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Epilepsy
Short report
Sodium valproate is associated with cortical thinning of disease-specific areas in juvenile myoclonic epilepsy
  1. Bernardo Crespo Pimentel1,2,3,4,
  2. Giorgi Kuchukhidze1,3,
  3. Fenglai Xiao2,4,
  4. Lorenzo Caciagli2,4,5,
  5. Julia Höfler1,3,
  6. Lucas Rainer1,6,
  7. Martin Kronbichler3,7,
  8. Christian Vollmar8,
  9. John S Duncan2,4,
  10. Eugen Trinka1,3,9,10,
  11. Matthias Koepp2,4,
  12. Britta Wandschneider2,4
  1. 1Department of Neurology, Neurointensive Care and Neurorehabilitation, Christian Doppler University Hospital, Paracelsus Medical University, Centre for Neuroscience Salzburg, Member of the European Reference Network, EpiCARE, Salzburg, Austria
  2. 2Department of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, London, UK
  3. 3Neuroscience Institute, Christian Doppler University Hospital, Centre for Cognitive Neuroscience, Salzburg, Austria
  4. 4Chalfont Centre for Epilepsy, Chalfont St. Peter, Buckinghamshire, UK
  5. 5Department of Neurology, Inselspital, Sleep-Wake-Epilepsy-Center, Bern University Hospital, University of Bern, Bern, Switzerland
  6. 6Department of Child and Adolescence Psychiatry, Christian Doppler University Hospital, Paracelsus Medical University, Salzburg, Austria
  7. 7Department of Psychology, University of Salzburg, Salzburg, Austria
  8. 8Department of Neurology, Epilepsy Center, University Hospital of the Ludwig-Maximilians-University of Munich, Munich, Germany
  9. 9Department of Public Health, Health Services Research and Health Technology Assessment, University of Health Sciences, Medical Informatics and Technology, Hall in Tirol, Austria
  10. 10Karl Landsteiner Institute for Neurorehabilitation and Space Neurology, Salzburg, Austria
  1. Correspondence to Dr. Bernardo Crespo Pimentel; bcpimentel93{at}gmail.com; Dr Britta Wandschneider; b.wandschneider{at}ucl.ac.uk

Abstract

Background Juvenile myoclonic epilepsy (JME) is associated with cortical thinning of the motor areas. The relative contribution of antiseizure medication to cortical thickness is unknown. We aimed to investigate how valproate influences the cortical morphology of JME.

Methods In this cross-sectional study, individuals with JME with and without valproate, with temporal lobe epilepsy (TLE) with valproate and controls were selected through propensity score matching. Participants underwent T1-weighted brain imaging and vertex-wise calculation of cortical thickness.

Results We matched 36 individuals with JME on valproate with 36 individuals with JME without valproate, 36 controls and 19 individuals with TLE on valproate. JME on valproate showed thinning of the precentral gyri (left and right, p<0.001) compared with controls and thinning of the left precentral gyrus when compared with JME not on valproate (p<0.01) or to TLE on valproate (p<0.001). Valproate dose correlated negatively with the thickness of the precentral gyri, postcentral gyri and superior frontal gyrus in JME (left and right p<0.0001), but not in TLE.

Conclusions Valproate was associated with JME-specific and dose-dependent thinning of the cortical motor regions. This suggests that valproate is a key modulator of cortical morphology in JME, an effect that may underlie its high efficacy in this syndrome.

  • EPILEPSY
  • IMAGE ANALYSIS
  • MRI

https://doi.org/10.1136/jnnp-2024-333703

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    Footnotes

    • MK and BW are joint senior authors.

    • X @pepperbern, @Fenglai1989

    • MK and BW contributed equally.

    • Contributors BCP, MK, BW, ET and GK designed the study, drafted a significant proportion of the manuscript and contributed to the acquisition and analysis of data. FX, JH, LC, CV, MK, LC and JD contributed to data acquisition. All authors reviewed and approved the final manuscript.

    • Funding This research was funded by an Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) grant awarded to ET (project number KLI 969), a Wellcome Trust grant awarded to MJK (079474) and a Henry Smith Charity grant awarded to MJK and BW (20133416).

    • Competing interests BCP was supported by a scholarship from the Austrian Society of Epileptology, which was not directly related to this project. ET reports personal fees from EVER Pharma, Marinus, Argenx, Arvelle/Angelini, Medtronic, Bial-Portela and Cª, NewBridge, GL Pharma, GlaxoSmithKline, Hikma, Boehringer Ingelheim, LivaNova, Eisai, UCB, Biogen, Genzyme Sanofi, GW Pharmaceuticals/Jazz and Actavis outside the submitted work; his institution has received grants from Biogen, UCB Pharma, Eisai, Red Bull, Merck, Bayer, the European Union, FWF Osterreichischer Fond zur Wissenschaftsforderung, Bundesministerium für Wissenschaft und Forschung and Jubilaumsfond der Österreichischen Nationalbank outside the submitted work. MK has received honoraria from Biocodex, Bial, GE, GSK, LivaNova, Eisai, UCB, Jazz Pharmaceuticals, and research funding from MRC, the Wellcome Trust, ER-UK, the Henry Smith Foundation and the Epilepsy Society. BW received salary support from the German Research Foundation (WA3135/1-1). The remaining authors have no conflicts of interest.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.