Sagittal sinus thrombosis with subarachnoid haemorrhage in a patient with COVID-19 infection.

A man in his late 50s was admitted with a 10-day history of right frontotemporal headache, left arm and leg weakness, and a sudden decline in visual acuity in the right eye. The patient had recent exposure to COVID-19 infection and tested positive for the same on admission. A CT scan of the head done on arrival demonstrated a subarachnoid haemorrhage in the right central sulcus with an underlying superior sagittal sinus thrombosis. No other known risk factors for central venous sinus thrombosis could be identified. The patient had a normal level of consciousness on admission clinically; however, he was in severe pain. A collective decision was made to administer anticoagulants to the patient with heparin after carefully deliberating the risk-to-benefit ratio of a superior sagittal thrombus with an associated subarachnoid haemorrhage. Our patient recovered and was discharged after 2 weeks on warfarin. We present this case to highlight the potential risks of hypercoagulable and neurotropic complications of COVID-19 infections, with special emphasis on cerebral venous thrombosis.

The role of anticoagulation for superior sagittal sinus thrombosis following craniotomy for resection of parasagittal/parafalcine meningiomas.

OBJECTIVE: The safety and efficacy of anticoagulation in managing superior sagittal sinus (SSS) thrombosis remains unclear. The present study investigated the relationship between anticoagulation and cerebrovascular complications in parasagittal/parafalcine meningioma patients presenting with post-surgical SSS thrombosis. METHODS: We analyzed 266 patients treated at a single institution between 2005 and 2020. Bivariate analysis was conducted using the Mann-Whitney U test and Fisher's exact test. Multivariate analysis was conducted using a logistic regression model. Blood thinning medications investigated included aspirin, warfarin, heparin, apixaban, rivaroxaban, and other novel oral anticoagulants (NOACs). A symptomatic SSS thrombosis was defined as a radiographically apparent thrombosis with new headaches, seizures, altered sensorium, or neurological deficits. RESULTS: Our patient cohort was majority female (67.3%) with a mean age ([Formula: see text] SD) of 58.82 [Formula: see text] 13.04 years. A total of 15 (5.6%) patients developed postoperative SSS thrombosis and 5 (1.9%) were symptomatic; 2 (0.8%) symptomatic patients received anticoagulation. None of these 15 patients developed cerebrovascular complications following observation or anticoagulative treatment of asymptomatic SSS thrombosis. While incidence of any other postoperative complications was significantly associated with SSS thrombosis in bivariate analysis (p = 0.015), this association was no longer observed in multivariate analysis (OR = 2.15, p = 0.16) when controlling for patient age, sex, and anatomical location of the tumor along the SSS. CONCLUSIONS: Our single-institution study examining the incidence of SSS thrombosis and associated risk factors highlights the need for further research efforts better prognosticate this adverse outcome. Conservative management may represent a viable treatment strategy for patients with SSS thrombosis.

Vaccine-Induced Immune Thrombotic Thrombocytopenia with Disseminated Intravascular Coagulation and Death following the ChAdOx1 nCoV-19 Vaccine.

Coronavirus is a novel human pathogen causing fulminant respiratory syndrome (COVID-19). Although COVID-19 is primarily a disease of the lungs with florid respiratory manifestations, there are increasing reports of cardiovascular, musculoskeletal, gastrointestinal, and thromboembolic complications. Developing an effective and reliable vaccine was emergently pursued to control the catastrophic spread of the global pandemic. We report a fatal case of vaccine-induced immune thrombotic thrombocytopenia (VITT) after receiving the first dose of the ChAdOx1 nCoV-19 vaccine. We attribute this fatal thrombotic condition to the vaccine due to the remarkable temporal relationship. The proposed mechanism of VITT is production of rogue antibodies against platelet factor-4 resulting in massive platelet aggregation. Healthcare providers should be aware of the possibility of such fatal complication, and the vaccine recipients should be warned about the symptoms of VITT.

