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Epilepticus
Kinds of Epilepticus Selected AbstractsIntravenous lidocaine for status epilepticus during childhoodDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2006Shin-ichiro Hamano MD; The clinical efficacy of lidocaine for convulsive status epilepticus in 53 convulsive episodes was examined in 37 children (17 males, 20 females). Mean age of patients receiving lidocaine was 3 years 7 months (SD 3y 5mo). Lidocaine administration achieved control of status epilepticus in 19 of 53 convulsive episodes (35.8%). Seizures ceased within 5 minutes of lidocaine administration in all 19 patients who were responsive to the drug. Regarding aetiology of status epilepticus and types of seizures, there was no statistical difference in effectiveness. Mild decrease of oxygen saturation, monitored by pulse oximetry, was observed in one patient, which improved by oxygenation using a mask. Lidocaine is a useful anticonvulsive agent; however, the response rate to lidocaine appears to be quite low, as less than half of the seizures were effectively controlled by lidocaine. Favourable properties of the drug include prompt responses, less alteration of consciousness, and fewer adverse effects, including less respiratory depression. [source] Withdrawal of older anticonvulsants for management of status epilepticus: implications for resource-poor countriesDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2005J M Wilmshurst No abstract is available for this article. [source] Neuronal plasticity: implications in epilepsy progression and managementDRUG DEVELOPMENT RESEARCH, Issue 8 2007Sherifa A. HamedArticle first published online: 12 FEB 200 Abstract Epilepsy is a common neurological disease. A growing number of research studies provide evidence regarding the progressive neuronal damage induced by prolonged seizures or status epilepticus (SE), as well as recurrent brief seizures. Importantly, seizure is only one aspect of epilepsy. However, cognitive and behavioral deficits induced by progressive seizures or antiepileptic treatment can be detrimental to individual function. The neurobiology of epilepsy is poorly understood involving complex cellular and molecular mechanisms. The brain undergoes changes in its basic structure and function, e.g., neural plasticity with an increased susceptibility in neuronal synchronization and network circuit alterations. Some of these changes are transient, while others are permanent with an involvement of both glutamatergic and ,-aminobutyric acid (GABA)ergic systems. Recent data suggest that impaired neuronal plasticity may underlie the cognitive impairment and behavioral changes associated with epilepsy. Many neurologists recognize that the prevention or suppression of seizures by the use of antiepileptic drugs (AEDs) alone is insufficient without clear predictions of disease outcome. Hence, it is important to understand the molecular mechanisms underlying epileptogenesis because this may allow the development of innovative strategies to prevent or cure this condition. In addition, this realization would have significant impact in reducing the long-term adverse consequences of the disease, including neurocognitive and behavioral adverse effects. Drug Dev Res 68:498,511, 2007. © 2008 Wiley-Liss, Inc. [source] Is the time overdue for an international reporting standard for convulsive paediatric status epilepticus?EMERGENCY MEDICINE AUSTRALASIA, Issue 1 2006Ronald A Dieckmann No abstract is available for this article. [source] Deletions in 16p13 including GRIN2A in patients with intellectual disability, various dysmorphic features, and seizure disorders of the rolandic regionEPILEPSIA, Issue 9 2010Constanze Reutlinger Summary Seizure disorders of the rolandic region comprise a spectrum of different epilepsy syndromes ranging from benign rolandic epilepsy to more severe seizure disorders including atypical benign partial epilepsy/pseudo-Lennox syndrome, electrical status epilepticus during sleep, and Landau-Kleffner syndrome. Centrotemporal spikes are the unifying electroencephalographic hallmark of these benign focal epilepsies, indicating a pathophysiologic relationship between the various epilepsies arising from the rolandic region. The etiology of these epilepsies is elusive, but a genetic component