World Health Organisation.
The fact that patients suffering from CCSVI tend to be classified, from the standpoint of
neurology, as instances of multiple sclerosis (MS), should not surprise on account of the
following:
(1) Regarding the pathomechanisms being indicated above, CCSVI must be expected to
usually comply with the clinical criteria underlying the neurological diagnosis of MS.
(2) The cerebrospinal fluid oligoclonal bands considered as the most important laboratory
finding supporting the clinical diagnosis of MS are also observed in traumatic and
vascular affections of brain and spinal cord (5). On this account we are also bound to
expect a development of oligclonal band in spinal and cerebral affections caused by
CCSVI.
(3) Both at post mortem and on MRI, findings which indubitably reflect - not only
regarding their location, but also in their form as well as manner and pattern of spread
- the kind of lesions that must be expected in CCSVI, have consistently been presented
as typical, even specific lesion pictures of MS (6, 7, 8, 9, 10, 11, 12).
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