A Rare Presentation of Neurobrucellosis in a 6-Year-Old Pediatric Patient with Sagittal Sinus Thrombosis.

Brucellosis is one of the most common zoonosis worldwide. It is still endemic in many regions of the world. A 6-year-old female was admitted to the emergency department (ED) due to a sudden change in consciousness, urinary incontinence, vomiting, and difficulty in walking. Neurological examination demonstrated abducens nerve paralysis, mild-to-moderate motor deficit in hemiparesis in the left arm. Brain magnetic resonance imaging showed a hemorrhagic focus at the right frontal lobe and thrombosis in the superior sagittal sinus of the brain. The diagnosis of neurobrucellosis was confirmed by identifying Brucella spp. in the blood culture on the day 6 of pediatric intensive care unit admission; thus, trimethoprim-sulfamethoxazole and rifampicin, and ceftriaxone were promptly initiated. Despite neuroprotective management and acetazolamide, the patient's neurological problems and high intracranial pressure (ICP) persisted. An external ventricular drainage tube and a Codman ICP monitor were placed to be on the consent vigilance of the patient's neurological condition. The patient's ICP continued to increase despite the current treatment regimen; therefore, a decompressive bitemporal craniectomy was performed. The ICP level of the patient returned to its normal range immediately after the craniectomy. The patient did not have any notable neurologic sequelae at the first-year follow-up. Neurobrucellosis is a rare complication of systemic brucellosis and may present as meningitis, encephalitis, myelitis, radiculitis, and/or neuritis. Herein, we describe a six-year-old girl with brucellosis complicated with cerebral vein thrombosis. This case illustrates the need for close monitoring of patients with unexplained neurological signs or symptoms for brucellosis in endemic areas.

Hyperthyroidism as a Precipitant Factor for Cerebral Venous Thrombosis: A Case Report.

Cerebral venous sinus thrombosis (CVT) is an uncommon yet serious condition. While CVT has many known precipitants and etiologies, hyperthyroidism as a precipitant of CVT is not well understood. This study reported a case of a 41-year-old male with a 4-year history of hyperthyroidism presented with seizure. Consequently, a diagnosis of superior sagittal sinus thrombosis was confirmed by computed tomography and magnetic resonance (MR) venograms. Extensive investigations yielded no apparent underlying cause, but laboratory findings were consistent with uncontrolled hyperthyroidism. The patient improved rapidly following anticoagulation. Follow-up MR and MRV scans 2 months after treatment revealed full recanalization of the superior sagittal sinus. This case report highlighted hyperthyroidism, as a procoagulant condition, resulting specifically in superior sagittal sinus thrombosis.

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.

A Case of Cerebral Venous Thrombosis and Deep Venous Thrombosis Due to Hyperthyroidism with Increased Factor VIII Activity.

A 48-year-old woman was admitted to our hospital because of headache and fever. She was diagnosed with aseptic meningitis. Five days later, she had a seizure and developed left hemiparesis. Magnetic resonance imaging showed hyperintensity in the right parietal area on fluid attenuated inversion recovery imaging. She was diagnosed as having cerebral venous thrombosis (CVT) because the suprasagittal sinus was invisible on the venographic studies. Moreover, deep venous thrombosis (DVT) was detected in her left lower extremity. Laboratory findings showed hyperthyroidism and markedly increased factor VIII activity. This is a rare case of concomitant CVT and DVT induced by high factor VIII activity due to hyperthyroidism under the presence of meningitis, an additional risk factor for thrombosis.

Dural Sinus Thrombosis with Nonsymptomatic Persistent Falcine Sinus: A Case Report.

