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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
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PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

Homocystinuria with elevated plasma homocysteine and methionine levels is the result of deficient activity of cystathionine synthetase, the enzyme catalyzing conversion of homocysteine to cystathionine. It is inherited as an autosomal recessive trait with a worldwide distribution. The major clinical manifestations result from the elevated plasma homocysteine level. The excitotoxic effect of homocysteic acid accounts for mental retardation and seizures. Interference with collagen cross-linking by sulfhydryl groups of homocysteine causes ectopia lentis and skeletal deformities. Sulfation factor-like effects contribute to disruption of vascular endothelium, which is followed by platelet thrombosis and widespread arterial and venous occlusions. Low methionine homocystinuria, with deficient remethylation of homocysteine, results from deranged vitamin B(12) metabolism and from deficient 5,10-methylene-tetrahydrofolate reductase. Administration of azaribine produces homocystinuria by mechanism not yet elucidated.
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PMID:Homocystinuria: pathogenetic mechanisms. 32 77

Three patients with left atrial myxoma presented with prominent neurologic symptoms and signs (cerebrovascular disease and/or syncope) within the past year. Two patients died because antemortem diagnosis was late or missed. One patient was successfully treated. Cardiac myxoma produces protean clinical manifestations that do not always include cardiac signs and symptoms. Neurologists may be called on for diagnostic consultation in patients who will prove to have cardiac myxoma. Unexplained transient ischemic attacks, cerebral infarction, or syncope (with possible features of seizure activity) are common neurologic manifestations of this disease. Additionally, systemic symptoms, signs, and laboratory data suggestive of collagen vascular disease or vasculitis are also often present. Echocardiography is a dependable noninvasive procedure for a confirmation of diagnosis in suspected cases.
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PMID:Cardiac myxoma: a diagnostic challenge for the neurologist. 98 13

The neurological manifestations of six cases of acquired central nervous system toxoplasmosis are compared with the 39 well-documented cases from the literature. Half of the patients had underlying systemic diseases (18 malignant neoplasms, two renal transplants, three collagen vascular diseases) treated with intensive immunosuppressive therapy. The remainder had primary toxoplasmosis. Three major neurological patterns were seen: (1) diffuse encephalopathy with or without seizures, (2) meningoencephalitis, and (3) singular or multiple progressive mass lesions. Routine neurological diagnostic studies were not helpful. The Sabin-Feldman dye test or IgM indirect fluorescent antibody test or both were effective in confirming the diagnosis. Twenty-seven patients died without a clinical diagnosis of toxoplasmosis. The diagnosis was made terminally in four additional patients. Thirteen of fourteen patients who received a full course of sulfadiazine or pyrimethamine or both did well. Toxoplasmosis should be considered in the immunosuppressed patient who appears with neurological involvement.
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PMID:Acquired toxoplasmosis. A neglected cause of treatable nervous system disease. 109 93

A case of giant aneurysm arising from the anterior communicating artery, 24 X 28 X 30 mm in diameter was found in a 30 year old man. About ten years ago he became blind and recently developed right anosmia and diencephalic seizures. No subarachnoid hemorrhage, however, was found. Radiograms and tomograms of the cranium showed a ring-like calcification, but by angiography it couldn't be recognized as a giant aneurysm. The right frontal craniotomy and partial resection, therefore, was performed. A histological study of the resected material revealed that it was a spontaneously thrombosed giant aneurysm. The inner layer of its wall had neither endothelium nor elastic lamina, but had deposits of calcium salt. The outer layer was composed of collagen fibers without cell infiltration. The aneurysm was thrombosed except for its neck but its organization occurred incompletely. We want to emphasize the importance of a correct preoperative diagnosis, as an erroneous operative procedure can result in disaster. Volume, viscosity and tension of flowing blood into the aneurysm as well as the size of its neck and dome regulate dynamic properties. These properties may determine the enlargement rate or growth of the aneurysm. The dynamic characteristics and features of the inner surface of the aneurysmal wall may regulate the formation of thrombosis in the aneurysm. The intraluminal thrombosis and strength of aneurysmal wall, for example, calcium deposits, may prohibit aneurysm from its rupture.
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PMID:[Giant anterior communicating artery aneurysm (author's transl)]. 123 24

