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)

A 13-year-old girl with preB-ALL was admitted because of headache during maintenance therapy including L-asparaginase. Magnetic resonance imaging revealed cerebral thrombosis. Coagulation studies showed decreased levels of fibrinogen, antithrombin-III and plasminogen. The patient was treated with antithrombin-III concentrates and fresh frozen plasma and recovered quickly. These findings suggest that coagulopathy induced by L-asparaginase is associated with the pathogenesis of cerebral thrombosis.
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PMID:[Cerebral thrombosis in a child with acute lymphocytic leukemia during L-asparaginase therapy]. 260 Oct 47

Sudden cerebrovascular insults occurred during or immediately following remission induction therapy in 4 children with acute lymphoblastic leukemia. In 3, cerebral infarction was due to thrombosis. In the fourth, an intracerebral hematoma developed representing either frank hemorrhaging or a hemorrhagic infarction. None of the patients had central nervous system leukemia or extreme leukocytosis at the time of diagnosis. Symptoms were obtundation, hemiparesis, seizures, and headache. The induction chemotherapy included L-asparaginase which causes deficiencies of antithrombin, plasminogen, fibrinogen, and factors IX and XI. These hemostatic abnormalities may explain the thromboses and bleeding observed in these children.
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PMID:Thrombotic and hemorrhagic strokes complicating early therapy for childhood acute lymphoblastic leukemia. 693 53

L-Asparaginase therapy for childhood acute lymphoblastic leukemia causes deficiencies of plasma hemostatic proteins, especially antithrombin, plasminogen, and fibrinogen. Severe thromboses and hemorrhages occurred in 18 children receiving vincristine, prednisone, and asparaginase therapy for ALL. Thirteen children had intracranial thrombosis or hemorrhage, four had extremity thrombosis, and one had both an intracranial hemorrhage and an extremity thrombosis. These events occur characteristically in the third and fourth weeks of therapy during or just after a three-week course of L-asparaginase. Symptoms of headache, obtundation, hemiparesis, and seizure were common for the intracranial events: local pain, swelling, and discoloration were common for the extremity thromboses. These complications have been recognized in 1 to 2% of children undergoing induction therapy which includes asparaginase.
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PMID:A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia. 695 21

It is well known that thromboembolism is 1 of the most serious side effects of oral contraceptives (OCs). In Japan, however, reports of thromboembolism following use of OCs are rare, since their clinical use in Japan is restricted to treatment of menstrual irregularities. We reported here on 2 patients affected with cerebrovascular occlusive diseases associated with the administration of OCs. The 1st case was that of a 32-year old woman who developed headaches, paresis, and dysesthesia of the right limbs following daily intake for 20 days of OCs (0.15 mg mestranol and 5 mg lynestrenol). Neurological symptoms as well as examinations led to the diagnosis of a kind of thalamic syndrome due to cerebral thrombosis. The 2nd case was that of a 37-year old woman who developed right hemiparesis following daily consumption over a 21 day period of OCs as administered above. Clinical symptoms and neurological examinations led to the diagnosis of right hemiparesis due to cerebral thrombosis. The pathogenesis of cerebral thrombosis caused by taking OCs was discussed mainly in connection with coagulation and fibrinolysis. Certain evidence suggesting that hypercoagulability may play a major role in the pathogenesis of thromboembolism during OC ingestion has been derived from the works of other investigators. It is true that estrogen in this compound may induce a state in which an increase in coagulation factors together with a decrease of antithrombin 3 combine to produce hypercoagulation; laboratory tests with our patients, however, produced nothing compatible with a state of hypercoagulability. (author's modified)
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PMID:[Cerebral thrombosis in woman receiving oral contraceptives: report of two cases (author's transl)]. 746 38

In patients with strong suspicion of SAH, CT is the initial diagnostic procedure of choice. A lumbar puncture (LP) should be done if a CT is not available. If the patient has no focal deficit or papilloedema there is a little risk in LP. When a CT is negative there can be indication to do a LP: small leaks can be overlooked by CT, and they are often important premonitory events preceding larger and severe haemorrhages. The accuracy of CT in documenting SAH diminishes after 24 hours: thereafter, diagnosis is often dependent on LP. In some cases LP can be useful because the procedure may alleviate headache and remove some blood. LP can also quantify cerebro-spinal fluid (CSF) pressure, provide a baseline for future CSF determination, and allow the study of some parameters like arachidonate metabolites, lactic acid, fibrinogen degradation products (FDP) and thrombin-antithrombin complex (TAT).
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PMID:[Reasons in favor of lumbar puncture diagnosis (or lavage)]. 977 40

