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.

Congenital dysfibrinogenemia in a Japanese family with fibrinogen Naples (BßAla68Thr) manifesting as superior sagittal sinus thrombosis.

: Congenital dysfibrinogenemia refers to the presence of a dysfunctional fibrinogen molecule, typically because of mutations in the fibrinogen gene. About 20% of fibrinogen gene mutations are responsible for thrombosis. Here, we described the case of a 17-year-old Japanese boy, who had a sudden stroke because of superior sagittal sinus thrombosis associated with dysfibrinogenemia. Genetic testing confirmed the presence of homozygous fibrinogen Naples (BßAla68Thr) mutation, which was previously reported as a causative mutation for thrombotic dysfibrinogenemia only in an Italian family. In this Japanese family, the patient's 12-year-old asymptomatic sister was also homozygous for this mutation. She, like her brother, was started on warfarin therapy. This report highlights the occurrence of fibrinogen Naples that has caused severe thrombotic complications in a young member of a Japanese family.

Comparison of anticoagulation and thrombolysis treatments in a rat model of superior sagittal sinus thrombosis.

Superior sagittal sinus thrombosis (SSST) is a form of cerebral venous sinus thrombosis (CVST) routinely treated with anticoagulation therapy. Anticoagulation and thrombolysis treatment effects on neurological function, venous recanalization and brain edema were compared after SSST in rats. Male Sprague-Dawley rats underwent non-fatal SSST induction and were divided into no treatment (control), anticoagulation (heparin), carotid artery thrombolysis and local thrombolysis groups (each n = 50). Within each group, an equal number of rats (n = 10) were treated with anticoagulation and thrombolysis at day 3 or weeks 1, 2, 3 or 4 following SSST. Magnetic resonance venography (MRV) was conducted within 24 h of anticoagulation and thrombolysis treatments to determine recanalization, structural abnormalities and cerebral edema quantitated by wet-dry methods. Neurological function (Rotarod test) and histological abnormalities were compared. Severe brain edema, flattened gyri and coronal swelling were observed following SSST. Recanalization rates in carotid artery and local thrombolysis were higher than in anticoagulation (both p < 0.001). Carotid artery and local thrombolysis brain water contents were 79.6±0.1% and 79.2±0.1%, respectively, significantly lower than 83.9±0.1% and 84±0.1% in anticoagulation and controls, respectively (all p < 0.05), after treatments at day 3 following SSST. Increasing SSST onset to treatment time worsened neurological function ( p < 0.05). Maximum treatment benefits were observed <2 weeks post-SSST using local thrombolysis and, to a lesser extent, carotid artery thrombolysis. Thrombolysis may produce better functional outcomes if employed early rather than as a second-line treatment following anticoagulant failure.

A new thrombosis model of the superior sagittal sinus involving cortical veins.

OBJECTIVE: Patients with cerebral sinus and cortical venous thrombosis develop venous infarcts in approximately 50% of cases, resulting in serious clinical symptoms. An animal model is needed to further clarify the underlying mechanisms and consequences surrounding cerebral venous sinus thrombosis, particularly for severe ones. METHODS: Adult male Sprague-Dawley rats were used to develop a new superior sagittal sinus thrombosis model involving cortical veins. The superior sagittal sinus was exposed and ligated. A microcatheter was inserted into the sinus, then both common carotid arteries were temporary occluded to reduce cerebral blood flow, and thrombin was injected into the sinus. Twenty-four hours later, after evaluating neurological function and obtaining a magnetic resonance imaging, animals were sacrificed and data pertaining to brain water content, infarct volume, and tissue histology was collected. RESULTS: Superior sagittal sinus thrombosis and brain infarction were detected in all rats (100%). Hemorrhagic infarction, when present, and brain edema were observed in the brain parenchyma of the parietal lobe. The rate of hemorrhage was 59%, which is similar to that seen clinically in patients with superior sagittal sinus thrombosis. Brain edema, as measured by brain water content percentage, was significantly increased in thrombosed animals compared with sham-operated animals (80.8% ± 0.55% vs. 78.8% ± 0.14%, P < 0.05). Infarct volumes were 53.02 ± 7.91 mm(3). CONCLUSIONS: We suggest that our modified model of superior sagittal sinus thrombosis, involving cortical veins, is suitable for the study of its underlying mechanisms, as well as therapeutic approaches directed at the disease.

