Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
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From 1988 to 1990, we observed five cases of aseptic dural sinus and cerebral venous thrombosis, all in non-smoking women (age 18 to 47 years) receiving low dose oral contraceptives. Treatment consisted of full anticoagulation over 2 to 6 months, over which time the neurologic symptoms disappeared almost completely. Extensive tests of the blood clotting system in 4 patients after 6 to 19 months revealed a reduction of free protein S in 2 patients with a history of contraceptive use over several years, and normal results in 2 patients in which the sinus thrombosis occurred within the first 6 weeks of use of the oral contraceptive. Whether the protein S deficiency was congenital or caused by the oral contraceptive cannot be decided retrospectively. Even modern oral contraceptives seem to lead to an increased incidence of sinus thrombosis. Initial symptoms of sinus thrombosis include headache and somnolence, followed either by focal neurologic deficits (often associated with focal seizures) or by signs of increased intracranial pressure. CT scans show venous infarcts or general brain edema and may specifically show the "empty triangle sign" and "delta sign". The CT scan may also be normal if focal neurologic deficits are absent. MRI is favoured as it can directly show the thrombosed sinus or veins. Differential diagnosis includes arterial stroke, brain tumor, encephalitis or "benign intracranial hypertension", which should only be diagnosed after sinus venous thrombosis has been appropriately ruled out. Recently, full anticoagulation has been recommended as therapy.
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PMID:[Aseptic cerebral sinus thrombosis. 5 cases and a review]. 194 57

A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
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PMID:Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus. 763 1

A 27-year-old woman suffered from a sudden onset of slight paralysis of the right side of her body and the inability to express herself by speech, writing, or signs. She was admitted to the National Rehabilitation Hospital in Washington, D.C., in the US. 6 months prior to these events, she had been in a motor vehicle accident and had since experienced headaches and generalized musculoskeletal pain. The only drug she took was an oral contraceptive (OC), which she took irregularly. Health workers could not arouse her upon admission. Clinical examination revealed symptoms consistent with a left hemispheric stroke. Cerebral computed tomography and magnetic resonance imaging revealed a left temporoparietal infarct. Her free protein S was only 27% on admission and 14% 11 days after admission (normal range, 55-125%). Over the next 72 hours, her physical condition deteriorated, entailing focal motor seizures, right Babinski's sign, loss of pain reflex response on her right side, and complete paralysis of the right side of her body. The left middle cerebral artery appeared to be constricted, which physicians first believed was caused by vasculitis but later found was the result of emboli. The patient developed right femoral vein deep thrombosis. The physicians treated her initially with heparin and followed with warfarin therapy. Nevertheless, embolus. Health workers placed a filter in her inferior vena cava and continued warfarin therapy. She did not experience any more thrombotic or embolic episodes during the rest of her hospital stay. OCs reduce circulating levels of free protein S which, along with activated protein C, inhibits clotting. OCs likely reduced her already existing low levels of free protein S. Deficiency of free protein S was likely responsible for the cerebral infarction and her thrombotic and embolic episodes.
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PMID:A case of cerebral infarction in association with free protein S deficiency and oral contraceptive use. 823 70

A 43-year-old man suffered generalized convulsions following severe headache. Initial angiography showed a dural arteriovenous fistula (DAVF) involving the right transverse-sigmoid sinus, and no contrast filling of the superior sagittal sinus, bilateral transverse sinuses, the left sigmoid sinus and the straight sinus. The diagnosis was extensive sinus thrombosis associated with DAVF. Transarterial embolization was performed for the DAVF. The follow-up angiography at 7 days postembolization showed no contrast filling of the DAVF. But the follow-up angiography at 6 months disclosed the appearance of multiple DAVF's involving the superior sagittal sinus, the left transverse sinus and the straight sinus. Each DAVF was supplied by different dural arteries. Coagulation tests revealed deficiency of plasma protein S. The pathogenesis of DAVF is controversial. But our case suggests that multiple isolated lesions indicated the presence of a congenital dural vascular abnormality, which was transformed to multiple DAVF's by sinus thrombosis.
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PMID:[Multiple dural arteriovenous fistulas following extensive sinus thrombosis: a case report]. 893 93

