Due to poor air quality, the Academy San Francisco offices will be closed Friday, Nov. 16. 

  • Written By: Michael Vaphiades, DO
    Neuro-Ophthalmology/Orbit

    The authors describe two patients with transverse sinus dural arteriovenous fistulas (DAVFs) who presented with headache and papilledema due to intracranial hypertension. They say the data from these patients supports the hypothesis that venous hypertension causes intracranial hypertension in DAVF. They note that an additional factor leading to intracranial hypertension could be stenosis of the fellow transverse sinus in these patients.

    The intracranial hypertension resolved in both patients after embolization of the DAVF. The authors propose that in these patients the lack of even one functioning transverse sinus allowed intracranial hypertension to develop.

    They report that in the first patient, after embolization, venous pressure remained mildly elevated due to the ongoing arterial supply to the DAVF and narrowing of the right transverse sinus. Yet treatment was sufficient to resolve the patient's tinnitus and papilledema. In the second patient, embolization not only terminated flow in the DAVF but also lessened stenosis in the contralateral transverse sinus. The patient's symptoms resolved, as did the papilledema and the venous hypertension.

    The authors say these results support the theory that intracranial hypertension in the setting of a transverse sinus DAVF is the result of decreased cerebrospinal fluid (CSF) absorption secondary to venous hypertension.

    They note that the flow of arterialized blood into the transverse sinuses added to the increase in venous pressure, leading to further venous hypertension and intracranial hypertension through decreased CSF absorption at the arachnoid villi. By embolizing the DAVFs, the venous hypertension improved, as did the intracranial hypertension and papilledema.

    They propose that if a patient has a DAVF of one transverse sinus and the other transverse sinus is functioning, significant venous hypertension and subsequent intracranial hypertension will not develop.

    They note that DAVFs with reflux into cortical veins pose great risk for hemorrhage and focal neurological damage. They believe that a DAVF with anterograde flow and reflux into the affected sinus also are not "benign" and may cause venous hypertension with papilledema and potential vision loss.

    They recommend that patients having arteriography for investigation of DAVFs be considered for venography and manometry. In patients in whom venous hypertension is identified, especially in the setting of only one functioning transverse sinus, a full ophthalmic evaluation should be performed, including visual acuity, visual fields and fundoscopy. Embolization should be considered if there is any indication of risk of visual loss.