Superior sagittal sinus thrombosis: A clinical and experimental study

Sinus-vein thrombosis is increasingly recognized as a much more frequent ne urological disorder than was anticipated before. We examined the pathophysi ology of superior sagittal sinus thrombosis (SSST) from 19 patients and a r at SSST model. We treated 19 cases with SSST who were diagnosed by angiogra phy. The symptoms of nine patients: who suffered multiple intracerebral hem orrhage: were abrupt. In another ten patients who recovered satisfactorily, the condition progressed slowly and they were treated with heparin and uro kinase, Multivariate analysis demonstrated that female, sudden onset (<24 h ours) and posterior 1/3 occlusion are related to bad outcome. Experimentall y, SSST was induced by ligation and slow injection of kaolin-cephalin suspe nsion into SSS in rats. Regional cerebral blood flow (rCBF) and tissue hemo globin oxygen saturation (Hb Sao,) using a "scanning" technique were measur ed at 48 locations, and fluorescence angiography was performed before and u ntil 90 min after SSST induction. After 48 hours the animals were sacrifice d for histological studies. Decrease of rCBF and tissue Hb SO2 and brain da mage were seen in group B (n = 10) with an extension of thrombosis from SSS into cortical veins. Brain injury was not observed in group A (n = 8) with SSS thrombus alone and sham-operated animals (n = 5). In conclusion, a bra in with acute extension of thrombus from SSS into cortical veins becomes cr itical for cerebral blood supply and metabolism. CBE tissue HbSO(2) and rep eated angiography can be helpful monitors for the early detection of critic al conditions after SSST. As to the therapy, restraint on the ongoing throm bus is essential to protect the brain with SSST, and we encourage the use o f combination therapy of heparin and urokinase as early as possible in case s without intracerebral hemorrhage.