Visual symptoms with dural arteriovenous malformations draining into occipital veins

Citation
Mj. Kupersmith et al., Visual symptoms with dural arteriovenous malformations draining into occipital veins, NEUROLOGY, 52(1), 1999, pp. 156-162
Citations number
22
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
52
Issue
1
Year of publication
1999
Pages
156 - 162
Database
ISI
SICI code
0028-3878(19990101)52:1<156:VSWDAM>2.0.ZU;2-S
Abstract
Objective: To determine the cause of the visual dysfunction and effect of t reatment on dural arteriovenous malformations (DAVMs) that secondarily invo lve the occipital lobe. Background: DAVMs are an infrequent cause of visual dysfunction that should be amenable to treatment if diagnosed before perma nent visual field loss. Methods: The records of seven patients with cerebra l visual disturbances associated with DAVMs were analyzed with attention to visual symptoms, visual field testing, and vascular anatomy. Results: Sudd en visual loss occurred in five patients, two with a hemorrhage and one wit h a venous infarct in the occipital lobe. Fortification images occurred in three patients, two of whom had palinopsia (one with de novo formed visual hallucinations). Homonymous quadrantic or hemianoptic field defects, some f luctuating, were found in six patients. Angiography revealed each DAVM was supplied solely by dural arteries and drained into occipital pial veins due to retrograde blood flow through the sites near or in the wall or lumen of the dural venous channels that normally drain the occipital lobe. Unlike D AVMs in other locations, only two patients had occlusion of an adjacent ven ous sinus. These patients, particularly the two with posterior fossa DAVMs remote to the occipital lobe, clearly demonstrate the visual and neurologic dysfunction resulting from venous hypertension. In six patients, intra-art erial embolization of the arterial feeders and nidus (one patient required additional surgery) resulted in resumption of normal occipital venous empty ing. No further visual episodes occurred in five of these six patients. The visual fields normalized in three patients and improved in one with venous infarct but were unchanged in both patients with a hemorrhage. Conclusions : DAVMs that drain into occipital veins cause field loss and other visual d isturbances because of venous hypertension in the occipital lobe, which can be reversed by occluding the DAVM nidus. If a venous infarct or hemorrhage has not caused irreversible damage, visual recovery should be complete.