Urokinase treatment of sagittal sinus thrombosis with venous hemorrhagic infarction

Background: Selective catheterization of the dural venous sinuses with local infusion of urokinase may be beneficial in patients with venous sinus thrombosis, and has been reported to be safe in patients with venous infarction. However, information regarding safety in the presence of hemorrhage is sparse. Methods: Three patients presented with severe, progressive focal neurological symptoms (National Institutes of Health Stroke Scales: 14, 22, and 12) resulting from superior sagittal sinus thrombosis, with evidence of hemorrhage on computed tomographic scans (two intraparenchymal, one subarachnoid). Selective venous catheterization was performed and low-dose urokinase was delivered directly into the thrombus by continuous infusion at 60,000 U/h. Intravenous heparin was administered concurrently. Results: Angiographic patency was restored in all patients. The total duration of urokinase infusion ranged from 36 to 84 hours. There was no major morbidity or mortality related to the procedure. All patients had dramatic clinical improvement during and after the course of therapy, and none had worsening of pre-existing hemorrhage. All patients were independent at 3 months, with minimal or no deficit (National Institutes of Health Stroke Scales: 2, 0, and 2). Conclusion: In selected patients with superior sagittal sinus thrombosis associated with venous hemorrhagic infarction, urokinase appears to be safe and may reverse progressive neurological deterioration. Future prospective study is warranted to further investigate this treatment option, and patients with severe deficits or pre-existing hemorrhages should not be excluded.     

Superior sagittal sinus thrombosis in a patient with protein S deficiency

A 30-year-old man presented with sagittal sinus thrombosis. He had a history of multiple thrombotic events since adolescence, and his father had had a similar history. Laboratory studies revealed the complete absence of free protein S in his plasma. Protein S deficiency, an autosomal dominant disorder, is an identifiable cause of cerebral thrombosis. The literature and our experience with this case suggest that long-term anticoagulant therapy may prevent thrombotic episodes in patients with this disorder.     

Late epileptic seizures after cerebral infarction

OBJECTIVES: To determine the profile of late epileptic seizures following cerebral infarcts and the predictive clinical and radiological factors associated with their development. METHODS: We compared 86 patients who developed late seizures after cerebral infarction with 285 similar patients who did not develop seizures for at least 1 year after their stroke. Patients who had seizures only at the onset of the stroke were excluded. Odds' ratios were used for statistical analysis. RESULTS: Simple partial, and mainly motor seizures, with or without secondary generalization, accounted for 80% of the classifiable seizures but it was not possible to determine the seizure type in half of the cases. Factors that appeared to be predictive of seizure development were the presence of large cortical infarcts and the presence of apparently preserved cerebral tissue within the infarcted area. Seizures were rare in patients with lacunar infarction but the presence of associated leukoaraiosis increased the risk. The risk was also increased in patients with other medical problems known to lower seizure threshold, such as renal failure.     

Superior sagittal sinus thrombosis after spinal anesthesia

Superior sagittal sinus thrombosis is an uncommon phenomenon that could occur in patients with a risk for thrombosis. It has been reported after spinal anesthesia with persistent cerebrospinal fluid leak. The current case is a young 29-year-old man who was complaining of persistent headache after spinal anesthesia for varicocelectomy and a new onset of blurred vision with a sign of papilledema. The diagnosis was confirmed with magnetic resonance imaging and proved to be superior sagittal sinus thrombosis. He was started on anticoagulant therapy and showed gradual improvement. No previous case has been reported in the literature in a patient without prothrombotic status risk. Received 8th January 2020. Accepted 26th March 2020.

