Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein C together with its plasmatic cofactor protein S and antithrombin III probably represent the most important plasmatic inhibitor in coagulation. Protein C deficiency constitutes a high risk factor for venous thrombosis. Cerebral venous thrombosis is a manifestation which is scarcely referred to in protein C deficiency. The case of a 32 year old patient with protein C deficiency is presented. The patient was admitted for an endocraneal hypertension syndrome. CT and MR demonstrated multiple hemorrhagic cerebral infarctions. Arteriography confirmed vertebral venous thrombosis. Only six cases sufficiently documenting cerebral venous thrombosis due to protein C deficiency were found in the literature. In most cases coadjuvant factors exist predisposing thromboembolic disease. The present clinical case demonstrates the importance of considering protein C deficiency in the diagnosis of cerebral venous thrombosis in young adults.
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PMID:[Cerebral venous thrombosis and hereditary protein C deficiency]. 159 2

A 35 year-old caucasian man suffered from paroxysmal nocturnal haemoglobinuria (PNH) or Marchiafava-Micheli's disease diagnosed in 1976 and complicated by several thrombotic episodes. He developed a benign intracranial hypertension. A digitalized intravenous angiography showed occlusion of both lateral sinuses. Partial improvement followed lombo-peritoneal shunting and steroid therapy. Cerebral venous thrombosis is a well-known complication of PNH but only a few cases have been radiologically and/or pathologically proven. It usually involves the superior longitudinal sinus and/or cortical veins resulting in hemorrhagic infarction of poor outcome. Benign intracranial hypertension due to a venous occlusion is rare. In 3 published cases, as in our own, the neurologic outcome was good. Steroid therapy seems useful. The risks of anticoagulant therapy are discussed.
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PMID:[Benign intracranial hypertension and Marchiafava-Micheli disease]. 382 10

Female hormones are linked to migraine. Women who have had menstrual migraine and migraine onset at menarche tend to experience no migraine during pregnancy. Not all migraines improve during pregnancy, however. Some women experience migraine for the first time during pregnancy. Migraine developing during pregnancy may indicate an underlying structural or functional disorder, e.g., cerebral aneurysms. Headaches caused by cerebral arteriovenous malformations often present as migraine with aura. Cerebral venous thrombosis (common during pregnancy and the puerperium) may manifest with migraine-like visual disturbance and headache. Idiopathic intracranial hypertension or intracranial hypertension secondary to cerebral venous thrombosis or coincidental brain mass can manifest as a continuous and increasing headache. Physicians need to intensively evaluate such cases to achieve an accurate diagnosis. Spinal procedures linked to delivery can cause a low pressure headache. Oral contraceptive use is linked to migraine. Decreasing estrogen levels appear to precipitate migraine. Estradiol and progesterone therapy for menstrual migraine maintains high estrogen levels during the menstrual epoch, which generally prevents migraine. High but stable estrogen levels prevent migraine. Thus, migraines who do not suffer from migraine during pregnancy benefit from high estrogen levels. Pregnant women with migraine should not take drugs unless the frequency and severity of migraine is life threatening to the mother or fetus. Acetaminophen can be used to relieve pain. Meperidine suppositories can relieve severe pain. Pregnant women should not use aspirin, nonsteroidal anti-inflammatory drugs, or vasoconstrictors. Fluid replacement and acceptable antiemetic drugs can treat dehydration and vomiting. Behavioral modification, identification, and elimination of foods that trigger attacks, magnesium supplementation, and low doses of propranolol 3-4 times/day in severe cases may prevent migraine in pregnant women.
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PMID:Migraine and pregnancy. 829 77

Cerebral venous thrombosis is a treatable and under-recognised cause of a benign intracranial hypertension syndrome, and may also cause focal signs, seizures, and depression of consciousness.
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PMID:Cerebral venous thrombosis. 887 55

Cerebral venous thrombosis shows remarkable clinical polymorphism: isolated intracranial hypertension, cerebrovascular accident or focal, subacute cerebral lesion. Magnetic resonance imaging permits easy identification of the thrombosis and its tissular consequences as well as long-term follow-up. Search for the cause should be meticulous, given the multiple possibilities, presently dominated by prothrombotic states (postpartum, haemostasis anomalies, systemic affections, haematologic diseases, birth control pill, etc.). The development of neuro-imaging is changing the classic severity of cerebral venous thrombosis. Anti-coagulant treatment is widely used, including during haemorrhagic infarction. This treatment probably contributes to improving the survival and functional prognosis.
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PMID:[Cerebral venous thrombosis]. 978 Dec 27