A 24-year-old woman was admitted to our hospital after convulsive status epilepticus. A cerebral magnetic resonance venography revealed a persistent fetal falcine sinus. Additionally, the posterior third of the superior sagittal sinus was hypoplastic and the abnormal deep venous drainage was accompanied. These abnormalities had already been detected by magnetic resonance imaging several years ago. In the present scan, we discovered a sinus thrombosis in the hypoplastic superior sagittal sinus. In the cerebral angiography, we observed delayed venous return in the left parieto-occipital lobe and hypothesized that cerebral venous stasis due to the thrombus caused the convulsive status epilepticus. The patient was treated with intravenous administration of heparin along with an antiepileptic drug, and she recovered with no neurological defects. In the present case, the falcine sinus and the anomalous venous return were likely congenital while the status epilepticus was derived from thrombosis in the hypoplastic superior sagittal sinus. Although the falcine sinus functioned as an alternative pathway for the superior sagittal sinus, the hypoplastic superior sagittal sinus itself may also play an important role as a venous drainage channel.

Superior sagittal sinus thrombosis as a rare complication of spontaneous intracranial hypotension syndrome: a case report and review of the literature.

In addition to an orthostatic headache, spontaneous intracranial hypotension syndrome can lead to subdural hematoma and diffusion, subarachnoid hemorrhage, and brain sag. However, cerebral venous sinus thrombosis is rarely reported in patients with spontaneous intracranial hypotension. We present the case of a 35-year-old male who developed an orthostatic headache, nausea, vomiting, and photophobia for 5 days. An enhanced brain magnetic resonance image showed extensive linear pachymeningeal enhancement in the bilateral cerebral hemispheres. Lumbar puncture showed that cerebrospinal fluid pressure was 80 mmH2O. Subsequent magnetic resonance scans demonstrated subdural effusion of the bilateral frontoparietal lobes, hyperintense T1-weighted images, and T2WI lesions within the superior sagittal sinus in 17 days. The patient was given low molecular weight heparin and adverse events occurred. Head computed tomography showed cerebral external fluid accumulation in the bilateral frontoparietal lobes. Then, digital subtraction angiography was performed at 22 days, which confirmed superior sagittal sinus thrombosis, and the patient recovered fully after therapy. The evolution of the disease and radiological findings support the diagnosis of spontaneous intracranial hypotension with superior sagittal sinus thrombosis. To the best of our knowledge, there are very few case reports describing superior sagittal sinus thrombosis as a complication of spontaneous intracranial hypotension. When spontaneous intracranial hypotension and cerebral venous thrombosis occur together, difficult practical questions arise regarding the treatment of these two conditions.

Treatment of the superior sagittal sinus and transverse sinus thrombosis associated with intracranial hemorrhage with the mechanical thrombectomy and thrombolytics: Case report.

RATIONALE: The superior sagittal sinus (SSS) and transverse sinus are the major dural sinuses that receive a considerable amount of venous drainage. The occlusion of them has been suggested to cause intracranial hypertension, hemorrhage, and lead to potentially fatal consequences. PATIENT CONCERNS: We reported a 35-year-old woman with headache presented to our emergency department with a decreased level of consciousness and epileptic seizures. The examination of speech, higher mental function, and cranial nerve were normal. Computed tomography (CT) demonstrated both subarachnoid and intraparenchymal hemorrhage and brain edema at the right temporal lobe accompanied by high density shadow in the right transverse sinus. Digital subtraction angiography (DSA) revealed extensive thrombosis of the SSS and bilateral transverse sinus. DIAGNOSES: The SSS and transverse sinus thrombosis, accompanied by right temporal lobe hemorrhage, subarachnoid hemorrhage (SAH). INTERVENTIONS: An emergent mechanical thrombectomy by placed Solitair AB stent in the SSS, respectively, passed left and right sigmoid sinus-transverse sinus route. We removed the most clots, DSA revealed recanalization of the SSS and left transverse sinus was seen with normalization of the venous outflow, the occlusion of right transverse sinus was still present. There were 4 hours after patient back to neurosurgical intensive care unit (NICU), patient appeared anisocoria (R/L:4.0/2.5 mm), bilateral light reflexes disappeared, then we took a CT reexamination revealed intraparenchymal hemorrhage increased, brain edema was aggravated at the left temporal lobe, and mild midline shift. Subsequently, we performed decompressive hemicraniectomy and puncture the hematoma supplemented by B ultrasonic. Anticoagulation treatment was initiated 24 hours after surgery, and follow-up DSA showed gradually improved patency in the SSS and bilateral transverse sinus. OUTCOMES: Despite occlusion of the SSS and bilateral transverse sinus, patient's symptoms resolved after the operations and he was discharged without complications. LESSONS: The favorable clinical outcome after complete occlusion of the SSS and transverse sinus, accompanied by right temporal lobe hemorrhage, SAH has rarely been reported and it might be explained by our timely surgical intervention and development of compensatory cerebral collateral circulation.

