Objectives: The aim of this report is to assess the safety of endovascular treatment for chronic cerebrospinal venous insufficiency (CCSVI). Although balloon angioplasty and stenting seem to be safe procedures, there are currently no data on the treatment of a large group of patients with this vascular pathology. Methods: A total of 564 endovascular procedures (balloon angioplasty or, if this procedure failed, stenting) were performed during 344 interventions in 331 CCSVI patients with associated multiple sclerosis. Results: Balloon angioplasty alone was performed in 192 cases (55.8%), whereas the stenting of at least one vein was required in the remaining 152 cases (44.2%). There were no major complications (severe bleeding, venous thrombosis, stent migration or injury to the nerves) related to the procedure, except for thrombotic occlusion of the stent in two cases (1.2% of stenting procedures) and surgical opening of femoral vein to remove angioplastic balloon in one case (0.3% of procedures). Minor complications included occasional technical problems (2.4% of procedures): difficulty removing the angioplastic balloon or problems with proper placement of stent, and other medical events (2.1% of procedures): local bleeding from the groin, minor gastrointestinal bleeding or cardiac arrhythmia. Conclusions: The procedures appeared to be safe and well tolerated by the patients, regardless of the actual impact of the endovascular treatments for venous pathology on the clinical course of multiple sclerosis, which warrants long-term follow-up.

Under the auspices of the International Society for Neurovascular Disease (ISNVD), four expert panel committees were created from the ISNVD membership between 2011 and 2012 to determine and standardize noninvasive and invasive imaging protocols for detection of extracranial venous abnormalities indicative of chronic cerebrospinal venous insufficiency (CCSVI). The committees created working groups on color Doppler ultrasound (US), magnetic resonance (MR) imaging, catheter venography (CV), and intravascular US. Each group organized a workshop focused on its assigned imaging modality. Non-ISNVD members from other societies were invited to contribute to the various workshops. More than 60 neurology, radiology, vascular surgery, and interventional radiology experts participated in these workshops and contributed to the development of standardized noninvasive and invasive imaging protocols for the detection of extracranial venous abnormalities indicative of CCSVI. This ISNVD position statement presents the MR imaging and intravascular US protocols for the first time and describes refined color Doppler US and CV protocols. It also emphasizes the need for the use of for noninvasive and invasive multimodal imaging to diagnose adequately and monitor extracranial venous abnormalities indicative of CCSVI for open-label or double-blinded, randomized, controlled studies.

Multiple sclerosis is an autoimmune disease characterized by multifocal areas of inflammation and demyelination within the central nervous system. The mechanism that triggers the disease remains elusive. However, recent findings may indicate that multiple sclerosis, at its source, could be a hemodynamic disorder. It has been found that multiple sclerosis patients exhibit significant stenoses in extracranial veins draining the central nervous system (in azygous and internal jugular veins), which are associated with significant pressure gradients measured across strictures. Such anatomic venous abnormalities were not found in the control group of healthy subjects. In this review, it is hypothesized that pathological refluxing venous flow in the cerebral and spinal veins increases the expression of adhesion molecules, particularly intercellular adhesion molecule-1 (ICAM-1), by the cerebrovascular endothelium. This, in turn, could lead to the increased permeability of the blood-brain barrier. Inflamed and activated endothelium could secrete proinflammatory cytokines, including GM-CSF and TGF-beta. In these settings, monocytes could transform into antigenpresenting cells and initiate an autoimmune attack against myelin-containing cells. Consequently, a potential therapeutic option for multiple sclerosis could be pharmacotherapy with either substances that strengthen the tight-junctions barrier, or with agents that reduce the expression of adhesion molecules. In addition, surgical correction could be an option in some anatomical variants of pathologic venous outflow. We are optimistic that a hemodynamic approach to the multiple sclerosis pathogenesis can open a new chapter of investigations and treatment of this debilitating neurologic disease.