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)

We report two cases of oligodendroglioma-like meningioma revealed by symptoms of increased intracranial pressure, progressive hemiparesia and partial epileptic seizures. Brain CT-scan or scintigraphy and carotid arteriography were suggestive of a convexity meningioma. One patient had received radiation treatment for scalp tinea capitis 25 years previously. In spite of complete surgical removal, the tumor recurred in both cases respectively 17 years and 18 months later. The two patients were operated again, and one underwent a complementary radiotherapy. Pathologic diagnosis was particularly difficult in the first case where the pattern at conventional histologic technics was that of oligodendroglioma. On the occasion of recurrence, immuno-histochemistry and ultrastructural studies were performed. The tumor was positive for epithelial membrane antigen (E.M.A) and cytokeratin, but was negative for glial fibrillary acidic (G.F.A.) protein, S 100 protein (S 100), neuron-specific enolase (N.S.E.), vimentin, anti-LEU-7 (N.H.K.1), and neurofilaments (N.F.). Electron microscopy showed closely adjacent cells with tonofilaments and numerous desmosomes. These findings permitted to establish the diagnosis of oligodendroglioma-like meningioma instead of oligodendroglioma. In the second case, the histologic pattern was also reminiscent of oligodendroglioma, but presence of few cellular whorls in some part of the tumor permitted the correct diagnosis. The pathogenesis of this atypical form of meningioma, its tendency for recurrence, and usefulness of radiotherapy are discussed and literature is reviewed.
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PMID:[Pseudo-oligodendrogliomatous meningioma. Report of 2 cases and review of the literature]. 178 19

Neuron-specific enolase (NSE) has recently proved to be a useful marker of neuron damage. We determined NSE levels in the serum and CSF of 117 children with various neurological disorders (43 with febrile convulsion, 25 with seizure disorder, 32 with meningitis, 3 with brain tumor, 2 with Reye syndrome, 3 with congenital CNS malformation and 9 with other disorders). The purpose of this study is to assess the potential usefulness of NSE in diagnosis and prognosis. Twenty CSF and serum samples of children without neurological problem served as a control. The mean values of the NSE levels in the CSF and serum of the control group were 5.00 +/- 1.65 ng/ml and 8.34 +/- 4.40 ng/ml respectively. The peak values were found in cases with brain tumor. A patient died of Reye syndrome didn't show a very high level of NSE in the serum or CSF. However, we found significant differences in NSE levels between the patients with febrile convulsions and those with seizure disorders (non-febrile, abnormal EEG). Most of our patients with febrile convulsions were cases of simple febrile convulsion, and their NSE levesin the CSF and serum were 4.55 +/- 1.00 and 8.06 +/- 3.18 ng/ml. Cases with non-febrile seizure disorders had significantly higher level of NSE in both CSF and serum (P less than 0.05). Patients with purulent meningitis usually had higher levels than those with aseptic meningitis. Our study can be summarized thus: 1. A normal level of NSE does not exclude severe neuron damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of neuron-specific enolase levels in serum and cerebrospinal fluid of children with neurological diseases. 234 56

Serum neuron-specific enolase (s-NSE), a marker of brain injury and acute seizures, was increased in 2 patients with nonconvulsive SE. Neither patient had an acute neurologic insult other than nonconvulsive SE (NCSE) accounting for s-NSE changes. Increase in s-NSE provides further in vivo evidence of transient brain injury after NCSE.
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PMID:Neuron-specific enolase is increased after nonconvulsive status epilepticus. 761 25

We report changes in CSF and serum neuron-specific enolase (NSE) before and after methohexital infusion during electrocorticography in three patients undergoing epilepsy surgery. NSE is a critical enzyme for energy metabolism that accounts for 1.5% of all soluble brain protein and is an accepted marker of neuronal injury. CSF NSE rose three- to fourfold from baseline within 60 minutes after methohexital activation. Serum NSE was unchanged. This report supports evidence that CSF NSE rises acutely after induction of epileptiform activity and suggests that CSF NSE is a marker of seizure activity.
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PMID:CSF neuron-specific enolase after methohexital activation during electrocorticography. 864 98

Expression of the cell cycle regulatory proteins RB and p34cdc2 was examined in the adult rat brain, with special emphasis on proliferation and neuronal differentiation in the hippocampal formation and olfactory bulb. RB-like immunoreactivity (RB-IR) was detected throughout the brain, with particularly intense staining observed in hippocampal pyramidal cells, pyriform cortex, and cerebellar Purkinje cells. Intense RB-IR and cdc2-IR were also detected in proliferating neuronal precursor cells in the subgranular region of the dentate gyrus and in the subependymal region extending from the anterior lateral ventricle into the olfactory bulb. Many of these cells developed into neurons as assessed by the expression of neuron-specific enolase (NSE) and, in the hippocampal formation, the expression of Fos-IR following pentylenetetrazol-induced seizure activity. A good correlation was observed between the number of proliferating cells expressing intense nuclear RB-IR staining and the number of thymidine-labeled cells that had differentiated into functional hippocampal neurons. A substantial decrease in RB-IR during differentiation was also observed and occurred prior to the expression of NSE. The possibility that the loss of RB may be necessary for neuronal differentiation to proceed is discussed.
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PMID:RB and Cdc2 expression in brain: correlations with 3H-thymidine incorporation and neurogenesis. 833 81