is assumed given the heritability of the characteristic electrographic trait. Herein we report on three patients with intellectual disability, various dysmorphic features, and epilepsies involving the rolandic region, carrying previously undescribed deletions in 16p13. The only gene located in the critical region shared by all three patients is GRIN2A coding for the alpha-2 subunit of the neuronal N -methyl- d -aspartate (NMDA) receptor. [source] Febrile infection,related epilepsy syndrome (FIRES): A nonencephalitic encephalopathy in childhoodEPILEPSIA, Issue 7 2010Andreas Van Baalen Summary Encephalitis is generally presumed, even when seizures follow banal febrile infection, and pathogen detection in cerebrospinal fluid fails. This retrospective multicenter case series reports on 22 previously healthy children aged 3,15 years (median 6.5 years) with prolonged or recurrent seizures occurring 2,14 days (median 5 days) after fever onset (19 children with respiratory or nonspecific infections). Cerebrospinal fluid studies revealed 2,42 cells/,l (median 5 cells/,l) and no pathogens. Electroencephalography showed diffuse slowing or multifocal discharges. Neuroimaging demonstrated normal findings in 10 children. Brain biopsies were performed in seven children showing gliosis but no inflammation. Anesthetic barbiturates were used in 14 children with refractory status epilepticus, and immunotherapy in 9. Two children died, eight remained in a state of impaired consciousness, eight developed therapy-refractory epilepsies, two had behavioral disturbances, and two recovered. The lack of evidence for encephalitis suggests another infection-related pathogenesis of this disastrous epileptic encephalopathy. Therefore, we propose the term "febrile infection,related epilepsy syndrome" (FIRES). [source] Distinct caspase pathways mediate necrosis and apoptosis in subpopulations of hippocampal neurons after status epilepticusEPILEPSIA, Issue 2010Maria-Leonor Lopez-Meraz Summary Status epilepticus in the immature brain induces neuronal injury in the hippocampal formation, but the mode and mechanism of death are poorly understood. Our laboratory has recently investigated the role of caspase-3, -8, and -9 in neuronal injury, using a lithium,pilocarpine model of status epilepticus in 2-week-old rat pups. Our results showed that dying neurons in the dentate gyrus and CA1-subiculum area do not share the same mechanism of death. In CA1-subiculum, caspase-8 upregulation preceded caspase-3 activation in morphologically necrotic neurons. The pan-caspase inhibitor Q-VD-OPH reduced CA1 damage, showing that caspases contribute to status epilepticus,induced necrosis. In the dentate gyrus, dying neurons were caspase-9 and -3 immunoreactive and morphologically apoptotic. It is not clear why the same seizures cause different types of cell death in neurons that are connected in series along the same hippocampal circuit, but the apoptotic dentate neurons express doublecortin, and do not express calbindin-D28k, suggesting that their immaturity may be a factor in producing an apoptotic mode of death. [source] De novo epileptic confusion in the elderly: A 1-year prospective studyEPILEPSIA, Issue 6 2010Olivier Veran Summary Purpose:, Nonconvulsive status epilepticus (NCSE) is clinically difficult to diagnose, especially in old patients without epilepsy, and requires electroencephalography (EEG) for diagnosis. Its incidence among elderly patients with confusion of unknown origin (CUO) remains undetermined. Methods:, A 1-year prospective study was conducted in patients aged 60 years or older, for whom EEG was requested because of confusion considered to be of unknown origin after initial clinical, biologic, and imaging investigations. Diagnosis criteria included a validated clinical assessment scale to confirm confusion. Results:, Of 44 patients with confirmed CUO, 7 presented with de novo NCSE. NCSE population had a mean age of 76 years (range, 60,97 years). No statistically significant differences were found between NCSE patients and others for age, drugs, presence of myoclonia, eyelid myoclonia, tachycardia, or agitation. In contrast, an acute onset (<24 h), gender (100% female among NCSE patients), and lack of clinical response to simple commands were significantly associated with NCSE. No differences