ReviewEpilepsia2001
Progress in the genetics of the partial epilepsies.
Review in Epilepsia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 24 citations in OpenAlex.
- Tantrums, Emotion Reactions and Their EEG Correlates in Childhood Benign Rolandic Epilepsy vs. Complex Partial Seizures: Exploratory Observations.Frontiers in behavioral neuroscience · 2018Article
- Recruitment for genetic studies of epilepsy.Epilepsy research · 2012Article
- A Locus Identified on Chromosome18P11.31 is Associated with Hippocampal Abnormalities in a Family with Mesial Temporal Lobe Epilepsy.Frontiers in neurology · 2012Article
- Idiopathic mesial temporal lobe epilepsy: a syndrome with complex inheritance?Journal of neurology · 2009Article
- 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
1 author at 1 institution in 1 country.
Funding
Abstract
The importance of genetic contributions to the partial epilepsies is now well established. Evidence for this genetic contribution has come from familial aggregation studies, twin studies, positional cloning of specific genes that raise risk, and clinical descriptions of families. Familial aggregation studies are consistent in showing an increased risk of epilepsy in the relatives of patients with partial epilepsies that occur in the absence of environmental insults to the central nervous system. Susceptibility genes have been localized in five syndromes: autosomal dominant nocturnal frontal lobe epilepsy (20q, 1q, and 15q), autosomal dominant partial epilepsy with auditory features (10q), familial partial epilepsy with variable foci (22q), benign epilepsy of childhood with centrotemporal spikes (15q), and benign familial infantile convulsions (19q). In nocturnal frontal lobe epilepsy, the genes on chromosome 20q and 1q have been identified as subunits of the neuronal nicotinic acetylcholine receptor.
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.