Chronic cerebrospinal venous insufficiency and multiple sclerosis: history and background.
Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) most commonly characterized by focal areas of myelin destruction, inflammation and axonal transection. The multicentric inflammation and demyelination of the brain and spinal cord are associated with variable neurologic symptoms ranging from mild dysfunction to debilitating. Typically, these symptoms are marked by episodes of clinical worsening followed by improvement. The cause of this disease remains unclear currently, but the underlying etiology is generally considered to be immunologically based. Other factors, including genetic, environmental and infectious influences have been implicated, as well. Now recent studies have proposed that extracranial venous obstruction, termed chronic cerebrospinal venous insufficiency (CCSVI) may have a role in the pathogenesis of MS or many of its associated clinical manifestations. It is postulated that venous narrowing affecting one or more of the jugular veins and/or the azygous vein in the chest may be responsible for abnormal blood flow in the veins draining the brain and spinal cord. The abnormal flow may initiate and/or sustain a local inflammatory response at the blood-brain barrier that promote pathological changes within the CNS. This review presents the history of the relationship between the vascular system and MS and explores the background of basic and clinical investigations that led to the concept of CCSVI.
Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5407, USA. mddake@stanford.edu
Michael D
MD
Dake
D002550:Cerebral Veins / Q000503:physiopathology*; D002908:Chronic Disease; D006801:Humans; D009103:Multiple Sclerosis / Q000150:complications / Q000503:physiopathology*; D013116:Spinal Cord / Q000098:blood supply* / Q000503:physiopathology*; D014689:Venous Insufficiency / Q000150:complications / Q000503:physiopathology*