In utero magnetic resonance imaging for diagnosis of dural venous sinus ectasia with thrombosis in the fetus.

BACKGROUND: Dural venous sinus ectasia with thrombosis (DVSET) in the fetus is a rare condition that can be diagnosed prenatally with the use of fetal MR imaging, yet with limited indication of long-term clinical significance. OBJECTIVE: To describe and evaluate the diagnostic value of fetal MR imaging in the prenatal diagnosis of dural venous sinus ectasia with thrombosis and its clinical significance. MATERIALS AND METHODS: We report a series of nine fetuses with dural venous sinus ectasia with thrombosis. The mothers, located in four feto-maternal centres, were referred for fetal MR imaging due to space occupying lesions identified on second-trimester antenatal ultrasound. RESULTS: In all but one case the dural venous sinus ectasia with thrombosis was in the vicinity of the venous confluence (VC) with various extension in the posterior dural sinuses. Antenatal follow-up imaging was performed in seven cases and showed progression in one, stable appearances in one and regression in five cases. Three pregnancies were terminated. In the remaining six cases there was no reported neurological deficit at up to 44 months of clinical follow-up. CONCLUSION: This is among the largest series of postnatal clinical follow-up in cases of prenatal diagnosis of dural venous sinus ectasia with thrombosis in the literature. Clinical follow-up suggests a good prognosis when antenatal follow-up shows partial or complete thrombus resolution.

Post-traumatic sagittal sinus thrombosis: case report.

Post-traumatic superior sagittal sinus thrombosis is rare. The usual presentation is raised intracranial pressure symptoms. We report a case of post-traumatic superior sagittal sinus thrombosis in which the computed tomography (CT) scan revealed depressed fracture of the vertex with parasagittal contusions. Despite surgical elevation of the fracture and repair of the superior sagittal sinus, the patient developed thrombosis of the anterior half of the superior sagittal sinus with bilateral hemorrhagic infarcts in the motor strip. This case is reported for its rarity and to highlight the importance of careful postoperative observation of such patients. In such settings, timely diagnosis and anticoagulant therapy are rewarding.

Sinus thrombosis in a patient with intracranial hypotension: a suggested hypothesis of venous stasis. a case report.

We describe the case of a 26-year-old man with orthostatic headache. Cerebral angiography revealed thrombosis in the sagittal sinus. Spine MRI showed cerebrospinal fluid collection at the C1-2 level. We performed blood patch and the symptoms disappeared. We report a rare case of intracranial hypotension caused by CSF leak and describe our hypothesis that SIH can change the velocity of cerebral blood flow and cause thrombosis.

Development of a new model of transvenous thrombosis in the pig superior sagittal sinus using thrombin injection and balloon occlusion.

PURPOSE: To establish an experimental model of superior sagittal sinus (SSS) thrombosis using a transvenous route, and thrombin and balloon occlusion, in pigs. METHODS: The SSS was catheterized transvenously in six pigs. Thrombin was injected into the pigs' SSS to induce thrombosis. Magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) confirmed successful SSS thrombosis. MRI and MRV were also used to observe the evolution of thrombus and accompanying brain parenchymal changes before thrombus induction postoperatively on Days 1, 3, and 7. The pigs were sacrificed for histological examination at the follow-up. RESULTS: SSS thrombosis was successfully achieved in all six pigs. On Day 1 postoperatively, MRV confirmed SSS thrombosis and MRI revealed brain edema in each animal. On Day 3, venous infarction was noted in two cases, one of which appeared to be hemorrhagic. On Day 7, MRV showed partial recanalization of the SSS in one pig. Brain edema was significantly relieved in four cases while, in two other cases, the extent of venous infarction was reduced. Histological examination confirmed SSS thrombosis in all animals, with recanalization in only one case. In two of the animals, bilateral parasagittal infarction was seen, including one with petechial hemorrhage. In the other four animals, bilateral parasagittal edema was observed. CONCLUSION: The development of an experimental model of SSS via the transvenous route is feasible in pigs using thrombin and balloon occlusion. This model closely resembles SSS thrombosis in humans, and can be applied in the clinical study of this phenomenon as well as in clinical therapeutic applications.

