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Jeroen Van Schependom

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5 papers

1 author row

YNICL Journal 2021 Journal Article

Increased brain atrophy and lesion load is associated with stronger lower alpha MEG power in multiple sclerosis patients

Jeroen Van Schependom
Diego Vidaurre
Lars Costers
Martin Sjøgård
Diana M. Sima
Dirk Smeets
Marie Beatrice D'hooghe
Miguel D'haeseleer

In multiple sclerosis, the interplay of neurodegeneration, demyelination and inflammation leads to changes in neurophysiological functioning. This study aims to characterize the relation between reduced brain volumes and spectral power in multiple sclerosis patients and matched healthy subjects. During resting-state eyes closed, we collected magnetoencephalographic data in 67 multiple sclerosis patients and 47 healthy subjects, matched for age and gender. Additionally, we quantified different brain volumes through magnetic resonance imaging (MRI). First, a principal component analysis of MRI-derived brain volumes demonstrates that atrophy can be largely described by two components: one overall degenerative component that correlates strongly with different cognitive tests, and one component that mainly captures degeneration of the cortical grey matter that strongly correlates with age. A multimodal correlation analysis indicates that increased brain atrophy and lesion load is accompanied by increased spectral power in the lower alpha (8-10 Hz) in the temporoparietal junction (TPJ). Increased lower alpha power in the TPJ was further associated with worse results on verbal and spatial working memory tests, whereas an increased lower/upper alpha power ratio was associated with slower information processing speed. In conclusion, multiple sclerosis patients with increased brain atrophy, lesion and thalamic volumes demonstrated increased lower alpha power in the TPJ and reduced cognitive abilities.

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YNIMG Journal 2019 Journal Article

Do the posterior midline cortices belong to the electrophysiological default-mode network?

Martin Sjøgård
Xavier De Tiège
Alison Mary
Philippe Peigneux
Serge Goldman
Guy Nagels
Jeroen Van Schependom
Andrew J. Quinn

The default-mode network (DMN) and its principal core hubs in the posterior midline cortices (PMC), i. e. , the precuneus and the posterior cingulate cortex, play a critical role in the human brain structural and functional architecture. Because of their centrality, they are affected by a wide spectrum of brain disorders, e. g. , Alzheimer's disease. Non-invasive electrophysiological techniques such as magnetoencephalography (MEG) are crucial to the investigation of the neurophysiology of the DMN and its alteration by brain disorders. However, MEG studies relying on band-limited power envelope correlation diverge in their ability to identify the PMC as a part of the DMN in healthy subjects at rest. Since these works were based on different MEG recording systems and different source reconstruction pipelines, we compared DMN functional connectivity estimated with two distinct MEG systems (Elekta, now MEGIN, and CTF) and two widely used reconstruction algorithms (Minimum Norm Estimation and linearly constrained minimum variance Beamformer). Our results identified the reconstruction method as the critical factor influencing PMC functional connectivity, which was significantly dampened by the Beamformer. On this basis, we recommend that future electrophysiological studies on the DMN should rely on Minimum Norm Estimation (or close variants) rather than on the classical Beamformer. Crucially, based on analytic knowledge about these two reconstruction algorithms, we demonstrated with simulations that this empirical observation could be explained by the existence of a spontaneous linear, approximately zero-lag synchronization structure between areas of the DMN or among multiple sources within the PMC. This finding highlights a novel property of the neural dynamics and functional architecture of a core human brain network at rest.

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YNICL Journal 2018 Journal Article

