PubMed Health⌕ Search

PubMed · 16037984

Generic head models for atlas-based EEG source analysis.

Abstract

We describe a method for using a generic head model, in the form of an anatomical atlas, to produce EEG source localizations. The atlas is fitted to the subject by a nonrigid warp using a set of surface landmarks. The warped atlas is used to compute a finite element model (FEM) of the forward mapping or lead-fields between neural current generators and the EEG electrodes. These lead-fields are used to localize current sources from the subject's EEG data and the sources are then mapped back to the anatomical atlas. This approach provides a mechanism for comparing source localizations across subjects in an atlas-based coordinate system, which can be used in the large fraction of EEG studies in which MR images are not available. The Montreal brain atlas was used as the reference anatomical atlas and 10 individual MR volumes were used to evaluate the method. The atlas was fitted to each subject's head by a thin-plate-spline (TPS) warp. The spatial locations of a generic 155-electrode configuration were used to constrain the warp. For the purposes of evaluation, dipolar sources were placed on the inner cortical surface in the atlas geometry and transferred to each subject's brain space using a polynomial warp. The parameters of the warp were computed using an intensity-based matching of the atlas and subject brains, thus ensuring that the sources were placed at approximately the same anatomical location in each case. Data were simulated in the subject geometry and a dipole fit was performed on these data using an FEM of the TPS warped atlas. The source positions found in the warped atlas were transferred back to the original atlas and compared to the original position. Sources were simulated at 972 locations evenly distributed over the inner cortical surface of the atlas. The mean error over all 10 subjects was 8.1 mm in the subject space and 15.2 mm in the atlas space. In comparison, using an affine transformation of the electrodes into atlas space and an FEM model generated from the atlas produced mean errors of 22.3 mm in subject space and 19.6 mm in atlas space. With a standard three-shell spherical model the errors were 27.2 mm in the subject space and 34.7 mm when mapped to atlas space.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Felix Darvas, John J Ermer, John C Mosher, Richard M Leahy. 2006. Generic head models for atlas-based EEG source analysis.. https://doi.org/10.1002/hbm.20171

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A MAGIBU-based model for pediatric and juvenile CNS tumors: an in-house epigenetic decision-support framework compared with online DNA methylation classifiers.

Background: DNA methylation profiling is a tool that provides key support for central nervous system (CNS) tumor classification. However, diagnostically ambiguous pediatric cases may result in discordant outputs across classifiers. We developed MAGIBU, a cross-platform, projection-based framework that embeds individual methylomes into a fixed CNS reference landscape, ranking diagnostic entities by local epigenetic proximity to support clinician-led integrative diagnosis. Methods: As a proof-of-concept, we evaluated MAGIBU in eight morphologically challenging pediatric/juvenile CNS tumors with unresolved diagnoses after institutional and central pathology review. To establish a benchmark in the absence of a definitive histopathological ground truth, a consensus epigenetic reference was defined a priori for cases showing concordant results between the Heidelberg CNS Tumor Methylation Classifier and Methylscape Analysis. Comparisons were also performed with Epigenomic Digital Pathology (EpiDiP). To validate MAGIBU beyond this discovery cohort, performance was assessed at the family level across the CNS methylation spectrum (n = 678, 28 methylation families), on non-array platforms (whole-genome bisulfite sequencing and Oxford Nanopore), and in a focused analysis of the low-grade glioma and diffuse midline glioma compartment across four independent cohorts (n = 670). Results: In the discovery cohort, MAGIBU achieved high concordance with the consensus reference (Cohen's κ = 0.855), outperforming EpiDiP (κ = 0.278), which frequently placed low-grade tumors in proximity to higher-grade reference regions. Conclusions: MAGIBU provides a stable, quantitative differential diagnosis framework that mitigates the limitations of rigid categorical assignments. By leveraging a distance-based proximity metric, it offers a transparent decision-support tool that integrates effectively with clinical, radiological, and molecular data. While performance is inherently dependent on reference atlas composition, MAGIBU represents a robust complementary approach for the diagnostic workup of ambiguous CNS tumors.

Brain↗

1q21.1 distal copy number variants are associated with cerebral and cognitive alterations in humans.

Low-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48% male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers-the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.

Brain↗