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Vos, S. B.

Publications and source records attributed to Vos, S. B..

3 recordsLinked to original sources

The European Prevention of Alzheimer's Dementia (EPAD) MRI Dataset and Processing Workflow

The European Prevention of Alzheimer Dementia (EPAD) is a multi-center study that aims to characterize the preclinical and prodromal stages of Alzheimers Disease. The EPAD imaging dataset includes core (3D T1w, 3D FLAIR) and advanced (ASL, diffusion MRI, and resting-state fMRI) MRI sequences. Here, we give an overview of the semi-automatic multimodal and multisite pipeline that we developed to curate, preprocess, quality control (QC), and compute image-derived phenotypes (IDPs) from the EPAD MRI dataset. This pipeline harmonizes DICOM data structure across sites and performs standardized MRI preprocessing steps. A semi-automated MRI QC procedure was implemented to visualize and flag MRI images next to site-specific distributions of QC features -- i.e. metrics that represent image quality. The value of each of these QC features was evaluated through comparison with visual assessment and step-wise parameter selection based on logistic regression. IDPs were computed from 5 different MRI modalities and their sanity and potential clinical relevance were ascertained by assessing their relationship with biological markers of aging and dementia. The EPAD v1500.0 data release encompassed core structural scans from 1356 participants 842 fMRI, 831 dMRI, and 858 ASL scans. From 1356 3D T1w images, we identified 17 images with poor quality and 61 with moderate quality. Five QC features -- Signal to Noise Ratio (SNR), Contrast to Noise Ratio (CNR), Coefficient of Joint Variation (CJV), Foreground-Background energy Ratio (FBER), and Image Quality Rate (IQR) -- were selected as the most informative on image quality by comparison with visual assessment. The multimodal IDPs showed greater impairment in associations with age and dementia biomarkers, demonstrating the potential of the dataset for future clinical analyses.

neuroscience↗

Tractography dissection variability: what happens when 42 groups dissect 14 white matter bundles on the same dataset?

White matter bundle segmentation using diffusion MRI fiber tractography has become the method of choice to identify white matter fiber pathways in vivo in human brains. However, like other analyses of complex data, there is considerable variability in segmentation protocols and techniques. This can result in different reconstructions of the same intended white matter pathways, which directly affects tractography results, quantification, and interpretation. In this study, we aim to evaluate and quantify the variability that arises from different protocols for bundle segmentation. Through an open call to users of fiber tractography, including anatomists, clinicians, and algorithm developers, 42 independent teams were given processed sets of human whole-brain streamlines and asked to segment 14 white matter fascicles on six subjects. In total, we received 57 different bundle segmentation protocols, which enabled detailed volume-based and streamline-based analyses of agreement and disagreement among protocols for each fiber pathway. Results show that even when given the exact same sets of underlying streamlines, the variability across protocols for bundle segmentation is greater than all other sources of variability in the virtual dissection process, including variability within protocols and variability across subjects. In order to foster the use of tractography bundle dissection in routine clinical settings, and as a fundamental analytical tool, future endeavors must aim to resolve and reduce this heterogeneity. Although external validation is needed to verify the anatomical accuracy of bundle dissections, reducing heterogeneity is a step towards reproducible research and may be achieved through the use of standard nomenclature and definitions of white matter bundles and well-chosen constraints and decisions in the dissection process.

neuroscience↗

Node abnormality predicts seizure outcome and relates to long-term relapse after epilepsy surgery

ObjectiveWe assessed pre-operative structural brain networks and clinical characteristics of patients with drug resistant temporal lobe epilepsy (TLE) to identify correlates of post-surgical seizure outcome at 1 year and seizure relapses up to 5 years.\n\nMethodsWe retrospectively examined data from 51 TLE patients who underwent anterior temporal lobe resection (ATLR) and 29 healthy controls. For each patient, using the pre-operative structural, diffusion, and post-operative structural MRI, we generated two networks: pre-surgery network and surgically-spared network. The pre-surgery network is the whole-brain network before surgery and the surgically-spared network is a subnetwork of the pre-surgery network which is expected to remain unaffected by surgery and hence present post-operatively. Standardising these networks with respect to controls, we determined the number of abnormal nodes before surgery and expected to remain after surgery. We incorporated these 2 abnormality measures and 13 commonly acquired clinical data from each patient in a robust machine learning framework to estimate patient-specific chances of seizures persisting after surgery.\n\nResultsPatients with more abnormal nodes had lower chance of seizure freedom at 1 year and even if seizure free at 1 year, were more likely to relapse within five years. In the surgically-spared networks of poor outcome patients, the number of abnormal nodes was greater and their locations more widespread than in good outcome patients. We achieved 0.84 {+/-} 0.06 AUC and 0.89 {+/-} 0.09 specificity in detecting unsuccessful seizure outcomes at 1-year. Moreover, the model-predicted likelihood of seizure relapse was significantly correlated with the grade of surgical outcome at year-one and associated with relapses up-to five years post-surgery.\n\nConclusionNode abnormality offers a personalised non-invasive marker, that can be combined with clinical data, to better estimate the chances of seizure freedom at 1 year, and subsequent relapse up to 5 years after ATLR.

neuroscience↗