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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe six cases of cerebral venous thrombosis in patients with systemic lupus erythematosus. In one patient, cerebral venous thrombosis was the initial manifestation of lupus; in the five others, it occurred 1-33 years after the diagnosis of lupus. The main clinical features of cerebral venous thrombosis were persistent headache in all six patients, focal symptoms in four, and seizures in three; papilledema was present in only one patient. Cerebral venous thrombosis was diagnosed based on angiography or magnetic resonance imaging. Both the transverse (in five patients) and the superior sagittal (in three) sinuses were involved. Extracranial arterial and/or venous thrombosis were present in three patients, abortion in two, thrombocytopenia in four, and lupus anticoagulant in three. The neurologic symptoms resolved rapidly in five patients treated with steroids and heparin. Cerebral venous thrombosis should be suspected in patients with lupus who complain of persistent headache, especially in the presence of neurologic symptoms.
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PMID:Cerebral venous thrombosis in systemic lupus erythematosus. 200 96

A 9-year-old girl with recurrent episodes of unconsciousness, with or without convulsions, was reported. The episodes, which have been observed 9 times over the last 6 years, were characterized by generalized or hemi-convulsions, associated features of headache and vomiting, disturbance of consciousness lasting for a few days, slow activity on EEG continuing for a few weeks after the episodes and no prophylactic effect of anticonvulsants. Repeated EEG examinations revealed no epileptic discharges. Cerebral angiography showed corkscrew-like veins in the frontal region. Cerebral venous thrombosis is strongly suggested as the underlying cause of her episodes.
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PMID:Cerebral venous thrombosis associated with recurrent epilepsy-like attacks. 281 99

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

We report a series of nine patients younger than 45 years with angiographically-documented cerebral venous thrombosis, consecutively referred to our Stroke Unit from 1988 to 1994. Two of them were men and seven were women. Eight patients initially complained of headache, often associated with other symptoms of increased intracranial pressure. Seven patients had focal motor deficits and four suffered from epileptic seizures. None of the patients died. Only one patient remained severely disabled, whereas the others recovered self-sufficiency within two months. The use of oral contraceptives was closely associated with the occurrence of venous thrombosis in the women. Cerebral venous thrombosis is to be kept in mind in the differential diagnosis of stroke in the young.
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PMID:Cerebral venous thrombosis in young adults. Experience in a stroke unit, 1988-1994. 897 48

Cerebral venous thrombosis (CVT) is less frequent than arterial thrombosis, however, it is still frequently overlooked. Pathophysiologically it is characterized by a disturbance of the equilibrium between endogenous thrombogenic and fibrinolytic factors. In addition, the time course depends on the presence or absence of efficient venous collaterals. A wide variety of clinical symptoms do occur, however, they may be grouped into at least four relatively typical syndromes: a) the pseudotumor cerebri syndrome, b) the combination of headache and focal neurologic deficit, c) the combination of focal epileptic seizure (with or without Todd's paresis) and headache, and d) deep CVT characterized by headache, nausea, bilateral long-tract symptoms and usually a rapidly progressing decline in the level of consciousness. Two diagnostic routes are generally accepted, the one consisting of cranial computed tomography plus radiographic angiography, the other one consisting of magnetic resonance imaging and magnetic resonance angiography. The mainstay of therapy is partial thromboplastin time-effective anticoagulation (PTT at least doubled, target PTT between 80 and 100 secs). Anticoagulation should be performed even if intracranial hemorrhage is present. In cases where deterioration occurs despite effective heparin treatment and in subjects presenting with stupor or coma, more aggressive therapy, e.g., local fibrinolysis during venous angiography, may be considered.
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PMID:Dural sinus and cerebral venous thrombosis. 943 85

