ArticleBMJ paediatrics open2026
Exploratory bidirectional Mendelian randomisation analysis of cerebrospinal fluid metabolites associated with cerebral palsy and epilepsy.
Article in BMJ paediatrics 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCerebral palsy (CP) and epilepsy are prevalent neurodevelopmental disorders with shared aetiological complexities. This study employs bidirectional Mendelian randomisation (MR) to investigate associations consistent with potential causal effects between cerebrospinal fluid (CSF) metabolites and the pathogenesis of CP and epilepsy.
methodsWe conducted a two-sample MR analysis using genome-wide association study (GWAS) data from FinnGen, including 482 CP cases, 11 740 epilepsy cases and European ancestry controls. Instrumental variables for 338 CSF metabolites were selected using a relaxed threshold (p<1×10
resultsSix CSF metabolites showed nominal significant associations with CP risk in inverse variance weighted analyses, after FDR correction, three remained significant: 3-hydroxypyridine sulfate (OR=1.23, Q=0.040), isoleucine (OR=0.49, Q=0.046) and sphingomyelin (OR=1.12, Q=0.040). 17 metabolites were linked to epilepsy, of these, five remained significant after FDR correction, including 2,3-dihydroxy-5-methylthio-4-pentenoate (OR=0.81, Q=0.009) and 3-ureidopropionate (OR=1.09, Q=0.024). γ-Glutamylvaline showed nominally significant associations with both disorders but in opposite directions (CP: OR=1.25, p=0.040; epilepsy: OR=0.95, p=0.031); neither survived FDR correction. Reverse MR analyses did not support reverse associations for CP (all p>0.05), although genetic liability to epilepsy was associated with two CSF metabolites. Sensitivity analyses did not detect evidence of directional pleiotropy.
conclusionsThese findings provide hypothesis-generating evidence regarding metabolic pathways potentially involved in CP and epilepsy and may inform future experimental and clinical investigations. Independent validation and functional studies are required before clinical application can be considered.
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.