Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Records of 108 patients with lupus erythematosus beginning in childhood (1953-1990) were reviewed; 25 had recorded neurologic findings. This is the largest group of childhood lupus erythematosus patients with neurologic disease that has been reported. The average age of children at the time of diagnosis of lupus was 154 months. There were 22 girls and 3 boys in the group. All patients met at least four of the 1982 American Rheumatism Association criteria for the classification of systemic lupus erythematosus. Average age at onset of neurologic difficulties was 168 months. In 4 patients, the neurologic symptoms preceded the diagnosis: 1 month (spastic diplegia), 1 month (bilateral weakness and spasticity), 24 months (chorea), and 26 months (chorea), respectively. Four patients had neurologic symptoms coincident with the diagnosis of lupus erythematosus. In those patients whose symptoms followed the diagnosis of lupus erythematosus, the average elapsed time until symptoms appeared was 33 months; the single lowest and highest outliers were discounted. Most frequent findings were headache (16/25) and behavioral aberrations (10/25). All behavioral manifestations were depression except in 1 patient. Other prevalent findings included hemichorea or chorea (7/25), cerebrovascular accident with hemiplegia or diplegia (7/25), seizures (5/25), visual loss (3/25), and cranial neuropathy (2/25). Vertigo and myelopathy occurred in 1 patient each. All patients were treated primarily with corticosteroids and azathioprine; in the presence of active disease, the drug dosages were increased with significant improvement in neurologic symptoms. Resolution usually occurred from days to months; most improved in a few days to a few weeks; 3-4 months was the longest period until symptoms subsided.
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PMID:Neurologic characteristics of childhood lupus erythematosus. 855 56

The paradox of aerobic life, or the 'Oxygen Paradox', is that higher eukaryotic aerobic organisms cannot exist without oxygen, yet oxygen is inherently dangerous to their existence. This 'dark side' of oxygen relates directly to the fact that each oxygen atom has one unpaired electron in its outer valence shell, and molecular oxygen has two unpaired electrons. Thus atomic oxygen is a free radical and molecular oxygen is a (free) bi-radical. Concerted tetravalent reduction of oxygen by the mitochondrial electron-transport chain, to produce water, is considered to be a relatively safe process; however, the univalent reduction of oxygen generates reactive intermediates. The reductive environment of the cellular milieu provides ample opportunities for oxygen to undergo unscheduled univalent reduction. Thus the superoxide anion radical, hydrogen peroxide and the extremely reactive hydroxyl radical are common products of life in an aerobic environment, and these agents appear to be responsible for oxygen toxicity. To survive in such an unfriendly oxygen environment, living organisms generate--or garner from their surroundings--a variety of water- and lipid-soluble antioxidant compounds. Additionally, a series of antioxidant enzymes, whose role is to intercept and inactivate reactive oxygen intermediates, is synthesized by all known aerobic organisms. Although extremely important, the antioxidant enzymes and compounds are not completely effective in preventing oxidative damage. To deal with the damage that does still occur, a series of damage removal/repair enzymes, for proteins, lipids and DNA, is synthesized. Finally, since oxidative stress levels may vary from time to time, organisms are able to adapt to such fluctuating stresses by inducing the synthesis of antioxidant enzymes and damage removal/repair enzymes. In a perfect world the story would end here; unfortunately, biology is seldom so precise. The reality appears to be that, despite the valiant antioxidant and repair mechanisms described above, oxidative damage remains an inescapable outcome of aerobic existence. In recent years oxidative stress has been implicated in a wide variety of degenerative processes, diseases and syndromes, including the following: mutagenesis, cell transformation and cancer; atherosclerosis, arteriosclerosis, heart attacks, strokes and ischaemia/reperfusion injury; chronic inflammatory diseases, such as rheumatoid arthritis, lupus erythematosus and psoriatic arthritis; acute inflammatory problems, such as wound healing; photo-oxidative stresses to the eye, such as cataract; central-nervous-system disorders, such as certain forms of familial amyotrophic lateral sclerosis, certain glutathione peroxidase-linked adolescent seizures, Parkinson's disease and Alzheimer's dementia; and a wide variety of age-related disorders, perhaps even including factors underlying the aging process itself. Some of these oxidation-linked diseases or disorders can be exacerbated, perhaps even initiated, by numerous environmental pro-oxidants and/or pro-oxidant drugs and foods. Alternatively, compounds found in certain foods may be able to significantly bolster biological resistance against oxidants. Currently, great interest centres on the possible protective value of a wide variety of plant-derived antioxidant compounds, particularly those from fruits and vegetables.
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PMID:Oxidative stress: the paradox of aerobic life. 866 Mar 87