Cerebral venous thrombosis is a rare disorder with highly variable and nonspecific clinical presentations. For these reasons, specific treatment should be given only when the diagnosis has been firmly established. Etiologic diagnosis should begin in the emergency department to identify underlying conditions that require specific treatment. The mainstay of treatment is anticoagulation with heparin, even in the case of cerebral hemorrhage, followed as soon as possible by oral anticoagulant administration. The optimal duration of oral anticoagulation has not been established. By analogy with systemic venous thrombosis, it should be prolonged 3 to 6 months. When a high risk of recurrence is present, treatment should be continued until the risk disappears. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation even when the clinical situation seems desperate. For the same reason, aggressive treatment of intracranial hypertension and seizures or status epilepticus is warranted. Screening for extraneurologic venous thrombosis should be done by means of clinical examination and, if necessary, specific imaging procedures. Local thrombolysis is not yet of proven efficacy and safety. It can be used in patients with clinical worsening related to documented extension of the venous thrombosis despite anticoagulation and in the absence of cerebral hematoma. Surgical treatment is limited to external ventricular drainage and suboccipital craniotomy in the very rare cases of cerebellar vein thrombosis with edematous cerebellar infarct.
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PMID:Cerebral Venous Thrombosis. 1109 59

Cerebral venous thrombosis is a clinical condition of difficult diagnosis, and poor prognosis when treatment is not started early. There is a long list of causes, and hereby we describe a case associated to prothrombin G20210 mutation. A 53-year-old man, white, was admitted with status epilepticus. After seizures control, he developed intracranial hypertension, with headache and vomiting, and bilateral papilledema. His past medical and familial history were unremarkable. He was a nonsmoker, no drug and alcohol user. CT scan and MRI showed right temporal and parietal infarct with hemorrhagic transformation. Spinal tap with opening pressure of 500 mmH2O showed normal CSF examination. MRI angiography disclosed superior sinus, right transverse and sigmoid sinus complete thrombosis. He was started with heparin and oral warfarin. In spite of anticoagulation, two months later he developed deep right inferior limb thrombosis. All the initial tests were normal, and test for prothrombin G20210 mutation was positive. He needed a much higher than conventional daily dose of warfarin to keep him asymptomatic.
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PMID:[Cerebral and systemic venous thrombosis associated to prothrombin G20210 mutation: case report]. 1476 16

Cerebral venous thrombosis is an infrequent condition characterized by extreme variability in its clinical presentation and mode of onset. The combination of magnetic resonance imaging and magnetic resonance angiography is currently the best method for diagnosis. The proportion of cases of unknown etiology remains high. The prognosis, although better than previously thought, remains unpredictable. Treatment, which should be started as soon as the diagnosis is established, consists of reversing the underlying cause when known, control of seizures and intracranial hypertension, and the use of antithrombotics. Heparin should be the first-line antithrombotic agent. Recent studies have confirmed its safety even in patients with hemorrhagic parenchymal lesions. Local thrombolysis is indicated in the very rare cases that deteriorate despite adequate anticoagulation. Cerebrospinal fluid diversion or optic nerve fenestration is used for vision-threatening papilledema when intracranial pressure control is difficult.
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PMID:Cerebral venous thrombosis. 1517 70

Cerebral venous thrombosis is a relatively uncommon but serious neurologic disorder that is potentially reversible with prompt diagnosis and appropriate medical care. Because the possible causal factors and clinical manifestations of this disorder are many and varied, imaging plays a primary role in the diagnosis. Magnetic resonance (MR) imaging, un-enhanced computed tomography (CT), unenhanced time-of-flight MR venography, and contrast material-enhanced MR venography and CT venography are particularly useful techniques for detecting cerebral venous and brain parenchymal changes that may be related to thrombosis. To achieve an accurate diagnosis, it is important to have a detailed knowledge of the normal venous anatomy and variants, the spectrum of findings (venous sinus thrombi and recanalization, parenchymal diffusion or perfusion changes or hemorrhage), other potentially relevant conditions (deep venous occlusion, isolated cortical venous thrombosis, idiopathic intracranial hypertension), and potential pitfalls in image interpretation.
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PMID:Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. 1705 May 15

Cerebral venous thrombosis, also known as cortical venous, cerebral sinus, cerebral venous sinus, or dural sinus thrombosis, results from clot formation in one of the many outflow tracts of the brain. Obstruction of flow causes venous hypertension, which is responsible for clinical findings associated with this condition. Signs and symptoms of cerebral venous thrombosis include headache, nausea, mental status changes, seizures, and focal neurologic deficits. Although cerebral venous thrombosis can occur at any time during life, women are particularly vulnerable before delivery and during the postpartum period because of the hypercoagulable state that accompanies pregnancy. This case study describes the challenging clinical course of one postpartum patient who developed venous thrombosis of the sagittal sinus.
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PMID:A case of postpartum cerebral venous thrombosis. 1706 63


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