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)

An examination has been carried out of 46 patients (33 females, 13 males, a mean age 40) with Sneddon's syndrome characterized by cerebrovascular disturbances and marked livedo. A clinical spectrum of the syndrome included miscarriage and intrauterine death of the fetus (20 cases), peripheral vein thromboses (12 cases), coronary heart disease (18 cases), thrombocytopenia (8 cases), arterial hypertension (27 cases), headache (39 cases), epileptic seizures (5 cases). Similar manifestations are usually seen in antiphospholipid syndrome (AFLS). Antibodies to phospholipids, those to cardiolipin, lupus anticoagulant were detectable in 78, 50 and 61% of the cases, respectively. Clinical and immunological signs of AFLS in the absence of SLE-typical symptoms provided grounds for considering them primary AFLS. Similar clinical patterns in 36 patients with cardiolipin antibodies and/or lupus anticoagulant and 10 patients without the antibodies and anticoagulant suggest these cases to be AFLS too.
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PMID:[Sneddon's syndrome and the primary antiphospholipid syndrome]. 805 89

We report a 47-year-old woman with SLE, who developed meningeal signs and consciousness disturbance. She noted an onset of fever, and swelling and pain in her face, hands and feet in 1990. She was seen in another hospital and the diagnosis of SLE was made. She was treated with prednisolone with marked improvement in her symptoms. She was well with 5 mg of oral prednisolone daily until January of 1991, when she developed fever, myalgia and weakness in her legs. She was admitted to the medical service of our hospital on August 5. She was receiving 15 mg of prednisolone daily. Gram positive rods were cultured from her blood on August 5. She became incoherent 2 days later, and had a convulsive episode on August 8. After the convulsion, she lost consciousness from which she did not recover. Her CSF contained 304/3 microliters cells, 29 of which were neutrophils, 6 lymphocytes, 90 others, and 179 destructed cells. The CSF protein content was 345 mg/dl, and glucose 23 mg/dl. A neurological consultation was asked on August 9. Physical examination at that time revealed a semicomatous woman. Respiration was 30/min and regular. BP 132/82 mmHg, heart rate 122/min and regular, and BT 39.6 degrees C. General physical examination was unremarkable. Pertinent neurologic findings were positive Kernig sign and spasticity in all four limbs. Brain stem reflexes were retained. Upon painful stimulation, withdrawal response was elicited both lower extremities. She was treated with pipiracillin, latamoxef and phenobarbital, however, she had frequent seizures. She was deeply comatose on December 10. She became flaccid and no more meningeal signs were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 47-year-old woman with meningeal signs and consciousness disturbance]. 821 15

Magnetic resonance imaging (MRI) of the brain is a sensitive method to detect parenchymal tissue lesions. Its value in the diagnosis of central nervous system (CNS) lupus is disputed. To address this question, we have conducted an open and prospective study in a population of 44 SLE patients. We investigated 24 patients (mean age 33 +/- 13 yr) with past or active CNS lupus (group A) that included organic brain syndrome (12), migraine (8), focal neurological signs (7), seizures (2), myelopathy (1) and narcolepsy-cataplexy (1), and 20 patients (mean age 32 +/- 12 yr) without CNS lupus (group B). Health controls comprising nine females and one male aged 31 +/- 9 yr were also studied for comparison (group C). MRI was performed using sagittal T1-weighted images, axial and coronal spin density, and T2-weighted images. All scans were read blindly. Thirteen patients in group A and 10 in group B had well-identified lesions on sequences with long repetition time. Lesions were mostly multiple, small, punctate areas of increased signal at periventricular or subcortical white matter of both cerebral hemispheres. The number and location of lesions were not significantly different in both groups. None of the group C patients had MRI lesions. The presence of lesions was significantly associated with age at study and disease duration, but not with the presence of CNS lupus. In summary, MRI abnormalities are detected in neurologically asymptomatic SLE patients. Whether this represents subclinical brain involvement remains unknown.
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PMID:Magnetic resonance imaging of the brain in systemic lupus erythematosus. 854 7

A 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.
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PMID:[Renal vascular lesion and microangiopathic hemolytic anemia in systemic lupus erythematosus]. 953 30

The Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index is a validated instrument specifically designed to ascertain damage in SLE; this instrument has been applied mainly to Caucasians and African-American SLE patients. The objective of this study was to assess damage using the SLICC/ACR Damage Index in Mexican SLE patients. The SLICC/ACR Damage Index was applied to 210 consecutive SLE patients with disease of variable duration. The SLICC/ACR Damage Index was assessed by review of hospital clinical records, interview and physical examination. One hundred and seventeen (55.5%) patients had some damage. The proportion of patients with damage increased significantly with disease duration (33% at 1-60 months, 66% at 61-120 months and 70% at > or = 121 months, P < 0.001). The main organ systems involved were musculoskeletal (osteonecrosis), neuropsychiatric (neuropathy, seizures), gonadal (amenorrhea prior to age 40 years), ocular (cataracts), renal (glomerular filtration < 50%) and peripheral vascular (permanent damage by venous thrombosis). Damage was frequent, increased over time, particularly for ocular, renal, musculoskeletal and gonadal. Patients who experienced damage were older, had a longer disease duration, a greater number of ACR criteria at diagnosis, and were more likely to have renal involvement and antibodies to dsDNA. The damage occurred in many different domains and started to develop early after disease onset. Mexican patients had more peripheral vascular and gonadal involvement compared with published data from non-Hispanic SLE populations.
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PMID:Measurement of damage in 210 Mexican patients with systemic lupus erythematosus: relationship with disease duration. 958 Mar 42

