Abstract
AS recently as ten years ago, spinal cord arteriovenous malformations (AVM) were considered by some neurosurgeons to be practically untreatable lesions. 1 A more aggressive and hopeful attitude toward these anomalies is now evidenced by the recent publication of several surgically treated series. 2-6 Despite this, we are not certain how these lesions become symptomatic and how they are related to and interact with the normal vascular supply of the cord. Because of these deficits in our understanding of such lesions, we have to date, only approximate guidelines to surgical therapy. 6 One hypothesis suggests that the blood supply to the anomaly and to the cord are separate and that symptoms are caused by pressure effects 3,5,6 This leads to the recommendation of excision of the bulk of the lesion or selective ligation of the arterial supply. An alternative hypothesis has recently been suggested by Chatterjee 7 (personal communication).
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