An 18-year-old female with 7 years' history of epilepsy was admitted for developing malar rash. She had been treated with hydantoin for 7 years. Laboratory examinations revealed leukopenia and high titer of anti-dsDNA antibodies. Renal biopsy also showed diffuse segmental mesangial proliferative glomerulonephritis. A diagnosis of systemic lupus erythematosus (SLE) was made, and she received 40 mg of prednisolone daily. At follow up 4 months later since her first visit, she developed choreiform movements involving the right upper and lower limbs, despite no signs of increase in her disease activity. Neither biological false positive testing for syphilis nor the lupus anticoagulant (LAC) was detected. MRI demonstrated no signal abnormalities in the brain. Administration of haloperidol was started and the choreiform movements were decreased. Anticonvulsants are associated with drug-induced lupus. On the other hand, seizure is known to be one of the first manifestations of SLE. In drug-induced lupus, positive testing for anti-dsDNA, anti-Sm antibodies, hypocomplementemia and renal involvement are not a frequent as in SLE. In this case, laboratory findings showed high titer of anti-dsDNA antibodies, positive testing for antihistone, anti-SSA, anti-Ki antibodies, and hypocomplementemia. And mesangial proliferative glomerulonephritis was detected. So we diagnosed her as SLE and suggested that epileptic seizure developed 7 years ago had been the first manifestations of SLE. Neurologic complications of SLE are common, but chorea has been rarely reported. Since it is known that LAC is associated with thrombosis, it has been suggested that small infarctions in the basal ganglia may play a part in the pathogenesis of chorea in SLE. In this case, the LAC was negative and MRI showed no detectable abnormalities. As a result another mechanism may be attributed to chorea in this case.
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PMID:[A case of systemic lupus erythematosus diagnosed 7 years after epileptic seizure and developed chorea during prednisolone treatment]. 877 91

To examine the association between anticardiolipin (aCL) antibodies and epilepsy, we investigated the serum titers of aCL antibodies in a total 252 systemic lupus erythematosus (SLE) patients recruited in a prospective study. Twenty-one cases with epilepsy which were not attributable to any causes other than SLE were identified after being followed-up for five years. The clinical manifestations were recorded and blood samples were tested for the presence of aCL antibodies (IgG, IgM and IgA isotypes). Among 21 patients with epilepsy, 12 (57.1%), 2 (9.5%) and 2 (9.5%), respectively, had elevated baseline serum levels of IgG, IgM and IgA aCL antibodies. There was a dose-response relationship between risk of seizure and the baseline serum level of aCL antibodies (P < 0.01). The odds ratio of developing seizure were 3.7 for those who had a high level of aCL antibodies compared with those without a detectable level of aCL antibodies as the referent. Our results indicate that epilepsy as a primary neuropsychiatric event among lupus patients is associated with a high titer of aCL antibodies.
Lupus 1996 Aug
PMID:Elevated levels of anticardiolipin antibodies and epilepsy in lupus patients. 922 72

Antiphospholipid antibodies (aPL) have been associated with a variety of neurological disorders, mostly linked to focal neuroparenchymal ischemia or infarction. Cerebral ischemia associated with the antiphospholipid syndrome (APS) occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and high positive GPL values are usually linked to the presence of a lupus anticoagulant. When other features of the syndrome are not present and cerebral ischemia occurs only associated with anticardiolipin immunoreactivity, there appears to be no discerning features of these patients unless GPL > 40 for which recurrent thrombo-occlusive events appear to occur more frequently. Other neurological manifestations associated with aPL include cerebral venous sinus thrombosis, ocular ischemia, dementia, including ischemic encephalopathy, and chorea. The role of aPL in migrainous events is controversial and may not play a role in recent, large case-controlled studies. Most seizures in patients harboring aPL are associated with focal brain infarction.
Lupus 1996 Oct
PMID:Neurological aspects of antiphospholipid antibody syndrome. 890 59

Antiphospholipid' (aPL) antibodies are of important clinical significance because of their association with thrombosis both arterial and venous, recurrent foetal loss, specific neurological sequelae like seizures and chorea, cardiac valvular abnormalities and thrombocytopenia. Traditionally these autoantibodies have been assayed using phospholipid (PL) dependent tests and are classified as lupus anticoagulants (LA) and anticardiolipin (aCL) antibodies based on the method of detection. The antibodies thus, had been thought to bind PLs but it has now become clear that the true antigens are PL-binding proteins. The major protein consistently found as the target antigen for these autoantibodies is beta 2-glycoprotein I (beta 2-GPI). Other candidate PL-binding proteins have also been investigated including prothrombin, protein C and protein S but thus far appear to play less important roles in the binding of these antibodies.
Lupus 1996 Oct
PMID:beta 2-Glycoprotein I: target antigen for autoantibodies in the 'antiphospholipid syndrome'. 890 65

