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)

This report addresses the verification of the hypothesis that arginine-vasopressin affects the formation of hyperthermia-evoked convulsions in early ontogenesis in rats on days 3, 5, 7, and 9 of postnatal life. The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin. Arginine-vasopressin (10 microg/rat) and PACAP (0.01 microg/rat) decreased the latency of generalized tonic-clonic convulsions and the time of truncal generalization of convulsive activity on days 3 and 5 of rat development. Animals given arginine-vasopressin (0.1-10 microg/rat) sowed significant increases in the duration of generalized convulsions to the level of status epilepticus on day 9 of life. Conversely, administration of higher doses of PACAP (0.1 microg/rat) increased the threshold of tonic-clonic convulsions on days 3 and 5 and decreased it on days 7 and 9 of postnatal development. The indirect involvement of PACAP in the mechanisms of experimental febrile convulsions is suggested to act via changes in arginine-vasopressin neurosecretion.
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PMID:Peptidergic mechanisms of hyperthermia-evoked convulsions in rats in early postnatal ontogenesis. 1240 2

We aimed to investigate the possible convulsant action of arginine vasopressin (AVP) in both a febrile convulsion model in rat pups and a temporal lobe epilepsy model in adult rats and to define the receptor type which mediates this effect. In rat pups, 125 ng V2 receptor antagonist significantly prevented hyperthermic seizures, but did not affect seizure latency. In adult rats, the only effective dose and agent was 125 ng V2 receptor antagonist, which prevented pilocarpine-induced status epilepticus, extended the status epilepticus latency and improved the 24 h survival rate. These data suggest that AVP has a convulsant activity in febrile convulsions and also in seizures independent of fever, and this effect is mediated by V2 receptors.
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PMID:Arginine vasopressin in the pathogenesis of febrile convulsion and temporal lobe epilepsy. 1243 23

Multiple types of insults, such as status epilepticus, hypoxia and trauma, may alter the central nervous system. Strategies to protect the brain against insults remain a very difficult and challenging problem. Damage to the central nervous system can be modulated via excessive excitatory and reduced inhibitory neurotransmission. In addition, increased sodium and calcium loading through impaired voltage-sensitive channels, as well as alterations in the acid-base balance can contribute to both excitotoxic and apoptotic cell death. Epilepsy treatment has always been related to neuroprotection, since it aims to reduce the duration or totally suppress seizures. Although the debate on the capacity of simple seizures to induce neuronal injury is still ongoing, no doubt persists on the disastrous effects of prolonged episodes of status. The next step would be to prevent epilepsy. Several animal models have been used to study the various aspects of the epileptogenic process. In humans, one of the most compelling examples of a series of epileptogenic events is temporal lobe epilepsy (TLE). Temporal lobe epilepsy is often attributed to prolonged febrile convulsions in childhood resulting in mesial temporal sclerosis. However, the relationship between TLE, seizures in childhood and hippocampal sclerosis may not be apparent as initially believed. Furthermore, it is well recognized that in a number of patients there is a delay from a specific insult to the onset of seizures. This "latent period" could be an opportunity for effective intervention, provided that the underlying mechanisms are understood and that appropriate means for a beneficial modification of the disease process become available. The present review discusses the various steps of temporal lobe epilepsy and provides illustrations of the various mechanisms implicated in neuronal death. Data from animal models is also presented and illustrated with video sequences. Finally, on the basis of what is known on mechanisms of action of available antiepileptic drugs, some suggestions are put forward. Basic science and research are guided by clinical queries and from ongoing dialogue. The present illustrated review deals with only a small part of the important amount of work related to epilepsy and neuroprotection. As such it is necessarily schematic or even simplistic. The review is designed to inform clinicians about the basic issues related to the subject, thus allowing them to follow the ongoing debate and participate with pertinent questions. (Published with video sequences).
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PMID:Epilepsy and neuroprotection: an illustrated review. 1244 19

Mesial temporal sclerosis (MTS) has been linked to prolonged febrile seizures. The sequence of changes in the temporal lobe/hippocampus following prolonged febrile seizures and status epilepticus is beginning to be elucidated. We obtained repeated magnetic resonance imaging (MRI) volumetric analysis of the hippocampi in a 23-month-old boy after a prolonged focal febrile seizure. Three days after a prolonged left focal febrile seizure, brain MRI showed increased T2 weighted signal and increased volume (swelling) of the right hippocampus. Repeat MRI 2 months later demonstrated sclerosis of the right hippocampus. Review of the literature shows four other children with prolonged focal seizures associated with the MRI sequence of temporal lobe swelling followed by sclerosis. All had left focal seizures followed by right MTS. Our patient demonstrates a shorter interval for the radiologic development of hippocampal sclerosis compared to other reports.
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PMID:From swelling to sclerosis: acute change in mesial hippocampus after prolonged febrile seizure. 1276 72

