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)

An increased incidence of cerebral thromboembolic events has been reported in young patients with inflammatory bowel disease (IBD). It has been suggested that a hypercoagulable state is associated with clinical activity of the disease, with elevation of factors V, VIII, fibrinogen and platelets and a lowering of anti-thrombin III. We present the case of a 35 y/o male with refractory Crohn's disease who complained of headaches, blurred vision and tonic-clonic seizures. The studies demonstrated an ischemic stroke of the left cerebral hemisphere, without vascular abnormalities. Elevation of factor VIII, platelets, and antithrombin III were found. The symptoms were relieved with medical treatment and the patient has continued in good health after resection of the diseased terminal ileum.
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PMID:Cerebral thrombosis associated with active Crohn's disease. 988 77

Mast cells (MC) are multipotent hemopoietic effector cells producing diverse mediators like histamine, heparin, or tissue type plasminogen activator. We report a 75-year-old male patient with myelodysplastic syndrome (MDS) of recent onset (3 months' history) associated with a massive leukemic spread of immature tryptase+ MC (tentative term: myelomastocytic leukemia). The patient presented with pancytopenia, bleeding, hypofibrinogenemia, and an increased cellular tryptase level. Moreover, an excessive elevation of plasmin-antiplasmin complexes (9,200 ng/ml; normal range: 10-150), an elevated D-dimer, and an increase in thrombin-antithrombin III complexes were found. The identity of the circulating MC was confirmed by immunophenotyping (CD117/c-kit+, CD123/IL-3R alpha-, CD11b/C3biR-), biochemical analysis (cellular ratio [ng:ng] of tryptase to histamine >1), and electron microscopy. Bone marrow (bm) examination showed trilineage dysplasia (17% blasts), 30% diffusely scattered MC, and a complex karyotype. No dense, compact MC infiltrates (mastocytosis) were detectable in bm sections. Despite hyperfibrinolysis and mediator syndrome (flushing, headache), the patient received remission induction polychemotherapy (DAV) followed by two cycles of consolidation with intermediate dose ARA-C (2 x 1 g/m2/day on days 1, 3, and 5). He entered complete remission after the first chemotherapy cycle without evidence of recurring MDS. Moreover, in response to chemotherapy, the hyperfibrinolysis and mediator syndrome resolved, and the circulating c-kit+ MC disappeared. We suggest consideration of polychemotherapy as a therapeutic option in patients with high-risk MDS of recent onset, even in the case of MC lineage involvement.
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PMID:Hyperfibrinolysis in a case of myelodysplastic syndrome with leukemic spread of mast cells. 1033 14

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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PMID:A case with cerebral thrombosis receiving tamoxifen treatment. 1178 61

Hereditary hypercoagulability has been identified as risk factor in approximately 30% of cerebral venous thrombosis cases. We report three females with this association. A 38 years old female with a history of deep venous thrombosis of the lower limb, presented with headache, vomiting and a generalized seizure. Magnetic resonance angiography showed a partial thrombosis of the left lateral and superior longitudinal venous sinuses. Coagulation study showed a resistance to activated C protein and factor V Leyden. A 42 years old woman with a history of deep venous thrombosis, presented a right hemiplegia during a hospitalization. Magnetic resonance showed a left lateral hemorrhagic infarction. Magnetic resonance angiography showed an absence of signal in three venous sinuses. Coagulation study showed a protein C deficiency. A 17 years old woman presented a right hemiparesis in the sixth day of puerperium. CAT scan showed a left frontoparietal subcortical venous infarction. Coagulation study showed an antithrombin III deficiency.
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PMID:[Status of hereditary hypercoagulability and cerebral venous thrombosis. Report of 3 cases]. 1196 66

