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)

Programmed cell death pathways have been implicated in the mechanism by which neurons die following brief and prolonged seizures, but the significance of proapoptotic Bcl-2 family proteins in the process remains poorly defined. Expression of the death agonist Bcl-2-interacting mediator of cell death (Bim) is under the control of the forkhead in rhabdomyosarcoma (FKHR) transcription factors. This prompted us to examine the response of this pathway to experimental seizures and in hippocampi from patients with intractable temporal lobe epilepsy. A short period of status epilepticus in rats that damaged the hippocampus activated FKHR/FKHRL-1 and induced a significant increase in expression of Bim. Blocking of FKHR/FKHRL-1 dephosphorylation after seizures improved hippocampal neuronal survival in vivo, and Bim antisense oligonucleotides were neuroprotective against seizures in vitro. Inhibition of Akt increased the FKHR/Bim response and DNA fragmentation within the normally resistant cortex. Analysis of hippocampi from patients with intractable epilepsy revealed that Bim levels were significantly lower than in controls and FKHR was inhibited; we were able to reproduce these results experimentally in rats by evoking multiple brief, noninjurious electroshock seizures. We conclude that Bim expression may be a critical determinant of whether seizures damage the brain, and that its control may be neuroprotective in status epilepticus and epilepsy.
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PMID:Bim regulation may determine hippocampal vulnerability after injurious seizures and in temporal lobe epilepsy. 1505 1

Non-convulsive status epilepticus (NCSE) can present with heterogeneous clinical manifestations including prolonged confusion. MRI of the brain may demonstrate enhancing signal abnormalities that can mimic various pathologies including disease progression in patients with brain tumour. These neuroimaging changes are usually reversible and have been attributed to a combination of cytotoxic and vasogenic oedema. We report an interesting patient with a past history of prostatic rhabdomyosarcoma and brain metastasis presenting with NCSE where brain MRI demonstrated marked left hemispheric signal abnormalities, raising concerns about tumour recurrence. However the neuroimaging changes resolved following treatment with intravenous anticonvulsants, confirming that they were an effect rather than the cause of seizures. Recognition of seizure-related imaging abnormalities is important to institute prompt appropriate treatment, and to avoid diagnostic ambiguity and unnecessary treatment and/or investigations.
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PMID:Seizure-induced MRI changes mimicking metastatic brain disease. 2418 75