between the two groups were evidenced for mortality and morbidity (length of hospitalization, social outcome, and so on). Discussion:, Almost 16% of patients aged 60 or older with confusion of unknown origin had NCSE, according to this first prospective study. Female patients with rapid onset (<24 h) of symptoms and lack of response to simple commands were at a higher risk of presenting with NCSE. [source] Topiramate overdose: A case report of a patient with extremely high topiramate serum concentrations and nonconvulsive status epilepticusEPILEPSIA, Issue 6 2010Christian Brandt Summary We report the case of a 21-year-old man with idiopathic generalized epilepsy who ingested about 8,000 mg of topiramate (TPM) in a suicide attempt. On admission to the hospital he had a nonconvulsive status epilepticus and received 4 mg lorazepam i.v. He recovered rapidly despite an initial TPM concentration of 144.6 ,g/ml. To our knowledge, this is the first report of a patient who survived such a high TPM concentration. The case indicates that nonconvulsive status epilepticus could be a manifestation of TPM intoxication. [source] Protective effects of naloxone in two-hit seizure modelEPILEPSIA, Issue 3 2010Lu Yang Summary Purpose:, Early life status epilepticus (SE) could enhance the vulnerability of the immature brain to a second SE in adulthood (two-hit seizure model). Naloxone has been proved to possess inflammation inhibitory effects in nervous system. This study was designed to evaluate the dose-dependent protective effects of naloxone in kainic acid (KA),induced two-hit seizure model. Methods:, After KA-induced SE at postnatal day 15 (P15), Sprague-Dawley rats were infused with either saline or different doses (1.92, 3.84, 5.76, and 7.68 mg/kg) of naloxone continuously for 12 h. De novo synthesis of cytokines (interleukin-1, [IL-1,], S100B) was assessed by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) at 12 h after P15 SE. Glial activation states were analyzed by western blotting of glial markers (glial fibrillary acidic protein [GFAP], S100B, Iba1) both at 12 h after P15 SE and at P45. After a second SE at P45, cognitive deteriorations were evaluated by Morris water tests and neuron injuries were evaluated by TdT-mediated dUTP nick end labeling (TUNEL) assays. Results:, Naloxone reduced IL-1, synthesis and microglial activation most potently at a dose of 3.84 mg/kg. Attenuation of S100B synthesis and astrocyte activation were achieved most dramatically by naloxone at a dose of 5.76 mg/kg, which is equal to the most powerful dose in ameliorating cognitive injuries and neuron apoptosis after second SE. Conclusions:, Naloxone treatment immediately after early life SE could dose-dependently reduce cytokine production, glial activation, and further lower the vulnerability of immature brains to a second hit in adulthood. [source] Antiepileptic drugs combined with high-frequency electrical stimulation in the ventral hippocampus modify pilocarpine-induced status epilepticus in ratsEPILEPSIA, Issue 3 2010Manola Cuellar-Herrera Summary Purpose:, To evaluate the effects of high-frequency electrical stimulation (HFS) in both ventral hippocampi, alone and combined with a subeffective dose of antiepileptic drugs, during the status epilepticus (SE) induced by lithium-pilocarpine (LP). Methods:, Male Wistar rats, stereotactically implanted in both ventral hippocampi, were injected with pilocarpine (30 mg/kg, i.p.) 24 h after lithium (3 mEq/kg) administration. One minute following pilocarpine injection, HFS (pulses of 60 ,s width at 130 Hz at subthreshold intensities and applied during 3 h) was applied alone or combined with subeffective doses of antiepileptic drugs. Results:, HFS alone reduced the incidence of severe generalized seizures. This effect was not evident when HFS was combined with phenytoin (33.3 mg/kg, i.p.). HFS combined with diazepam (0.41 mg/kg, i.p.) or phenobarbital (10 mg/kg, i.p.) reduced the incidence of severe generalized seizures and mortality rate, and augmented the latency to first forelimb clonus, generalized seizure, and status epilepticus (SE). When combined with gabapentin (46 mg/kg, i.p.), HFS reduced the incidence of severe generalized seizures, enhanced latency to SE, and decreased mortality rate. Discussion:, Subeffective doses of antiepileptic drugs that