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.

Idiopathic Hypertrophic Pachymeningitis Mimicking Meningioma with Occlusion of Superior Sagittal Sinus: Case Report and Review of Literature.

BACKGROUND: Idiopathic hypertrophic pachymeningitis is a rare inflammatory condition with diffuse thickening of the dura mater, which may cause a compressive effect or vascular compromise. CASE DESCRIPTION: A 40-year-old Chinese man presented with persistent headache for 6 months and a sudden epileptic seizure 2 days ago. Magnetic resonance imaging demonstrated a large (71 × 34 × 27 mm) extra-axial mass at the right frontal convexity with severe edema mimicking meningioma. The lesion and peripheral dura mater showed contrast enhancement. Additionally, the skull near the lesion was eroded. Meningioma was diagnosed, and the patient underwent surgery. During the operation, we found the lesion texture was very tough, and the superior sagittal sinus was occluded. Histopathologic findings revealed a large number of infiltrated lymphocytes with fibrosis and microabscess formation; intracranial idiopathic hypertrophic pachymeningitis was diagnosed. Follow-up magnetic resonance imaging performed 3 months after surgery demonstrated the enhancement was notably alleviated. CONCLUSIONS: Idiopathic hypertrophic pachymeningitis should be part of the differential diagnosis of some cases of meningioma.

[Cerebral venous thrombosis misinterpreted as migraine].

A 23-year-old woman with known tension-type headache and in treatment with oral contraceptives was hospitalized with headache, nausea and vomiting during two weeks. Prior to hospitalization the symptoms had been interpreted as migraine. Blood samples including D-dimer were normal. A computed tomography showed cerebral venous thrombosis (CVT), so the patient was treated with anticoagulation drugs and her symptoms remitted slowly. CVT is a dangerous condition, and the symptoms can have a fluctuating course which can mask the diagnosis. D-dimer cannot be used to exclude CVT, and attention should be paid to the risk factors.

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.

A Very Rare Cerebral Complication of Chemotherapy in a Young Girl: A Difficult Diagnosis.

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.

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.

Acquired pial and dural arteriovenous fistulae following superior sagittal sinus thrombosis in patients with protein S deficiency: a report of two cases.

Two patients with protein S deficiency with acquired multiple pial and dural arteriovenous fistulae (AVFs) following superior sagittal sinus (SSS) thrombosis are reported. Case 1 is a 38-year-old male with protein S deficiency who developed generalized seizure due to SSS thrombosis. Local fibrinolysis was achieved in the acute stage. His 10-month follow-up angiogram revealed an asymptomatic acquired dural AVF arising from the middle meningeal artery and the anterior cerebral artery with drainage to the thrombosed cortical vein in the right frontal lobe. Furthermore, his 2-year follow-up angiogram revealed a de novo pial AVF from the middle cerebral artery in the Sylvian fissure with drainage to the cortical vein initially thrombosed. However, this asymptomatic pial AVF caused bleeding in the ipsilateral cerebral hemisphere 12 years after onset, whereas the dural AVF spontaneously disappeared. Surgical disconnection was successfully performed to eliminate the source of hemorrhage. Case 2 is a 50-year-old male with a past history of SSS thrombosis with protein S deficiency who developed pulsatile tinnitus and generalized seizure. His angiogram showed a cortical dural AVF in the left parietal lobe and a sporadic dural AVF involving the right sigmoid sinus. The parietal lesion was eliminated by transarterial embolization followed by craniotomy. However, a de novo pial AVF emerged from the middle cerebral artery adjacent to the previously treated lesion. Of four cortical AVFs in two patients, thrombosis of cortical veins caused by protein S deficiency might play an important role in their formation. Long-term follow-up is required because this peculiar disorder has an unusual clinical course.

Right atrial thrombosis associated with sagittal sinus thrombosis caused by protein C-S deficiency.

Right atrial thrombi may develop within the right atrium or may have peripheral venous origins that, on their way to the final destination site lodge in, right atrium. Right atrial thrombosis is classified as two type: A (mobile, thin) and B (non mobile and attached to atrial wall) that they are probably of cardiac origin due to local pathology, indwelling catheter, atrial fibrillation, stasis, rheumatological or hematological disease like protein C or S deficiency. Protein C deficiency has been reported to be a risk factor for thrombosis in multiple organs as a result of inactivation of factor of Va. We describe a case of a huge right atrial thrombus with cerebral sagittal sinus thrombosis, in a protein C-S deficient patient, in which right atrial clot was successfully removed surgically and sagittal vein treated conservatively with full recovery of his central neurologic symptom. Magnetic Resonance Imaging demonstrated thrombosis in those regions.

