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

A simple model of filtration and macromolecule transport through microvascular walls