A case of a dural arteriovenous malformation with prominent localizing neurological deficits is reported. The venous drainage of the lesion and the lack of a significant pial supply implicate venous hypertension as the mechanism of neurological dysfunction. This mechanism is supported further by the angiographic changes and the prompt resolution of the deficits after endovascular treatment. This case illustrates the potential for this frequently postulated but rarely confirmed pathophysiological mechanism to cause reversible neurological dysfunction.