OBJECTIVE: To systematically evaluate the efficacy and safety of levetiracetam (LEV) versus phenytoin (PHT) as second-line drugs for the treatment of convulsive status epilepticus (CSE) in children. METHODS: English and Chinese electronic databases were searched for the randomized controlled trials comparing the efficacy and safety of LEV and PHT as second-line drugs for the treatment of childhood CSE. RevMan 5.3 software was used for data analysis. RESULTS: Seven studies with 1 434 children were included. The Meta analysis showed that compared with the PHT group, the LEV group achieved a significantly higher control rate of CSE ( CONCLUSIONS LEV has a better clinical effect than PHT in the treatment of children with CSE and does not increase the incidence rate of adverse events.
Anticonvulsants/adverse effects* ; Child ; Humans ; Levetiracetam/therapeutic use* ; Pharmaceutical Preparations ; Phenytoin/adverse effects* ; Status Epilepticus/drug therapy*

OBJECTIVES: To study the effect of gap junction blockers, quinine (QUIN) and carbenoxolone (CBX), on hippocampal ripple energy expression in rats with status epilepticus (SE). METHODS: A total of 24 rats were randomly divided into four groups: model, QUIN, valproic acid (VPA), and CBX ( RESULTS: Ripple expression was observed in the hippocampal CA1, CA3, and dentate gyrus regions of normal rats. After 10 minutes of PILO injection, all groups had a gradual increase in mean ripple energy expression compared with 1 day before modeling, with the highest expression level before chloral hydrate injection in the model, VPA and CBX groups ( CONCLUSIONS The change in ripple energy can be used as a quantitative indicator for early warning of seizures, while it cannot predict seizures in the interictal period. Gap junction blockers can reduce ripple energy during seizures.
Animals ; Gap Junctions ; Hippocampus ; Pilocarpine ; Rats ; Seizures ; Status Epilepticus/drug therapy*

OBJECTIVE: To study the clinical features of electrical status epilepticus during sleep (ESES) in children, as well as the clinical effect of methylprednisolone pulse therapy in children with ESES. METHODS: A retrospective analysis was performed using the clinical data of 78 children with ESES. Among these children, 56 children who had had the failure of antiepileptic drugs were treated with methylprednisolone pulse therapy at a dose of 15-20 mg/(kg·d) for three courses. Each course of treatment was 3 days, followed by oral prednisone [1-2 mg/(kg·d)] for 3 days. The role of methylprednisolone pulse therapy in eliminating ESES, controlling clinical seizures, and improving intelligence and behaviors was analyzed. RESULTS: The mean age of onset of epilepsy in 78 children was 6.8±2.4 years, and the mean age for the first occurrence of ESES was 7.6±2.5 years. Compared with normal children, children with ESES had delayed intelligence development and higher scores of some behavior problems. Methylprednisolone pulse therapy had an overall response rate of 73% (41/56) on clinical seizures, and the overall response rate on electroencephalography (EEG)/spike-wave index was 70% (39/56) after treatment. There were significant improvements in verbal intelligence quotient, performance intelligence quotient and full intelligence quotient, and significant reductions in the scores of learning problems, impulse-hyperactivity and hyperactivity index after treatment (P<0.05). The overall recurrence rate after 1-year follow-up was 29% (11/38). CONCLUSIONS ESES often presents around school age and impairs children's intelligence and behaviors. Methylprednisolone pulse therapy has a marked efficiency in reducing clinical seizures and EEG discharges in children with ESES and can improve intelligence and behavior development, but the recurrence rate remains high.
Anticonvulsants ; Child ; Child, Preschool ; Electroencephalography ; Follow-Up Studies ; Humans ; Methylprednisolone ; therapeutic use ; Retrospective Studies ; Sleep ; Status Epilepticus ; drug therapy

OBJECTIVETo study the effect of a microRNA-132 antagonist on lithium-pilocarpine-induced status epilepticus (SE) in young Sprague-Dawley (SD) rats.

METHODSForty-five 3-week-old SD rats were randomly and equally divided into epilepticus model group, microRNA-132 antagonist group, and microRNA-132 antagonist negative control group. The young SD rat model of SE was established using lithium-pilocarpine. For the microRNA-132 antagonist group and the negative control group, pretreatment was performed 24 hours before the model establishment. Behavioral observation was performed to assess the latency of SE and success rate of induction of SE. The scale of Lado was used to evaluate the seizure severity. Electroencephalography (EEG) was used to assess the frequency and amplitude of epileptiform discharges. The mortality rate was calculated in each group.

RESULTSThere was no significant difference in the success rate of induction of SE between the three groups (P>0.05). Compared with the microRNA-132 negative control group and the epilepticus model group, the microRNA-132 antagonist group had significantly prolonged SE latency after model establishment (P<0.05), a significantly lower Lado score of seizure (P<0.05), significantly lower frequency and amplitude of epileptiform discharges on EEG (P<0.05), and a slightly reduced mortality rate.

CONCLUSIONSThe treatment with the microRNA-132 antagonist shows an inhibitory effect on the development and progression of lithium-pilocarpine-induced SE in young SD rats. The inhibition of microRNA-132 is likely to be a potential target or direction for drug treatment of SE.

