The Pathology of the Internal Jugular Vein Wall in Multiple SclerosisMassimo Pedriali1 and Paolo Zamboni2*
- *Corresponding Author:
- Paolo Zamboni
Vascular Diseases Center, University of Ferrara
Via Aldo Moro 8, 44124 Cona, Ferrara, Italy
E-mail: [email protected]
Received date: September 29 , 2015; Accepted date: November 23, 2015; Published date: November 30, 2015
Citation: Pedriali M, Zamboni P (2015) The Pathology of the Internal Jugular Vein Wall in Multiple Sclerosis. J Mult Scler (Foster City) 2:160. doi:10.4172/2376-0389.1000160
Copyright: © 2015 Pedriali M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In the last years it has been described a condition named Chronic Cerebrospinal Venous Insufficiency (CCSVI), frequently but not exclusively associated to Multiple Sclerosis (MS), which generated a strong scientific controversy about the epidemiological prevalence and the possible role in the complex, multi-factorial MS ethio-pathogenesis. However, CCSVI description also stimulated a considerable research activity on the extracranial veins. Among the fields of interest, the pathology of the Internal Jugular Veins (IJVs) was deeply investigated by some groups, so improving our knowledge in an underestimated field of MS research. Currently, the available papers clearly show the presence of abnormalities in the IJV wall of MS patient’s respect to control tissue. In the tunica intima a significant derangement and loss of the endothelial cells have been described. Interestingly scanning electronic microscopy showed absence of endothelium in the defective jugular valves. In the adventitia it has been described an inverted ratio between type I and type III collagen, with prevalence of the latter. Finally, in the adventitia layer it has been found the presence of calcifications arranged around the vena venarum. Assessment of immune cells in the three IJV layers did not demonstrate increased infiltration. Current studies do not clarify the origin of the pathology of the IJV in patients with MS. Congenital, infectious, or even post thrombotic ethiology have been advocated. Finally, the review summarizes studies which link the CCSVI pathophysiology to the complex MS pathogenesis, and particularly to the impact of restricted brain outflow on the cerebral spinal fluid dynamics and cerebral perfusion.