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

A 55-year-old man presented with a rare case of multiple isolated sinus dural arteriovenous fistulas (AVFs) associated with antithrombin (AT) III deficiency manifesting as sudden onset of headache and gait disturbance. Increased arterial shunting flow had caused intraventricular hemorrhage after incomplete repeated transarterial embolization procedures for dural AVFs. Multiple isolated sinus dural AVFs were located in the anterior superior sagittal sinus (SSS) and transverse sinus, which were completely embolized by direct packing of the isolated sinuses via the SSS. The development of dural AVF is complicated and associated with a number of factors, such as congenital abnormality, head trauma, craniotomy, radiation, hematological abnormality, and sinus thrombosis. Hematological abnormality is a risk factor of sinus thrombosis. In the present case, the multiple isolated sinus dural AVFs might have resulted from the aggravation of multiple dural AVFs and the coagulative tendency due to AT III deficiency. Direct sinus packing should be considered if transvenous catheterization is difficult or fails.
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PMID:Multiple isolated sinus dural arteriovenous fistulas associated with antithrombin III deficiency--case report--. 1894 80

Cerebral venous thrombosis (CVT) is a rare disease. It has numerous and complex etiologies. Inherited or acquired prothrombotic states play a key role in the development of this disease, such as factor V G1691A mutation (FV Leiden). A 15-year-old girl presented to the Department of Neurology with a complaint of severe headache with visual blurring. The diagnosis of CVT was not initially suspected because of the patient's condition on presentation. An MRI showed thrombosis in the superior sagittal sinus, confirming venous stroke. Anticardiolipin and antiphospholipid antibodies were assessed. In addition, inherited prothrombotic defects, such as protein C, protein S, and antithrombin deficiencies, and genetic mutations for FV Leiden, prothrombin gene G20210A (FII G20210A), and methyltetrahydrofolate reductase C677T (MTHFR C677T) were studied. All results were unremarkable except for the unique homozygous FV Leiden mutation, which likely contributed to this prothrombotic situation. This study highlights the fact that FV Leiden may play a significant role in the onset of CVT in young patients.
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PMID:Cerebral venous thrombosis associated with homozygous factor V Leiden mutation in a 15-year-old girl of Tunisian origin. 2204 15

A systematic study of thrombophilia markers in a large series of patients with cerebral venous thrombosis (CVT) from India is scarce. The present study was undertaken to know the prevalence of common hereditary thrombophilia in a large series of CVT patients from India. Six hundred and twelve (354 men, 219 women and 39 children) consecutive patients with CVT admitted to various hospitals in Mumbai between 2001 and 2010 were investigated for the common thrombophilia markers, that is, protein C (PC), protein S, antithrombin (AT), and factor V Leiden (FVL) mutation. The main presenting clinical manifestations included papilledema (62%), headache (62%), hemiparesis (48%), seizures (31%), and cranial nerve palsy (7%). All the patients were managed with heparin followed by warfarin during the succeeding 6 months. Superior sagittal sinus thrombosis was the commonest site (74%) followed by cortical venous thrombosis (15%). Associated clinical pathologies were dehydration, sepsis, pregnancy and puerperium, malaria, and tuberculosis; but in the majority of patients, there was no obvious cause. Eighteen percent of the patients had any of the thrombophilia markers studied; PC deficiency was the commonest thrombophilia marker followed by deficiency of protein S, FVL mutation and AT deficiency. The men below 45 years with PC deficiency (P=0.03) and women with protein S deficiency were significantly higher (P=0.04). In conclusion, CVT is not an uncommon cause of neurological deficit as was presented in earlier reports. Pregnancy and puerperium-related CVT was much less common. Thrombophilia markers accounted for approximately one-fifth of the patients. Death due to CVT has shown remarkable reduction (13%) because of early diagnosis and appropriate anticoagulation.
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PMID:Hereditary thrombophilia in cerebral venous thrombosis: a study from India. 2437 May 83

The clinical symptoms, causative factors, and prognosis in Japanese patients with cerebral venous thrombosis have not been adequately characterized. The present study describes these features in patients in Japan. Twenty-two patients with cerebral venous thrombosis were retrospectively identified. Diagnosis was confirmed by either digital subtraction angiography, magnetic resonance venography, or contrast-enhanced computed tomography. Demographic data and clinical and radiological features were recorded and analyzed for each patient. Prognosis was evaluated by the modified Rankin scale (mRS) at the time of hospital discharge. The most frequent symptom of cerebral venous thrombosis was headache (59.1 %). Causative factors included congenital thrombophilia (31.8 %), acquired thrombophilia (27.3 %), and iron-deficiency anemia (13.6 %). Of seven patients with congenital thrombophilia, four had mutations in the protein S gene, two had mutations in the protein C gene, and one had mutations in the antithrombin gene. All patients were alive at discharge from hospital. Nineteen of the 22 patients (86.4 %) recovered completely or exhibited only mild residual symptoms (mRS 0-2). However, three patients (13.6 %) had a poor prognosis (mRS 3-5). Cerebral venous thrombosis in Japanese patients is frequently associated with congenital thrombophilia and protein S gene mutation.
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PMID:Clinical features and underlying causes of cerebral venous thrombosis in Japanese patients. 2459 15


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