Multiple sclerosis: a chronic infective cerebrospinal venulitis?
Abstract
The aetiology proposed for the development
of chronic cerebrospinal venous insufficiency (CCSVI) associated with
multiple
sclerosis (MS) has been the presence of congenital
truncular venous malformations. However, this hypothesis is not
consistent
with the epidemiology or geographical incidence of
MS and is not consistent with many of the ultrasonographic or
radiographical
findings of the venous disturbances found in MS
patients. However, the probability of a venous aetiology of MS remains
strong
based on evidence accumulated from the time the
disorder was first described.
The method used in this review was to
search PubMed for all past medical publications related to vascular,
venous, haematological,
epidemiological, biochemical, and genetic
investigations and treatments of MS.
Epidemiological and geographical findings
of prevalence of MS indicate the involvement of an infective agent. This
review
of the venous pathology associated with MS
describes a hypothesis that the pathogenesis of the venous disease could
be initiated
by a respiratory infective agent such as Chlamydophila pneumonia,
which causes a specific chronic persistent venulitis affecting the
cerebrospinal venous system. Secondary spread of the
agent would initially be via the lymphatic system
to specifically involve the azygos, internal jugular and vertebral
veins.
The hypothesis proposes mechanisms by which an
infective venous vasculitis could result in the specific neural damage,
metabolic,
immunological and vascular effects observed in MS.
The hypothesis described is consistent with many of the known facts of
MS pathogenesis and therefore provides a framework
for further research into a venous aetiology for the disease.
If MS does result from a chronic infective venulitis rather than a syndrome involving congenital truncular venous malformations,
then additional therapies to the currently used angioplasties will be required to optimize results.
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