ArticleExperimental neurology2026
Etiology-specific trajectories of longitudinal functional connectivity and network topology in posttraumatic and mesial temporal lobe epileptogenesis.
Article in Experimental neurology, 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
8 authors.
Funding
Abstract
The latent period of epileptogenesis represents a critical window for early diagnosis and preventive intervention before the disease progresses. Among epilepsy subtypes, posttraumatic epilepsy (PTE) and mesial temporal lobe epilepsy (mTLE) account for a significant proportion of cases. However, it remains unclear whether these two subtypes share common longitudinal network biomarkers during the latent phase. To address this question, we performed longitudinal functional and structural MRI in rat models of PTE induced by lateral fluid percussion injury (LFPI) and mTLE induced by intrahippocampal kainic acid (KA). The final dataset included 31 rats, comprising 18 KA/mTLE rats and 13 LFPI/PTE rats, with available MRI scans at pre-induction baseline, 1 week, and/or 8 weeks post-induction. We quantified lesion volume (LV), resting-state functional connectivity (rsFC), network topology, longitudinal changes, and rsFC-LV associations. In mTLE model, hippocampal rsFC increased at 1 week relative to baseline (p = 0.024) and declined globally at 8 weeks. Hippocampal rsFC was negatively associated with LV in the left hippocampus (week 1, p = 0.036), right hippocampus (week 8, p = 0.02), and sensorimotor cortex (week 8, p = 0.041). Network topology showed an early reduction followed by a later increase in clustering coefficient. In contrast, the PTE model displayed progressive rsFC reductions from baseline at both post-induction time points and higher clustering coefficient than mTLE. Despite overall rsFC declines in both models, mTLE retained greater prefrontal rsFC but lower hippocampal rsFC than PTE at 8 weeks. Etiology-specific LV differences were observed in hippocampus and sensorimotor cortex at week 8 (mTLE < PTE, p < 0.037). These findings demonstrate distinct, etiology-specific trajectories of rsFC, topology, and structure-function coupling in established rodent models of epileptogenesis.
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.