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)

Increased levels of neuron-specific enolase (NSE), a key glycolytic enzyme, in either the cerebrospinal fluid or the serum is correlated with both the duration and the outcome of status epilepticus. To further understand the molecular basis of seizure-induced elevations in NSE protein, we investigated NSE mRNA expression in the adult rat brain following systemic administration of kainic acid. The findings demonstrated either no change or a decrease in NSE gene expression during, and following, status epilepticus, suggesting that posttranscriptional mechanisms are responsible for seizure-induced increases in NSE protein.
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PMID:Expression of neuron-specific enolase in adult rat brain following status epilepticus. 1048 1

Epileptogenesis was evaluated in 60 patients with acute encephalitis and in 10 patients with acute encephalopathy. Forty-seven patients have been seizure-free during for more than three years' follow-up (Group III). On the other hand, 23 patients developed epilepsy. Among them, 18 patients developed epilepsy after a latent period of 1 month to 2 3/12 years (Group I). In Group I, a younger age of the onset, a long period of disturbed consciousness and a high activity of CSF neuron-specific enolase (NSE) was associated with refractory epilepsy. The other five patients had continuous seizures from the acute phase of encephalitis without a latent period (Group II). They had more than 2 types of partial motor seizures which occurred frequently during the acute phase of encephalitis. The NSE activity in the CSF of patients in Group II was less than 50 ng/ml, being similar to those in Group III. The epilepsy in Group II, however, was the most refractory. The reason for the development of this continuous refractory epilepsy remained obscure.
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PMID:[Epileptogenesis of acute encephalitis and acute encephalopathy: epilepsy with its onset in the acute phase and without a latent period]. 1082 79

If febrile seizures cause significant compromise of neuronal metabolism (whether permanent or reversible), this should be reflected in an increase in the cerebrospinal fluid concentrations of neuron-specific enolase (NSE) and/or adenosine triphosphate (ATP) breakdown products. In the present study, AMP, IMP, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid and NSE concentrations were determined in the cerebrospinal fluid of 90 children 1 h after febrile seizure (73 simple febrile seizures (SFS); 17 complex febrile seizures (CFS)), and in a control group of 160 children. There was no statistically significant difference between the SFS group and the control group for any of the substances determined, suggesting that SFS neither significantly depletes neuronal ATP concentration, nor significantly increases NSE concentration; thus, SFS do not appear to constitute a threat to neuronal integrity. However, patients with CFS showed significantly lower IMP concentrations and significantly higher adenine concentrations than controls, and significantly higher AMP concentrations than SFS patients; these results suggest that CFS may affect energy metabolism in the brain. However, NSE concentrations were normal in the cerebrospinal fluid of both SFS and CFS patients, suggesting that neither type of seizure causes significant neuronal damage, at least early after the seizure.
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PMID:Cerebrospinal fluid purine metabolite and neuron-specific enolase concentrations after febrile seizures. 1110 27

The GAL879-881QQQ mutation in the cytoplasmic S4-S5 linker of domain 2 of the rat brain IIA sodium channel (Na(v)1.2) results in slowed inactivation and increased persistent current when expressed in Xenopus oocytes. The neuron-specific enolase promoter was used to direct in vivo expression of the mutated channel in transgenic mice. Three transgenic lines exhibited seizures, and line Q54 was characterized in detail. The seizures in these mice began at two months of age and were accompanied by behavioral arrest and stereotyped repetitive behaviors. Continuous electroencephalogram monitoring detected focal seizure activity in the hippocampus, which in some instances generalized to involve the cortex. Hippocampal CA1 neurons isolated from presymptomatic Q54 mice exhibited increased persistent sodium current which may underlie hyperexcitability in the hippocampus. During the progression of the disorder there was extensive cell loss and gliosis within the hippocampus in areas CA1, CA2, CA3 and the hilus. The lifespan of Q54 mice was shortened and only 25% of the mice survived beyond six months of age. Four independent transgenic lines expressing the wild-type sodium channel were examined and did not exhibit any abnormalities. The transgenic Q54 mice provide a genetic model that will be useful for testing the effect of pharmacological intervention on progression of seizures caused by sodium channel dysfunction. The human ortholog, SCN2A, is a candidate gene for seizure disorders mapped to chromosome 2q22-24.
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PMID:A gain-of-function mutation in the sodium channel gene Scn2a results in seizures and behavioral abnormalities. 1116 17