Protein S deficiency, epileptic seizures, sagittal sinus thrombosis and hemorrhagic infarction after ingestion of dimenhydrinate.

Congenital protein S deficiency is associated with an increased risk of venous thrombosis. A14-year-old boy presented with epileptic seizures and thrombosis of the superior sagittal sinus and frontal hemorrhagic venous infarction after ingestion of 50 mg of dimenhydrinate, an antiemetic drug. The patient was found to be heterozygous for the factor V Leiden mutation and had a functional protein S deficiency. He recovered completely within a month after conservative treatment. Dimenhydrinate may have disrupted a subclinical pre-existing condition in this case.

Thrombosis of sinus sagitalis during puerperium caused by thrombophilic gene mutation.

Cerebral veno-sinus thrombosis (CVT) during puerperium may have fatal consequences. A nonspecific clinical picture must be complete with computed tomography of the brain and digital substract angiography of the brain blood vessels, and, once the clinical diagnosis is confirmed, coagulation tests and genetic analysis of the coagulation factor are to be made as well. Genetic polymorphisms associated with thrombophilia such as factor V Leiden, prothrombin G20210A, MTHFR C677T, ACE and PIA1/A2 may be the cause of the hypercoagulability that results in CVT.

A new model of reversible superior sagittal sinus thrombosis in rats.

To investigate the characteristics of the thrombus at different time points after thrombosis of the intracranial venous sinus, we have developed a new reversible superior sagittal sinus (SSS) model in rats. In this new model, thrombosis was induced by slow injections of the thrombogenic agent into the SSS using a microcatheter. The success of SSS thrombosis was confirmed by magnetic resonance images (MRI), magnetic resonance venographs (MRV), and electron microscopy. T2-weighted MRI and MRV were performed every week for 4 weeks to investigate the process of SSS occlusion. We also examined thrombus formation and the surrounding tissue pathology, as well as endothelial cell injury following SSS occlusion. SSS occlusion occurred at the beginning of the injection of the partial thromboplastin time reagent, and the occluded SSS reopened at the beginning of the second week. MRI images revealed that T2 signals were detected in the parieto-occipital lobes 24 h after SSS thrombosis and disappeared at the end of week two. During week two, the rate of thrombus organization was evident and increased significantly in week three. Thrombus calcification was detected in week three and increased significantly in week four. Electron microscopy examination showed the damaged endothelial cell detected at week three following SSS thrombosis. All of these findings suggest that this reversible SSS thrombosis model is feasible and reproducible. The occlusion state can be maintained for at least 4 weeks, providing an opportunity to study the mechanisms of SSS thrombosis.

Superior sagittal sinus thrombosis and bilateral sixth-nerve palsy in a child with nephrotic syndrome.

We report on a patient with nephrotic syndrome who developed superior sagittal sinus thrombosis. He presented with double vision due to bilateral sixth-nerve palsy and papilledema. The thrombosis resolved with intravenous heparin and oral corticosteroids. A month later there were no signs of ocular movement paresis, and both optic nerves were normal.

[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis].

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.

Chronic superior sagittal sinus thrombosis with phlebosclerotic changes of the subarachnoid and intracerebral veins.

An autopsy case of chronic thrombotic occlusion of the superior sagittal sinus (SSS) with an unusually protracted clinical course is reported. The patient was an 84-year-old man without any predisposing conditions for thrombosis. The clinical features were atypical and were characterized by recurrent cerebral subcortical hemorrhages. The autopsy revealed a large, organized thrombus in the SSS and extensive hemorrhagic infarction of the bilateral parasagittal region of the cerebral hemispheres. The hemorrhagic infarction was comprised of the aggregation of numerous minute foci of coagulation necrosis associated with petechial hemorrhages. Marked phlebosclerotic changes were observed in the subarachnoid and intracerebral veins, which were considered to be reactive changes of the venous walls against a persistent elevation in peripheral venous pressure caused by thrombosis of the SSS.