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.

Sagittal sinus thrombosis in JAK2-V617F mutation without overt myeloproliferative disorder.

We describe a case of a man aged 41 years who presented with a history of generalised headaches for 1 week and an acute episode of tonic-clonic seizures. He had no history of medical illness, was non-smoker, with an extensive family history of haematological disorders. Initial CT brain with contrast did not show any abnormalities in brain parenchyma. X-ray and CT right shoulder showed shoulder dislocation secondary to trauma associated with seizure prior to hospital admission. Subsequently, MRA and MRV brain was arranged, which revealed extensive expansible occlusive filling defect dominating the middle of superior sagittal sinus with left frontal cortical and subcortical acute oedema. He was promptly started on anticoagulation therapy. Considering the unusual site and unprovoked nature of thrombosis, further investigations including JAK2 mutation were arranged which revealed latent myeloproliferative disorder. He was referred to haematology services for further follow-up and monitoring of latent myeloproliferative disorder.

Multiple Dural and Pial Arteriovenous Fistulae in a Twenty-Four-Year-Old Woman in the Setting of Superior Sagittal Sinus Thrombosis: Case Report and Review of Literature.

CASE: A 24-year-old woman presented with headache, nausea, and vomiting, and was found to have chronic superior sagittal sinus (SSS) thrombosis and multiple dural arteriovenous fistulae (dAVFs). Despite anticoagulant therapy and successful recanalization of her sinus, her fistulae persisted, and she developed additional separate pial arteriovenous fistulae (pAVFs). Her fistulae were treated with staged endovascular embolization, open clipping, and gamma knife radiosurgery over the course of 10 months. Complete resolution of SSS thrombosis and all arteriovenous fistulae (AVFs) was noted on cerebral angiogram performed 18 months from initial presentation. DISCUSSION: dAVFs have frequently been associated with venous sinus thrombosis. Sinus thrombosis resulting after endovascular or surgical treatment of dural arteriovenous fistulous connections has been reported in literature and is considered a possible complication of treatment. Multiple dAVFs and pAVFs are rare and often require multimodal staged approaches for definitive treatment. CONCLUSION: We report a case of chronic sagittal sinus thrombosis resulting in multiple AVFs requiring staged multimodal treatment with successful resolution of the fistulous connections. Furthermore, upon reviewing the literature addressing multiple dAVFs and the treatment of such lesions using endovascular, microsurgical, and stereotactic radiosurgery techniques, we elucidate the success a multimodal approach to therapy can afford for the unique challenges associated with multiple lesions.