A granular cell tumor involving the pituitary gland, optic chiasm and ventral pyriform lobes was discovered in a 12-year-old Labrador Retriever. Clinical signs included acute blindness, seizures, ataxia, weakness, and behavioral changes. The diagnosis was established by histopathologic and ultrastructural examination of neoplastic tissues collected at necropsy. Granular cell tumors involving the central nervous system are well documented in humans but rarely have been described in dogs. The location of the neoplasm and the clinical symptoms seen in this dog closely parallel those of a rare syndrome in humans commonly described as symptomatic parasellar or pituitary granular cell tumors. The cell of origin for these tumors is still highly debated, and attempts to characterize human granular cell tumors through immunohistochemistry have produced conflicting results. An immunohistochemical profile of this neoplasm revealed focal positive staining for vimentin with a lack of staining for neuron-specific enolase, glial fibrillary acidic protein, S-100, and synaptophysin. All neoplastic cells were strongly positive with the periodic acid-Schiff reaction.
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PMID:Symptomatic granular cell tumor involving the pituitary gland in a dog: a case report and review of the literature. 1135 66

As chemokines and their receptors are primarily expressed by glial cells in brain parenchyma, a model of glial cell proliferation may be useful to study the regulation of their expression in the brain. The well-established kainic acid seizure model was used in this study, focusing on the expression of the CCR5 chemokine receptor. Adult Sprague-Dawley rats were injected intraperitoneally with kainic acid (12 mg/kg), and in situ hybridization of CCR5 mRNA was performed at 12 h, 1, 3, or 7 days, posttreatment. Autoradiographic films and wet photographic emulsions demonstrated the very low expression of CCR5 mRNA in normal brain parenchyma, as well as in the microvasculature and ventricular/choroid plexus systems. After kainic acid treatment, brain CCR5 mRNA expression increased progressively from 12 h to 7 days, especially in the olfactory system, amygdaloid complex, thalamus, hippocampal formation, septum, and neocortex. This increase paralleled that of activated microglial cells as shown, using the microglial marker, OX-42. Moreover, CCR5 mRNA ISH combined with neuron-specific enolase immunocytochemistry showed that, in addition to its glial expression, CCR5 mRNA is expressed in neurons in the normal brain and, to a lesser extent, after kainate treatment due to neuronal losses. Finally, CCR5 protein is detected by immunocytochemistry in neurodegenerative areas in numerous glial cells, as well as in neurons, as clearly shown in the hippocampal formation. In summary, the chemokine receptor CCR5 is expressed by neuronal and non-neuronal cell types in the normal brain and is upregulated in both cell types after an insult.
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PMID:Systemic administration of kainic acid in adult rat stimulates expression of the chemokine receptor CCR5 in the forebrain. 1175 11

Neuron-specific enolase, a marker for neuronal injury, is elevated following seizures in adults, but relatively few data exist on postictal neuron-specific enolase levels in children. This study measured cerebrospinal fluid (CSF) neuron-specific enolase levels after seizures in 49 consecutive pediatric patients and investigated the role of seizure type, duration, and etiology in influencing neuron-specific enolase. Overall, there was no significant difference in neuron-specific enolase levels between patients with seizures and a control group. However, 4 of the 49 seizure patients (8%) had neuron-specific enolase levels clearly above the normal range. Seizure patients with symptomatic etiologies had significantly increased neuron-specific enolase compared to cryptogenic/idiopathic or febrile seizures. The four individual patients with elevated cerebrospinal fluid neuron-specific enolase all had identified metabolic or genetic etiologies and presented with medically refractory status epilepticus. No individuals with cryptogenic/idiopathic or febrile seizures had abnormal neuron-specific enolase. There was no significant effect of seizure duration or type on cerebrospinal fluid neuron-specific enolase. In contrast to adults, acute seizure-induced neuronal injury in children as detected by neuron-specific enolase is rare and may occur primarily with severe symptomatic etiologies. Children with cryptogenic, idiopathic, or febrile seizures, including status epilepticus, are at relatively low risk for neuronal damage following seizures.
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PMID:Cerebrospinal fluid neuron-specific enolase following seizures in children: role of etiology. 1208 80

