Abstract

Chronic cerebrospinal venous insufficiency (CCSVI) is a theory that has attempted to link venous outflow obstruction from the central nervous system (CNS) with neurologic abnormalities such as multiple sclerosis (MS). In some ways, it has been unfortunate that CCSVI was initially described in the context of a disease such as MS. Enthusiastic and optimistic patients and physicians embraced the early findings of Zamboni et al (1) as an ‘‘explanation’’ and ‘‘cure’’ for this debilitating condition. Venous disease was identified on venography and treated with angioplasty, leading to patient-reported symptomatic improvement. Understandably, this type of fundamental paradigm shift regarding an important disease such as MS was unsettling to many, and some neurologists countered these claims with a very reasonable demand for evidence. This led to additional studies that largely centered on the noninvasive diagnosis of CCSVI and the inconsistency of Doppler ultrasound (US) in identifying CCSVI in patients with MS (2–4). Unfortunately, the deep investment in current thinking regarding an autoimmune basis of MS led these investigators to conclude that, if a noninvasive imaging test cannot diagnose CCSVI, then CCSVI must not exist. In my opinion, these conclusions about noninvasive imaging should have led to a call for additional study and not the condemnation of an entire theory. Instead, this is exactly what happened, and the effect was to significantly dampen the enthusiasm surrounding CCSVI. So let’s back up. This phenomenon started with an observation made by Zamboni et al (5) of a venous outflow obstruction in patients with MS. On the basis of that observation, angioplasty and stent placement have been

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