Animals ; Electroencephalography ; Male ; MicroRNAs ; antagonists & inhibitors ; Pilocarpine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; chemically induced ; drug therapy

OBJECTIVETo study the effect of cyclooxygenase -2 selective inhibitor celecoxib on the expression of major vault protein ( MVP) in the brain of rats with status epilepticus and its possible roles in the treatment of refractory epilepsy.

METHODSSixty adult male Sprague-Dawley rats were randomly assigned to blank control (n=16), epilepsy model (n=22) and celecoxib treatment groups (n=22). After the status epilepticus was induced in rats by injecting lithium and pilocarpine, each group had 16 rats enrolled as subjects. Immunohistochemical method and Western blot method were used to detect the expression of MVP in the frontal cortex and hippocampus.

RESULTSThe expression of MVP was significantly higher in the epilepsy model group than in the control group (P<0.01). The expression of MVP in the celecoxib treatment group was significantly decreased compared with the epilepsy model group, but it was still higher than in the control group (P<0.01).

CONCLUSIONSCelecoxib could decrease the expression of MVP in brain tissue of rats with status epilepticus, suggesting that it is promising for the treatment of intractable epilepsy.

Animals ; Blotting, Western ; Brain ; metabolism ; Celecoxib ; pharmacology ; therapeutic use ; Cyclooxygenase 2 Inhibitors ; pharmacology ; Immunohistochemistry ; Male ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; drug therapy ; metabolism ; Vault Ribonucleoprotein Particles ; analysis

OBJECTIVETo investigate the effect of licorice flavonoid (LF) on kainic acid (KA)-induced seizure in mice and its mechanism.

METHODSMale adult ICR mice were injected with 25 mg/kg KA to induce temporal lobe seizure. LF was administrated 7 d before seizure induction (pre-treatment) or 24 h after seizure induction (post-treatment) for 7 d. Acute seizure latency, seizure stage and duration were observed and compared between LF- and vehicle-treated mice. From d2 on, mice with status epilepticus were video-monitored for spontaneous seizures, 10 h/d for 6 w. Immunohistochemical analysis of BrdU and Timm staining was conducted to detect the neurogenesis and mossy fiber sprouting, respectively.

RESULTSNo significant difference was observed in acute seizure latency, seizure stage and duration between LF-and vehicle-treated mice. KA-induced acute seizure resulted in spontaneous seizure in mice, and the seizure frequency was increased with time. Pre- and post-treatment with LF decreased seizure frequency from w3 after modeling [(0.58±0.15)/d, (0.38±0.38)/d vs (1.23±0.23)/d, P <0.05]. Furthermore, KA-induced seizure resulted in robust neurogenesis and mossy fiber sprouting, while treatment with LF both pre- and post- KA injection significantly inhibited neurogenesis (15.6±2.6, 17.1±3.1 vs 28.9±3.5, P <0.05) and mossy fiber sprouting (1.33±0.31, 1.56±0.42 vs 3.0±0.37, P <0.05).

CONCLUSIONLF has no significant anti-seizure effect. However, it can decrease epileptogenesis through inhibition of neurogenesis and mossy fiber sprouting.

Animals ; Disease Models, Animal ; Flavonoids ; pharmacology ; Glycyrrhiza ; chemistry ; Kainic Acid ; adverse effects ; Male ; Mice ; Mice, Inbred ICR ; Mossy Fibers, Hippocampal ; drug effects ; Neurogenesis ; drug effects ; Seizures ; chemically induced ; drug therapy ; Status Epilepticus ; drug therapy

OBJECTIVETo evaluate the therapeutic effect of methylprednisolone for electrical status epilepticus during sleep (ESES) in children.

METHODThe clinical and EEG data of 82 epilepsy patients with ESES, which included benign childhood epilepsy with centro temporal spikes (BECT) variants, epilepsy with continuous spikes and waves during slow sleep (CSWS) , Landau-Kleffner syndrome (LKS) collected from department of pediatrics, Peking University First Hospital were analyzed from July 2007 to September 2012. During ESES period, all patients received methylprednisolone treatment for three courses, which included methylprednisolone intravenous infusion for three days, followed by oral prednisone for four days every time. After three courses, prednisone [1-2 mg/(kg × d)] were taken by all patients for 6 months. The ESES phenomenon and seizures were observed before and after treatment. The efficacy of corticosteroid on ESES suppression, seizure control of three epilepsy syndrome were analyzed.

RESULTThirty-nine cases were male and 43 cases were female. The epilepsy syndromes included 49 patients diagnosed as benign childhood epilepsy with centrotemporal spike (BECT) variants, 27 patients diagnosed as epilepsy with continuous spikes and waves during slow sleep (CSWS), and 6 patients diagnosed as LKS. Age of onset ranged from 1 year and 4 months to 11 years. The age of ESES newly monitored was from 2 years to 10 years and 8 months. The total effective rate of corticosteroid was 83% (68/82) for ESES, BECT variants was 82% (40/49), CSWS was 81% (22/27), LKS was 100% (6/6). There was no statistically significant difference in effective rates between the front two (χ² = 0.09, P > 0.05). The seizures were improved in the first month after methylprednisolone treatment in 3 epilepsy syndromes. The recurrence rate of BECT variants was 47% (23/49) , CSWS was 59% (16/27) , LKS was 50% (3/6) after 1 year follow up. There was no association between disease parameters, including age at seizure onset, duration of ESES and the treatment effect of ESES examined by Kruskal-Wallis method (χ² = 3.585, 0.932, P > 0.05).