Cerebral venous sinus thrombosis (CVT) is an uncommon alarming pathological process. Moreover, women affected more commonly than men and the incidence in annual basis is about 0.9 per 100,000.1,2 It commonly occurs secondarily to a genetic or acquired hypercoagulable state such as pregnancy, malignancy, infection, trauma, mechanical heart valve, and oral contraceptive use.3 Cerebral venous sinus thrombosis has variable clinical presentations. The most common presenting symptom is headache that can be accompanied with vomiting, papilledema, visual disturbance, and/or focal neurological syndrome such as focal neurological deficit with or without seizures. It can also associate with mental status changes such as stupor or with coma in some occasions.2,3The positional headache considered as the common presenting neurological symptoms after spinal anesthesia, and it occurs in 10 to 30% of patients. The mechanism behind it, is secondary to persistent cerebrospinal fluid leakage after epidural anesthesia. The course of the headache is usually benign in nature with almost complete recovery a few weeks. A rare complication can occur, which is secondary to brain stem compression such as subdural hygroma and neurological deficits.4 It has been reported that CVT rarely occurs in post-partum women after epidural anesthesia who have a tendency for thrombosis secondary to hypercoagulable state.4 Herein, we report a rare occurrence of superior sagittal sinus thrombosis in a healthy young man without prothrombotic status who underwent a day surgery procedure with microscopic varicocele ligation, which was performed under spinal anesthesia.     

Superior sagittal sinus thrombosis with infarction in sickle cell trait

An adolescent female with sickle cell trait presented with acute neurologic deterioration during treatment for pseudotumor cerebri. Cranial computed tomography, initially normal, subsequently revealed multiple hemorrhagic infarctions. Suspected superior sagittal sinus thrombosis was confirmed by cerebral angiography. Superior sagittal sinus thrombosis associated with sickle cell trait is exceedingly rare, and the accompanying increased intracranial pressure may require aggressive management.     

Risk and predictors of early epileptic seizures in acute cerebral venous and sinus thrombosis

We assessed the risk and determined predictors of early epileptic seizures (ES) in patients with acute cerebral venous and sinus thrombosis (CVST). A prospective series of 194 consecutive patients with acute CVST admitted to neurological wards in two German university hospitals was analysed for frequency of ES and in-hospital mortality. Demographic, clinical and radiological characteristics during the acute stage were retrospectively analysed for significant association with ES in univariate and multivariate analyses. During the acute stage, 19 patients (9.8%) died. Early symptomatic seizures were found in 86 patients (44.3%). Status epilepticus occurred in 11 patients (12.8%) of whom four died. Amongst patients with epileptic seizures, mortality was three times higher in those with status than in those without (36.4% and 12%, respectively). In multivariate logistic regression analysis, motor deficit [odds ratio (OR) 5.8; 95% CI 2.98–11.42; P  < 0.001], intracranial haemorrhage (OR 2.8; 95% CI 1.46–5.56; P  = 0.002) and cortical vein thrombosis (OR 2.9; 95% CI 1.43–5.96; P  = 0.003) were independent predictors of early epileptic seizures. Status epilepticus was an important source of morbidity and early mortality in patients with CVST in this study. Patients with focal motor deficits, cortical vein thrombosis and intracranial haemorrhage carried the highest risk for ES. Prophylactic antiepileptic treatment may be an option for these patients.     

Myelodysplastic syndrome and sagittal sinus thrombosis.

After a 5-day illness beginning with severe headache, a 46-year-old man with myelodysplastic syndrome died of complications from cerebral venous thrombosis. Considering the underlying hematologic abnormality, multiple therapies, and potential for leukemic transformation, we suggest that patients with myelodysplastic syndrome may be at increased risk for developing cerebral venous thrombosis.     

Congenital protein C deficiency and superior sagittal sinus thrombosis causing isolated intracranial hypertension.

The first case of a superior sagittal sinus thrombosis causing isolated intracranial hypertension as a result of congenital protein C deficiency is reported. Such a possibility must not be overlooked. Anticoagulation is recommended as a treatment for cerebral venous thrombosis. In the case of congenital protein C deficiency, vitamin K antagonists must be started cautiously due to the risk of skin necrosis.     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).     

矢状窦切开置管抗凝治疗颅内静脉窦血栓形成

颅内静脉窦通常因大脑的血液循环血流较快,不易造成血栓形成,但在外伤及一些高凝状态等情况下也可发生颅内静脉窦血栓形成(cranial venous sinUS thrombosis,CYST).