Fig 1.
(a) TLE-MTS atrophy distribution. As expected, the hippocampus has the highest atrophy, consistent with TLE-MTS. (b) Pearson correlation R between Φ1 and measured atrophy vs. the number of eigen-modes used. Peak R is reached when eigen-modes u2–68 are used. (c) Atrophy distribution estimated using Model 1 using eigen-modes u2 − u68. Model 2: (d) Correlation R obtained when each node is seeded (model Φ2). The highest R is obtained when the hippocampus is seeded. (e) R vs. graph diffusion depth. Hippocampus seeding leads to the highest R is obtained at t = 5.56, followed by amygdala and the hypothalamus. (f) Estimated TLE-MTS atrophy obtained from Model 2 when the hippocampus is seeded.
Table 1.
Eigen-modes ∣u5∣ and ∣u2∣ (Fig 2(a) and 2(b)), and their dominant regions (Model 1).
Fig 2.
Model 1: Atrophy distribution via exitotoxicity.
(a) Eigen-mode u5 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 u2 recovers features of the TLE-no when the temporal lobe is bilaterally seeded. (c) Plot of R vs the eigen-mode index for TLE-MTS when each eigen-mode ui is correlated with the group atrophy. (d) Plot of R vs. the eigen-mode index for the TLE-no when eigen-modes ui are each correlated with the group atrophy.
Table 2.
Subcortical Pearson correlation R of the estimated atrophy and the t-statistics for both epilepsy types.
“Max” refers to the overall highest R and the corresponding region, all located in the ipsilateral hemisphere.
Fig 3.
TLE-no case, Model 1: (a) Cortical/subcortical atrophy obtained from t-statistics of epileptic and healthy groups’ volumetrics. (b) R vs. the number of eigen-modes Eq (10) used for neuronal atrophy estimation. (c) Atrophy distribution estimated using Model 1 and eigen-modes u2 − u27. Model 2: (d) Correlation R of group atrophy and Φ2 obtained when each node is seeded. (e) R vs. graph diffusion depth t. Left paracentral gives the maximum R, followed by the left post central and the left frontal pole. (f) Neuronal atrophy estimate obtained from Model 2 when the paracentral lobe is seeded.
Fig 4.
Scatter plots for each model and epilepsy type of the measured neuronal atrophy vs. the neuronal atrophy as estimated by the two models.
Empirical vs. estimated neuronal atrophy for the case of TLE-MTS; Model 1 (a), and Model 2 (b); and measured vs. estimated neuronal atrophy for the case of TLE-no; Model 1 (c), and Model 2 (d). For both types of epilepsy, Model 2 outperforms Model 1.
Fig 5.
Histograms of R resulting from 1,000 instances of random permutations of the neuronal atrophy for each type of epilepsy and for both models.
From the histograms, the estimated neuronal atrophy is likely to be specific to the atrophies obtained from both epilepsy groups, more so in the case of Model 2 where high R is obtained for both types of epilepsy. Histograms of R resulting from random permutation of neuronal atrophy, (a) TLE-MTS Model 1, (b) TLE-MTS, Model 2. Histogram of R resulting from TLE-no neuronal atrophy random permutation, (c) Model 1, and (d) Model 2.
Table 3.
Summary of the variables and definitions used in this text.