ArticleEpilepsia open2026
Neurometabolite abnormalities and associations with epilepsy duration and cognition in patients with idiopathic generalized epilepsies.
Article in Epilepsia open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
objectiveThis study investigated whether idiopathic generalized epilepsies (IGEs) are associated with neuroinflammation by measuring neurometabolite levels and brain temperature using whole-brain magnetic resonance spectroscopy imaging (MRSI). We compared patients with IGEs to healthy controls (HCs), and in IGEs examined relationships with seizure control, MRSI markers, epilepsy duration, and cognitive performance.
methodsSeventeen patients with IGEs and 15 HCs underwent 3T-MRI scans. IGEs were also administered the Montreal Cognitive Assessment (MoCA) and Flanker test. Whole-brain
resultsCompared with HCs, IGEs showed higher MI/Cr in the parietal cortex, PCC, and thalamus; higher hippocampus Glx/Cr; and lower parietal cortex NAA/Cr. Brain temperature did not differ between groups. IGE- exhibited higher hippocampal NAA/Cr and better MoCA scores than IGE+. Longer epilepsy duration was associated with lower NAA/Cr in the ACC and PCC, and parietal cortex, as well as lower Glx/Cr in the ACC, PCC, parietal cortex, and hippocampus. Lower NAA/Cr in the ACC, PCC, hippocampus, and thalamus, together with higher thalamus MI/Cr, was associated with lower MoCA scores in IGEs. Lower NAA/Cr in the ACC, thalamus, and hippocampus was associated with poorer Flanker performance in IGEs. SIGNIFICANCE: We provide novel evidence of neurometabolic abnormalities in IGEs. The associations between metabolite levels and clinical and cognitive variables suggest potential biomarkers for disease progression and treatment response. Furthermore, these results highlight the roles of abnormal glial activation, neuronal loss, and hyperexcitability in IGE pathophysiology. PLAIN LANGUAGE SUMMARY: We compared patients with idiopathic generalized epilepsies (IGEs) to healthy controls (HCs) to investigate brain chemistry and temperature differences and their relationships to seizure control, epilepsy duration, and cognitive performance. We found group differences in brain N-acetylaspartate (NAA; neuronal marker), myo-inositol (MI; glial cell marker), and glutamate/glutamine (Glx; excitatory neurotransmission) levels, but not in brain temperature. Longer epilepsy duration was associated with brain chemistry levels. In IGEs, lower NAA levels and higher MI levels were associated with worse cognitive performance. This study highlights the roles of abnormal glial activation, neuronal loss, and hyperexcitability in epilepsy duration and cognition in IGEs.
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.