Phasic oral contraceptives (OCs) provide a physiological approach to contraception and most closely approximate the ideals of a combined OC with the lowest possible doses to avoid the metabolic risks of estrogens and progestins, maximal contraceptive protection, and satisfactory cycle control. Earlier studies have demostrated the decline in myocaridal infarct and thromboembolic disease with reduction of ethinyl estradiol (EE) from 50 to 30 mcg, the correlation between progestin dose and cardiovascular and cerebrovascular deaths, and the effects of progestins derived from 19 nortestosterone in reducing the beneficial high density lipoprotein (HDL) cholesterol. The preparation SH B 264 AB for example provides a 1st phase daily dose of 30 mcg EE and 50 mcg levonorgestrel, a sufficient dosage because of the low probability of ovulation but 1 which attempts to mimic the follicular secretion needed for endometrial growth. Daily doses in the 2nd phase increase to 40 mcg EE and 75 levonorgestrel, each of which is capable alone of inhibiting ovulation. The progestin causes a supplementary hypothalamic inhibition and renders the cervical mucus too viscous for sperm penetration, while the EE augments the hypothalamic inhibitory effect of the progestin, prevents release of luteinizing hormone releasing hormone, and suppresses the luteinizing hormone peak by increasing the pituitary threshold to hypothalamic stimulation. The total dose of SH B 264 AB is at least 30% less than that of other OCs. The Pearl index is 0.0-0.6, not quite as good as that of normal dosed OCs. The duration of menstrual bleeding appears unchanged even after prolonged use, while the amount of bleeding is slightly decreased. Amenorrhea and intermenstrual bleeding are rare. The good cycle control occurs because the steroid levels administered in the triphasic pill mimic those of ovarian secretion, leading to better endometrial development. The effects of triphasic pills on glycemia and insulin levels are very weak and are not statistically significant, while their slight estrogen dominance means that they have very slight effects on the level of HDL cholesterol. They cause a slight increase in triglyceride levels, minimal variation in coagulation parameters, a weak variation in factors VII, VIII, X, and plasminogen, and a slight decrease of antithrombin III. Triphasic OCs induce minimal augmentation in activity of the renin-angiotensin system, and in most cases do not affect blood pressure. Because of their estrogenic dominance, triphasic pills improve acne but may be associated with breast problems, water retention, dysmenorrhea, and premenstrual syndrome with irritability, nervousness, and headache. Triphasic pills are indicated for women beginning OCs, women with poor cycle control under other OCs, women at high cardiovascular risk, women with acne, and women whose current OCs cause oily skin, hirsutism, reduced libido or other symptoms. Contraindications for the triphasic pill in addition to the usual factors include benign breast disease, premenstural syndrome, dysmenorrhea, or polycystic ovarian syndrome.
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PMID:[Pros and cons of triphasic oral contraception]. 1226 12

A 27-year-old woman was admitted to our hospital because of headache, fever and right neck pain. Neurological examination revealed mild meningeal signs, and hyper-reflexia in all extremities. In the laboratory tests, white-cell count was 13,000/mm3, rheumatoid factor(RF) and C-reactive protein(CRP) were positive. The cerebro-spinal fluid showed pleocytosis (56/mm3, neutorophils and lymphocytes were 26 and 28, respectively). Thus, she was diagnosed as aseptic meningitis. A few days later, she had weakness and dysesthesia of the right face and the left extremities. Pulse therapy with intravenous methylprednisolone was started. A magnetic resonance imaging (MRI) of the brain showed a hemorrhagic infarction in the right parietal lobe. In hemostatic markers, thrombin-antithrombin III complex(TAT; 106 ng/dl), D-dimer 1234 ng/dl, prothrombin fragment 1 + 2(F1 + 2; 2.36 nmol/L), beta-thromboglobulin (beta TG; 4,300 ng/dl) and platelet factor 4 (PF-4; 1,770 ng/dl) were extremely elevated. On duplex ultrasonography, a low echo lucent plaque was observed at the right internal carotid artery and the mean blood flow velocity in the right carotid artery was decreased. She was placed on oral prednisolone and warfarin for suspected stroke due to hypercoagulability associated with vasculitis. Afterwards, she discharged from our hospital. Two months later, she was readmitted to our hospital because of irregular menses and vaginal bleeding. Endometrial uterus biopsy was conducted, which revealed a grade I endometrioid adenocarcinoma. She was under total uterectomy without tumor recurrence. After the radical operation, white-cell count, RF, CRP, TAT, D-dimer, F1 + 2, and beta TG were normalized, and the mean flow velocity of the right common carotid artery was increased. Thereafter, she did not experience stroke recurrence. Therefore, we speculated that she had stroke due to hypercoagulability in association with malignancy, that is Trousseau's syndrome. We also assumed that aseptic meningitis, brainstem encephalitis associated with vasculitis in this patient are other clinical variants of paraneoplastic syndrome through immunological mechanisms associated with malignancy. We emphasize that patients with Trousseau's syndrome can be associated with other paraneoplastic manifestations such as vasculitis as seen in this patient.
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PMID:[A young patient with endometrioid adenocarcinoma who suffered Trousseau's syndrome associated with vasculitis]. 1247 93