Dr. Pfausler and colleagues report in this issue of Journal of Travel Medicine a series of patients with an interesting and potentially fatal neurovascular disorder; they raise the question, is this condition more frequent in travelers? Over a period of 18 months, Dr. Pfausler and colleagues identified five of fifteen consecutive patients presenting with occlusion of the cerebral veins who had been traveling on long distance flights. Some of these patients also had a history of diarrhea, and exposure to heat or dehydration associated with their air travel. It is important to note that their air travel experience was also associated with other precipitating factors in several of the cases. One patient had been mountaineering at high altitude and also had donated plasma. Another had severe diarrhea. A third patient was taking oral contraceptives. Whereas more than a coincidental link appears to be related to air travel, some of the authors' statements implying causality should be qualified in the absence of a larger, more formal, epidemiologic analysis. How might air travel lead to cerebral venous thrombosis? In clinical practice, thrombosis of the cerebral veins most commonly occurs after trauma or infection of the head and neck. However, thrombosis is also seen in conditions of heightened coagulability or viscosity. One could conjecture that prolonged air travel in a cabin, pressurized to the equivalent of high altitude, might lead to compensatory hemoconcentration and heightened blood viscosity, which could be aggravated further by other conditions such as diarrhea or oral contraceptive use. A critical point made by the authors is that the clinical presentation of cerebral venous thrombosis differs from that of conventional stroke. Patients with venous occlusion often present with headache and behavioral abnormalities, which often lead to a mistaken diagnosis of psychogenic illness before seizures or signs of increased intracranial pressure become obvious. Neurologists are trained to have a high index of suspicion for this condition in patients with trauma, infection, or in the peri-partal period. If the observations of Pfausler et al are confirmed, we should add prolonged air travel to the list of predisposing conditions. Cerebral venous thrombosis is a very treatable type of stroke. Major morbidity is due to increased intracranial pressure, which can be relieved by steroids or dehydrating agents. Treatment of underlying infection or hypercoagulability is critical. In the past, most patients were given anticoagulants, despite the risk of hemorrhage into a venous infarct. If the major draining veins of the brain are affected - in particular, the sagittal sinus - a malignant form of increasing intracranial pressure with high morbidity ensues. Recently, direct infusion of thrombolytic agents in the venous sinuses through a retrograde placed catheter has been used in patients with this condition. Cerebral venous thrombosis can be diagnosed readily with magnetic resonance imaging and angiography, which have largely replaced conventional angiography in suspected cases. The development of thrombolytic therapy for acute occlusive stroke and the demonstration of its efficacy and relative safety in carefully selected patients1 have focused attention on the need for ultra-fast recognition and treatment of cerebrovascular disease. As stroke enters the era of emergency therapy, all health professionals, including those who care for air travelers, should be aware of the various presentations of stroke syndromes and the need for urgent therapy.
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PMID:Cerebral Venous Thrombosis - a new diagnosis in travel medicine. 981 40

Cerebral venous thrombosis (CVT) is being diagnosed more frequently with the use of advanced radiologic imaging. The presentation of CVT includes a wide spectrum of nonspecific symptoms with headache predominating. We present a case with acute, severe headache. The evaluation included a head computed tomography (CT) scan that was normal. The presence of opacified sinuses led to treatment for sinusitis. The patient returned the following day with a generalized tonic-clonic seizure. A magnetic resonance imaging (MRI) study identified an isolated cortical venous thrombosis. This patient was treated with anticonvulsant and anticoagulation therapy. A CVT is an unusual cause of headache and should be considered in patients with atypical presentation or associated seizure, or who are refractory to current therapy. Diagnosis may be made with MRI. Resolution and complete recovery are possible with appropriate therapy.
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PMID:Headache: cortical vein thrombosis and response to anticoagulation. 1033 37

Venous infarcts are uncommon and frequently misdiagnosed as arterial infarcts, intracerebral haemorrhages or tumours on CT. Cerebral venous thrombosis is a condition with large variety of causes. However, in 20 to 35% of causes, no cause is found. The clinical features depend on the location of venous thrombosis. Clinical signs are mainly headache, hemiparesis, cranial nerves paresis, epilepsy, TIA. The question about the proper way of treatment and duration of treatment remains open.
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PMID:[Venous infarcts]. 1125 82

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 (CVT) associated with minor or trivial head trauma has only been described in a few cases so far. We report two patients who developed CVT after a sudden intracranial pressure increase and head acceleration. A 49-year-old woman jumped from a small rock, 1 m in height, and developed instantaneous occipital headaches. Magnetic resonance imaging (MRI) confirmed confluens sinuum thrombosis. Risk factors consisted of smoking and oral contraceptives. Our second patient, an 18-year-old woman, experienced instantaneous headaches after a sneezing attack. Superior sagittal and right-sided transverse sinus thrombosis were confirmed by venous computed tomography angiography. She took oral contraceptives as an additional risk factor. In about 20% of CVT cases the cause remains unclear. As minor head trauma may not have been recognized during history taking, this may represent a so far under-recognized precipitating factor for CVT.
Headache 2004 Sep
PMID:Sinus thrombosis after a jump from a small rock and a sneezing attack: minor endothelial trauma as a precipitating factor for cerebral venous thrombosis? 1533 Aug 29


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