RESUMO
BACKGROUND: Cerebral venous sinus thrombosis (CVST) can infrequently lead to chronical intracranial hypertension (IH) due to the altered venous drainage. The aim of this study was to ascertain the risk of IH after CVST and to stratify underlying risk factors. METHODS: We performed a retrospective cohort analysis of all cases treated for acute CVST at our department between 2013 and 2019. IH was diagnosed at follow-up according to the modified Dandy criteria. CVST-patients with and without IH were descriptively compared conforming to available clinical and radiological data as well as outcomes. RESULTS: Our study included 102 patients with acute CVST. In 70 cases complete follow-up data was available (68.6%). Seven of these patients developed symptomatic intracranial hypertension (10%; N = 7, n = 70) within a median follow-up of 6 months. Four of these patients (57.1% (N = 4, n = 7) vs. 3.2% (N = 2, n = 63); p < 0.001) presented recurrent sinus thrombosis in the further course. There were no significant differences between patients with or without IH concerning gender, age, risk factors, occluded vessels and treatment for their CVST. However the presence of visual deterioration at initial admission was higher in patients who developed IH afterwards (57.1% (N = 4, n = 7) vs. 20.6% (N = 13, n = 63); p = 0.03). Patients with chronic IH after CVST showed significantly less likely recanalization of the occluded vessel on follow-up MRI (no recanalization in 28.6% (N = 2, n = 7) vs. 4.8% (N = 3, n = 63); p = 0.02). All patients with IH had a good outcome (mRS 0-2) at discharge and follow-up. CONCLUSION: IH occurred in around 10% after CVST. Insufficient recanalization status may facilitate IH. Patients with visual disturbances seem to develop more likely IH afterwards. Patients who present IH after CVST may develop recurrent cerebral venous thrombosis.
RESUMO
BACKGROUND AND PURPOSE: Thrombosis of cerebral veins and sinus (cerebral venous thrombosis) is a rare stroke pathogenesis. Pharmaceutical treatment is restricted to heparin and oral anticoagulation with vitamin K antagonists (VKAs). METHODS: Between January 2012 and December 2013, we recorded data from our patients with cerebral venous thrombosis. The modified Rankin scale was used to assess clinical severity; excellent outcome was defined as modified Rankin scale 0 to 1. Recanalization was assessed on follow-up MR angiography. Patients were then divided into 2 treatment groups: phenprocoumon (VKA) and a novel factor Xa inhibitor. Clinical and radiological baseline data, outcome, recanalization status, and complications were retrospectively compared. RESULTS: Sixteen patients were included, and 7 were treated with rivaroxaban. Overall outcome was excellent in 93.8%, and all patients showed at least partial recanalization. No statistical significant differences were found between the groups, except the use of heparin before start of oral anticoagulation (P=0.03). One patient in the VKA and 2 patients in the factor Xa inhibitor group had minor bleeding (P=0.55) within the median (range) follow-up of 8 months (5-26). CONCLUSIONS: Factor Xa inhibitor showed a similar clinical benefit as VKA in the treatment of cerebral venous thrombosis. Further systematic prospective evaluation is warranted.