L-asparaginase is frequently used in combination therapy for the treatment of lymphoid malignancies. We report 5 children aged between 8 and 14 years with neurologic complications presenting with headache and seizures during the first three weeks of L-asparaginase treatment. Three patients had venous thrombosis, one presented a parenchymal hemorrhage, and one showed a peculiar encephalopathy with extended cortical and subcortical lesions suggesting a neurotoxic reaction. Decreased fibrinogen and antithrombin III levels were found. Early MRI is critical even in cases with mild neurologic symptoms. Diagnosis should be followed by early cessation of l-asparaginase application.
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PMID:Cerebrovascular complications of L-asparaginase in the therapy of acute lymphoblastic leukemia. 1279 28

Migraine is a common and chronic disorder. It is considered benign but several studies have suggested it as a rare risk factor for ischaemic stroke. The association is still conflicting and seems to be restricted to particular subgroups of patients (i.e., women under the age of 45, with migraine with aura, and particularly ones who smoke and use oral contraceptives). The pathogenetic mechanisms underlying this condition are not known. We describe 6 cases of migrainous stroke fully meeting the diagnostic criteria of the International Headache Society (IHS). For each patient, demographic and anamnestic data, clinical features, results of laboratory tests and neuroimaging findings were recorded. Five of the 6 cases were women (median age of 29, range from 23 to 40). The man was 36. All patients fulfilled the IHS criteria for migraine with aura. At the time of the event, 2 patients were taking oral contraceptives and smoked, one patient smoked and three patients had no vascular risk factors. The stroke manifested as homonymous hemianopia in 3 patients, lower homonymous quadrantopia in 1 patient and sensory symptom in 1 patient. The neurological examination was normal in 1 case. All patients underwent several tests with negative results: blood test (antithrombin III, protein C or S, autoantibodies), transthoracic and transoesophageal echocardiography, extracranial and intracranial Doppler sonography, and angiography which was not performed in 1 patient. All patients had a cerebral infarct visible on neuroimaging study (MRI): posterior cerebral artery in 4, middle cerebral artery in 1 and anterior cerebral artery in 1. We support the findings reported by others that migrainous stroke is more common in young women affected by migraine with aura. In consideration of the high prevalence of migraine in the population, further research is indicated and necessary to establish if migraine is independent from other vascular risk factors.
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PMID:Migrainous cerebral infarction: case reports. 1554 69

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

We encountered a 10-year-old girl with fluctuating sensorineural hearing loss, episodic headache, and white matter stroke. Strenuous exercise, febrile illness, and general anesthesia all temporarily worsened hearing. Audiologic findings were asymmetric: left-sided retrocochlear dysfunction consistent with auditory neuropathy contrasted with cochlear hearing loss in the right ear. Platelets obtained during a headache-free period showed excessive responsiveness to collagen in vitro, while episodic elevations of thromboxane B(2) and thrombin-antithrombin III complex were noted in blood sampled during headache. Treatment of hyperaggregability of platelets with aspirin and antioxidant vitamins relieved headache, while adenosine triphosphate administration improved hearing thresholds. In this patient, hearing impairment and white matter strokes appeared to respectively related to impaired blood flow to the cochlea and white matter caused by platelet dysfunction triggered by physiologic stresses.
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PMID:Fluctuating hearing loss, episodic headache, and stroke with platelet hyperaggregability: coexistence of auditory neuropathy and cochlear hearing loss. 1616


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