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Using ferric chloride (FeCl3) to induce experimental superior sagittal sinus (SSS) thrombosis might interfere with magnetic resonance imaging (MRI)-assisted visualization and evaluation of the thrombus, the brain parenchyma, and the quality of the occlusion. The aim of this study was to investigate whether aluminum chloride (AlCl3)-induced thrombosis of the SSS has comparable properties to those of FeCl3 without causing artifacts in MRI. SSS thrombosis was induced in 14 male Wistar rats by exposure of the SSS and subsequent topical application of a filter paper strip soaked in AlCl3 (n = 7) or FeCl3 (n = 7) over a period of 15 min. The animals with AlCl3-induced SSS thrombosis showed a constant and complete occlusion with in histological analysis large thrombi. Blood flow measurements indicated a significant reduction on the first and seventh postoperative day compared to preoperative measurements. MRI enabled visualization and subsequent evaluation of the thrombus and the surrounding parenchyma. In comparison, FeCl3-induced SSS thrombosis could not be evaluated by MRI due to artifacts caused by the paramagnetic properties and increased susceptibility of FeCl3. The occluded sinus and the surrounding area appeared hypointense. The quality of SSS occlusion by AlCl3 was comparable to that of FeCl3. AlCl3 therefore represents a significant alternative substance in experimental SSS thrombosis ideally suited for studies using MRI., (© 2024. The Author(s).)

Rationale: Cosmetic hyaluronic acid injections for facial soft tissue augmentation are gaining popularity because of their convenience and favorable outcomes. Several associated complications have been described; however, ophthalmic artery occlusion (OAO) combined with superior sagittal sinus thrombosis (SSST) has been rarely reported., Patient Concerns: A 21-year-old woman presented with sudden loss of vision and severe pain in the left eye, right upper limb weakness, and headache immediately after hyaluronic acid injection on the left side of her forehead., Diagnosis: Clinical manifestations and multimodal imaging, including spectral-domain optical coherence tomography, fundus fluorescein angiography, and digital subtraction angiography, indicated OAO and SSST., Interventions: Various clinical examinations were performed, and the patient was treated by thrombolysis, corticosteroids, oxygen therapy, a formula for the nourishment of the optic nerve, and measures for improving the microcirculation., Outcomes: The treatment response was closely observed. The intracerebral hemorrhages were absorbed after 2 weeks of treatment, while the clinical manifestations, including ocular pain, headache, and limb dysfunction, were gradually alleviated. However, the visual acuity in the left eye remained at no light perception., Lessons: Cosmetic hyaluronic acid injection can result in emergent and catastrophic complications that require immediate treatment. Thus, the development of appropriate prevention and management protocols for such scenarios is considered crucial.

Superior sagittal sinus thrombosis (SSST) is a very rare but life-threatening complication in leukemia patients. SSST is very rare in acute myeloid leukemia (AML). In leukemia patients, several risk factors for SSST have been reported such as administration of L-asparaginase, disseminated intravascular coagulation, congenital thrombophilia, meningeal leukemia, and intrathecal chemotherapy (IT). Lumbar puncture itself and corticosteroid administration have also been acknowledged as risk factors. We describe herein our clinical experience with SSST in a 29-year-old Japanese man suffering from AML with t(8;21)(q22;q22), who presented with abrupt onset of loss of consciousness, left hemiplegia, and seizure soon after IT and high-dose cytarabine (HD-AraC) with dexamethasone for post remission consolidation. Despite the presence of intracranial hemorrhage (ICH) due to SSST rupture, we conducted anticoagulant therapy with heparin. Although ICH worsened temporarily, his clinical condition gradually improved with resolution of the SSST, and he eventually became fully ambulatory. There were no deficiencies of natural anticoagulants. Three additional cycles of HD-AraC without IT therapy were conducted, but no neurological complications recurred with the concomitant use of warfarin. He was discharged free of neurological deficits. In our case, there is a possibility that IT and the administration of corticosteroids along with HD-AraC triggered SSST.

Background: Oral contraceptive pills (OCPs) are a well-established precipitant of thrombosis. The local release of hormone from the vaginal ring still results in systemic administration and therefore predisposes users to increased risk of venous thrombosis. Although representing only 1% of strokes, cerebral venous sinus thrombosis is eight times more likely in women taking OCPs than in nonusers, and the incidence of cerebral venous sinus thrombosis associated with the vaginal ring is unknown but is likely to be increased., Cases: We report four cases of cerebral venous sinus thrombosis in women using hormonal vaginal rings with negative thrombophilia testing who presented to our facility over a 2-year period. Three of the four women required mechanical thrombectomy in addition to anticoagulation, but all four women recovered and were discharged home with minimal or no neurologic deficits., Conclusions: Increased recognition of the thrombogenic potential of hormonal vaginal rings may promote earlier venous imaging and result in better clinical outcomes.

