old article (1989)

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

old article (1989)

Postby frodo » Sat Jul 07, 2012 7:34 am

PERIVENTRICULAR LESIONS IN MULTIPLE SCLEROSIS:
THEIR PERIVENOUS ORIGIN AND RELATIONSHIP TO
GRANULAR EPENDYMITIS

http://www.direct-ms.org/pdf/CCSVI/Adam ... S%2087.pdf

The part that catched my attention was:

Increased permeability of the inflamed ependyma constitutes a possible abnormal entry route from plaque to CSF
or, in reverse, from CSF to brain.

could this be the link between CCSVI and the CSF flow hipotheses?
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Re: old article (1989)

Postby Cece » Sun Jul 08, 2012 1:48 pm

Granular ependymitis is distinct from the plaque, both in site (i.e.
sometimes distant from plaques), and also in time of onset (i.e. less associated
with lymphocytic infiltration and the early non-confluent perivenous lesion).
Granular ependymitis is not an early feature of the disease and is not specific
for multiple sclerosis; for example, it is seen in association with ventricular
dilatation or meningitis (see Results). Nevertheless. it does seem to provide a
possible route in multiple sclerosis for movement of inflammatory agents (e.g.
IgG and C3) between CNS lesion and CSF, or vice versa. This could explain
the 23% incidence of raised albumin in the CSF in multiple sclerosis (Walsh
& Tourtellotte, 1983), as well as the increase therein of myelin constituents,
such as basic myelin protein (Cuzner et al., 1978).

It does seem that barriers which should not be permeable are permeable.
Would impaired flow or stasis of the cerebrospinal fluid cause that increase in permeability?
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