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)

Seizures do not often strike randomly but may occur in circadian patterns. We compared daily times of partial seizures determined by continuous electroencephalography among patients with mesial temporal lobe epilepsy (MTLE; n = 64), those with extratemporal lobe (XTLE; n = 26) or lesional temporal lobe epilepsy (LTLE; n = 8), and a rat model similar to MTLE in which rats become epileptic after electrically induced limbic status epilepticus (postlimbic status [PLS]; n = 20). Rats were maintained on a 12-hour light/dark cycle with lights on at 0700 hours. The distributions of seizures were fitted by cosinor analysis to determine time of peak seizure incidence +/- 95% confidence interval (95% CI). The mean fraction +/- SD of seizures recorded during light was 63 +/- 17% in PLS animals and 60 +/- 21% in humans. Peak incidence of seizures for PLS rats (547 seizures) was 1645 (95% CI = 1448,1830) and for MTLE subjects (774 seizures) was 1500 (95% CI = 1324,1636). Seizures from XTLE (465 seizures) and LTLE (48 seizures) did not fit a cosinor model and occurred no more frequently during light than dark. In conclusion, limbic seizures in humans and PLS rats occur more often during light than dark and have similar cosinor daily distributions. The chronological similarity between human MTLE and PLS rat epilepsy suggests that limbic seizure occurrence has a relation to the circadian regulatory system.
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PMID:Temporal distribution of partial seizures: comparison of an animal model with human partial epilepsy. 962 44

This work presents a model combining quantitative proton HRMAS NMR data and PLS-DA for neuropathology and neuroprotection evaluation. Metabolic data were also confronted to histopathological results obtained using the same experimental conditions. Soman, when not lethal, can induce status epilepticus (SE), brain damage, histological lesions, and profound cerebral metabolic disorders as revealed using (1)H HRMAS NMR. Our challenge was to evaluate delayed treatments, which could control refractory SE and avoid brain lesions. For this aim, we have built a statistical model of soman intoxication describing brain metabolite evolution during 7 days. We have then used this model to evaluate the efficiency of a combination of ketamine/atropine (KET/AS) administrated 1 and 2 h after SE induction, compared to the immediate anticonvulsant therapy midazolam/atropine sulfate (MDZ/AS). Furthermore, quantitation of HRMAS NMR data allowed us to follow individual evolution of 17 metabolites. N-Acetylaspartate, lactate, or taurine presented a long lasting disruption, while glutamine, alanine, glycerophosphocholine and myo-inositol showed disruptions for 3 days with a reversion at day 7. These changes were completely normalized by the administration of MDZ/AS. Interestingly, they were also almost completely reversed by KET/AS 1 h postsoman. This work suggests further the predictive interest of HRMAS and PLS-DA for neuropathology/neuroprotection studies and also confirms, on the metabolic aspects, the neuroprotective potentials of KET/AS combinations for the delayed treatment of soman-induced SE.
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PMID:Prediction of neuroprotective treatment efficiency using a HRMAS NMR-based statistical model of refractory status epilepticus on mouse: a metabolomic approach supported by histology. 2262 46