Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report clinical findings, risk factors and neurological and cognitive long-term outcome in three Italian children aged 7, 8 and 5, respectively, who experienced cerebral venous sinus thrombosis (CVST). All children presented with headache, associated to nausea, vomiting and papilloedema. None suffered from epileptic seizures. In two of them a paresis of the sixth cranial nerve with diplopia was found. Diagnosis was confirmed by magnetic resonance imaging angiography (angio MRI) in all cases. In all patients plasma levels of protein C, protein S, antithrombin III (AT III), antiphospholipid antibodies (ApA) and homocysteine were detected. Furthermore, factor V Leiden mutation, prothrombin mutation G20210A and MTHFR mutation were searched for. A Protein C reduction was detected in all patients at onset; this finding, however, was not confirmed at follow-up in all of them. At one-year follow-up, neurological examination was normal in all children and neuropsychological assessment, aimed at excluding linguistic and non-linguistic cognitive deficits, revealed normal performances in two of them. In the third child, cognitive assessment confirmed a previously diagnosed developmental dyslexia.
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PMID:Cerebral venous sinus thrombosis in childhood: clinical aspects and neurological and cognitive long-term outcome in three cases. 1562 88

A 39 year-old man was admitted to our hospital because of severe headache with fever continuing over two weeks. Three days after admission he developed aphasia and right hemiparesis, when his CT revealed subarachnoid hemorrhage at the left sylvian fissure. He was diagnosed as suffering from cerebral venous thrombosis because empty delta sign was positive on the enhanced brain CT. Suprasagittal sinus and bilateral transverse sinuses were not detected on the cerebral angiography. He was also diagnosed as having Graves' disease for the first time on the basis of free T3 13.56 pg/ml, free T4 4.65 ng/dl, TSH < 0.01 IU/ml, anti-TSH receptor antibody 4.3 IU/l, and thyroid stimulating antibody 224%. On the examination, homocystine and activities of antithrombin III, protein C, and protein S were normal. Antinculear, anti-DNA, anti-Sm, anticardiolipin beta2GP-I antibodies, and PR3ANCA were negative. Factor VIII activity, however, markedly increased over 300%, which has been known to increase in the cases of hyperthyroidism. He recovered well after the treatment with thiamazole in addition to warfarin followed by intravenous heparin. There are only six cases of cerebral venous thrombosis due to hyperthyroidism with increased factor VIII level. All of those cases were female, and 5 of them were taking oral contraceptives. This is a first Japanese male case.
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PMID:[Case of cerebral venous thrombosis due to graves' disease with increased factor VIII activity]. 1676 94

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53

We report the case of a 27-year-old parturient who developed a headache within 12 hours of delivery and who subsequently seized. Further examination, including magnetic resonance imaging and computed tomographic scan, showed a partial thrombosis of a transversal venous sinus, the underlying cause being an activated protein C resistance caused by a heterozygote factor V Leiden mutation and heterozygote prothrombin-gene mutation G20210A. Seven months after delivery, the patient is in good health, showing no neurocognitive disability.
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PMID:Postpartum seizures after epidural analgesia: a patient with a mutation of the factor V Leiden and prothrombin gene. 1806 13

An increased risk of venous thromboembolism has been demonstrated following renal transplantation. Commonly reported sites have been deep vein thrombosis, pulmonary thromboembolism and vascular thrombosis involving the graft. Cerebral venous thrombosis (CVT) has not been reported in literature so far. A 36-year-old male patient, transplanted in Jan 2005 with normal graft functions, was admitted with history of headache, blurring of vision and vomiting. Examination revealed papilledema and no neurological deficits. Baseline investigations and analysis of cerebrospinal fluid were normal. Cerebral magnetic resonance venogram revealed extensive CVT involving superior sagittal sinus, bilateral transverse sinuses and the right sigmoid sinus. He was investigated for a thrombophilic disorder; serum homocysteine, protein C and S levels, antiphospholipid antibody and antithrombin-III levels were done despite which no conclusive diagnosis could be arrived at. To our knowledge, this is the first report of extensive CVT described in a transplant recipient. No definite prothrombotic or predisposing factors could be identified in our patient and the cause of CVT remains unclear.
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PMID:Extensive cerebral venous thrombosis in a renal allograft recipient. 1808 32

