Ragucci, Monica (2016) Contrast-enhanced ultrasound study of Internal Jugular vein blood flow in Multiple Sclerosis patients. Imaging study of cerebral venous system in mouse. [Tesi di dottorato]

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The underlying mechanism of the widespread axonal degeneration in Multiple Sclerosis (MS) is not yet fully understood. The patterns of demyelination are different between different subgroups of patients with MS, suggesting that the disease is heterogeneous. It is known that the development of a chronic inflammatory reaction in the brain requires additional factors and that the impairment associated with relapsing-remitting clinical form is primarily caused by inflammation and demyelination, whereas the accumulation of irreversible neurological deficit, typical of the progressive forms, is caused mainly by axonal destruction and neuronal loss. Other mechanisms may contribute in determining brain damage during the course of the disease. One hypothesis is that immune factors interacting with the vascular system may secondarily induce changes in cerebral perfusion that are detectable in both early stage of disease and advanced disease and that may cause neuronal damage. The higher frequency of ischemic stroke in patients with MS may be due to several factors such as inflammation, oxidative stress, and increase of thrombophilic factors such as homocysteine. Recently it has been suggested that alterations of cerebral venous outflow in MS patients could determine perivenular extravasations of erythrocytes, iron overload and activation of the immune response. Vascular dysfunction could be one of the factors involved in the complex pathogenesis of MS. However, available data to support the presence and importance of vascular dysfunction are still insufficient to draw definitive conclusions. A first part of research project was to study the Internal Jugular Veins dynamics in MS patients compared with healthy controls using contrast-enhanced ultrasonography. The patients with MS showed a significantly reduction of wash-out rate compared to healthy controls [22.2% (2.7%-65.9%) vs. 33.4% (16.2%-76.8%); P<0.005]. Then we decided to explore the effect of cerebral outflow reduction on cerebral nervous system in experimental animal model. Therefore, the second part of research project was dedicated to the characterization the anatomy of the cerebral veins of the mouse brain using different imaging techniques. This work was preliminary to the development of a mice model of cerebral outflow occlusion to assess the correlations between venous stasis and the development of neurological disease.

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