OBJECTIVE: To characterize the neuro-ophthalmologic manifestations of impaired cranial venous outflow. DESIGN: A retrospective study of 20 patients who developed increased intracranial pressure as the result of impaired cerebral drainage. SETTING: Three neuro-ophthalmologic referral centers. PATIENTS: Ten patients had noncompressive thrombosis of sagittal or lateral sinuses (noncompressive group), four had compression of the sagittal sinus or jugular veins (compressive group), and six had transient sinus thrombosis following surgical procedures (iatrogenic group). INTERVENTIONS: Medical and/or surgical treatment of increased intracranial pressure and of underlying conditions predisposing to venous obstruction. MAIN OUTCOME MEASURES: Symptoms (headache and esodeviation) and signs (visual acuity, visual fields, and optic disc appearance) of increased intracranial pressure. RESULTS: Headache was more severe, esodeviation was more prevalent, and onset was more abrupt in the noncompressive group than in the compressive and iatrogenic groups. Among the 10 patients with noncompressive thrombosis, factors predisposing to thrombosis were present in seven patients but sometimes overlooked. Following treatment, visual outcome was generally favorable in all three groups. All patients had 20/30 or better visual acuity in at least one eye, and substantial visual field loss was present in both eyes of only two patients. CONCLUSIONS: The clinical manifestation of impaired cerebral venous outflow vary depending on the underlying mechanism. Although most patients maintain good vision, more aggressive treatment is sometimes indicated in patients with thrombosis or compression. The abrupt onset and marked severity of symptoms in patients with thrombosis should help to differentiate these patients from those with idiopathic intracranial hypertension.
OBJECTIVE: To characterize the neuro-ophthalmologic manifestations of impaired cranial venous outflow. DESIGN: A retrospective study of 20 patients who developed increased intracranial pressure as the result of impaired cerebral drainage. SETTING: Three neuro-ophthalmologic referral centers. PATIENTS: Ten patients had noncompressive thrombosis of sagittal or lateral sinuses (noncompressive group), four had compression of the sagittal sinus or jugular veins (compressive group), and six had transient sinus thrombosis following surgical procedures (iatrogenic group). INTERVENTIONS: Medical and/or surgical treatment of increased intracranial pressure and of underlying conditions predisposing to venous obstruction. MAIN OUTCOME MEASURES: Symptoms (headache and esodeviation) and signs (visual acuity, visual fields, and optic disc appearance) of increased intracranial pressure. RESULTS:Headache was more severe, esodeviation was more prevalent, and onset was more abrupt in the noncompressive group than in the compressive and iatrogenic groups. Among the 10 patients with noncompressive thrombosis, factors predisposing to thrombosis were present in seven patients but sometimes overlooked. Following treatment, visual outcome was generally favorable in all three groups. All patients had 20/30 or better visual acuity in at least one eye, and substantial visual field loss was present in both eyes of only two patients. CONCLUSIONS: The clinical manifestation of impaired cerebral venous outflow vary depending on the underlying mechanism. Although most patients maintain good vision, more aggressive treatment is sometimes indicated in patients with thrombosis or compression. The abrupt onset and marked severity of symptoms in patients with thrombosis should help to differentiate these patients from those with idiopathic intracranial hypertension.