The author presents and discusses the anaesthetic implications of a four-month-old infant with Menkes' syndrome who required tracheostomy. Menkes' syndrome is an X-linked recessive disorder of copper absorption and metabolism. Defective processing of copper results in abnormalities of several enzyme systems leading to severe dysfunction of multiple organ systems. Due to the progressive nature of this disorder and its severe effects on several different organ systems, most importantly the central nervous system, these children frequently require anaesthetic care during imaging procedures such as MRI or during various surgical operations. The high prevalence of seizure disorders, gastroesophageal reflux with the risk of aspiration, and airway complications related to poor pharyngeal muscle control are of concern to the anaesthetist. In addition, defective collagen formation, similar to that seen in Ehlers-Danlos syndrome, may be present. Identification of these associated conditions during the preoperative examination will guide the selection of appropriate, safe anaesthetic care for these children.
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PMID:Anaesthetic considerations in the child with Menkes' syndrome. 139 61

Discussed is an 8-year-old girl with a history of convulsive seizures. A sharply demarcated tumor, measuring 3 X 4 cm, was located in the right frontal lobe. The mass grey and cystic in the center, and microscopic specimen demonstrated bizarre, irregular, giant cell with a long vesicular nuclei and spindle-shaped cell. A perivascular pseudo-rosette formation also was seen, and silver impregnation revealed reticulin network and extracellular collagen fibers. The pathological entity of an intracranial giant celled glioblastoma remains controversial. This entity is considered a giant celled glioblastoma by some and a monstrocellular sarcoma by others. In this that the authors experienced, a CT scan showed a ring that formed a high density area and low density in the center at the right frontal lobe. Also reviewed and discussed are the historical aspects of a giant celled glioblastoma and radiologic problems that have been encountered.
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PMID:[A giant cell glioblastoma--a case report]. 270 40

We describe a series of experiments in which a subhuman primate model was used to create temporary and permanent cerebral ischemia by three separate mechanisms. In the first group of five baboons, a hemodynamic model was produced by creating unilateral and bilateral carotid stenotic lesions of varying degrees with and without associated reduction in systemic perfusion pressure. Only global ischemic changes and no focal changes resulted. In the second group of three baboons, a macroembolic model was produced by introducing solid particulate material into the extracranial circulation. No reversible contralateral focal neurologic changes resulted. In the third group of 11 baboons, cerebral ischemia was produced by introducing agents known to cause platelet aggregation (arachidonic acid, adenosine diphosphate, and collagen) into the extracranial arterial circulation. Arachidonic acid caused seizures, adenosine diphosphate caused severe postural hypotension, and only collagen fibrils produced a picture resembling a transient ischemic attack. We propose a theory that intravascular activation of the prostaglandin cascade by chemical initiation may result in the pathophysiologic changes of transient cerebral ischemia.
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PMID:Pathogenesis of transient ischemic attacks and stroke in baboons. 292 78

Although many systemic disorders involve the nervous system and may cause seizures, certain clinical features are unique to some illnesses. This article reviews seizures associated with collagen vascular disorders, vasculitidis, fluid and electrolyte disturbances, endocrine diseases, porphyrias, renal and hepatic disorders, and drugs. Emphasized are features associated with each systemic disorder that may aid in diagnosis and therapy.
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PMID:Seizures as a manifestation of systemic disease. 309 2

A case of false-negative Tc-99m MDP bone scintigrams, taken at one and two weeks for pathologic fractures in a patient with metabolic bone disease and a super-scan appearance, is described. The patient had renal osteodystrophy, and postparathyroidectomy hypocalcemia. Postoperative seizures caused multiple pathologic fractures. Initial scans were negative for focal tracer localization in the presence of a continued super-scan appearance. After months of calcium and vitamin D replacement therapy, fracture sites became positive on Tc-99m MDP imaging. The observations in this case lend credence to the hypothesis of Tc-99m MDP binding by immature collagen in the production of a super scan in metabolic bone disease, as well as that of Tc-99m MDP chemisorption to calcium hydroxyapatite crystal in fracture healing. In addition, aluminum toxicity, common in chronic renal osteodystrophy, may have played a role in the delayed fracture healing.
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PMID:Pathologic fractures in a patient with renal osteodystrophy. Failure of early detection on bone scans. 360 30


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