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)

1. Among patients with SLE, 71 (51%) had significant neuropsychiatric problems during the course of the disease. In 52 (37%), the nervous system manifestations were secondary to SLE. 2. The most frequent manifestations were psychiatric dysfunction, seizures, long tract signs, cranial neuropathy, and peripheral neuropathy. 3. Psychiatric abnormalities secondary to SLE were characterized by organic features (present in 22 of 24) and by the association of neurologic lesions which were often diffuse or multifocal. 4. An abnormal cerebrospinal fluid was found in 32% of neuropsychiatric episodes in which specimens were obtained. The most frequently abnormal study was the electroencephalogram (71%), and the least frequent was the brain scan (8%). These studies did not correlate with specific clinical patterns. 5. In 63% of the patients, NP manifestations preceded the diagnosis of SLE or occurred within the first year of diagnosed disease, and in most episodes were associated with evidence of clinical and/or serologic activity of the underlying illness. 6. Only two clinical features showed significant and striking correlations with neuropsychiatric involvement, namely vasculitis and thrombocytopenia. The possible pathogenic implications have been discussed. 7. Only 2 of the 140 patients were felt to have steroid-induced psychoses. In approximately one-half of the NP episodes secondary to SLE, patients were receiving no corticosteriods on presentation. Of those developing while patients were on steroids, the majority occurred on low doses or after tapering from higher levels. 8. The immediate prognosis for improvement in neuropsychiatric function was good with 84% of episodes showing complete or partial resolution. Corticosteroids appeared to be of benefit in a substantial number of patients although their precise role is difficult to quantitate. 9. Five and 10 years survivals for the overall population were 94% and 82%, respectively. There were no significant differences in survival for patients with or without nervous system involvement.
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PMID:Neuropsychiatric manifestations of systemic lupus erythematosus: diagnosis, clinical spectrum, and relationship to other features of the disease. 78 66

To elucidate the clinical significance of MRI on CNS-SLE, MRI and CT scans were performed in 35 patients with SLE, of 18 patients who had CNS manifestations at the time of MRI examinations. The investigations were also carried out with 17 patients without CNS-SLE. The rate of detection of abnormal findings on MRI in patients with CNS-SLE was 77.2% (14/18), which was high, as compared with the rate of those on CT scans (50%: 9/18). Especially, all of 4 patients with seizure and 3 patients with encephalopathy showed abnormal MRI findings, although respectively 50% and 33.3% of them had abnormal CT scan findings. MRI findings were classified into 4 groups as below: 1) Large focal are as of increased signal intensity at T2 weighted image. These were observed in 2 of 4 patients with seizure and 1 of 3 patients with encephalopathy, which were completely resolved after treatment. 2) Patchy subcortical foci of increased signal intensity at T2 weighted image. These were observed in 11 of 18 CNS-SLE and 7 of 17 without CNS-SLE, which were not detected by CT scan. 3) All of six patients with cerebral infarctions showed high signal intensity areas at T2 weighted image and low signal intensity areas at T1 weighted image. 4) Normal findings were observed in 4 of 18 CNS-SLE (22.2%). We concluded that MRI is useful for the evaluation of CNS-SLE and provides more information than CT scan.
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PMID:[Abnormal findings of magnetic resonance imaging (MRI) in patients with systemic lupus erythematosus involving the brain]. 152 21

