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Neurology 1999;52:156
© 1999 American Academy of Neurology


Articles

Visual symptoms with dural arteriovenous malformations draining into occipital veins

M. J. Kupersmith, MD, A. Berenstein, MD, P. K. Nelson, MD, H. T. ApSimon, MD and A. Setton, MD

From the Institute of Neurology and Neurosurgery at Beth Israel Medical Center (Drs. Kupersmith, Berenstein, and Setton), New York, NY; New York University School of Medicine (Drs. Kupersmith and Nelson), New York, NY; and Royal Perth Hospital (Dr. ApSimon), Perth, Western Australia.

Address correspondence and reprint requests to Dr. Mark J. Kupersmith, INN, Beth Israel North, 170 East End Avenue, New York, NY 19128.

OBJECTIVE: To determine the cause of the visual dysfunction and effect of treatment on dural arteriovenous malformations (DAVMs) that secondarily involve the occipital lobe.

BACKGROUND: DAVMs are an infrequent cause of visual dysfunction that should be amenable to treatment if diagnosed before permanent visual field loss.

METHODS: The records of seven patients with cerebral visual disturbances associated with DAVMs were analyzed with attention to visual symptoms, visual field testing, and vascular anatomy.

RESULTS: Sudden visual loss occurred in five patients, two with a hemorrhage and one with 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 fluctuating, 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 DAVMs in other locations, only two patients had occlusion of an adjacent venous 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-arterial embolization of the arterial feeders and nidus (one patient required additional surgery) resulted in resumption of normal occipital venous emptying. 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 disturbances 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.




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H. D. Pomeranz and S. Lessell
Palinopsia and polyopia in the absence of drugs or cerebral disease
Neurology, February 22, 2000; 54(4): 855 - 859.
[Abstract] [Full Text] [PDF]




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