Cases reported "Intracranial Thrombosis"

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1/24. Traumatic intracerebral venous thrombosis associated with an abnormal golf swing.

    OBJECTIVES: To describe the occurrence of cerebral venous thrombosis in a 40-year-old man whose cerebral event was induced by a poor golf swing, to review the literature on possible mechanisms producing venous thrombosis, and to compare this case with the literature. BACKGROUND: Headache is the most frequent symptom in patients with cerebral venous thrombosis. However, patients presenting with a headache due to cerebral venous thrombosis are uncommon. The known risk factors for thrombosis include both acquired and genetic factors. When the interaction of these two groups occurs, the magnitude of this interaction is thought to produce a dynamic state that can favor thrombosis. Our case report illustrates that moderate levels of anticardiolipin antibodies together with the mild trauma of a golf swing can induce a cerebral venous thrombosis. This case also suggests that although headache is rarely due to cerebral venous thrombosis, it should be excluded by good medical acumen and testing. RESULTS: Minor trauma induced by a poor golf swing was chronologically related to the development of a progressive cerebral venous thrombosis. The patient had none of the risk factors associated with a predisposition to venous thrombosis: hypercoagulable state, concurrent infection, pregnancy/puerperium, collagen vascular disorder, malignancy, migraine, false-positive VDRL, previous deep vein thrombosis, renal disease, factor v Leiden, or a hematological disorder. There was no anatomical abnormality that would predispose the patient to a cerebral venous thrombosis. The only laboratory abnormality was a moderate anticardiolipin antibody level (25 GPL). The patient was placed on warfarin sodium therapy and is currently without clinical sequela from the venous thrombotic event. CONCLUSIONS: Under certain circumstances, minor trauma can induce cerebral venous thrombosis. A review of the literature indicates that cerebral venous thrombosis in the presence of anticardiolipin antibodies and in the absence of systemic lupus erythematosus is a rare event. Previously, only major traumatic events have been reported to be associated with cerebral venous thromboses. The chronological development of cerebral venous thrombosis after a faulty golf swing strongly indicates that given a background of moderate levels of anticardiolipin antibodies, even minor trauma can induce a venous thrombotic event.
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2/24. case reports: sudden worsening of cluster headache: A signal of aneurysmal thrombosis and enlargement.

    We report a 55-year-old man presenting with symptoms of cluster headache, including throbbing pain behind the left eye, tearing, and rhinorrhea. magnetic resonance imaging and magnetic resonance angiography revealed no abnormalities. Two days of intravenous dihydroergotamine resolved his pain. His headaches were somewhat relieved with a treatment regimen of 100 mg of imipramine each night, 40 mg of propranolol twice a day, 250 mg of divalproex three times a day, and dihydroergotamine nasal spray for breakthrough headaches. Two months later, the severity of his pain increased dramatically. Repeat imaging revealed a large thrombosed left posterior communicating artery aneurysm. Following obliterative surgery, his headaches are infrequent and mild and resemble tension headaches. Dramatic changes in headache characteristics can be an indicator of aneurysmal enlargement and thrombosis. This case illustrates the importance of repeat imaging when a patient's headache significantly worsens.
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3/24. diffusion-weighted MRI suggests the coexistence of cytotoxic and vasogenic oedema in a case of deep cerebral venous thrombosis.

    We report a 20-year-old woman who suffered headaches before presenting with a state of fluctuating vigilance. MRI showed diffuse high signal in the basal ganglia bilaterally on diffusion- and T2-weighted images, which had areas of both low and high apparent diffusion coefficient, presumed to correspond to cytotoxic and vasogenic oedema. MR venography showed no flow in the deep cerebral veins or straight sinus. heparin was given, with clinical recovery. On follow-up MRI, the appearances became normal.
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4/24. Giant intracranial aneurysm of the anterior communicating artery treated by direct surgical approach. Case report.

    We report the singular case of an exceptionally large giant communicating artery aneurysm successfully treated with a direct surgical approach. The clinical presentation was a relatively short history of frontal headache. In the pre- and postcontrast CT scans the lesion mimicked an intracranial tumor. At surgery the intraluminal thrombus was partially removed with an ultrasonic surgical aspirator; the decompression allowed the isolation and subsequent temporary dipping of the tracts A1 and A2 of both the anterior cerebral arteries. It was then possible to complete the thrombectomy and to dip the neck of the aneurysm. The report emphasizes the indispensable role of MRI for the accurate diagnosis of giant intracranial aneurysms and the recent improvement of the surgical results concerning this category of aneurysms (mainly related to the present wider availability of technical surgical instrumentation).
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5/24. Cerebral venous thrombosis associated with tentorial subdural hematoma during oxymetholone therapy.

    Androgen was reported to cause cerebral venous thrombosis (CVT) during replacement therapy for aplastic anemia. oxymetholone, a synthetic androgen analogue, has been widely used in the treatment of aplastic anemia. A 40-year-old woman with aplastic anemia visited our hospital because of severe headache, nausea, vomiting, blurred vision and diplopia for a period of 1 month. She had taken oxymetholone for 2 years. Neurological examination revealed bilateral papilledema and bilateral sixth nerve palsies. brain magnetic resonance imaging (MRI), performed at the time of admission, demonstrated left-sided tentorial SDH, and focal cerebral thrombosis of the left superficial sylvian vein and sigmoid sinus. MR venography revealed multiple irregularities in the superior sagittal sinus and left transverse sinus. CVT with tentorial subdural hematoma (SDH) caused by oxymetholone was strongly suggested. oxymetholone was immediately discontinued, and her symptoms and signs disappeared. Because of the thrombocytopenia, anticoagulation was not started. She was discharged and visited the outpatient clinic without neurological symptoms for 6 months. This report supports the cautions given about the risk of CVT with oxymetholone supplementation in aplastic anemia. To the best of our knowledge, this is the first report of CVT associated with tentorial SDH that was probably caused by oxymetholone.
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6/24. Treatment of deep cerebral venous thrombosis by local infusion of tissue plasminogen activator.