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

Mesial temporal sclerosis (MTS) is the most common lesion in patients who require epilepsy surgery, and approximately 50% of patients with MTS have a history of prolonged febrile convulsion (PFC) in childhood. The latter led to the hypothesis that convulsive status epilepticus, including PFC, can cause MTS. Our recently published data on children investigated within 5 days of a PFC showed that children investigated by MRI within 48 h of a PFC had large hippocampal volumes and prolongation of T2 relaxation time. Patients investigated >48 h from a PFC had large hippocampal volumes and normal T2 relaxation time. These data are strongly suggestive of hippocampal oedema that is resolving within 5 days of a PFC, but do not exclude the possibility of a pre-existing hippocampal lesion. Fourteen children from the original study had follow-up investigations carried out 4-8 months after the acute investigations. Of the 14 patients, four have had further seizures. Two had short febrile convulsions, one had PFC and one had non-febrile seizures. There was a significant reduction in hippocampal volume and T2 relaxation time between the first and second investigations, and there is now no difference in hippocampal volume or T2 relaxation time in patients compared with a control population. Moreover, there is a significant increase in hippocampal volume asymmetry in patients at follow-up when compared with initial data. Five out of 14 patients had asymmetry outside the 95th percentile for control subjects and, of these, three had one hippocampal volume outside the lower 95% prediction limit for control subjects. A reduction in hippocampal volume or T2 relaxation time, into or below the normal range between the first and second scans, indicates that the earlier findings are temporary and are strongly suggestive of hippocampal oedema as the abnormality in the initial investigations. The change in hippocampal symmetry in the patient group is consistent with injury and neuronal loss associated with a PFC, especially in the three individuals who now have a single small hippocampus. However, as there is no T2 relaxation time abnormality, the hippocampi do not meet the criteria for MTS. There may be a lag period of several years between a PFC and the onset of epilepsy, and therefore some of these patients may be developing MTS. Alternatively, the asymmetry could represent return (post-acute oedema) to a pre-existing hippocampal abnormality similar to that identified in family members of patients with MTS and a history of PFC.
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PMID:Hippocampal abnormalities after prolonged febrile convulsion: a longitudinal MRI study. 1293 81

The prevalence and psychopathologic features of psychiatric adverse events (PAE) in 517 patients taking levetiracetam (LEV) were investigated. Fifty-three (10.1%) patients developed PAE. A significant association was found with previous psychiatric history, history of febrile convulsions, and history of status epilepticus, whereas lamotrigine co-therapy had a protective effect. PAE were not related to the titration schedule of LEV, and certain patients seem to be biologically more vulnerable.
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PMID:Psychiatric adverse events during levetiracetam therapy. 1296 70

Temporal lobe epilepsy (TLE) is associated with febrile convulsions and childhood status epilepticus (SE). Since the initial precipitating injury, triggering epileptogenesis, occurs during this SE, we aimed to examine the metabolic and morphological cerebral changes during the acute phase of experimental SE noninvasively. In the rat lithium-pilocarpine model of SE, we performed quantified T(2)- and isotropic-diffusion-weighted (DW) magnetic resonance imaging (MRI) at 3 and 5 h of SE and acquired single-voxel (1)H MR spectra at 2, 4 and 6 h of SE. T(2) was globally decreased, most pronounced in the amygdala (Am) and piriformic cortex (Pi), in which also a significant decrease in apparent diffusion coefficient (ADC) was found. In contrast, ADC values increased transiently in the hippocampus (HC) and thalamus (Th). MR spectra showed a decrease in N-acetylaspartate (NAA) and choline (Cho) and an increase of lactate in a hippocampal voxel. The T(2) decrease, attributed to raised deoxyhemoglobin, and the presence of lactate both indicate a mismatch between oxygen demand and delivery. The ADC decrease, indicative of excitotoxicity, confirms that the amygdala and piriformic cortex are particularly vulnerable to lithium-pilocarpine-induced seizures. The transient ADC increase in the thalamus may reflect the breakdown of the blood-brain barrier (BBB), which is shown to occur in this region at these time points. Neuronal damage and failure of energy-dependent formation of NAA are likely causes of an observed decrease in NAA, while the decrease in Cho is possibly due to depletion of the cholinergic system. This study illustrates that relative hypoxia, excitotoxicity and concomitant neuronal damage associated with SE can be probed noninvasively with MR. These pathological phenomena are the first to contribute to the pathophysiology of spontaneous recurrent seizures in a later stage in this animal model.
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PMID:In vivo 1H magnetic resonance spectroscopy, T2-weighted and diffusion-weighted MRI during lithium-pilocarpine-induced status epilepticus in the rat. 1556 33