increase the ,-aminobutyric acid (GABA)ergic neurotransmission may represent a therapeutic tool to augment the HFS-induced anticonvulsant effects. [source] High seizure frequency prior to antiepileptic treatment is a predictor of pharmacoresistant epilepsy in a rat model of temporal lobe epilepsyEPILEPSIA, Issue 1 2010Wolfgang Löscher Summary Purpose:, Progress in the management of patients with medically intractable epilepsy is impeded because we do not fully understand why pharmacoresistance happens and how it can be predicted. The presence of multiple seizures prior to medical treatment has been suggested as a potential predictor of poor outcome. In the present study, we used an animal model of temporal lobe epilepsy to investigate whether pharmacoresistant rats differ in seizure frequency from pharmacoresponsive animals. Methods:, Epilepsy with spontaneous recurrent seizures (SRS) was induced by status epilepticus. Frequency of SRS was determined by video/EEG (electroencephalography) monitoring in a total of 33 epileptic rats before onset of treatment with phenobarbital (PB). Results:, Thirteen (39%) rats did not respond to treatment with PB. Before treatment with PB, average seizure frequency in PB nonresponders was significantly higher than seizure frequency in responders, which, however, was due to six nonresponders that exhibited > 3 seizures per day. Such high seizure frequency was not observed in responders, demonstrating that high seizure frequency predicts pharmacoresistance in this model, but does not occur in all nonresponders. Discussion:, The data from this study are in line with clinical experience that the frequency of seizures in the early phase of epilepsy is a dominant risk factor that predicts refractoriness. However, resistance to treatment also occurred in rats that did not differ in seizure frequency from responders, indicating that disease severity alone is not sufficient to explain antiepileptic drug (AED) resistance. These data provide further evidence that epilepsy models are useful in the search for predictors and mechanisms of pharmacoresistance. [source] The impact of diazepam's discovery on the treatment and understanding of status epilepticusEPILEPSIA, Issue 9 2009Howard P. Goodkin Summary The fortuitous discovery of the benzodiazepines and the subsequent application of these agents to the treatment of status epilepticus (SE) heralds in the modern age of treating this neurologic emergency. More than 50 years after their discovery, the benzodiazepines remain the drugs of first choice in the treatment of SE. However, the benzodiazepines can be ineffective, especially in those patients whose seizures are the most prolonged. The benzodiazepines act by increasing the affinity of ,-aminobutyric acid (GABA) for GABAA receptors. A receptor's subunit composition affects its functional and pharmacologic properties, trafficking, and cellular localization. The GABAA receptors that mediate synaptic inhibition typically contain a ,2 subunit and are diazepam-sensitive. Among the GABAA receptors that mediate tonic inhibition are the benzodiazepine-insensitive , subunit,containing receptors. The initial studies investigating the pathogenesis of SE demonstrated that a reduction in GABA-mediated inhibition within the hippocampus was important in maintenance of SE, and this reduction correlated with a rapid modification in the postsynaptic GABAA receptor population expressed on the surface of the hippocampal principal neurons. Subsequent studies found that this rapid modification is, in part, mediated by an activity-dependent, subunit-specific trafficking of the receptors that resulted in the reduction in the surface expression of the benzodiazepine-sensitive ,2 subunit,containing receptors and the preserved surface expression of the benzodiazepine-insensitive , subunit-containing receptors. This improved understanding of the changes in the trafficking of GABAA receptors during SE partially accounts for the development of benzodiazepine-pharmacoresistance and has implications for the current and future treatment of benzodiazepine-refractory SE. [source] Hemiconvulsion,hemiplegia syndrome in a patient with severe myoclonic epilepsy in infancyEPILEPSIA, Issue 9 2009Takafumi Sakakibara Summary We report a 2-year-old girl who had repeated febrile or afebrile