    BACKGROUND: Treatment of extensive intracranial venous sinus thrombosis with thrombolytic drugs is described, although the indications for and most efficacious technique for achieving thrombolysis remain uncertain. We report the successful lysis of superficial and deep venous system thrombosis by infusion of recombinant human tissue-type plasminogen activator (rt-PA) into the anterior superior sagittal sinus. CASE DESCRIPTION: A 34-year-old man presented with headaches followed by decreased level of consciousness and left hemiplegia. Angiography showed thrombosis of the superior sagittal and both transverse and straight sinuses with extension into the internal cerebral veins. The superior sagittal sinus was catheterized via a transfemoral route and rt-PA, 25 mg, was infused. There was no significant change in the thrombosis. The catheter was left in place and rt-PA was infused at 1 mg/minute for 19 hours. Repeat angiography showed resolution of the thrombosis. The patient was placed on heparin and then coumadin. He recovered completely. CONCLUSIONS: This report suggests that superselective infusion of thrombolytics into thrombosed intracranial venous sinuses can lyse intracranial venous sinus thrombosis. The thrombolytic agent must be infused for hours. The apparent successful lysis of clot in the deep venous system when infusion was into the superior sagittal sinus might be related to diffusion of rt-PA throughout the intracranial venous system or to improved venous outflow caused by lysis of clot in superficial dural sinuses.
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7/24. Intracranial venous thrombosis and pulmonary embolism with antiphospholipid syndrome in systemic lupus erythematosus.

    The presence of antiphospholipid antibodies is associated with arterial and venous thrombosis. A 14-year-old girl, with systemic lupus erythematosus (SLE), developed headache and cough and was found to have intracranial venous sinus thrombosis with secondary pulmonary embolism associated with antiphospholipid syndrome. Clinical and radiological improvement occurred with anticoagulation therapy. Because SLE is commonly associated with antiphospholipid antibodies, thromboembolic events should be considered in the differential diagnosis of both cough and headache in children with SLE.
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8/24. Peripheral hemodialysis shunt with intracranial venous congestion.

    BACKGROUND: Intracranial venous congestion is often caused by local venous thrombosis or brain arteriovenous fistulas. Hemodialysis shunts are known to cause venous enlargement in the arm or chest but have not been related to intracranial vascular pathology. Case Description- A 59-year-old woman who presented with increasing headache, gait instability, and memory loss was a renal transplant recipient who still carried a left upper arm shunt. Cranial CT scan showed enlarged veins in the posterior fossa with incipient hydrocephalus. Extracranial duplex sonography revealed reversed flow in the left internal jugular vein, which normalized on cuff inflation around the shunt-carrying arm. The reversed flow, intracranial venous congestion, and neurological status improved after surgical shunt ligation. CONCLUSIONS: To our knowledge, this is the first case description of an intracranial venous outflow obstruction caused by a peripheral arteriovenous shunt.
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9/24. A case with cerebral thrombosis receiving tamoxifen treatment.

    Cerebral sinus thrombosis (CST) is known to be related to a number of underlying aetiologies including otitis media, trauma, pregnancy, birth control pills, tumours, malnutrition, dehydration, haematologic disorders and malignancy (Fishman, 2000; Raizer and Abbott, 2000). We present the case of a patient with breast cancer receiving the antioestrogen drug tamoxifen who developed CST. A 40-year-old female presented as an emergency with a 10-day history of headache and left sided weakness. On questioning her past medical history included a diagnosis of breast cancer 3 years ago treated by radical mastectomy and tamoxifen 20 mg daily. At the time of admission, neurologic examination revealed a mild left sided hemiparesis and a present Babinksi sign. Non-contrast enhanced tomography was normal. magnetic resonance imaging (MRI) showed thrombosis in the superior sagittal sinus, right lateral sinus and jugular vein in addition venous infarction in the right temporal lobe was present (Figs 1a and b). Routine haematology and biochemistry was normal. Anticoagulation tests, antithrombin iii, protein s and C levels were also found to be normal. She was treated with anticoagulation therapy and her hemiparesis improved within 3 days. Control MRI showed the resorption of the venous infarction and resolution of the thrombosis (Fig. 1c).
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10/24. Concomitant heterozygous factor v Leiden mutation and homozygous prothrombin gene variant (G20210A) in patient with cerebral venous thrombosis.

    BACKGROUND: factor v Leiden mutation represents the most common genetic risk factor of venous thrombosis in Caucasian population. A common mutation in prothrombin gene, which is due to G-->A transition at position 20210, is also associated with elevated prothrombin concentration and thrombosis. Both this mutations may constitute concomitant risk factors for deep venous thrombosis. CASE REPORT: A 29-years old woman was admitted in the Emergency Department because of severe headache with vomiting that she suffered for a few days without any neurological deficits. In the Emergency she presented first in her life tonic-clonic seizures followed by right hemiparesis and aphasia and than was admitted to hospital. CT and MR scan showed a large lesion in the left fronto-parietal region with extent edema, which was first diagnosed as tumor. Following MR showed more lesions and typical signs of sinus thrombosis. She improved quickly after stroke without any anticoagulant treatment. Genetic study revealed factor v Leiden mutation and homozygous mutation G20210A in prothrombin gene. CONCLUSIONS: Both mutations found in this case, alone, are not a high risk factors for venous thrombosis but together may increase 5-10 fold risk of venous thrombosis. Venous stroke must be considered always in acute neurological events with organic brain lesions, especially in young
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