CONCLUSIONMethylprednisolone was effective for improving ESES and seizures in 3 epilepsy syndromes combined with ESES. There was no significant correlation between age at seizure onset, duration of ESES and treatment effect of ESES.

Adrenal Cortex Hormones ; therapeutic use ; Child ; Child, Preschool ; Electroencephalography ; Female ; Humans ; Infant ; Landau-Kleffner Syndrome ; drug therapy ; physiopathology ; Male ; Methylprednisolone ; therapeutic use ; Pediatrics ; Seizures ; prevention & control ; Sleep ; physiology ; Status Epilepticus ; drug therapy ; physiopathology ; Treatment Outcome

OBJECTIVETo study the efficacy of levetiracetam (LEV) combined with short-term clonazepam (CZP) in the treatment of electrical status epilepticus during sleep (ESES) in children with benign childhood epilepsy with centrotemporal spikes (BECCT).

METHODSFifteen children (9 boys and 6 girls) diagnosed with BECCT with ESES, who had continuous spike-and-wave accounting for over 85% of the non-rapid eye movement sleep as monitored by 24-hours ambulatory EEG or 3-hours video EEG, were enrolled. The clinical manifestations and EEG characteristics of patients were retrospectively analyzed. These children received two months of CZP treatment in addition to oral LEV [20-40 mg/(kg·d)]. All patients were followed up for 6-18 months.

RESULTSThe 15 children were orally given LEV in the early stage, but showed no improvement when reexamined by EEG or had seizures during treatment. Then, they received LEV in combination with short-term CZP. Re-examinations at 1 and 6 months after treatment showed that 14 cases had significantly reduced discharge (only little discharge in the Rolandic area) or no discharge, as well as completely controlled seizure; one case had recurrent ESES and two epileptic seizures during follow-up. The recurrent case received the combination therapy again, and re-examinations 1 and 6 months later revealed normal EEG; no seizure occurred in the 8 months of follow-up.

CONCLUSIONSLEV combined with short-term CZP is effective and has few side effects in treating ESES syndrome among children with BECCT.

Anticonvulsants ; administration & dosage ; Child ; Child, Preschool ; Clonazepam ; administration & dosage ; Drug Therapy, Combination ; Electroencephalography ; Epilepsy, Rolandic ; drug therapy ; physiopathology ; Female ; Humans ; Male ; Piracetam ; administration & dosage ; analogs & derivatives ; Retrospective Studies ; Sleep ; physiology ; Status Epilepticus ; drug therapy ; physiopathology

2-Aminoadipic Acid ; analogs & derivatives ; analysis ; Aldehyde Dehydrogenase ; genetics ; Anticonvulsants ; therapeutic use ; Biomarkers ; analysis ; Brain ; pathology ; DNA Mutational Analysis ; Electroencephalography ; Epilepsy ; diagnosis ; drug therapy ; genetics ; Genetic Association Studies ; Humans ; Infant ; Infant, Newborn ; Magnetic Resonance Imaging ; Mutation, Missense ; Prognosis ; Pyridoxine ; therapeutic use ; Seizures ; diagnosis ; drug therapy ; genetics ; Status Epilepticus ; diagnosis ; drug therapy ; genetics

OBJECTIVETo study the efficacy of levetiracetam (LEV) in the treatment of electrical status epilepticus during sleep (ESES) in children.

METHODSThe clinical data of 27 children who were newly diagnosed with ESES and treated with LEV between August 2009 and March 2011 and who were followed up for at least 6 months were retrospectively studied.

RESULTSThe onset age of the 27 children ranged from 9 months to 9 years and 7 months. Partial motion seizures were found in 81% of the children in the early stage. Twenty-three children received LEV treatment after ESES was definitely diagnosed. Of the 23 children, 19 were diagnosed as epilepsy syndrome of benign childhood epilepsy with centrotemporal spikes (BECT). The age of the patients at the beginning of LEV treatment ranged from 1 year and 8 months to 11 years and 9 months. The follow- up duration was 7 to 19 months. The effective rate of LEV for seizure control was 82% and for EEG recovery it was 78% (P<0.05). The other 4 children received LEV treatment before the occurrence of ESES. Seizure control and EEG recovery were noted in two of the 4 children.

CONCLUSIONSLEV treatment is efficacious, to some extent, for both seizure control and EEG recovery in children with ESES.

Adolescent ; Anticonvulsants ; therapeutic use ; Child ; Child, Preschool ; Electroencephalography ; drug effects ; Female ; Humans ; Infant ; Male ; Piracetam ; analogs & derivatives ; therapeutic use ; Retrospective Studies ; Status Epilepticus ; drug therapy ; physiopathology