seizures since infancy. Prolonged left/right hemiconvulsions and myoclonus of the eyelids/extremities with generalization to tonic,clonic seizures, were refractory to antiepileptic agents. At age 1 year and 4 months, she contracted rotavirus infection, and developed status epilepticus with persistent right hemiclonic seizures. Left unilateral brain edema with subsequent emergence of cortical laminar necrosis and white matter lesions, and progressive atrophy of the left cerebral hemisphere were noted during this period. She showed residual right hemiparesis and mild intellectual disability, and had generalized/eyelid myoclonia and hot water epilepsy after a 5-month seizure-free period. Analysis for SCN1A, the gene encoding the neuronal voltage-gated Na+ channel ,1 subunit revealed a nonsense mutation, R1892X. These indicate the potential risk in patients with severe myoclonic epilepsy in infancy (SMEI) to develop hemiconvulsion,hemiplegia (HH) syndrome. SCN1A mutations may need to be further explored in patients with HH syndrome without features of SMEI. [source] The effects of intracerebroventricular AM-251, a CB1-receptor antagonist, and ACEA, a CB1-receptor agonist, on penicillin-induced epileptiform activity in ratsEPILEPSIA, Issue 7 2009Ramazan Kozan Summary Purpose:, Several results support the conclusion that the cannabinoid system has a role in generation and cessation of epileptic seizures. The aim of this study was to evaluate the effects of intracerebroventricular AM-251 [N -(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide], a CB1-receptor antagonist, and ACEA (arachidonyl-2-chloroethylamide), a CB1-receptor agonist, on penicillin-induced epileptiform activity in rats. Methods:, In the first set of experiments, 30 min after penicillin injection, AM-251, at doses of 0.125, 0.25, 0.5, and 1 ,g, was administered intracerebroventricularly (i.c.v.). In the second set of experiments, 30 min after penicillin injection, ACEA, at doses of 2.5, 5, 7.5, and 15 ,g (i.c.v.), was administered. In the third set of experiments, AM-251, at doses of 0.125 and 0.25 ,g (i.c.v.), was administered 10 min before ACEA (7.5 ,g, i.c.v.) injection. Results:, ACEA, at a dose of 7.5 ,g, significantly decreased the frequency of penicillin-induced epileptiform activity without changing the amplitude. ACEA, at doses of 2.5, 5, and 15 ,g, had no impact on either frequency or amplitude of epileptiform activity. AM-251, at doses of 0.25 and 0.50 ,g, significantly increased the frequency of epileptiform activity. AM-251, at a dose of 0.25 ,g (i.c.v.), was the most effective in changing the frequency of penicillin-induced epileptiform activity, and it also caused status epilepticus,like activity. AM-251, at doses of 0.125 and 0.25 ,g, 10 min before ACEA (7.5 ,g), reversed the anticonvulsant action of ACEA. Discussion:, The results of the present study provide electrophysiologic evidence for the role of CB1 receptors in regulating the frequency of epileptiform activity in the model of penicillin-induced epilepsy. To elucidate the precise mechanism of cannabinoid action in the brain during seizure, more advanced electrophysiologic and neurochemical studies are required. [source] Aphasic or amnesic status epilepticus detected on PET but not EEGEPILEPSIA, Issue 2 2009Christine Dong Summary Purpose:, To describe five patients with ictal aphasia and one patient with ictal amnesia, who had focal positron emission tomography (PET) hypermetabolism but no clear ictal activity on electroencephalography (EEG). Methods:,18F-Fluorodeoxyglucose (FDG),PET scans with concomitant EEG were obtained in five patients with suspected ictal aphasia or ictal amnesia without ictal activity on EEG. We reviewed medical history, EEG, imaging data, and treatment outcome. Results:, Brain magnetic resonance imaging (MRI) showed no structural abnormalities in any of the patients. EEG showed left temporal irregular delta activity in three patients, with aphasia and nonspecific abnormalities in two other patients, all without clear ictal pattern. All patients demonstrated focal hypermetabolism on PET scan. The hypermetabolism was in the left frontotemporal region in patients with ictal aphasia and in the bilateral hippocampal region in the patient with amnesia. Three patients who received intravenous benzodiazepines during