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[Cerebral thrombophlebitis].
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[Cerebral fat embolism].
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[Persistent cerebral damage by fat embolism].
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[Electroencephalography in cerebral thrombophlebitis and thrombosis].
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THE ELECTROENCEPHALOGRAM IN CEREBRAL FAT EMBOLISM.
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WEEKLY clinicopathological exercises: coronary artery disease with cerebral and pulmonary embolism and infarction.
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Occlusive disease of the cerebral vessels.
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[Budd-Chiari syndrome with cerebral sinus involvement].
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[Thrombosis and thrombophlebitis of the cerebral veins].
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[Cerebral thrombosis and hypotension].
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[Thrombosis of the cerebral veins and sinus].
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[Comparative study of cerebral arterial thromboses with and without pseudotumoral form].
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Significance of atrial septal aneurysm: report of a case.
Postoperative stroke can have many etiologies including cerebral thrombosis, embolism, and hemorrhage. If there is a right-to-left intracardiac shunt, paradoxical embolism may also occur. Atrial septal aneurysm has been diagnosed with increasing frequency because of the accuracy of transesophageal echocardiography (TEE). Atrial septal aneurysm is also associated with patent foramen ovale and atrial septal defects. We report a case of a patient who developed a postoperative stroke one day after coronary artery bypass surgery. TEE performed in the intensive care unit revealed an atrial septal aneurysm with a right-to-left interatrial shunt, which may have resulted in paradoxical systemic embolism.
[Cerebral venous & sinus thrombosis].
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[Clinical and arteriographical aspects of cerebral thrombosis].
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Protein S deficiency in middle-aged women with stroke.
We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.
[EXPERIMENTAL EMBOLI OF THE VERTEBRO-BASILAR SYSTEM. I. NEUROLOGIC CHANGES].
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