Neurocytoma is an unusual neuronal tumor especially affecting young people. It commonly arises in the ventricles and has a benign outcome. Herein, we report on a rare case of extraventricular neurocytomas (right parietal lobe) in a young girl admitted to hospital for a cranial trauma subsequent to a seizure. The tumor, radiologically well-circumscribed, cystic and enhancing, was surgically excised. The patient, who received no post surgical treatment, is alive and well after 18 months of follow-up. Pathological examination showed a well-differentiated lesion composed of uniform, round cells with perinuclear halos in a neuropil background and immunohistochemically positive for neuronal markers (synaptophysin, neuron-specific enolase, neurofilaments). The authors emphasize the role of the morphological and immunohistochemical evaluations to recognize this rare tumor.
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PMID:Extraventricular neurocytoma: morphological and immunohistochemical considerations on differential diagnosis. 1244 Jul 86

Compared to publications of elevated levels of neuron-specific enolase (NSE) in adult patients with single seizures or epilepsy, data in children are rare. We studied serial NSE serum concentrations in children after febrile convulsions (FC). In addition, the predictive value of NSE levels in serum for recurrence of FC or further development of epilepsy was determined. Serum NSE levels were determined at (1) 0-2 h, (2) 6-8 h and (3) 20-24 h after a first or second FC in children aged 4 months to 6 years. Eighty-two patients (35 female, 47 male) aged four months to 5.7 years were included. Seventy-one children had generalized, and seven focal FC. The seizures in the remaining four patients could not be properly classified. During the follow-up of 14-28 months 13 patients had at least one more FC and in five epilepsy due to recurrent afebrile seizures was diagnosed. There was no statistically significant elevation of NSE concentration in the group of children with FC or the group with recurrent FC or epilepsy. The comparison of the NSE values at different times after FC did not show any significant differences either. It seems from our results that NSE activity cannot be used as a predictor for possible brain damage caused by FC and that it is not of predictive value considering further FC or development of epilepsy. We cannot confirm the published results of the elevation of NSE serum levels in adults with single seizures or status epilepticus.
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PMID:Serum neuron-specific enolase in children with febrile seizures: time profile and prognostic implications. 1276 59

Patients who undergo coronary artery bypass grafting (CABG) are at increased risk for brain injury. Surgical techniques have advanced so that the risk of neurological sequelae is decreased, but there remains significant morbidity and mortality related to the postoperative period as well as to the surgery itself. In addition, patients who undergo CABG have comorbidities or demographic factors that may increase their likelihood of developing neurological complications. Pathophysiological mechanisms of cerebral injury after CABG range from hemodynamic compromise to embolization, either intraoperatively or postoperatively. Biochemical markers such as S100 and neuron-specific enolase may play a role in the prediction of outcome after CABG, and because of this may help elucidate other potential risk factors. Specific neurological sequelae are discussed, such as stroke, with summaries of the apparent risk factors, as well as encephalopathy, seizure, and both short- and long-term cognitive deficits. Changes in surgical technique have led to some improvements, but there is no definitive information yet as to the role of some of these, such as the use of off-pump CABG. Other techniques such as the use of an arterial filter are discussed, as are their potential benefits in the prevention of neurological complications.
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PMID:Brain injury from cardiac bypass procedures. 1696 44


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