The medical records of 478 SLE patients were reviewed. Ninety-five patients (19.9%) with a history of seizures were identified. EEG reports were available on 62. EEGs were interpreted as normal in 8 (12.9%) and abnormal in 54 (87.1%). Abnormal EEGs were reviewed for the presence of unilateral and bilateral abnormalities. Left hemisphere abnormalities were identified in 43 (79.6%), right hemisphere abnormalities in 4 (7.4%), and bilateral abnormalities in 7 (13.0%) patients with SLE. Abnormalities included theta and delta slowing and sharp wave activity. In 32 of the 43 (74.4%) patients with left hemisphere abnormalities, the abnormalities were localized to the left temporal leads. These findings suggest selective damage to the left temporolimbic region in patients with SLE.
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PMID:EEG abnormalities in systemic lupus erythematosus. 966 13

In a cross-sectional study of 21 children with Systemic Lupus Erythematosus, 15 (71%) were found to have neuropsychiatric manifestations. The most common finding was generalised seizures (42.8%) followed by encephalopathy (19%) and hallucinations (19%). One child (4.76%) had hemichorea. In 3 children neurological manifestations were the first symptom of SLE. Computerised Axial Tomograms (CAT scans) showed cerebral atrophy in 7 of 12 scans available for review. Ten children had abnormal EEGs. Although none of the children had clinical evidence of a peripheral neuropathy, 8 had neurophysiological evidence of a neuropathy. One child died of intracranial haemorrhage. Six children had residual neuropsychiatric sequalae.
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PMID:Neurological manifestations of children with systemic lupus erythematosus. 1122 Nov 57

The aim of this study was to examine whether the clinical features of antiphospholipid antibody syndrome are associated with anti-cardiolipin and anti-beta2 glycoprotein I antibodies in Indian patients with SLE. Seventy-six patients (71 females), who fulfilled 1982 ACR criteria for SLE, were prospectively studied for the clinical features of antiphospholipid antibody syndrome (APS), and their sera were analysed for the presence of IgG/IgM/IgA anti-cardiolipin antibodies (aCL) by an in-house ELISA and, in 65 of them, for the presence of IgG anti-beta2 glycoprotein I antibodies (anti-beta2 GPI) by a commercial kit. Thirty-nine (51%) patients were positive for aCL, all of which were positive for IgG aCL, either alone (79.6%) or along with IgM and/or IgA. Twenty-seven (69.3%) out of 39 aCL-positive and seven (26.9%) out of 26 aCL-negative sera were positive for IgG antibodies to beta2 GPI. There was a significant correlation (r = 0.66, P < 0.05) between the levels of aCL and anti-beta2 GPI antibodies. Forty-one patients had features of definite or suggestive APS. Thrombocytopenia, recurrent pregnancy loss and CNS manifestations (seizures eight, infarct one) were seen in 20, 13 and nine patients, respectively. Thrombosis of the peripheral vessels was seen in only one patient. Only the presence of seizures was significantly associated with the presence of aCL and anti-beta2 GPI antibodies (P < 0.05). The characteristic association of definite APS (recurrent pregnancy loss and arterial/venous thrombosis) was lacking.
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PMID:Anti-cardiolipin and anti-beta2 glycoprotein I antibodies in Indian patients with systemic lupus erythematosus: association with the presence of seizures. 1124 9

We describe a case of St. Louis encephalitis in a 19-day-old infant who presented with fever and seizure activity. To our knowledge, this is the youngest case of St. Louis encephalitis ever reported.
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PMID:St. Louis encephalitis in early infancy. 1560 96

Autoantibodies (Ab's) to the "B" peptide (amino acids 372-395) of glutamate/AMPA receptor subtype 3 (GluR3) are found in serum and cerebrospinal fluid of some patients with different types of epilepsy. Since such anti-GluR3B Ab's can activate and/or kill neurons in vitro and in vivo, they may contribute to epilepsy. To investigate whether anti-GluR3B Ab's may also be relevant to epilepsy when it accompanies some autoimmune-diseases, we tested for these Ab's in patients suffering from epilepsy that accompanies anti-phospholipid syndrome (APS) or Sneddon's syndrome (SNS), both being autoimmune-diseases with frequent neurological complications. We tested 77 pediatric patients whose epilepsy is their main disease; 31 adult patients whose epilepsy accompanies APS (primary or SLE-associated) or SNS; 45 epilepsy-free APS and SNS patients; and 90 healthy controls. Compared to the controls, significantly elevated anti-GluR3B Ab's were found in 22/77 (29%) patients whose epilepsy is their main disease, but in none of the patients whose seizures accompany APS or SNS. Yet, all the APS and SNS patients harbored the characteristic anti-phospholipid Ab's (aPL), directed against cardiolipin and beta2-glycoprotein I, and had lupus anti-coagulant. Thus, anti-GluR3B Ab's are not crossreactive with aPL, and not produced as a non-specific consequence of seizures on the one hand, or autoimmune-diseases on the other. Taken together with new findings accumulated recently in our lab, we suggest that anti-GluR3B Ab's are produced primarily in the periphery due to specific/non-specific "irritation" of the immune system, and that once they reach the brain via a leaky blood-brain barrier they may cause neuronal/glial damage and facilitate the outburst of epilepsy and additional neurological abnormalities. In contrast, the presence of anti-GluR3B Ab's does not seem to increase the probability of developing APS, SNS or the seizures that often accompany these autoimmune-diseases. These findings may have important diagnostic and therapeutic implications.
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PMID:Antibodies to glutamate receptor subtype 3 (GluR3) are found in some patients suffering from epilepsy as the main disease, but not in patients whose epilepsy accompanies antiphospholipid syndrome or Sneddon's syndrome. 1627 46


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