Evidence map›Paper›PMID 35361967›Full record

ReviewNature reviews. Neurology2022

The metabolic basis of epilepsy.

Jong M Rho, Detlev Boison

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 3 pooled it
27.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

164 citing papers in PubMed, 3 syntheses or guidelines pooled it, 255 citations in OpenAlex.

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  19. GABACellular and molecular neurobiology · 2026
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104 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Jong M RhoDepartment of Neuroscience, University of California San Diego, San Diego, CA, USA. jrho@health.ucsd.edu.ORCID http://orcid.org/0000-0001-9886-9924
Detlev BoisonDepartment of Neurosurgery, Robert Wood Johnson Medical School and New Jersey Medical School, Rutgers University, Piscataway, NJ, USA.
Rutgers, The State University of New Jersey · USUC San Diego Health System · US

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Therapies for Epilepsy Prevention - Focus on AdenosineR01NS127846 · NINDS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Detlev Boison · 2022 to 2026
$2.1M
Adenosine receptor mediated therapies for SUDEPR01NS103740 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI BOISON, DETLEV · 2018 to 2022
$1.7M
Metabolic role of the neuronal Na+-dependent citrate transporter implicated in epilepsyR21NS104513 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI METALLO, CHRISTIAN MICHAEL, RHO, JONG MIN · 2018 to 2019
$426k
NINDS NIH HHS R01 NS065957NINDS NIH HHS R01 NS103740NINDS NIH HHS R01 NS127846NINDS NIH HHS R21 NS104513
6 · The paper itself

Abstract

The brain is a highly energy-demanding organ and requires bioenergetic adaptability to balance normal activity with pathophysiological fuelling of spontaneous recurrent seizures, the hallmark feature of the epilepsies. Recurrent or prolonged seizures have long been known to permanently alter neuronal circuitry and to cause excitotoxic injury and aberrant inflammation. Furthermore, pathological changes in bioenergetics and metabolism are considered downstream consequences of epileptic seizures that begin at the synaptic level. However, as we highlight in this Review, evidence is also emerging that primary derangements in cellular or mitochondrial metabolism can result in seizure genesis and lead to spontaneous recurrent seizures. Basic and translational research indicates that the relationships between brain metabolism and epileptic seizures are complex and bidirectional, producing a vicious cycle that compounds the deleterious consequences of seizures. Metabolism-based treatments such as the high-fat, antiseizure ketogenic diet have become mainstream, and metabolic substrates and enzymes have become attractive molecular targets for seizure prevention and recovery. Moreover, given that metabolism is crucial for epigenetic as well as inflammatory changes, the idea that epileptogenesis can be both negatively and positively influenced by metabolic changes is rapidly gaining ground. Here, we review evidence that supports both pathophysiological and therapeutic roles for brain metabolism in epilepsy.

Indexed as

EpilepsyStatus EpilepticusBrainEnergy MetabolismHumansSeizures

Identifiers

PMID35361967
PMCPMC10259193
OpenAlexW4220970567

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.