Venous hypertensive encephalopathy.

Dural arteriovenous fistulae (DAVFs) in adults are generally regarded to be acquired lesions that may follow trauma, surgery, or thrombosis of a dural sinus (1, 2). Normal dural sinuses contain small arteriovenous anastomoses which do not appear to create any problem (3). In a setting of venous hypertension possibly in association with local angiogenic factors or congenital abnormalities of the dura, however, there can be enlargement of these preexisting arteriovenous anastomoses. The arteriovenous shunting then exacerbates the venous hypertension. Venous hypertension can then be even further compounded by vessel wall hypertrophy or thrombosis of the draining veins in response to the abnormal high flow in these vessels, which can cause stenosis or occlusion of these draining veins. This whole process can result in a wide spectrum of clinical presentations, and the fistulae can vary from asymptomatic lesions to those which are severely disabling or even life-threatening. In this issue of The American Journal of Neuroradiology, Hurst et al (page 1267) describe a series of patients with dementia related to DAVFs. Unlike patients with parenchymal arteriovenous malformations who may present with dementia, patients with dural fistulae have only minimal, if any, arterial contribution from pial arteries to the arteriovenous shunt. Therefore there is no likelihood that arterial steal is the source of these symptoms. Venous hypertension is the culprit, and this is well demonstrated by angiography and even, as in this series, by pathologic findings. All patients had angiographic evidence of venous occlusive disease with redistribution of flow. Extensive congestion of cerebral cortical and deep veins could be seen, with marked slowing of the arteriovenous transit time. Cross sectional imaging showed parenchymal edema remote from the fistula site. Autopsy results found in one patient provided pathologic evidence of chronic venous hypertension. With all these pathologic changes, it is no wonder these patients exhibited signs of impaired cognitive function. By angiographic criteria alone, these DAVFs have characteristics of aggressive lesions. Awad et al (4) have shown that leptomeningeal venous drainage, variceal or aneurysmal venous dilatation, or involvement of the deep venous system are features strongly correlated with progressive neurologic deficits and even intracranial hemorrhage. Other authors have described focal central nervous system deficits associated with DAVFs (4–6). These types of symptoms are much less common than bruit, headache, and visual changes, but, like intracranial hemorrhage, appear to be associated with drainage of the fistula to cortical or deep cerebral veins. In vein of