  Multiple Sclerosis (MS) is a disorder that usually appears in adults in their
thirties. It has a prevalence that ranges between 2 and 150 per 100 000.
Epidemiological studies of MS have provided hints on possible causes for the
disease ranging from genetic, environmental and infectious factors to other
factors of vascular origin. Despite the tremendous effort spent in the last few
years, none of the hypotheses formulated so far has gained wide acceptance and
the causes of the disease remain unknown. From a clinical point of view, a high
correlation has been recently observed between MS and Chronic Cerebro-Spinal
Venous Insufficiency (CCSVI) in a statistically significant number of patients.
In this pathological situation CCSVI may induce alterations of blood pressure
in brain microvessels, thereby perturbing the exchange of small hydrophilic
molecules between the blood and the external cells. In the presence of large
pressure alterations it cannot be excluded also the leakage of macromolecules
that otherwise would not cross the vessel wall. All these disorders may trigger
immune defenses with the destruction of myelin as a side effect. In the present
work we investigate the role of perturbed blood pressure in brain microvessels
as driving force for an altered exchange of small hydrophilic solutes and
leakage of macromolecules into the interstitial fluid. With a simplified, yet
realistic, model we obtain closed-form steady-state solutions for fluid flow
and solute transport across the microvessel wall. Finally, we use these results
(i) to interpret experimental data available in the literature and (ii) to
carry out a preliminary analysis of the disorder in the exchange processes
triggered by an increase of blood pressure, thereby relating our preliminary
results to the hypothesised vascular connection to MS.