Papiledema secundario a trombosis del seno sagital superior. Cuadro paraneoplásico de un linfoma del manto / Papilledema secondary to a superior sagittal sinus thrombosis. Mantle cell lymphoma paraneoplastic syndrome

CASO CLÍNICO: Se presenta el caso de un varón de 46 años con disminución de la visión del ojo izquierdo de meses de evolución. Se diagnostica de papiledema por trombosis del seno sagital superior gracias a la angiorresonancia. En busca de la etiología de la trombosis se descubre un linfoma del manto. DISCUSIÓN: La trombosis venosa cerebral es una causa poco frecuente de papiledema. Puede deberse a cuadros de hiperviscosidad en el contexto de un síndrome paraneoplásico

CLINICAL CASE: A 46 year old patient presented with visual loss in the left eye during the previous months. Ophthalmoscopic examination and magnetic resonance angiography found the presence of papilledema due to thrombosis in superior sagittal sinus. The examination findings revealed a mantle cell lymphoma. DISCUSSION: Cerebral venous thrombosis is an unusual cause of papilledema. This type of thrombosis may be secondary to hyper-viscosity within a context of a paraneoplastic síndrome

Superior Sagittal Sinus Thrombosis Related to the Use of Tamoxifen: A Case Report and Review of Literature.

Tamoxifen is a selective estrogen- receptor modulator commonly associated with an increased risk of thrombotic events, including cere- bral venous thrombosis. Ihe superior sagittal sinus appears to be the most affected site of cerebral venous thrombosis in patients with a history of malignancy. However, the underlying mechanism of tamoxifen- induced hypercoagulability and location of cerebral venous thrombosis are notwellunderstood. Here, we present a case of a 47-year-old female with a history of breast cancer, on tamoxifen for 10 months, found to have superior sagittal sinus thrombosis with additional thrombosis of the draining cortical veins. Furthermore, we review similar cases published in literature. We recommend that physicians should be aware ofthe potential of developing superior sagittal sinus thrombosis in patients who take tamoxifen and warn patients of this adverse event when prescribing the medication.

[Progressive Intracranial Hypertension due to Superior Sagittal Sinus Thrombosis Following Mild Head Trauma: A Case Report].

Cerebral venous sinus thrombosis after mild head trauma without skull fracture or intracranial hematoma is exceptionally rare. We describe an unusual case of progressive intracranial hypertension due to superior sagittal sinus thrombosis following mild head trauma. A 17-year-old boy presented with nape pain a day after a head blow during a gymnastics competition (backward double somersault). On admission, he showed no neurological deficit. CT scans revealed no skull fractures, and there were no abnormalities in the brain parenchyma. However, his headache worsened day-by-day and he had begun to vomit. Lumbar puncture was performed on Day 6, and the opening pressure was 40 cm of water. After tapping 20 mL, he felt better and the headache diminished for a few hours. MR venography performed on Day 8 revealed severe flow disturbance in the posterior third of the superior sagittal sinus with multiple venous collaterals. Because of the beneficial effects of lumbar puncture, we decided to manage his symptoms of intracranial hypertension conservatively with repeated lumbar puncture and administration of glycerol. After 7 days of conservative treatment, his symptoms resolved completely, and he was discharged from the hospital. Follow-up MR venography performed on Day 55 showed complete recanalization of the superior sagittal sinus. The exact mechanism of sinus thrombosis in this case is not clear, but we speculate that endothelial damage caused by shearing stress because of strong rotational acceleration or direct impact to the superior sagittal sinus wall may have initiated thrombus formation.

Cerebral venous thrombosis as a complication of neuropsychiatric systemic lupus erythematosus.

A 51-year-old woman undergoing steroid treatment for systemic lupus erythematosus (SLE) was admitted to our hospital after developing a fever, consciousness disturbance and seizures, leading to a diagnosis of SLE-induced meningoencephalitis. Although steroid therapy improved her symptoms, she complained of post-lumbar puncture thunderclap headaches during follow-up, and cerebral venous thrombosis (CVT) was subsequently diagnosed on magnetic resonance venography and cerebral angiography. This is a rare case of neuropsychiatric SLE complicated by CVT during treatment for aseptic meningoencephalitis. The onset of aseptic meningoencephalitis and administration of the lumbar puncture and steroid therapy may have induced the development of the patient's CVT symptoms.