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

Abdelnour F, Mueller S, Raj A - PLoS Comput. Biol. (2015)

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Radiology, Weill Cornell Medical College, New York, New York, United States of America.

ABSTRACT
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 (R = 0.586 for TLE-MTS, R = 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.

No MeSH data available.


Related in: MedlinePlus

(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.
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pcbi.1004564.g001: (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.

Mentions: The TLE-MTS measured atrophy reflected in Fig 1(a) indicates, as expected, pronounced atrophy in the hippocampus, with less marked atrophy ipsilaterally in pars orbitalis, amygdala, VDC, pallidum, thalamus and inferior temporal gyrus. Contralateral temporal pole, transverse temporal gyrus, entorhinal cortex (ERC) and pars opercularis also reveal some atrophy.


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

Abdelnour F, Mueller S, Raj A - PLoS Comput. Biol. (2015)

(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.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4626097&req=5

pcbi.1004564.g001: (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.
Mentions: The TLE-MTS measured atrophy reflected in Fig 1(a) indicates, as expected, pronounced atrophy in the hippocampus, with less marked atrophy ipsilaterally in pars orbitalis, amygdala, VDC, pallidum, thalamus and inferior temporal gyrus. Contralateral temporal pole, transverse temporal gyrus, entorhinal cortex (ERC) and pars opercularis also reveal some atrophy.

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Radiology, Weill Cornell Medical College, New York, New York, United States of America.

ABSTRACT
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 (R = 0.586 for TLE-MTS, R = 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.

No MeSH data available.


Related in: MedlinePlus