Neuropsychiatric symptoms are recognized to occur in a significant percentage of systemic lupus erythematosus patients and to be a leading cause of morbidity and morality in lupus. Recent findings regarding the clinical presentation, diagnosis, pathogenesis, and treatment of neuropsychiatric lupus erythematosus are reviewed. The study of neurocognitive deficits and psychosocial functioning in systemic lupus erythematosus patients continues to be an area of great research interest worldwide. Severe neuropsychiatric manifestations can be divided into diffuse, focal, and seizure presentations, which can each have a different etiopathogenesis. New techniques for magnetic resonance imaging and single-photon emission CT of the brain may improve the utility and sensitivity of these neuroradiographic tests. Certain combinations of serologic, cerebrospinal fluid, and neuroimaging tests appear to be most useful diagnostically when ordered based on the patient's neurologic presentation. The role of complement, cytokines, and endothelial cell activation in causing the vascular pathology observed in the brains of neuropsychiatric lupus erythematosus patients is an area of promising research. Treatment remains empiric, but intravenous pulse cyclophosphamide and intrathecal administration of immunosuppressive medications are new approaches that have been used successfully to treat patients with severe and refractory symptoms.
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PMID:Lupus and the central nervous system. 894 43

A 31-year-old woman with systemic lupus erythematosus presented with respiratory and renal symptoms followed by abdominal pain and seizure. Clinical diagnoses of lupus pneumonitis, nephritis, vasculitis, and cerebritis were made. The patient had a progressively downhill course with pancytopenia and hemolysis treated with aggressive immunosuppressive therapy and extended plasmapheresis. Lupus pneumonitis leading to diffuse alveolar damage was the immediate cause of death. Diffuse proliferative lupus nephritis was seen in the biopsy, and the autopsy demonstrated thrombotic microangiopathy. Extra-renal complications of lupus and response to therapy are discussed in the format of a Tulane Clinicopathologic Conference.
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PMID:A 31-year-old woman with lupus erythematosus and fatal multisystem complications. 915 Jun 65

Neonatal seizures in the neonatal period are symptoms of numerous underlying disorders of the neonate. We present a case in which neonatal seizures due to cerebral infarction led to a diagnosis in the mother. Neonatal convulsions caused by cerebral artery thrombosis is relatively rare in the neonatal period and is often secondary to indwelling intravascular catheters that cause thromboembolism, but may be associated with many conditions.1 Cerebral artery thrombosis in newborns, in which antiphospholipid antibodies (APA) were found in the mother, has been described in three case reports. Two of these premature infants were born with other risk factors for thrombosis. APA could not be identified in any of these three infants. In the two cases reported by Silver et al the diagnosis was made several months after birth. This case is unique in the fact that no other risk factors for thrombosis could be identified to explain the infarction, and that APA were found in the offspring of an apparently healthy mother. Whether the prior fetal death was caused by APA remains unclear. The finding of lupus anticoagulant in her child led to the diagnosis of antiphospholipid antibody syndrome in her. We believe that in case of cerebral artery thrombosis in a neonate, with no trivial cause such as an indwelling catheter or sepsis, both mother and infant should be tested for presence of APA, even when the mother seems healthy.
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PMID:An unusual cause of neonatal seizures in a newborn infant. 931 May 41

The first case of systemic lupus erythematosus (SLE) was reported from India in 1995 followed by two more case reports and further, a series of eight cases, till 1969. Since the establishment of a clinical immunology laboratory at a major teaching institution in New Delhi in 1968, SLE was extensively studied and reported from that centre. From mid-1980 onwards several other centres in different regions in India including Chennai (old name Madras), Mumbai (old name Bombay), Calcutta and Hydrabad, also published their regional experience on SLE. Based on these data, the present report describes the clinical and laboratory characteristics of 1366 SLE patients seen in different regions of India. Arthritis, rash, photosensitivity, seizures and psychosis were seen in comparable proportions to other racial groups. Similarly, ANA and anti-DNA antibody positivity was also within the range seen in other racial groups. When compared with other series, however, alopecia, renal lupus, oral ulcers and neurological involvement was seen in higher proportions, reaching statistically significant figures in comparison to some racial groups. In contrast, haematological manifestations were seen in significantly less proportions in comparison to some of the racial groups. Serositis and discoid lesions were also seen in lower proportions than in most of other races. The proportion of those with anti-Sm antibodies was in between two extremes of highest among Africans and Israelis and lowest among Chinese and Europeans. Other manifestations were comparable to most other racial groups. Compared to North American and European reports, significantly low 5 and 10 year survival was observed among patients from India. This could be related to the general public health situation in the country including less than optimal management facilities in hospitals, delay in diagnosis due to lack of awareness of the disease, referral bias where only serious patients reach major city hospitals, or a truly severe disease among Indians, or a combination of these genetic, environmental and/or sociocultural factors. The Main causes of death were irreversible renal damage, infections and neurological involvement. Despite a comparable prevalence of anticardiolipin antibodies (aCL) and lupus anticoagulants (LAC), clinical antiphospholipid syndrome was significantly less common. Genetic studies showed appreciable increase of HLA DR4 (37.5%) among patients compared with controls (18%). Additionally the haplotype B8-DR3 was encountered frequently in the patient group.
Lupus 1997
PMID:Systemic lupus erythematosus in India. 941 83


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