Abstract

Hyperperfusion has been reported after carotid endarterectomy or stenting for stenosis of the internal carotid artery. Because few reports have examined postoperative hyperperfusion after treatment for dural arteriovenous fistulae (DAVFs), we present a case describing a patient who manifested this clinical entity. The patient was a 63-year-old man with a DAVF in the left transverse sigmoid sinus with retrograde leptomeningeal venous drainage. He experienced slowly progressive disorientation lasting for several months. Preoperative single-photon emission computed tomography with (123)I-labeled N-isopropyl-p-iodoamphetamine revealed an area of hyperintensity on T2-weighted magnetic resonance imaging (MRI) scans that coincided with the hypoperfusion area; it was not increased after acetazolamide challenge. Complete DAVF obliteration was achieved by embolization, then sinus isolation. After treatment, he experienced frequent generalized convulsions that were terminated by 2-day barbiturate therapy. On T2-weighted MRI scans obtained 3 days after surgery, the hyperintense area not only persisted but had expanded to the left parietal lobe. Moreover, a subcortical hyperintense lesion was recognized on T1-weighted MRI scans; this was considered to reflect cortical laminar necrosis. Single-photon emission computed tomography revealed hyperperfusion in the left parietal lobe; it changed to hypoperfusion a month after treatment. In patients with DAVFs with preoperative findings of marked low perfusion and a poor perfusion reserve, postoperative study may reveal hyperperfusion on single-photon emission computed tomography or cortical laminar necrosis on MRI. This may be evidence of severe perfusion disturbance as a result of venous infarction. In these patients, careful blood pressure control and early treatment of seizures are important after DAVF treatment.

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