Cases reported "Intracranial Thrombosis"

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1/6. Emergent decompressive craniectomy in patients with fixed dilated pupils due to cerebral venous and dural sinus thrombosis: report of three cases.

    OBJECTIVE AND IMPORTANCE: Cerebral venous and dural sinus thrombosis is a rare cause of stroke. Although morbidity and mortality have greatly decreased in recent years as a result of early diagnosis and timely medical treatment, when coma occurs the prognosis remains poor. We evaluated whether emergent decompressive craniectomy has a role in the treatment of patients with brain herniation from dural sinus thrombosis and hemorrhagic infarct. CLINICAL PRESENTATION: Three patients developed large hemorrhagic infarct with coma and bilaterally fixed and dilated pupils resulting from aseptic dural sinus thrombosis. INTERVENTION: Two patients underwent emergent surgical decompression as soon as brain herniation developed, and these patients had complete functional recovery. One underwent delayed surgical decompression and remained severely disabled. CONCLUSION: Our results provide preliminary evidence that emergent decompressive craniectomy is effective in patients with brain herniation from dural sinus thrombosis, provided that the clinical onset is recent. We therefore recommend consideration of this aggressive surgical technique for such patients, who may survive with good outcomes.
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2/6. Disseminated cerebral thrombotic microangiopathy in a patient with adult's still disease.

    OBJECTIVE: The aim of this report is to describe a fatal disseminated thrombotic micoangiopathy with renal, pancreatic, and cerebral involvement in a patient with recently diagnosed adult's Still disease (ASD). CASE REPORT: A previously healthy 15 year old girl was admitted to our hospital. According to the clinical and laboratory data the diagnosis of adult's still disease was established. The treatment was begun and few days after an initial improvement a sudden neurologic deterioration with coma and seizures has occurred. Hours later the patient died. Clinical, laboratorial, and pathologic data will be presented. CONCLUSION: To our knowledge this is the second description of a fatal disseminated cerebral thrombotic microangiopathy in a patient with adult's Still disease, but with a much more fulminating evolution than previously reported. Some etiopathogenic mechanisms could be shared in these two disorders explaining this coexistence.
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3/6. Cerebral venous and dural sinus thrombosis in severe falciparum malaria.

    Common causes of coma in falciparum malaria are cerebral malaria, hypoglycaemia and electrolyte disturbances. Focal deficits due to arterial infarcts may sometimes occur in children, but are rare in adults. Three adults with falciparum malaria who had fever, altered consciousness and focal neurological deficits (one of whom also had seizures) are being reported here. CT scan of the brain revealed haemorrhagic infarction of the cerebral cortex and subcortical white matter with surrounding oedema suggestive of venous infarction in all three patients. The diagnosis of cerebral venous thrombosis was missed in the first patient, and was detected only at autopsy. In the next two patients, superior sagittal sinus thrombosis was confirmed angiographically. Only one patient survived; the other two died of increased intracranial pressure. Two of the three patients also had plasmodium vivax co-infection. A hypercoagulable state resulting from severe malaria may be responsible for this rare and potentially fatal complication. Cerebral malaria may be associated with raised intracranial pressure due to cerebral oedema. Cerebral venous thrombosis may worsen this and adversely affect outcome. This diagnosis should be suspected in patients with severe malaria who develop focal neurological deficits and confirmed by appropriate imaging; judicious use of local thrombolytic therapy may help improve outcome.
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4/6. Intracranial pseudoaneurysm due to rupture of a saccular aneurysm mimicking a large partially thrombosed aneurysm ("ghost aneurysm"): radiological findings and therapeutic implications in two cases.

    Intracranial pseudoaneurysm formation due to ruptured non-traumatic saccular aneurysm is extremely rare. We experienced two cases of large pseudoaneurysm formation due to rupture of a saccular aneurysm. The neuroradiological ghost-like appearance of the aneurysms led to misdiagnoses as large partially thrombosed aneurysm. Two cases of large intracranial pseudoaneurysm formation due to rupture of a saccular aneurysm occurred in a 77-year-old comatose woman with an aneurysm on the anterior wall of the internal carotid artery and a 73-year-old comatose woman with an anterior cerebral artery (azygos) aneurysm. Both patients suffered subarachnoid hemorrhage associated with intracerebral and intraventricular hematomas. angiography showed peculiar "ghost-like" appearance of the aneurysm including delayed filling, changing shape, retention of the contrast material after the venous phase, and unclear location of neck. neck clipping surgeries were performed, but were difficult because of the preoperative misdiagnosis as large partially thrombosed aneurysm. The entity of "ghost aneurysm" caused by rupture of a saccular aneurysm should be considered in the clinical diagnosis.
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5/6. Intravascular papillary endothelial hyperplasia in an intracranial thrombosed aneurysm: 3T magnetic resonance imaging and angiographical features.

    Enhancement of intracranial thrombosed aneurysms is an uncommon finding on magnetic resonance (MR) imaging, and can present diagnostic difficulties and complicate management decisions. We report a 46-year-old man who had an enhancing thrombosed intracranial aneurysm observed on 3T MR imaging. There was angiographical correlation, with follow-up serial MR imaging documenting regression and improvement. Findings are typical for benign intravascular papillary endothelial hyperplasia. Differential diagnoses of giant serpentine intracranial aneurysm and malignant angiosarcoma are discussed.
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6/6. Systemic hemostasis with recombinant-activated factor vii followed by local thrombolysis with recombinant tissue plasminogen activator in intraventricular hemorrhage.

    INTRODUCTION: A 51-year-old woman on warfarin thromboprophylaxis for transient ischemic attacks developed sudden onset nausea, vomiting, and decreased mental status, rapidly becoming comatose. head computed tomography (CT) showed intracerebral hemorrhage, extending into all ventricular chambers, and acute obstructive hematocephalus requiring urgent ventricular drainage. CT angiogram showed no evidence of an aneurysm or vascular malformation. methods: The pretreatment international normalized ratio (INR) of 4.9 was rapidly corrected with recombinant activated factor vii and an external ventricular drain was placed. Despite accurate positioning, the ventriculostomy thrombosed and became nonfunctional. Recombinant tissue plasminogen activator was given intraventricularly and resulted in partial ventricular decompression within 24 hours, with dramatic improvement in the patient's level of consciousness. RESULTS: Repeated intraventricular fibrinolysis resulted in further reduction of the intraventricular hematoma within a few days and a good patient outcome. The patient did not require permanent ventricular shunt. CONCLUSION: To our knowledge, this is the first reported case of combined systemic enhancement of hemostasis and local fibrinolysis as a life-saving measure in intracranial hemorrhage.
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