In order to study spatial interactions during low magnesium induced epileptiform activity, changes in extracellular potassium concentration ([K+]0) and associated slow field potentials (f.p.'s) were recorded in thin rat temporal cortex slices (400 microns) containing the neocortical temporal area 3 (Te3), the entorhinal cortex (EC) and the hippocampal formation with the dentate gyrus, area CA3 and CA1 and the subiculum (Sub). The epileptiform activity was characterized by short recurrent epileptiform discharges (40 to 80 ms, 20/min) in areas CA3 and CA1 and by interictal discharges and tonic and clonic seizure like events (SLE's) (13-88s) in the EC, Te3 and Sub. While interictal discharges occurred independent of each other in the different subfields, the three areas became synchronized during the course of a SLE. The EC, Te3 and Sub all could represent the "focus" for generation of the SLE's. This initiation site for SLE's sometimes changed from one area to another. The characteristics of the rises in [K+]0 and subsequent undershoots were comparable to previous observations in in vivo preparations. Interestingly, rises in [K+]0 could start before actual onset of seizure like activity in secondarily recruited areas. The epileptiform activity could change its characteristics to either a state of recurrent tonic discharge episodes or to a continuous clonic discharge state reminiscent of various forms of status epilepticus. We did not observe, in any of these states, active participation by area CA3 in the epileptiform activity of the EC in spite of clear projected activity to the dentate gyrus. Even after application of picrotoxin (20 microM), area CA3 did not actively participate in the SLE's generated in the entorhinal cortex. When baclofen (2 microM) was added to the picrotoxin containing medium, SLE's occurred both in the entorhinal cortex and in area CA3, suggesting that inhibition of inhibitory interneurons by baclofen could overcome the "filtering" of projected activity from the entorhinal cortex to the hippocampus.
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PMID:Regional and time dependent variations of low Mg2+ induced epileptiform activity in rat temporal cortex slices. 178 28

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

A 21-year-old male with SLE developed seizure, loss of consciousness and focal signs referable to involvement of the front-temporal brain regions. MRI (magnetic response imaging) image revealed high signal areas in the temporal lobes. By these findings, herpes simplex encephalitis (HSE) was suspected at first. But neither isolation of herpes simplex virus nor HSV specific IgM by ELISA was detected. Acyclovir administration by intravenous infusion was'nt effective but corticosteroid pulse therapy was effective. The level of anticardiolipin antibody was very high. Finally, the diagnosis of CNS-lupus with HSE-like characteristics was made in this case.
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PMID:[A case of systemic lupus erythematosus with the central nervous system manifestations (CNS-lupus) mimicking herpes simplex encephalitis (HSE)]. 194 88

Clinical and pathological studies were made on 5 patients (1 male and 4 females; average age, 58.2 years) with primary malignant lymphoma of the brain. One case had received long-term immunosuppressive therapy for SLE. The most common initial signs and symptoms were non-specific and non-localized. They included headache, disorientation and consciousness disturbance. During the course, the signs and symptoms consisted of consciousness disturbance (5 cases), hemiparesis (4 cases), headache (3 cases), dementia (2 cases), seizures (2 cases), and diplopia (1 case). The tumors on CT scans appeared as slight hyperdense areas in 3 cases, and as isodense areas in 1 case with enhancement following contrast media infusion, which was compatible with previously reported results. However, the other case showed diffuse hypodense areas without enhancement which has rarely been reported. Multiple lesions were found in 4 cases. Three cases underwent cerebral angiography which demonstrated avascular masses. Pathologically, the tumors were located in the cerebral hemispheres in 5 cases, the basal ganglia and thalamus in 3 cases, the brain stem in 2 cases, and the cerebellum in 2 cases. Three cases were classified as of the diffuse, large cell type, 1 case as small cleaved cell and 1 case as immunoblastic. Thus, the clinical diagnosis of primary malignant lymphoma of the brain still remains difficult because the symptoms and CT findings are so varied.
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PMID:Primary malignant lymphoma of the brain--clinical and pathological investigations. 272 42

The clinical and computed tomographic (CT) findings in 17 patients with neurological manifestations of systemic lupus erythematosus were analyzed. Two patients presented with stroke syndromes; they did not have systemic manifestations of SLE at the time the neurological disturbances developed. Of 15 patients with prominent systemic evidence of SLE, 9 presented with stroke syndromes or seizures. CT showed a hypodense lesions representing infarction (7 cases) or hyperdense lesions representing intracerebral hematomas (2 cases). Six patients with gradual onset of neurobehavioral symptoms showed cerebral atrophy without infarction or hemorrhage.
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PMID:The cranial computed tomographic findings in patients with neurologic manifestations of systemic lupus erythematosus. 395 92