Sagittal sinus thrombosis (SST) induced by chemotherapy is exceptional. We describe here a new case following the fourth cure of chemotherapy based on cisplatin, bleomycin and etoposide in a 16-year-old patient with no obvious risk factors. Through this uncommon case which forms part of cerebral venous sinus thrombosis (CVST), we propose to study the pathophysiology, the diagnosis and the management of this entity. The exclusion of the other causes of CVST is important not only for the therapeutic implication but also for the prognosis. Then, accurate documentation of each case induced by chemotherapy is needed to further understanding.

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., (Copyright 2009 Elsevier Masson SAS. All rights reserved.)

A 16-year-old girl was diagnosed with widely distributed dural sinus thrombosis (DST) and a haemorrhagic infarct in the left parietal lobe. Despite of heparin treatment, pronounced aggravation of symptoms was observed. Through a femoral vein approach a micro-catheter was advanced into the superior sagittal sinus and rt-PA was infused slowly, directly into the thrombus over 24 hours. A follow up angiogram showed recanalisation of sinus. The patient recovered almost completely, with only few remaining cognitive symptoms. This treatment remains experimental, but should be kept in mind for DST-patients unresponsive to heparin treatment.

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.

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.

Objective: The causes of cerebral sinus and vein occlusion and the accompanying parenchymal changes remain largely unexplained. The clinical variability and low incidence of the disease complicate systematic clinical investigations. Animal studies are indispensable; however, existing animal models of sinus thrombosis do not allow for long-term follow-up studies and are not suitable for pharmacological recanalization because sinus thrombosis is induced by ligation and injection of thrombogenic substances and does not resemble sinus thrombosis in humans., Methods: We induced thrombosis of the superior sagittal sinus (SSS) by careful topical application of ferric chloride onto the SSS of rats, leading to highly reproducible occlusions. Magnetic resonance imaging was performed immediately after initiation of thrombosis and on postoperative Days 1, 2, and 7. Diffusion- and T2-weighted images allowed for calculation of the apparent diffusion coefficient and T2 relaxation time. Vascular status was assessed by venous magnetic resonance angiography. Neurological deficits were assessed with the rotarod test., Results: Seven days after induction of thrombosis, partial recanalization (50.7% of the SSS remaining occluded) was accompanied by a resolution of early generalized changes of the apparent diffusion coefficient and of T2 relaxation time, indicating edema of the entire brain parenchyma. Compared with sham-treated animals, clinical skills in the experimental group improved over time, which was statistically independent from the degree of recanalization. Histopathological analysis revealed no signs of cerebral infarction., Conclusion: This is the first animal model of SSS thrombosis that offers the possibility to investigate pathophysiological aspects of the disease as well as the influence of therapy on the nature of disease progression.

Background: Cerebral venous sinus thrombosis is an infrequent disease with a variety of causes. Pregnancy, puerperium, contraceptive pills and intracranial infections are the most common causes. The patient may present with headache, focal neurological deficits and seizures.The clinical outcome is highly variable and treatment with heparin is advised., Case Presentation: The patient is a 22 year old male who presented with headache, repeated vomiting and papilledema.He was a bodybuilder doing exercise since 5 years ago, who had used nandrolone decaonoate 25 milligrams intramuscularly during the previous 5 months. Brain MRI and MRV showed superior sagital and transverse sinus thrombosis and extensive investigations did not reveal any known cause., Conclusions: We suggested that androgen was the predisposing factor in our patient. Androgens may increase coagulation factors or platelet activity and cause arterial or venous thrombosis. As athletes may hide using androgens it should be considered as a predisposing factor for thrombotic events in such patients.

A 55-year-old man, who had been medicated with carbamazepine, phenobarbital, and sodium valproate for 12 years' duration, presented with severe headache, nausea, and transient diplopia. The neurological examination revealed mild disturbance of consciousness and postural tremor. He also complained of severe continuous headache but no throbbing pain. Enhanced head CT showed empty delta sign and irregular pooling of contrast agent around the superior sagittal sinus. Head MRI did not show the flow void in the superior sagittal sinus. Cerebral angiography demonstrated incomplete occlusion of the superior sagittal sinus and well-developed colateral channels. He was diagnosed having superior sagittal sinus thrombosis, and was placed on anticoagulant and antiplatelet drugs. He did not have any other risk factors such as inflammatory disease, infection, malignancy, and oral contraceptives. However, he had been medicated with some anticonvulsants including carbamazepine, which is known to induce venous thrombosis in the leg. Therefore, the association between superior sagittal sinus thrombosis and long term medication with carbamazepine was suspected. This is the first case report of anticonvulsant-associated cerebral venous thrombosis. It suggests that long-term medication with carbamazepine should be considered to be one of the risk factors for cerebral venous thrombosis.