The superior vena cava (SVC) syndrome is due to obstruction of the SVC and may present by dyspnea, chest pain, cough, headache, dysphasia, and symptoms of increased intracranial pressure; however, the affected patients can be asymptomatic. Numerous collateral veins are often seen on the upper chest, arms and neck. The syndrome may be caused by prolonged use of indwelling catheters, but is an infrequently reported complication in the hemodialysis patients. We report two patients who developed SVC syndrome several months after removal of hemodialysis indwelling catheters. The causes of this syndrome in our patients were stenosis in one patient and thrombosis in the other; venous endothelial injury and subnormal levels of protein C and S were possible contributory factors. These cases illustrate that SVC syndrome is a possible late complication after removal of hemodialysis indwelling catheters.
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PMID:The superior vena cava syndrome: late presentation after hemodialysis catheter removal. 1820 44

A 35-year-old healthy male with no history of any past medical illness developed severe headache, vomiting and drowsiness while at high altitude (4,572 m) in the eastern Himalayan ranges. He was evacuated to a tertiary-care hospital where he was diagnosed to have cerebral sinus venous thrombosis (CSVT) on magnetic resonance imaging, with deep vein thrombosis (DVT) of his right popliteo-femoral vein on color Doppler study. Investigation for thrombophilia revealed protein S (PS) deficiency in this patient. Family screening revealed low levels of PS in two elder brothers. One brother had a history of 'stroke in young' at the age of 20 years with the other being asymptomatic. This established the hereditary nature of PS deficiency. We are not aware of any previously published report on hereditary PS deficiency combined with CSVT and DVT occurring at high altitude. However, 1 case of protein C deficiency with CSVT has been reported previously.
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PMID:A case of hereditary protein S deficiency presenting with cerebral sinus venous thrombosis and deep vein thrombosis at high altitude. 1843 8

We present a case of hemorrhagic stroke after cesarean delivery under combined spinal-epidural anesthesia in an 35-year-old Hispanic patient treated with anticoagulants for protein C deficiency. She required vasopressor therapy for intraoperative hypotension and developed severe headache immediately after administration. To our knowledge, this is the first case of stroke occurring in a pregnant woman following vasopressor therapy for spinal anesthesia-induced hypotension. Although the exact cause of her hemorrhagic stroke is uncertain, the hypertensive response that may have led to the hemorrhagic stroke occurred following administration of commonly used doses of vasopressor agents. We discuss the possible causes of stroke.
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PMID:Hemorrhagic stroke following elective cesarean delivery. 1851 Dec 57

Cerebral venous thrombosis (CVT) is infrequent among cerebrovascular diseases. The simultaneous thrombosis involving both cerebral artery and venous sinus is even extremely rare. We reported a 41-year-old woman who presented with acute headache and left hemiparesis due to concomitant arterial ischemic stroke and recurrent CVT. Extensive investigation disclosed acquired protein C and protein S deficiency, iron deficiency anemia (IDA) and cryoglobulinemia. She was treated with intravenous injection of heparin followed by oral anticoagulant therapy. The headache rapidly subsided; however, left hemiparesis persisted over five months. The rare condition of simultaneous thrombosis of cerebral artery and venous sinus may be caused by the synergistic effect of coagulation disorders, IDA and cryoglobulinemia.
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PMID:Simultaneous thrombosis of cerebral artery and venous sinus. 1868 52

Postpartum cerebral vein thrombosis is a very rare entity (3-4 cases per million). Clinical manifestations vary, though persistent headache is almost always reported, meaning that differential diagnosis should be performed to rule out other causes of postpartum headache. Recognized risk factors for this disease are the prothrombotic state of pregnancy (third trimester), excess weight, and thrombophilia Accidental dural puncture, protein C and S deficiencies, factor V Leiden mutation, antiphospholipid syndrome, and the use of oral contraceptives have also been implicated. The diagnostic test of choice is magnetic resonance imaging, as it is convenient and harmless, though transcranial Doppler ultrasound can also be used. Pulmonary angiography is the gold-standard test. The treatment of choice is anticoagulant therapy with heparin (a treatment that is controversial, however, due to the high risk of rebleeding), followed by long-term treatment with antivitamin K drugs. We report a case of thrombosis of the upper longitudinal sinus associated with persistent postpartum headache and a history of a failed attempt at epidural puncture for analgesia during labor. The case posed interesting diagnostic questions.
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PMID:[Sagittal sinus thrombosis as a rare cause of postpartum headache: a case report]. 1885 84


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