their episodes had transient clinical improvement. With antiepileptic drug (AED) treatment, symptoms gradually resolved in all patients. Concomitant resolution of PET hypermetabolism was documented in three patients who had follow up scans. One patient with ictal aphasia later developed recurrent episodes, each with recurrent PET hypermetabolism. This patient and one other patient required immune-modulating therapy in addition to AEDs. Discussion:, FDG-PET imaging should be considered as a diagnostic tool in patients with suspected ictal aphasia or amnesia, who fail to show clear evidence of ictal activity on EEG. [source] Human herpes virus 6B: A possible role in epilepsy?EPILEPSIA, Issue 11 2008William H. Theodore Summary Human herpes virus 6 (HHV6) infection is nearly ubiquitous in childhood and may include central nervous system invasion. There are two variants, HHV6A and HHV6B. Usually asymptomatic, it is associated with the common, self-limited childhood illness roseola infantum and rarely with more severe syndromes. In patients with immune compromise, subsequent reactivation of viral activity may lead to severe limbic encephalitis. HHV6 has been identified as a possible etiologic agent in multiple sclerosis, myocarditis, and encephalitis. A preponderance of evidence supports an association between HHV6 and febrile seizures. An ongoing multicenter study is investigating possible links between HHV6 infection, febrile status epilepticus, and development of mesial temporal sclerosis (MTS). Investigation of temporal lobectomy specimens showed evidence of active HHV6B but not HHV6A replication in hippocampal astrocytes in about two-thirds of patients with MTS but not other causes of epilepsy. It has been suggested that HHV6B may cause "excitotoxicity" by interfering with astrocyte excitatory amino acid transport. Although conventional inflammatory changes are not found in most MTS specimens, inflammatory modulators may play a role in neuronal injury leading to MTS as well. If the link between early viral infection, complex or prolonged febrile seizures, and later development of intractable temporal lobe epilepsy is confirmed, new therapeutic approaches to a common intractable epilepsy syndrome may be possible. [source] The drug treatment of status epilepticus in Europe: Consensus document from a workshop at the first London Colloquium on Status EpilepticusEPILEPSIA, Issue 7 2008Simon Shorvon First page of article [source] Transatlantic similarities and differences in the management of status epilepticusEPILEPSIA, Issue 7 2008Thomas P. Bleck No abstract is available for this article. [source] Gene and protein expression in experimental status epilepticusEPILEPSIA, Issue 2007Katarzyna Lukasiuk First page of article [source] Status epilepticus: The past and the futureEPILEPSIA, Issue 2007Brian Meldrum No abstract is available for this article. [source] Clinical trial design in status epilepticus: problems and solutionsEPILEPSIA, Issue 2007Brian G. R. Neville No abstract is available for this article. [source] Intensive care unit management of patients with status epilepticusEPILEPSIA, Issue 2007Thomas P. Bleck Summary The intensive care unit management of status epilepticus focuses on patients who are refractory to initial treatment, who have an underlying condition that require critical care management, or who experience respiratory or cardiovascular complications of their therapies. The available data suggest that failure of a first-line anticonvulsant agent to terminate status should lead to the use of a definitive therapy in general anesthetic doses. Midazolam, propofol, and phenobarbital have been used most frequently; the place of newer agents (e.g., valproate, levetiracetam, or topiramate) remains to be determined. [source] Cognitive outcome of status epilepticus in adultsEPILEPSIA, Issue 2007Christoph Helmstaedter Summary There is no doubt that structural morphological brain lesions and malformations in epilepsy represent major etiological factors for the cognitive impairments seen in this disease. The role of epileptic activity and seizures for cognition and cognitive development, however, is less easily determined. Epileptic dysfunction ranges from interictal and periictal activity over self-terminating seizures to non-convulsive and convulsive status epilepticus, which