Callosal circularity as an early marker for Alzheimer's disease

Jeroen Van Schependom
Ellis Niemantsverdriet
Dirk Smeets
Sebastiaan Engelborghs

Background: Although brain atrophy is considered to be a downstream marker of Alzheimer's disease (AD), subtle changes may allow to identify healthy subjects at risk of developing AD. As the ability to select at-risk persons is considered to be important to assess the efficacy of drugs and as MRI is a widely available imaging technique we have recently developed a reliable segmentation algorithm for the corpus callosum (CC). Callosal atrophy within AD has been hypothesized to reflect both myelin breakdown and Wallerian degeneration. Methods: We applied our fully automated segmentation and feature extraction algorithm to two datasets: the OASIS database consisting of 316 healthy controls (HC) and 100 patients affected by either mild cognitive impairment (MCI) or Alzheimer's disease dementia (ADD) and a second database that was collected at the Memory Clinic of Hospital Network Antwerp and consists of 181 subjects, including healthy controls, subjects with subjective cognitive decline (SCD), MCI, and ADD. All subjects underwent (among others) neuropsychological testing including the Mini-Mental State Examination (MMSE). The extracted features were the callosal area (CCA), the circularity (CIR), the corpus callosum index (CCI) and the thickness profile. Results: CIR and CCI differed significantly between most groups. Furthermore, CIR allowed us to discriminate between SCD and HC with an accuracy of 77%. The more detailed callosal thickness profile provided little added value towards the discrimination of the different AD stages. The largest effect of normal ageing on callosal thickness was found in the frontal callosal midbody. Conclusions: To the best of our knowledge, this is the first study investigating changes in corpus callosum morphometry in normal ageing and AD by exploring both summarizing features (CCA, CIR and CCI) and the complete CC thickness profile in two independent cohorts using a completely automated algorithm. We showed that callosal circularity allows to discriminate between an important subgroup of the early AD spectrum (SCD) and age and sex matched healthy controls.

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YNICL Journal 2016 Journal Article

Reliability of measuring regional callosal atrophy in neurodegenerative diseases

Jeroen Van Schependom
Saurabh Jain
Melissa Cambron
Anne-Marie Vanbinst
Johan De Mey
Dirk Smeets
Guy Nagels

The Corpus Callosum (CC) is an important structure connecting the two brain hemispheres. As several neurodegenerative diseases are known to alter its shape, it is an interesting structure to assess as biomarker. Yet, currently, the CC-segmentation is often performed manually and is consequently an error prone and time-demanding procedure. In this paper, we present an accurate and automated method for corpus callosum segmentation based on T1-weighted MRI images. After the initial construction of a CC atlas based on healthy controls, a new image is subjected to a mid-sagittal plane (MSP) detection algorithm and a 3D affine registration in order to initialise the CC within the extracted MSP. Next, an active shape model is run to extract the CC. We calculated the reliability of most popular CC features (area, circularity, corpus callosum index and thickness profile) in healthy controls, Alzheimer's Disease patients and Multiple Sclerosis patients. Importantly, we also provide inter-scanner reliability estimates. We obtained an intra-class correlation coefficient (ICC) of over 0.95 for most features and most datasets. The inter-scanner reliability assessed on the MS patients was remarkably well and ranged from 0.77 to 0.97. In summary, we have constructed an algorithm that reliably detects the CC in 3D T1 images in a fully automated way in healthy controls and different neurodegenerative diseases. Although the CC area and the circularity are the most reliable features (ICC > 0.97); the reliability of the thickness profile (ICC > 0.90; excluding the tip) is sufficient to warrant its inclusion in future clinical studies.

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YNICL Journal 2014 Journal Article

Graph theoretical analysis indicates cognitive impairment in MS stems from neural disconnection

Jeroen Van Schependom
Jeroen Gielen
Jorne Laton
Marie B. D'hooghe
Jacques De Keyser
Guy Nagels

BACKGROUND: The mechanisms underlying cognitive impairment in MS are still poorly understood. However, due to the specific pathology of MS, one can expect alterations in connectivity leading to physical and cognitive impairment. AIM: In this study we aimed at assessing connectivity differences in EEG between cognitively impaired (CI) and cognitively preserved (CP) MS patients. We also investigated the influence of the measures used to construct networks. METHODS: We included 308 MS patients and divided them into two groups based on their cognitive score. Graph theoretical network analyses were conducted based on networks constructed using different connectivity measures, i.e. correlation, correlation in the frequency domain, coherence, partial correlation, the phase lag index and the imaginary part of coherency. The most commonly encountered network parameters were calculated and compared between the two groups using Wilcoxon's rank test. Clustering coefficients and path lengths were normalized to a randomized mean clustering coefficient and path length for each patient. False discovery rate was used to correct for the multiple comparisons and Cohen's d effect sizes are reported. RESULTS: Coherence analysis suggests that theta and delta connectivity is significantly smaller in cognitively impaired patients. Small-worldness differences are found in networks based on correlation, theta and delta coherence and correlation in the frequency domain. Modularity was related to age but not to cognition. CONCLUSION: Cognitive deterioration in MS is a symptom that seems to be caused by neural disconnections, probably the white matter tracts connecting both hemispheres, and leads to a wide range in network differences which can be assessed by applying GTA to EEG data. In the future, these results may lead to cheaper and more objective assessments of cognitive impairment in MS.

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