Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuron-specific enolase (NSE) is a sensitive marker of brain injury after stroke, global ischemia, and coma. We report changes in serum NSE (s-NSE) in 19 patients who sustained status epilepticus. s-NSE peaked within 24 to 48 hours after status epilepticus. The mean peak s-NSE level for the entire group was elevated compared with the levels for normal controls (24.87 ng/ml versus 5.36 ng/ml, p = 0.0001) and for epileptic controls (24.87 ng/ml versus 4.61 ng/ml, p = 0.0001). The mean peak s-NSE level for the 11 subjects without an acute neurologic insult (15.44 ng/ml) was also significantly increased compared with levels for normal and epileptic controls. Further, s-NSE was significantly correlated with outcome and duration. We conclude that s-NSE is a promising in vivo marker of brain injury in status epilepticus and warrants further study in larger populations.
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PMID:Serum neuron-specific enolase in human status epilepticus. 864 98

We determined the serum concentrations of neuron-specific enolase (s-NSE) in rat pups of 1, 2, 3, and 4 weeks of age and in adult rats that were subjected to lithium-pilocarpine status epilepticus (SE). Damage to brain regions was rated on a scale of 0 (no damage) to 5 (> 50% cell loss). Rat pups of 1-2 weeks of age had a higher baseline s-NSE than the adults. Following SE, 1 week old rat pups had no elevation of s-NSE and no histologic evidence of damage. At older ages the increases in NSE ranged from 18.9 +/- 0.8 ng/ml in the 2 week old (vs. 11.5 +/- 0.5 control) to 35.8 +/- 2.1 ng/ml in the 3 week old (vs. 12.1 +/- 0.8 control). In the adult rats s-NSE increased from 5.4 +/- 0.4 in the control animals to 30.4 +/- 1.3 after SE. The different brain regions examined had distinctive ontogenic profiles for SE-induced damage. Elevation of s-NSE after SE correlated with overall histologic evidence for damage.
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PMID:Serum neuron-specific enolase is a marker for neuronal damage following status epilepticus in the rat. 926 77

Neuron-specific enolase (NSE) is a sensitive marker of brain damage in stroke, global ischemia, and coma. Serum NSE is also correlated with the duration and outcome of status epilepticus (SE). CSF-NSE levels have not been previously reported in SE. We report the CSF concentrations of NSE in 11 patients with cryptogenic/remote symptomatic SE. CSF obtained within 24 hours of SE showed increased concentrations of NSE in 9 of 11 patients. The mean CSF-NSE for the group was elevated compared with the levels for normal control subjects (30.8 +/- 18.33 versus 10.76 +/- 3.08 ng/mL; p = 0.002). Further, CSF-NSE levels were elevated compared with simultaneous serum levels in the same group of patients (p = 0.01). In addition, the CSF/serum albumin ratio (QAlb), a measure of the integrity of the blood-brain barrier, was increased in SE patients compared with control individuals (33.4 versus 4.79 x 10(-3); p = 0.0001). An increase of QAlb correlated with CSF-NSE (rs = 0.66, p = 0.04) and serum NSE levels (rs = 0.83, p = 0.004). CSF-NSE is a promising in vivo marker for brain injury after SE.
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PMID:Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier. 959 92

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

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

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

Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N=11), patients with encephalic injuries associated with impairment of consciousness (ENC, N=7), patients with neurocysticercosis (N=25), and normal subjects (N=8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P=0.01) and albumin quotient (P=0.005), but not sNSE (P=0.14), levels than the other groups (Kruskal-Wallis test). Patients with lower GOS scores had higher cNSE levels (P=0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.
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PMID:Use of neuron-specific enolase for assessing the severity and outcome in patients with neurological disorders. 1468 39

Postanoxic coma is a state of unconsciousness caused by global anoxia of the brain, most commonly due to cardiac arrest. Outcome after postanoxic coma lasting more than several hours is generally, but not invariably, poor. Recovery of consciousness reported in the literature varies from 8% to 72% of patients, but is mostly thought to be around 20-30% in patients surviving in coma for at least 24 h. Research is directed at defining factors that reliably predict poor outcome in these patients. Favourable outcome proves impossible to predict. Studies on outcome prediction have focussed mostly on neurological examination, clinical neurophysiological tests and biochemical parameters. The most recent and extensive study in this respect was the PROPAC study in The Netherlands (407 patients). This study confirmed earlier findings that bilaterally absent early cortical response after median nerve somatosensory potentials (absent somatosensory evoked potentials) is the most reliable predictor of poor outcome (no recovery of consciousness). A serum neuron-specific-enolase level >33 microg L(-1) seemed equally reliable. In 2006, the American Practice Parameter on anoxic-ischaemic coma was published, summarizing the findings from the different studies. Poor outcome was defined as death, coma or severe disability after 6 months. The following factors were found to reliably predict this outcome: myoclonic status epilepticus within the first 24 h, absent pupillary responses after 24 h, absent corneal reflexes after 48 h, motor response to pain absent or extensor after 72 h and absent somatosensory evoked potentials (as defined above) after 1-3 days. Results for biochemical parameters (such as neuron-specific enolase) and neuroimaging are inconclusive.
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PMID:Postanoxic coma: how (long) should we treat? 1828 15

Most patients with post-anoxic coma after resuscitation have a poor prognosis. Reliable prediction of poor outcomes (death or vegetative state after 1 month; death, vegetative state or severe disability after at least 6 months) at an early stage is important for both family members and treating physicians. Poor outcome can be predicted with 100% reliability in the first 3 days after resuscitation in about 80% of patients using pupillary and corneal reflexes and motor response from the neurological examination, cortical responses from somatosensory evoked potentials and EEG. The predictive value of a status epilepticus or serum levels of neuron-specific enolase is uncertain at this time. In contrast to poor outcomes, good neurological recovery cannot be predicted reliably at this time.
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PMID:[Prognosis for patients in a coma following cardiopulmonary resuscitation]. 1859 66

Established markers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100), may increase after status epilepticus, but whether a single tonic-clonic or complex partial seizure induces elevation of these markers is not known. Furthermore, it is unclear whether the risk of seizure-related neuronal damage in temporal lobe epilepsy (TLE) differs from that in extratemporal lobe epilepsies (XTLE). The aim of this study was to analyze NSE and S-100 in patients with TLE and XTLE after acute seizures. The levels of NSE and S-100 were measured in serum before (0h) and at 3, 6, 12, and 24h after acute seizures in 31 patients during inpatient video-EEG monitoring. The patients were categorized into the TLE and the XTLE group based on video-EEG recordings and MRI findings. Fifteen patients had TLE and 16 XTLE. Index seizures were mainly complex partial seizures (n=21). In TLE mean+/-S.D. values for NSE levels (mug/L) were 8.36+/-2.64 (0h), 11.35+/-3.84 (3h), 13.48+/-4.49 (6h), 12.95+/-5.46 (12h) and 10.33+/-3.13 (24h) (p=0.006, ANOVA). In XTLE the changes were not significant (p=0.3). There was less increase in the levels of S-100 in TLE (p=0.05) and no significant change in XTLE (p=0.4). The levels of markers of neuronal damage were increased in patients with TLE, not only after tonic-clonic but also after complex partial seizures. These data suggest that TLE may be associated with brain damage.
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PMID:Elevated serum neuron-specific enolase in patients with temporal lobe epilepsy: a video-EEG study. 1859 63


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