Introduction ― Recently, a radically different concept regarding the pathogenesis of multiple sclerosis (MS) has been proposed. Termed chronic cerebrospinal venous insufficiency (CCSVI), it suggests that macro occlusive abnormalities of the extracranial venous drainage pathways of the brain and spinal cord can cause or contribute to MS.

As a consequence of this theory, it has been suggested that angioplasty and possibly stenting of the internal jugular and/or azygos veins can improve the signs and symptoms of MS. These interventions have been performed sporadically across the globe in an open label fashion and never in the context of a well designed, controlled, randomized and blinded clinical trial. Despite this, the procedure has been labeled by some as ‘liberation procedure’ and caused a firestorm of interest in the medical and MS communities, both for and against its utilization. The arguments on all sides are passionate, ranging from the belief that venous intervention is a miracle cure that must not be withheld from patients, to the feeling that the procedure is ineffective and unwarranted at best and dangerous at worst. The various camps commonly protest that those with differing views are not acting in the best interest of their patients.

As neurointerventionalists interested in interventional treatment of neurological disorders, it is time to take a thorough and objective look at CCSVI. This commentary will examine the origin of the CCSVI theory and discuss the data supporting and refuting its existence. An attempt will be made to critically analyze the available data and provide constructive recommendations about whether or not endovascular therapy represents a reasonable option at this point in time for patients with MS.

Brief review of multiple sclerosis
MS is a fearful and unpredictable disease that brings an enormous physical, emotional and financial burden on patients, family, relatives, friends and society in general. It is the most common cause of physical disability, with estimated 250 000–350 000 individual diagnosed with MS in the USA. The peak age at onset is 20–40 years. It affects women more so than men and is more common among Caucasians. MS can present with just about any neurological symptom in any part of the nervous system, sensory, motor, cranial nerves, visual, autonomic, coordination and myelopathic on different occasions with cumulative disability.1 Diagnosis is based on clinical and imaging criteria (McDonald criteria) to establish the dissemination in place (different CNS sites) and time (at least 30 days between clinical relapses and 90 days for new MRI lesion without clinical relapse). The clinical course of MS is most commonly relapsing remitting, with return to baseline after each relapse, followed by secondary progressive starting as relapsing remitting, then primary progressive MS.1 The most prevalent hypothesis regarding the pathophysiological basis for MS is that it is an autoimmune inflammatory disease triggered by environmental factors (toxic and infectious triggers) with genetic predisposition leading to myelin and axonal destruction in the brain and spinal cord by the immune system.1 To date, MS management has been limited to the indefinite administration of ‘disease modifying’ medications and immune modulating agents which may reduce the number and severity of relapses.1 These agents are not only costly but are associated with a wide spectrum of side effects ranging from mild to severe.