oh Charcot

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

oh Charcot

Postby Cece » Fri Nov 18, 2011 4:28 pm


Want to know why cerebral venous outflow has been a neglected topic? It's because of this guy:
Inadequate descriptions of collateral venous pathways
have influenced the development of explanatory
concepts in neuropathology. Charcot [2] suggested a topographical
distribution of brain diseases (haemorrhage
and encephalomalacia) according to the distribution of
arteries; but he paid little attention to veins. Until the
end of the 19th century some anatomy texts still provided
a careful description of cranial and vertebral venous
anatomy [3–7]. But the teachings of Charcot were
very influential in regard to the initial structuring of
neurological explanation and when, in the first half of
the 20th century, textbooks became standardised, they
gave extensive accounts of the cerebral arteries, with
only a brief and incomplete description of the anatomy
of the cerebral veins and vertebral venous plexuses. Insufficiency
of cerebral blood flow is interpreted as disturbance
of arterial inflow. That primary insufficiency of
venous outflow from the brain causes a similar reduction
in arterial inflow does not seem so self-evident; yet
it does not require experimental proof

And if that latter part is correct -- primary insufficiency of venous outflow from the brain causes a similar reduction in arterial inflow -- does not require experimental proof, then hot dang, why are we wasting time. Blood flow is a closed system. Treat us now, just as we would be treated if we had carotid artery stenoses or hemodialysis stenoses.
insufficient cranial venous outflow

ICVO, CCSVI...tomatoe, tomato....
The venous watershed between the periventricular and
subcortical white matter is not the only indication of the
separateness of the deep cerebral venous system.

It's only since learning of CCSVI that I even learned there was a venous watershed separating periventrucular white matter from subcortical white matter. With MS lesions tending to occur in the periventricular white matter, this is of interest.
However, in contrast,
Suzuki [45] reported CBF to be lowest in the neonatal
period. He used the intravenous xenon-133 clearance
method, in 80 normal children between 4 days and
15 years of age, and applied a two-compartment analysis.
From birth on, blood flow increased. After the 1st
week of life, average flow in the white matter quadrupled,
reaching its highest level at 6–8 month of age,
while average flow in grey matter more than tripled, towards
a maximum at age 3–4 years. Suzuki considered it
likely that the increase in white-matter blood flow during
the first few months of life represented mainly a response
to the increasing metabolic demands associated
with myelination, whereas grey-matter flow reflects the
establishment of higher cortical functions related to
standing, walking and speaking until 3–4 years of age.

If CCSVI is present since birth, then it might be affecting blood flow during these key early months when myelination is occurring. Maybe we have less myelin because of that. This would not explain the lesions, but it would leave us more susceptible if we have less white matter.

Men have more white matter than women and women are more likely to get MS. Compulsive liars have the most white matter of us all.

The anatomy and pathophysiology of the cerebral venous
system have long been neglected, due to theoretical
preoccupations with arterial blood supply and circulation
of CSF. According to philosophers of science, all
interpretations of data are hypotheses, which are used
until they can be replaced. Interpretations used for a
long time can become the basis of a vast literature, in
which the postulates are taken for granted, while proof
remained scanty. To make critical discussion possible,
the attempts at proof they consider best must be cited
specifically by anyone adhering to them. Uncritical,
generalised reference to the literature can prevent open,
rational discussion. Strict demands must be made not
only on new interpretations, but also on old ones, which
is much more difficult because of habit and loyalty.
The territory of the deep cerebral venous system offers
an extremely interesting field of investigation, because
as well as the periventricular white matter it includes
the basal ganglia and limbic system. Important
new techniques have become available to neuroradiologists,
for example: various methods of venography, improved
methods for assessing flow in the deep cerebral
venous system, and demonstration of brain oedema and
periventricular pathology of the white matter in the living
subject by means of CT and MRI. Great opportunities
have opened up for the acquisition of new insights.

Well said, all of this. When he mentions investigating periventricular pathology of the white matter by means of CT and MRI, that is directly applicable to us, the MS patient. New techniques and tools lead to new insights, particularly in the under-explored topic of cerebrospinal venous outflow.
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