The efficacy of a combination of midazolam and phenytoin in treating generalized convulsive status epilepticus in children was studied retrospectively. The patient group comprised all patients admitted for generalized convulsive status epilepticus to the pediatric intensive care unit over 7 years. Patients treated according to the protocol were included (N = 122). These patients were treated with the following regimen; each subsequent step was taken if clinical evidence of epileptic activity persisted: midazolam 0.5 mg/kg rectally or 0.1 mg/kg intravenously. After 10 minutes: midazolam 0.1 mg/kg intravenously. After 10 minutes: phenytoin 20 mg/kg intravenously in 20 minutes. After phenytoin load: midazolam 0.2 mg/kg intravenously followed by midazolam 0.1 mg/kg/hour continuously, increased by 0.1 mg/kg/hour every 10 minutes to maximum 1 mg/kg/hour. Phenobarbital 20 mg/kg intravenously or pentobarbital 2 to 5 mg/kg intravenous load, 1 to 2 mg/kg/hour continuously intravenously. Patients who received initial rectal diazepam were included. Patients were categorized according to the cause of generalized convulsive status epilepticus. These categories were then related to the level of antiepileptic therapy needed. Patients' ages ranged from 0.5 to 197.4 months. The cause of generalized convulsive status epilepticus was idiopathic or febrile convulsions in two thirds of cases. Most (89%) patients were managed on midazolam and phenytoin. Generalized convulsive status epilepticus was terminated with midazolam alone in 58 patients, with the addition of phenytoin in 19 patients and with continuous midazolam in 32 patients. Thirteen patients needed additional barbiturates. The relationship between the level of antiepileptic therapy and etiology was not significant. Fifty-two patients needed artificial ventilation. Seven patients died; no deaths were directly attributable to generalized convulsive status epilepticus itself. With the use of the proposed protocol, combining midazolam and phenytoin, 89% of the cases of generalized convulsive status epilepticus could be successfully managed.
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PMID:Status epilepticus: clinical analysis of a treatment protocol based on midazolam and phenytoin. 1599 95

A retrospective case note study of the aetiology and course of children in convulsive status epilepticus (CSE) admitted to a large paediatric intensive care unit (PICU) was undertaken between January 1999 and April 2004. Status epilepticus was defined as a prolonged (>30 min) tonic-clonic seizure irrespective of whether the seizure had stopped prior to admission to PICU. During this period, 137 (74 male) children aged 1 month to 15 years were admitted to PICU with 147 episodes of status epilepticus. Forty-seven of the 137 children (34%) were admitted following a prolonged febrile seizure. Thirty-eight of the 137 children (28%) had a remote symptomatic cause for the CSE, 24 (18%) were admitted for an acute symptomatic cause and 15 (11%) were admitted with an acute exacerbation of a pre-existing idiopathic/cryptogenic epilepsy. Six children had a progressive encephalopathy and no cause was identified in the remaining 7 of the 137 children (5%). Forty-nine (36%) of the 137 children had pre-existing epilepsy. The mean duration of CSE was 44 min. Forty-nine (36%) children admitted to PICU who had received a benzodiazepine with either phenobarbital or phenytoin, required further treatment to terminate the presenting episode of CSE. Forty-two of these 49 were treated with thiopentone anaesthesia and the remaining 7 with a continuous infusion of midazolam, successfully terminating status in all. No child died. Of the 70 children considered to be previously neurologically and developmentally normal prior to admission, only 1 child demonstrated a new gross neurological abnormality at the time of latest follow-up. Seven patients (5%) developed new or de novo epilepsy.
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PMID:Aetiology, course and outcome of children admitted to paediatric intensive care with convulsive status epilepticus: a retrospective 5-year review. 1729 36


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