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Event‐based modeling in temporal lobe epilepsy demonstrates progressive atrophy from cross‐sectional data.

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Title: Event‐based modeling in temporal lobe epilepsy demonstrates progressive atrophy from cross‐sectional data.
Authors: Lopez, Seymour M. (AUTHOR), Aksman, Leon M. (AUTHOR), Oxtoby, Neil P. (AUTHOR), Vos, Sjoerd B. (AUTHOR), Rao, Jun (AUTHOR), Kaestner, Erik (AUTHOR), Alhusaini, Saud (AUTHOR), Alvim, Marina (AUTHOR), Bender, Benjamin (AUTHOR), Bernasconi, Andrea (AUTHOR), Bernasconi, Neda (AUTHOR), Bernhardt, Boris (AUTHOR), Bonilha, Leonardo (AUTHOR), Caciagli, Lorenzo (AUTHOR), Caldairou, Benoit (AUTHOR), Caligiuri, Maria Eugenia (AUTHOR), Calvet, Angels (AUTHOR), Cendes, Fernando (AUTHOR), Concha, Luis (AUTHOR), Conde‐Blanco, Estefania (AUTHOR)
Source: Epilepsia (Series 4). Aug2022, Vol. 63 Issue 8, p2081-2095. 15p.
Subjects: Temporal lobe epilepsy, Cerebral cortical thinning, Disease duration, Mann Whitney U Test, Magnetic resonance imaging, Partial epilepsy
Abstract: Objective: Recent work has shown that people with common epilepsies have characteristic patterns of cortical thinning, and that these changes may be progressive over time. Leveraging a large multicenter cross‐sectional cohort, we investigated whether regional morphometric changes occur in a sequential manner, and whether these changes in people with mesial temporal lobe epilepsy and hippocampal sclerosis (MTLE‐HS) correlate with clinical features. Methods: We extracted regional measures of cortical thickness, surface area, and subcortical brain volumes from T1‐weighted (T1W) magnetic resonance imaging (MRI) scans collected by the ENIGMA‐Epilepsy consortium, comprising 804 people with MTLE‐HS and 1625 healthy controls from 25 centers. Features with a moderate case–control effect size (Cohen d ≥.5) were used to train an event‐based model (EBM), which estimates a sequence of disease‐specific biomarker changes from cross‐sectional data and assigns a biomarker‐based fine‐grained disease stage to individual patients. We tested for associations between EBM disease stage and duration of epilepsy, age at onset, and antiseizure medicine (ASM) resistance. Results: In MTLE‐HS, decrease in ipsilateral hippocampal volume along with increased asymmetry in hippocampal volume was followed by reduced thickness in neocortical regions, reduction in ipsilateral thalamus volume, and finally, increase in ipsilateral lateral ventricle volume. EBM stage was correlated with duration of illness (Spearman ρ =.293, p = 7.03 × 10−16), age at onset (ρ = −.18, p = 9.82 × 10−7), and ASM resistance (area under the curve =.59, p =.043, Mann–Whitney U test). However, associations were driven by cases assigned to EBM Stage 0, which represents MTLE‐HS with mild or nondetectable abnormality on T1W MRI. Significance: From cross‐sectional MRI, we reconstructed a disease progression model that highlights a sequence of MRI changes that aligns with previous longitudinal studies. This model could be used to stage MTLE‐HS subjects in other cohorts and help establish connections between imaging‐based progression staging and clinical features. [ABSTRACT FROM AUTHOR]
Copyright of Epilepsia (Series 4) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Event‐based modeling in temporal lobe epilepsy demonstrates progressive atrophy from cross‐sectional data.