Neuron-specific enolase (NSE) is a marker of brain injury after acute neurologic insults. We report changes in serum NSE (s-NSE) in 25 patients (15 with epilepsy and 10 patients with nonepileptic events) during continuous inpatient video/EEG monitoring. s-NSE was significantly increased as compared with baseline and normal controls after the first ictal event in the epileptic group, especially in patients with secondarily generalized tonic-clonic seizures (p = 0.01), but s-NSE was not increased in patients with nonepileptic events. These preliminary data indicate that s-NSE may be increased after complex partial seizures--and generalized tonic-clonic seizures (GTCS).
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PMID:Neuron-specific enolase is increased after single seizures during inpatient video/EEG monitoring. 863 21

Serum neuron-specific enolase (NSE) levels were studied by an enzymo-immunoassay method in 2 groups of patients: a group of epileptic patients, and a group of patients with refractory major depression after electroconvulsive therapy (ECT). In patients without organic neurological disease (n = 274) the mean serum NSE level (+/- S.D.) was 8.4 +/- 3.4 micrograms/l. No correlation with sex or age was observed. No significant difference was observed between epileptic patients without seizure or major electroencephalogram (EEG) abnormality, and a reference group. Significant increases were observed in 32 samples collected from patients with interictal EEG without spikes and waves before the 7th day after a seizure, in whom mean NSE was 21.5 +/- 9.4 micrograms/l, and in 26 samples from 4 patients without seizures but with spikes and waves in the interictal EEG, whose mean NSE was 20.6 +/- 11.5 micrograms/l. The increases of serum NSE levels in epileptic patients seem therefore to be linked to seizures and/or to EEG abnormalities. The consequences of these observations for the survey of epileptic patients, and for the diagnosis of cerebral tumors (mainly neuroblastoma) or for monitoring treatment after surgical resection, are discussed. In only 1 patient out of 6, an increase in serum NSE levels was observed with a peak about 12 h after ECT. No significant correlation with the ECT features (length of seizures, one- or two-sided electrodes) was observed.
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PMID:Increased serum levels of neuron-specific enolase in epileptic patients and after electroconvulsive therapy--a preliminary report. 871 37

Febrile seizures are the commonest acute neurological disorder of early childhood. Studies suggested that febrile seizures are previous acute events from a more serious neurological problem. Due to neuron-specific enolase is generally accepted as a marker for neuropathological processes in the brain, 16 pediatric patients were studied during their first seizures and a year after it. Neuron-specific enolase in cerebrospinal fluid and blood were analysed by an immune enzyme assay. Non pathological neuron-specific enolase values were obtained in both periods in the group of patients. There were no significative differences when paired series statistics test was performed with 95% of confidence. Neuron-specific enolase appears not to be a marker for febrile seizures because its concentration not be increased in cerebrospinal fluid in this group of patients.
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PMID:Non increased neuron-specific enolase concentration in cerebrospinal fluid during first febrile seizures and a year follow-up in pediatric patients. 985 Jul 47

Serum neuron-specific enolase (s-NSE) and s-100 protein (s-100) are sensitive markers of various brain diseases. We investigated both of these markers in nine patients within 5 min, 6 h, 12 h, and 48 h after a single tonic-clonic seizure. The mean peak s-NSE level was significantly higher after 5 min (11.97 +/- 8.56 microg/l) and 48 h (10.31 +/- 8.92 microg/l, P < 0.05) than the levels of seizure-free, age-matched controls. Five patients had increased s-NSE levels regarding the upper limit of normal as mean + 3 SD. s-100 was not detected either in controls or epileptic patients. These data indicate that s-NSE in contrast to s-100 may be an in vivo marker after generalized seizures in some patients.
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PMID:Serum levels of neuron-specific enolase and s-100 protein after single tonic-clonic seizures. 1043 71

In the brain, S100 protein and neuron-specific enolase (NSE) are mainly found in glial cells and neurons, respectively. We investigated concentrations of S100 protein and NSE in cisternal cerebrospinal fluid obtained during implantation of foramen ovale electrodes in eight patients with temporal lobe epilepsy (TLE). In addition, the meningeal markers cystatin-C and beta-trace as well as total protein were measured. Patients with trigeminal neuralgia (TN) undergoing glycerol rhizotomy served as controls. S100 protein and NSE levels ipsilateral to the site of seizure onset were significantly higher than in TN. Contralateral TLE values were also markedly but not significantly elevated. The meningeal markers cystatin-C and beta-trace protein as well as total protein did not differ in TLE and TN. We conclude that interictal temporal lobe dysfunction corresponds with neuronal and glial marker elevations in the extracellular space and that site-specific elevations may predict the site of seizure origin biochemically.
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PMID:Cisternal S100 protein and neuron-specific enolase are elevated and site-specific markers in intractable temporal lobe epilepsy. 1046 53


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