ReviewSeminars in pediatric neurology2010
Lessons from the laboratory: the pathophysiology, and consequences of status epilepticus.
Review in Seminars in pediatric neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Haploinsufficiency of X-linked intellectual disability gene CASK induces post-transcriptional changes in synaptic and cellular metabolic pathways.Experimental neurology · 2020Article
- Status epilepticus: Role for etiology in determining response to benzodiazepines.Annals of neurology · 2018Article
- Beneficial Effects of Selective Orexin-A Receptor Antagonist in 4-aminopyridine-induced Seizures in Male Rats.Advanced biomedical research · 2017Article
- Status epilepticus: Using antioxidant agents as alternative therapies.Experimental and therapeutic medicine · 2016Article
- Hypothermia for pediatric refractory status epilepticus.Epilepsia · 2013Article
- Expression of AMPA receptor subunits in hippocampus after status convulsion.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2012Article
- Status epilepticus.Indian journal of pediatrics · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Status epilepticus (SE) is the most common neurologic emergency of childhood. Experimental models parallel several clinical features of SE including (1) treatment is complicated by an increasing probability that benzodiazepines will fail with increasing seizure duration and (2) outcome varies with age and etiology. Studies using these models showed that the activity-dependent trafficking of GABA(A) receptors contributes in part to the progressive decline in GABA-mediated inhibition and the failure of the benzodiazepines. Furthermore, laboratory studies have provided evidence that age and inciting stimulus interact to determine the neuronal circuits activated during SE (ie, functional anatomy) and that differences in functional anatomy can partially account for variations in SE outcome. Future laboratory studies are likely to provide an additional understanding of the cellular and molecular mechanisms that underlie SE and its consequences. Such studies are necessary in the development of rational emergent therapy for SE and its long-term outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.