ArticleFrontiers in neuroscience2023
Spectral-based thickness profiling of the corpus callosum enhances anomaly detection in fetal alcohol spectrum disorders.
Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- The Role of HIF-1α and Its Association with BDNF Levels in Post-Stroke Cognitive Decline Following Prenatal Immune Activation and Maternal Hypoxic Stress in Adult Rat Offspring: A Sex Comparison Study.Molecular neurobiology · 2026Article
- Pattern of Deep Grey Matter Undersizing Boosts MRI-Based Diagnostic Classifiers in Fetal Alcohol Spectrum Disorders.Human brain mapping · 2025Article
- Callosal Injuries in Cytomegalovirus Fetopathy: A Neurosonographic Study.Fetal diagnosis and therapy · 2025Article
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Authors and funding
8 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: Fetal alcohol spectrum disorders (FASD) range from fetal alcohol syndrome (FAS) to non-syndromic forms (NS-FASD). The neuroanatomical consequences of prenatal alcohol exposure are mainly the reduction in brain size, but also focal abnormalities such as those of the corpus callosum (CC). We previously showed a narrowing of the CC for brain size, using manual measurement and its usefulness to improve diagnostic certainty. Our aim was to automate these measurements of the CC and identify more recurrent abnormalities in FAS subjects, independently of brain size reduction. Methods: We developed a fast, automated, and normalization-free method based on spectral analysis to generate thicknesses of the CC continuously and at singular points (genu, body, isthmus, and splenium), and its length (LCC). We applied it on midsagittal section of the CC extracted from T1-anatomical brain MRI of 89 subjects with FASD (52 FAS, 37 NS-FASD) and 126 with typically development (6-20 y-o). After adjusting for batch effect, we compared the mean profiles and thicknesses of the singular points across the 3 groups. For each parameter, we established variations with age (growth charts) and brain size in the control group (scaling charts), then identified participants with abnormal measurements (<10th percentile). Results: We confirmed the slimming of the posterior half of the CC in both FASD groups, and of the genu section in the FAS group, compared to the control group. We found a significant group effect for the LCC, genu, median body, isthmus, and splenium thicknesses ( Conclusion: We characterized size-independent anomalies of the posterior part of the CC in FASD, with an automated method, confirming and extending our previous study. Our new tool brings the use of a neuroanatomical criterion including CC damage closer to clinical practice. Our results suggest that an FAS signature identified in NS-FASD, could improve diagnosis specificity.
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