Pathophysiology
First described in 1926 by Foix and Alajouanine,the pathophysiology of venous hypertension was not elucidated until 1974 by Aminoff and Logue.10 In a SDAVF,
typically 1 (but sometimes multiple) feeding radiculomedullary artery enters the dura mater of the spinal cord at the dural root sleeve and forms a fistula with a medullary vein, thus arterializing the corona venous plexus surrounding the spinal cord. The resistance to venous outflow results in chronic venous hypertension/stagnation leading to chronic medullary ischemia. In the case patient, a feeding dorsal radiculomedullary artery formed an intradural arteriovenous fistula and arterialized the coronal venous plexus (Figures 2and 3). Hurst et al11 reported that a spinal cord biopsy from a patient with documented SDAVF demonstrated marked hypocellularity, small blood vessels with hyalinized walls, extensive vascular sclerosis and gliosis of the white matter, and focally enlarged, degenerating axons,findings that supported a pathophysiology of ischemic myelopathy due to increased venous pressure.