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A recent hypothesis1 implicated chronic cerebrospinal venous insufficiency (CCSVI) in the etiology of multiple sclerosis (MS). The postulated mechanism states that iron accumulation in the brains of patients with MS was caused by blockade of the cerebral veins, resulting in reduced blood flow, extravasation of erythrocytes, and iron deposition leading to oxidative tissue damage. This hypothesis left patients in a quandary: Should they pursue diagnosis and amelioration of vein blockade for treatment of MS, and must they avoid iron in order to improve their quality of life?
In this issue of Neurology®, Worthington et al.2 challenge this proposal, reasoning that if parenchymal brain iron deposition were present in MS, it should be reflected by increased CSF ferritin (the iron storage protein). Their study showed that while CSF ferritin levels were pathologically raised in patients with superficial siderosis and subarachnoid hemorrhage, a significantly lower number of patients with MS were affected by high ferritin levels. Furthermore, CSF ferritin did not increase in patients with MS over a …
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