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The diagnosis of spinal dural arteriovenous malformation (AVMs) remains elusive and characteristically defies an early recognition. Berenstein and Lasjaunias combined their se-ries with the reports by Djindjian, Merland, Rosenblum, and Symon to summarize the com-mon clinical presentations and findings (1–5). Patients usually present in the 4th to 6th decade with a slowly progressive thoracic myelopathy. Leg weakness, back pain, and/or radicular pain are the most common presenting problems. Stocking and/or saddle paraesthesias often de-velop in association with bladder, bowel, and sexual-function disturbances. Upper and lower motor neuron findings in the lower limbs sug-gest a low cord or conus lesion. Power usually is grade 4. Deep tendon reflexes may be in creased despite wasting of the buttocks and lower extremities. Clonus often is present. Loss of pain and temperature sensation as well as joint-position sense is frequent. The pathophysiology of spinal dural AVMs was elucidated by Aminoff and supported by the work of Kendall and Merland (3, 6, 7) Shunting into the perimedullary venous plexus results in a venous hypertension and chronic passive venous congestion of the cord. The pa tient’s signs and symptoms relate to dysfunc tion in the lower thoracic cord and conus, irre spective of the location of the shunt. Intracrania dural AVMs draining into the perimedullary ve nous plexus of the cord can produce a simila myelopathy (8–10). Magnetic resonance (MR) of the spinal cord now should be the first radiologic investigation of a myelopathy. Previous reports have shown the following MR findings in spinal dural AVM