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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

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.
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pcbi.1004564.g003: 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.

Mentions: The measured atrophy of TLE-no, Fig 3(a), reveals pronounced atrophy broadly, bilaterally distributed across cortical and subcortical regions, particularly in the frontal and temporal lobes. The region with the highest atrophy is the contralateral transverse temporal gyrus, with t-statistics of 3.74. Other regions with high atrophy include the contralateral precentral gyrus (t-statistics 3.29) and the postcentral gyrus (t-statistics 3.45).


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

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

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.
© Copyright Policy
Related In: Results  -  Collection

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

pcbi.1004564.g003: 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.
Mentions: The measured atrophy of TLE-no, Fig 3(a), reveals pronounced atrophy broadly, bilaterally distributed across cortical and subcortical regions, particularly in the frontal and temporal lobes. The region with the highest atrophy is the contralateral transverse temporal gyrus, with t-statistics of 3.74. Other regions with high atrophy include the contralateral precentral gyrus (t-statistics 3.29) and the postcentral gyrus (t-statistics 3.45).

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