Epileptic spasms related to neuronal differentiation factor 2 (NEUROD2) mutation respond to combined vigabatrin and high dose prednisolone therapy.


Journal

BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555

Informations de publication

Date de publication:
09 Dec 2022
Historique:
received: 28 12 2021
accepted: 25 11 2022
entrez: 9 12 2022
pubmed: 10 12 2022
medline: 15 12 2022
Statut: epublish

Résumé

Epileptic spasms are a devastating form of early infantile epileptic encephalopathy (EIEE) with various etiologies. Early diagnosis and a shorter lead time to treatment are crucial to stop the seizures and optimize the neurodevelopmental outcome. Genetic testing has become an integral part of epilepsy care that directly guides management and family planning and discovers new targeted treatments. Neuronal differentiation Factor 2 (NEUROD2) variants have recently been a cause of neurodevelopmental disorders (NDDs) and EIEEs with distinctive features. However, there is limited information about the clinical and electroencephalographic response of epileptic spasm treatment in NEUROD2-related NDD syndrome. We report a female patient of Southeast Asian ethnicity with global developmental delay and epileptic spasms commencing in the first few months of life. A novel de novo heterozygous pathogenic NEUROD2 variant, p. E130Q, was subsequently identified by whole-exome sequencing. Electroencephalogram before treatment showed multifocal independent spikes predominantly in both posterior head regions and demonstrated marked improvement following combined vigabatrin and high-dose prednisolone treatment. However, multiple courses of relapse occurred after weaning off the antiseizure medication. We propose that epileptic spasms related to de novo NEUROD2 pathogenic variant respond well to combined vigabatrin and high-dose prednisolone therapy. These findings may imply the benefit of using combination therapy to treat epileptic spasms in NEUROD2-related NDD syndrome.

Sections du résumé

BACKGROUND BACKGROUND
Epileptic spasms are a devastating form of early infantile epileptic encephalopathy (EIEE) with various etiologies. Early diagnosis and a shorter lead time to treatment are crucial to stop the seizures and optimize the neurodevelopmental outcome. Genetic testing has become an integral part of epilepsy care that directly guides management and family planning and discovers new targeted treatments. Neuronal differentiation Factor 2 (NEUROD2) variants have recently been a cause of neurodevelopmental disorders (NDDs) and EIEEs with distinctive features. However, there is limited information about the clinical and electroencephalographic response of epileptic spasm treatment in NEUROD2-related NDD syndrome.
CASE PRESENTATION METHODS
We report a female patient of Southeast Asian ethnicity with global developmental delay and epileptic spasms commencing in the first few months of life. A novel de novo heterozygous pathogenic NEUROD2 variant, p. E130Q, was subsequently identified by whole-exome sequencing. Electroencephalogram before treatment showed multifocal independent spikes predominantly in both posterior head regions and demonstrated marked improvement following combined vigabatrin and high-dose prednisolone treatment. However, multiple courses of relapse occurred after weaning off the antiseizure medication.
CONCLUSIONS CONCLUSIONS
We propose that epileptic spasms related to de novo NEUROD2 pathogenic variant respond well to combined vigabatrin and high-dose prednisolone therapy. These findings may imply the benefit of using combination therapy to treat epileptic spasms in NEUROD2-related NDD syndrome.

Identifiants

pubmed: 36494631
doi: 10.1186/s12883-022-02992-9
pii: 10.1186/s12883-022-02992-9
pmc: PMC9733267
doi:

Substances chimiques

Vigabatrin GR120KRT6K
Prednisolone 9PHQ9Y1OLM
Anticonvulsants 0
NEUROD2 protein, human 0
Neuropeptides 0
Basic Helix-Loop-Helix Transcription Factors 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

461

Informations de copyright

© 2022. The Author(s).

Références

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pubmed: 30323019
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pubmed: 18783433
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pubmed: 27146976
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pubmed: 25779538
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pubmed: 35323127
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pubmed: 11356028
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pubmed: 24781210
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pubmed: 27838190
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pubmed: 11701250
Am J Med Genet A. 2021 Apr;185(4):1076-1080
pubmed: 33438828

Auteurs

Kullasate Sakpichaisakul (K)

Department of Pediatrics, Queen Sirikit National Institute of Child Health, College of Medicine, Rangsit University, Bangkok, 10400, Thailand.

Rachata Boonkrongsak (R)

Department of Pediatrics, Queen Sirikit National Institute of Child Health, College of Medicine, Rangsit University, Bangkok, 10400, Thailand.

Punjama Lertbutsayanukul (P)

Department of Radiology, Neurological Institute of Thailand, Bangkok, Thailand.

Nareenart Iemwimangsa (N)

Centre for Medical Genomics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.

Sommon Klumsathian (S)

Centre for Medical Genomics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.

Objoon Trachoo (O)

Centre for Medical Genomics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand. objoon.tra@mahidol.ac.th.
Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, 270 Rama 6 Road, Ratchathewi, Bangkok, 10400, Thailand. objoon.tra@mahidol.ac.th.

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Classifications MeSH