SynthesisDrugs2001
Antiepileptogenic agents: how close are we?
Synthesis in Drugs, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 87 citations in OpenAlex.
- Innovative drug discovery strategies in epilepsy: integrating next-generation syndrome-specific mouse models to address pharmacoresistance and epileptogenesis.Expert opinion on drug discovery · 2024Review
- Article
- Developing Novel Experimental Models of m-TORopathic Epilepsy and Related Neuropathologies: Translational Insights from Zebrafish.International journal of molecular sciences · 2023Review
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
- Development of an antiepileptogenesis drug screening platform: Effects of everolimus and phenobarbital.Epilepsia · 2021Article
- Animal Models of Post-Traumatic Epilepsy.Diagnostics (Basel, Switzerland) · 2019Review
- A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy.PloS one · 2019Article
- Neuroinflammation in epileptogenesis: Insights and translational perspectives from new models of epilepsy.Epilepsia · 2017Article
- Differential effects of rapamycin treatment on tonic and phasic GABAergic inhibition in dentate granule cells after focal brain injury in mice.Experimental neurology · 2016Article
- Review
- Effects of Rapamycin Treatment on Neurogenesis and Synaptic Reorganization in the Dentate Gyrus after Controlled Cortical Impact Injury in Mice.Frontiers in systems neuroscience · 2015Article
- Oxidative stress and epilepsy: literature review.Oxidative medicine and cellular longevity · 2012Review
- Post-traumatic seizures exacerbate histopathological damage after fluid-percussion brain injury.Journal of neurotrauma · 2011Article
- Post-traumatic seizure susceptibility is attenuated by hypothermia therapy.The European journal of neuroscience · 2010Article
- Epilepsy following cortical injury: cellular and molecular mechanisms as targets for potential prophylaxis.Epilepsia · 2009Review
- A Drosophila systems model of pentylenetetrazole induced locomotor plasticity responsive to antiepileptic drugs.BMC systems biology · 2009Article
- Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat.Brain : a journal of neurology · 2005Article
- Post-traumatic epilepsy following fluid percussion injury in the rat.Brain : a journal of neurology · 2004Article
- Future prospects for the drug treatment of epilepsy.CNS drugs · 2001Review
- Article
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 2 institutions in 1 country.
Funding
Abstract
Epilepsy is a common neurological condition, affecting about 4% of individuals over their lifetime. Epilepsy can be idiopathic, secondary to an underlying genetic abnormality or unknown causes, or acquired. Known potential causes account for about one third of epilepsy. Control of epilepsy has primarily focused on suppressing seizure activity after epilepsy has developed. An intriguing possibility is to control acquired epilepsy by preventing epileptogenesis, the process by which the brain becomes epileptic. Many laboratory models simulate human epilepsy as well as provide a system for studying epileptogenesis. The kindling model involves repeated application of subconvulsive electrical stimulation to the brain, leading to spontaneous seizures. Other models include the cortical or systemic injection of various chemicals. These models suggest that many antiepileptic drugs, from phenobarbital and valproate (valproic acid) to levetiracetam and tiagabine, have antiepileptogenic potential. Some promising other possibilities include N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) antagonists as well as the neurotrophins and their receptors. Phenobarbital, phenytoin, valproate, carbamazepine and, to a very limited extent, diazepam have been evaluated in clinical trials to test whether they actually prevent epileptogenesis in humans. Results have been very disappointing. Meta-analyses of 12 different drug-condition combinations show none with significantly lower unprovoked seizure rates among those receiving the active drug. In 4 of the 12, the observed rate was actually slightly higher among treated individuals. None of the newer drugs have been evaluated in antiepileptogenesis trials. Until some drugs demonstrate a clear antiepileptogenic effect in clinical trials, the best course to reduce the incidence of epilepsy is primary prevention of the risk-increasing events--for example, wearing helmets, using seat belts, or decreasing the risk of stroke by reducing smoking.
Indexed as
Identifiers
What OpenQuestion holds
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.