Superior sagittal sinus thrombosis as a treatment complication of nonsyndromic Kleeblattschädel.

A patient with nonsyndromic Kleeblattschädel, who underwent a craniotomy involving a constricting calvarial ring and frontal calvarial remodeling, developed a superior sagittal sinus thrombosis. The superior sagittal sinus venous outflow was obstructed as a consequence of the rapid brain expansion, along with a conflict of a remaining posterior bone crest. A successful second operation was performed to remove the posterior bone crest and facilitate the venous outflow. Meticulous preoperative planning should be carried out before addressing this complex craniofacial deformity.

Transient ischaemic attack: an exceptional presenting syndrome of a superior sagittal sinus thrombosis.

We report a case of a transient ischaemic attack (TIA) as an exceptionally rare form of cerebral vein thrombosis. A 41-year-old man presented with a headache and five episodes of a transient left hemiparesis lasting approximately 10-15 min over the course of 2 weeks. Arterial origins of the disease were ruled out by detailed investigations. However, MR venography revealed a superior sagittal sinus thrombosis with numerous prominent collateral venous channels. No parenchymal lesion was seen. After medical therapy, no further transient neurological deficit occurred. Follow-up MR venography showed sinus recanalisation.

Headache in a young male: the clot thickens.

Cerebral venous sinus thrombosis  is a rare but serious cause of headache. In this report, we present a young man with poorly controlled Crohn's disease who presented with a 2-week history of headache and fluctuating left-sided sensory and motor symptoms. CT demonstrated changes consistent with either a subarachnoid haemorrhage or venous sinus thrombosis. The ensuing magnetic resonance venogram confirmed superior sagittal venous sinus thrombosis and an infarct of his right superior frontal lobe. The patient was started on low-molecular weight heparin and steroids. He required multi-disciplinary input from the stroke physicians, neurologists, gastroenterologists, dieticians and physiotherapists. He made a full neurological recovery and is now on long-term azathioprine. The purpose of this report is to highlight the consideration of venous sinus thrombosis in the diagnosis of headache and as a rare extraintestinal complication of Crohn's disease.

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.

Isolated inferior sagittal sinus thrombosis caused by a rare combination of elevated lipoprotein (a) and iron deficiency anemia.

A 21-year-old woman was admitted with right hemiparesis, bilateral papilledema, negative myoclonus of right upper extremity, and bilateral pyramidal findings. An MRI showed no venous flow in the inferior sagittal sinus. Lipoprotein a (Lp [a]) level was high and iron deficiency anemia (IDA) was found. The coexistence of IDA and Lp (a) in patients with cerebral venous thrombosis is a very rare condition in adult patients. These risk factors should be investigated in patients with cerebral venous thrombosis.

Bilateral optic disc swelling as a presenting sign of superior sagittal sinus thrombosis.

The case of a 59-year-old Caucasian man who presented with a 6-week history of intermittent blurring of vision and diplopia is reported. Fundoscopy revealed asymmetrical, bilateral optic disc swelling with peripapillary haemorrhages. An initial CT scan and D-dimer level were reported as normal. A subsequent MRI revealed a recanalising superior sagittal sinus thrombosis. Cerebral venous sinus thrombosis is a rare and potentially fatal condition. The author suggests that it should be part of the differential diagnosis of bilateral optic disc swelling and that a normal unenhanced CT scan and D-dimer would not rule out this potentially devastating condition.

An unusual case of transient cortical blindness with sagittal sinus thrombosis in a case of Henoch-Schonlein purpura.

INTRODUCTION: Henoch-Schonlein purpura (HSP) is one of the most common causes of small vessel vasculitis in children, but sometimes may have an atypical presentation. OBJECTIVE: To report an unusual case of transient cortical blindness in a patient with Henoch-Schonlein purpura. CASE: A 3-year-old female child was brought with the complaint of diffuse abdominal pain and hematochezia, which was preceded by high grade fever and cough. Three days later she developed hematuria, hematemesis, melena and hemoptysis along with palpable purpura. Four days later she became irritable and developed a few episodes of generalized tonic clonic seizure, followed by cortical blindness. The CT scan of the brain showed bilateral non-enhancing occipital hypodensity. The magnetic resonance venography showed thrombosis in transverse and sigmoid sinus. She was treated with corticosteroids and her mental status and vision improved. CONCLUSION: The HSP can cause transient cortical blindness, and recovery is good if therapy is initiated at the appropriate time.