SynthesisFrontiers in neurology2025
No reliable gray matter alterations in idiopathic dystonia.
Synthesis in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Brain network pathophysiology in dystonia.Dystonia (Lausanne, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The structural brain abnormalities associated with idiopathic dystonia (ID) remain inadequately understood. Previous voxel-based morphometry (VBM) studies examining whole-brain gray matter (GM) volume alterations in patients with ID have reported inconsistent and occasionally contradictory findings. Methods: We performed a coordinate-based meta-analysis (CBMA) using the latest seed-based d mapping with permutation of subject images (SDM-PSI) technique to identify consistent GM alterations in patients with ID at the whole-brain level. Additionally, meta-regression analyses were conducted to explore the potential moderating effects of age, gender, and disease duration on GM volume. Results: The CBMA incorporated 27 VBM studies, comprising 32 datasets with a total of 840 patients with ID and 834 healthy controls. Our analysis did not identify consistent or reliable GM alterations in patients with ID. The robustness of these findings was confirmed through a jackknife sensitivity analysis. Meta-regression analyses revealed that disease duration significantly influenced GM volume in the right insula. Conclusion: Based on the best practice guidelines for CBMA, we utilized the most recent SDM-PSI algorithm to perform a new CBMA that included a larger group of individuals with ID. However, in contrast to previous CBMAs, we did not observe any consistent alterations in GM in ID. The findings suggest that using GM volume assessed by VBM as an imaging marker for ID may not be reliable. This could be attributed to ID being a functional disorder, or the inconsistency in GM alterations may be influenced by demographic and clinical variations, differences in imaging protocols and analysis methods, or small sample sizes. It is imperative to control for subject characteristics, employ standardized VBM methodologies, and enhance sample sizes in future research.
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