Summary of the variables and definitions used in this text.

<p>Summary of the variables and definitions used in this text.</p

Eigen-modes ∣<b>u</b>₅∣ and ∣<b>u</b>₂∣ (Fig 2(a) and 2(b)), and their dominant regions (Model 1).

<p>Eigen-modes ∣<b>u</b>₅∣ and ∣<b>u</b>₂∣ (<a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1004564#pcbi.1004564.g002" target="_blank">Fig 2(a) and 2(b)</a>), and their dominant regions (Model 1).</p

Subcortical Pearson correlation <i>R</i> of the estimated atrophy and the <i>t</i>-statistics for both epilepsy types.

<p>“Max” refers to the overall highest <i>R</i> and the corresponding region, all located in the ipsilateral hemisphere.</p

Model 1: Atrophy distribution via exitotoxicity.

<p>(a) Eigen-mode <b>u</b>₅ captures the essentials of estimating network diffusion from the Laplacian’s eigen-modes for TLE-MTS when the ipsilateral hippocampus is seeded. (b) Eigen-mode <b>u</b>₂ recovers features of the TLE-no when the temporal lobe is bilaterally seeded. (c) Plot of <i>R</i> vs the eigen-mode index for TLE-MTS when each eigen-mode <b>u</b>_<i>i</i> is correlated with the group atrophy. (d) Plot of <i>R</i> vs. the eigen-mode index for the TLE-no when eigen-modes <b>u</b>_<i>i</i> are each correlated with the group atrophy.</p

Relating Cortical Atrophy in Temporal Lobe Epilepsy with Graph Diffusion-Based Network Models

<div><p>Mesial temporal lobe epilepsy (TLE) is characterized by stereotyped origination and spread pattern of epileptogenic activity, which is reflected in stereotyped topographic distribution of neuronal atrophy on magnetic resonance imaging (MRI). Both epileptogenic activity and atrophy spread appear to follow white matter connections. We model the networked spread of activity and atrophy in TLE from first principles via two simple first order network diffusion models. Atrophy distribution is modeled as a simple consequence of the propagation of epileptogenic activity in one model, and as a progressive degenerative process in the other. We show that the network models closely reproduce the regional volumetric gray matter atrophy distribution of two epilepsy cohorts: 29 TLE subjects with medial temporal sclerosis (TLE-MTS), and 50 TLE subjects with normal appearance on MRI (TLE-no). Statistical validation at the group level suggests high correlation with measured atrophy (<i>R</i> = 0.586 for TLE-MTS, <i>R</i> = 0.283 for TLE-no). We conclude that atrophy spread model out-performs the hyperactivity spread model. These results pave the way for future clinical application of the proposed model on individual patients, including estimating future spread of atrophy, identification of seizure onset zones and surgical planning.</p></div