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  Data: <searchLink fieldCode="AR" term="%22Lopez%2C+Seymour+M%2E%22">Lopez, Seymour M.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Aksman%2C+Leon+M%2E%22">Aksman, Leon M.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Oxtoby%2C+Neil+P%2E%22">Oxtoby, Neil P.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Vos%2C+Sjoerd+B%2E%22">Vos, Sjoerd B.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Rao%2C+Jun%22">Rao, Jun</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kaestner%2C+Erik%22">Kaestner, Erik</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Alhusaini%2C+Saud%22">Alhusaini, Saud</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Alvim%2C+Marina%22">Alvim, Marina</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bender%2C+Benjamin%22">Bender, Benjamin</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bernasconi%2C+Andrea%22">Bernasconi, Andrea</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bernasconi%2C+Neda%22">Bernasconi, Neda</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bernhardt%2C+Boris%22">Bernhardt, Boris</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bonilha%2C+Leonardo%22">Bonilha, Leonardo</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Caciagli%2C+Lorenzo%22">Caciagli, Lorenzo</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Caldairou%2C+Benoit%22">Caldairou, Benoit</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Caligiuri%2C+Maria+Eugenia%22">Caligiuri, Maria Eugenia</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Calvet%2C+Angels%22">Calvet, Angels</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Cendes%2C+Fernando%22">Cendes, Fernando</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Concha%2C+Luis%22">Concha, Luis</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Conde‐Blanco%2C+Estefania%22">Conde‐Blanco, Estefania</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Epilepsia+%28Series+4%29%22">Epilepsia (Series 4)</searchLink>. Aug2022, Vol. 63 Issue 8, p2081-2095. 15p.
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  Data: <searchLink fieldCode="DE" term="%22Temporal+lobe+epilepsy%22">Temporal lobe epilepsy</searchLink><br /><searchLink fieldCode="DE" term="%22Cerebral+cortical+thinning%22">Cerebral cortical thinning</searchLink><br /><searchLink fieldCode="DE" term="%22Disease+duration%22">Disease duration</searchLink><br /><searchLink fieldCode="DE" term="%22Mann+Whitney+U+Test%22">Mann Whitney U Test</searchLink><br /><searchLink fieldCode="DE" term="%22Magnetic+resonance+imaging%22">Magnetic resonance imaging</searchLink><br /><searchLink fieldCode="DE" term="%22Partial+epilepsy%22">Partial epilepsy</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Objective: Recent work has shown that people with common epilepsies have characteristic patterns of cortical thinning, and that these changes may be progressive over time. Leveraging a large multicenter cross‐sectional cohort, we investigated whether regional morphometric changes occur in a sequential manner, and whether these changes in people with mesial temporal lobe epilepsy and hippocampal sclerosis (MTLE‐HS) correlate with clinical features. Methods: We extracted regional measures of cortical thickness, surface area, and subcortical brain volumes from T1‐weighted (T1W) magnetic resonance imaging (MRI) scans collected by the ENIGMA‐Epilepsy consortium, comprising 804 people with MTLE‐HS and 1625 healthy controls from 25 centers. Features with a moderate case–control effect size (Cohen d ≥.5) were used to train an event‐based model (EBM), which estimates a sequence of disease‐specific biomarker changes from cross‐sectional data and assigns a biomarker‐based fine‐grained disease stage to individual patients. We tested for associations between EBM disease stage and duration of epilepsy, age at onset, and antiseizure medicine (ASM) resistance. Results: In MTLE‐HS, decrease in ipsilateral hippocampal volume along with increased asymmetry in hippocampal volume was followed by reduced thickness in neocortical regions, reduction in ipsilateral thalamus volume, and finally, increase in ipsilateral lateral ventricle volume. EBM stage was correlated with duration of illness (Spearman ρ =.293, p = 7.03 × 10−16), age at onset (ρ = −.18, p = 9.82 × 10−7), and ASM resistance (area under the curve =.59, p =.043, Mann–Whitney U test). However, associations were driven by cases assigned to EBM Stage 0, which represents MTLE‐HS with mild or nondetectable abnormality on T1W MRI. Significance: From cross‐sectional MRI, we reconstructed a disease progression model that highlights a sequence of MRI changes that aligns with previous longitudinal studies. This model could be used to stage MTLE‐HS subjects in other cohorts and help establish connections between imaging‐based progression staging and clinical features. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Epilepsia (Series 4) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/epi.17316
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        Text: English
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