Paired serum and cerebrospinal fluid specimens from 19 patients with SLE and central nervous system dysfunction were studied with respect to cerebrospinal fluid IgG index (a measure of intrathecal IgG synthesis), isoelectric focusing using immunoperoxidase staining techniques to detect oligoclonal IgG, and determination of the cerebrospinal fluid/serum albumin quotient (Q albumin) as a measure of blood-brain barrier integrity. Twenty-five patients without neurologic disease and 70 patients with a variety of non-SLE neurologic disorders were also studied for comparison. Of most interest was the observation that 42 percent of the patients with SLE had cerebrospinal fluid oligoclonal IgG, usually in association with elevation of the cerebrospinal fluid IgG index. In addition, two of the cerebrospinal fluid specimens that exhibited oligoclonal IgG also had increased titers of alpha-interferon. Q albumin was normal (under 9.0) in 12 of 13 patients with SLE, who had seizure, psychosis, or cranial neuropathy as principal central nervous system manifestations (mean +/- SD = 5.3 +/- 2.4), but was significantly elevated (mean +/- SD = 27.4 +/- 18.8, p less than 0.001) in five of six patients with diffuse, major central nervous system injury, for example, encephalopathy with coma, transverse myelopathy, paraparesis. Blood-brain barrier impairment was not correlated either with presence of circulating immune complexes or with other clinical or serologic evidence for extra-central nervous system disease activity. Taken together, the data suggest that, within the limitations of the techniques used, impairment of the blood-brain barrier in SLE may be secondary to the central nervous system lesion, rather than a result of systemic immune complex injury. In addition, substantial evidence is provided for an ongoing humoral immune response within the central nervous system in this disorder, which, in certain patients, may be associated with the production of intrathecal alpha-interferon.
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PMID:Intrathecal IgG synthesis and blood-brain barrier impairment in patients with systemic lupus erythematosus and central nervous system dysfunction. 683 7

Neurologic complications of systemic lupus erythematosus (neuro-SLE) are common. The most frequent manifestations of neuro-SLE are seizures, encephalopathy, and behavioral changes, but a wide variety of other neurologic abnormalities affecting the central and peripheral nervous system and muscle also occur. Although the prevalence of neuro-SLE is high, the diversity of clinical presentations, the multiple potential etiologies, and the absence of sensitive and specific diagnostic tests render diagnosis difficult. Recent advances in understanding mechanisms of neuronal dysfunction combined with advances in imaging techniques, including functional imaging, should help in diagnosis and management. The mechanisms of neurologic injury can be divided into three broad categories. First, neuronal dysfunction may result from direct effects of the immune system on brain cells such as autoantibody binding to cell surface, immune complex deposition with secondary inflammation, and effects of cytokines. Second, immune- mediated injury to supportive structures such as the vasculature may also affect the nervous system by producing ischemia. Finally, the neuraxis may be affected by any one of several immune and non- immune effects of infection, toxins, and metabolic disturbances.
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PMID:Systemic lupus erythematosus: immunopathogenesis of neurologic dysfunction. 748 26

Properties of low Mg2+ induced epileptiform activity were studied in isolated rat hippocampal slices or in combined slices containing the entorhinal cortex and hippocampus. Slices were prepared from rats which were 1, 2, 3 or more weeks of age. Field potentials and often also changes in [K+]0, [Ca2+]0 and [Mg2+]0 were recorded with appropriate ion selective microelectrodes. In isolated hippocampal and entorhinal cortex/hippocampal combined slices the latency to onset of epileptiform activity upon lowering of extracellular Mg2+ was shortest in the youngest age group and approached adult levels at about the fourth postnatal week. Washout kinetics of Mg2+ were fastest in slices from 1-week-old rats. The onset of low Mg2+ induced epileptiform activity occurred at higher Mg2+ levels in slices from young compared with those from adult animals. In isolated hippocampal slices the epileptiform discharges varied in appearance during development. Short discharges lasting for 40 to 80 ms were observed in hippocampal slices prepared from 1-week-old and adult animals. Seizure-like events (SLE's) characterized by slow negative potential shifts and characteristic elevations in [K +]0 and decreases in [Ca2+]0 lasting for up to 30 s were observed in a proportion of hippocampal slices prepared after the first, second and third postnatal week. In slices from week 2 and 3 seizure-like events often progressed into spreading depressions (SD's). In entorhinal cortex/hippocampal combined slices seizure-like events were observed in all age groups. The seizure-like events spread readily into dentate gyrus (DG), area CA3 and CA1 after week 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Properties of low Mg2+ induced epileptiform activity in rat hippocampal and entorhinal cortex slices during adolescence. 758 96


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