appear the most severe conditions along this continuum. The decisive question in this regard is as to whether cognitive impairments observed in the acute epileptic condition are reversible or not. Impairments from interictal or postictal epileptic dysfunction are reversible and may interfere at most with brain maturation and cognitive development in the young patient. Seizures and ictal dysfunction in contrast, even when reversible, can leave a permanent trace which extends the phase of postictal recovery. As for status epilepticus and subsequent cognitive decline it often remains open whether the epileptic condition itself or the underlying clinical condition is causative for the aftermath. While there is evidence for both possibilities, group data from neuropsychological cross sectional and longitudinal studies indicate that more severe mental impairments, which in turn indicate more severe clinical conditions, appear to be a risk factor for sustaining status epilepticus, rather than that status epilepticus causes the cognitive decline. Reviewing the literature the cognitive condition in patients with status epilepticus varies with the type of epilepsy, the etiology of epilepsy, severity of the status, and the age of the patient. [source] Outcome of status epilepticus in childrenEPILEPSIA, Issue 2007Alexis Arzimanoglou No abstract is available for this article. [source] Cognitive Deficits during Status Epilepticus and Time Course of Recovery: A Case ReportEPILEPSIA, Issue 10 2007Wim Van Paesschen Summary:, We describe a young woman with progressive cognitive and neurological deficits during a parietal lobe status epilepticus (SE). Ictal FDG-PET showed left parietal lobe hypermetabolism and frontal lobe hypometabolism with concomitant EEG slowing. Cognitive and neurological deficits fully reversed more than 1 year after seizure remission, and were associated with normalization of FDG-PET and EEG. Our findings suggest that ictal hypometabolism and EEG delta activity at a distance from the epileptic focus were seizure-related phenomena, possibly representing inhibition in seizure propagation pathways, which could be responsible for the epileptic encephalopathy. [source] The Epidemiology of Convulsive Status Epilepticus in Children: A Critical ReviewEPILEPSIA, Issue 9 2007Miquel Raspall-Chaure Summary:, There is ongoing debate regarding the most appropriate definition of status epilepticus. This depends upon the research question being asked. Based on the most widely used "30 min definition," the incidence of childhood convulsive status epilepticus (CSE) in developed countries is approximately 20/100,000/year, but will vary depending, among others, on socioeconomic and ethnic characteristics of the population. Age is a main determinant of the epidemiology of CSE and, even within the pediatric population there are substantial differences between older and younger children in terms of incidence, etiology, and frequency of prior neurological abnormalities or prior seizures. Overall, incidence is highest during the first year of life, febrile CSE is the single most common cause, around 40% of children will have previous neurological abnormalities and less than 15% will have a prior history of epilepsy. Outcome is mainly a function of etiology. However, the causative role of CSE itself on mesial temporal sclerosis and subsequent epilepsy or the influence of age, duration, or treatment on outcome of CSE remains largely unknown. Future studies should aim at clarifying these issues and identifying specific ethnic, genetic, or socioeconomic factors associated with CSE to pinpoint potential targets for its primary and secondary prevention. [source] Status Epilepticus in Children with Epilepsy: Dutch Study of Epilepsy in ChildhoodEPILEPSIA, Issue 9 2007Hans Stroink Summary:,Purpose: To study course and outcome of epilepsy in children having had a status epilepticus (SE) as the presenting sign or after the diagnosis. Methods: A total of 494 children with newly diagnosed epilepsy, aged 1 month through 15 years, were followed prospectively for 5 years. Results: A total of 47 Children had SE. Forty-one of them had SE when epilepsy was diagnosed. For 32 (78%), SE was the first seizure. SE recurred in 13 out of 41 (32%). Terminal remission at 5 years (TR5) was not significantly