Cerebral sinus thrombosis associated with protein S deficiency is rare to the best of our knowledge. We report here a 22-year-old female who presented sudden onset of headache, vomiting and disturbance of consciousness. Neuroradiological studies including computed tomography scan, magnetic resonance imaging and cerebral angiography disclosed a huge cerebral sinus thrombosis in the territory of the superior sagittal sinus, torcular herophili, lateral sinus and straight sinus. Hematological studies confirmed the diagnosis of protein S deficiency. We summarize the reported cases of cerebral sinus thrombosis associated with protein S deficiency. For young patients presenting occlusive cerebrovascular disease, we stressed the importance of doing extensive hematological investigation to detect possible etiological factors, such as protein S deficiency, protein C deficiency, antithrombin III deficiency. Once we discover the etiology of a disease, we may be able to designate the precise treatment or regimen for each patient.
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PMID:[Cerebral sinus thrombosis in a patient with protein S deficiency: a case report]. 914 7

A 24-year-old woman presented with headache of 6 days' duration, described as throbbing pain in the right periorbital region radiating to her right ear and neck. The pain was unresponsive to oral analgesics. She had no speech or hearing difficulties, no previous history of migraines, and no family history of neurologic disease. Her medications included oral contraceptives for 8 months' duration. This report describes the salient features of dural sinus thrombosis and recent advances in diagnostic and therapeutic procedures. The relationship between oral contraceptives and protein S levels is also discussed. Cerebral dural sinus thrombosis should be considered in the differential of new onset of headaches, seizures, or focal neurological deficits.
Headache
PMID:Transverse sinus thrombosis: an unusual cause of headache. 927 32

Migraine, particularly migraine with aura (MA), may be a risk factor for ischemic stroke (IS). The reasons for this association are unknown. We investigated the presence of genetic abnormalities of the protein C system in 83 MA patients, 31 IS patients, and 124 healthy controls, all aged under 45 years. We found an increased frequency of activated protein C resistance due to Arg506Gln factor V mutation, and of protein S deficiency in both disorders, with figures higher than those reported in the general population and significantly different from those found in controls. These prothrombotic genetic abnormalities may be shared risk factors in IS and MA, and may play a role in increasing the risk of cerebrovascular disease in migraineurs.
Cephalalgia 1998 Nov
PMID:Genetic abnormalities of the protein C system: shared risk factors in young adults with migraine with aura and with ischemic stroke? 987 85

The authors describe two cases of cerebral venous thrombosis (CVT) in patients with nephrotic syndrome. The main clinical features of CVT were persistent headache, hemiparesis, and seizure, and the diagnosis was based on magnetic resonance imaging and magnetic resonance angiography. Both showed acquired deficiency of free protein S. The neurologic symptoms remained stationary in the first patient, who received no anticoagulation therapy, but resolved rapidly in the second, treated with intravenous heparin and supplemented with fresh frozen plasma. CVT should be suspected in patients with nephrotic syndrome who present with symptoms of intracranial hypertension or any focal neurologic deficit.
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PMID:Cerebral venous thrombosis in patients with nephrotic syndrome--case reports. 1034 32

Moyamoya disease is a cerebrovascular disease with progressive occlusion of both internal carotid arteries and of their branches and formation of a new vascular network at the base of the brain. Because of the angiographic appearance, it is named as moyamoya. The clinical features are cerebral ischaemia, recurrent transient ischaemic attacks, sensorimotor paralysis, convulsions and migraine-like headaches. A 10-year-old child who acutely developed hemiparesis, weakness and aphasia was found to have moyamoya disease and heterozygous protein S deficiency. This case shows us that during the thromboembolic events the coexistence of protein S deficiency and moyamoya should be investigated.
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PMID:Moyamoya syndrome with protein S deficiency. 1100 63

Thrombosis of deep cerebral veins is a rare condition, and is associated with a poor prognosis. We report four new cases observed between 1994 and 1997. All four cases were women, aged less than 45 years. Initial symptoms associated alteration of consciousness, change in mental status, progressive headache and vomiting. We observed also uni or bilateral signs of long tract injury. In three cases, diagnosis initially suspected by CT scan was confirmed with encephalic MRI. For the last patient, conventional angiography was needed. Thrombosis affected straight sinus, vein of Galien and internal cerebral veins in all patients. Basilar veins were also affected in one patient, without dural sinuses extension. Lateral sinus was involved in two others cases, and superior sagittal in the last patient. Etiology remains undetermined in one patient, associated with post-partum, use of oral contraceptive pill, and familial protein S deficiency, one case each. Outcome was favorable in all four cases with anticoagulation therapy. Precocity of diagnosis is determinant and MRI is usefull in this issue. These observations show that evolution of deep veins thrombosis can be favorable, without needing fibrinolytic therapy.
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PMID:[Thrombosis of deep cerebral veins in form adults: clinical features and diagnostic approach]. 1103 13


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