worse for these 41 children: 31.7% had a TR5 <1 year versus 21.2% of 447 children without SE. They were not more often intractable. Five out of six children with first SE after diagnosis had a TR5 <1 year. Mortality was not significantly increased for children with SE. Independent factors associated with SE at presentation were remote symptomatic and cryptogenic etiology, and a history of febrile convulsions. Children with first SE after inclusion more often had symptomatic etiology. Conclusions: Although we find a trend for shorter TR5 in children with SE at presentation, outcome and mortality are not significantly worse. Etiology is an important factor for prognosis. Children with SE during the course of their epilepsy have a worse prognosis and a high recurrence rate of SE. This outcome is not due to the SE itself, but related to the etiology and type of epilepsy. The occurrence of SE is just an indicator of the severity of the disease. [source] A Large-scale Mutagenesis Screen to Identify Seizure-resistant ZebrafishEPILEPSIA, Issue 6 2007Scott C. Baraban Summary:,Methods: Seizures were induced with pentylenetetrazole (PTZ). Zebrafish were analyzed between 3 and 7 days postfertilization (dpf). Genome mutations were induced in founders by using N- ethyl-nitrosourea (ENU). Seizure behavior was monitored by using a high-speed camera and quantified by locomotion-tracking software. Electrographic activity was monitored by using a field-recording electrode placed in the optic tectum of agar-immobilized zebrafish. Results: Short-term PTZ exposure elicited a burst-suppression seizure pattern in 3-dpf zebrafish and more complex activity consisting of interictal- and ictal-like discharges at 7 dpf. Prolonged exposure to PTZ induced status epilepticus,like seizure activity and fatality in wild-type zebrafish larvae. With a PTZ survival assay at 6,7 dpf, we identified six zebrafish mutants in a forward-genetic screen covering nearly 2,000 F2 families. One mutant (s334) also was shown to exhibit reduced behavioral activity on short-term PTZ exposure and an inability to generate long-duration ictal-like discharge. Conclusions: Zebrafish offers a powerful tool for the identification and study of a genetic basis for seizure resistance. [source] Effect of Interictal Spikes on Single-Cell Firing Patterns in the HippocampusEPILEPSIA, Issue 4 2007Jun-Li Zhou Summary:,Purpose: The interictal EEG spike(s) is the hallmark of the epileptic EEG. While focal interictal spike (IS) have been associated with transitory cognitive impairment, with the type of deficit dependent on where in the cortex the IS arises, the mechanism by which IS result in transitory dysfunction is not known. The purpose of this study was to determine the effect of IS on single-cell firing patterns in freely moving rats with a prior history of seizures. Methods: We studied IS in two seizure models; pilocarpine-induced status epilepticus and recurrent flurothyl models. The effect of spontaneous hippocampal spikes on action potentials (APs) of CA1 cells in rats walking in a familiar environment was investigated using 32 extracellular electrodes. We also compared the effect of spikes on two types of hippcampal cells; place cells that discharge rapidly only when the rat's head is in a specific part of the environment, the so-called firing field, and interneurons, which are a main source of inhibition in the hippocampus. Results: IS were associated with a decreased likelihood of AP compared with IS-free portions of the record. Compared to pre-IS baseline, IS were followed by significant decreases in CA1 APs for periods up to 2 s following the IS in both models. When occurring in flurries, IS were associated with a pronounced decrease in APs. The response to IS was cell-dependent; IS resulted in decreases in AP firing after the IS in interneurons but not place cells. Conclusions: This study demonstrates that IS have substantial effects on cellular firing in the hippocampus and that these effects last far longer than the spike and slow wave. Furthermore, the effect of IS on cellular firing was cell specific, affecting interneurons more than place cells. These findings suggest that IS may contribute to seizure-induced cognitive impairment by altering AP firing in a cell-specific manner. [source] | |||||||||||||||||||||||||||||||