Evidence map›Paper›PMID 39235869›Full record

ArticleEpileptic disorders : international epilepsy journal with videotape2024

Epilepsy with eyelid myoclonia in a patient with ATP1A3-related neurologic disorder.

Ann Mertens, Maria T Papadopoulou, Matthildi Athina Papathanasiou Terzi, Gaëtan Lesca, Mateusz Biela, Robert Smigiel, Eleni Panagiotakaki

Abstract readCase Reports
In one paragraph

Article in Epileptic disorders : international epilepsy journal with videotape, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Clinical and Genetic Spectrum ofNeurology. Genetics · 2026
    Article
  2. Article
  3. Epilepsy with eyelid myoclonia in a patient with ATP1A3-related neurologic disorder.Epileptic disorders : international epilepsy journal with videotape · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Ann MertensDepartment of Pediatric Epileptology, Functional Neurology and Sleep Disorders, Hôpital Femme Mère Enfant, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Lyon, France.ORCID https://orcid.org/0000-0003-2357-9556
Maria T PapadopoulouDepartment of Pediatric Epileptology, Functional Neurology and Sleep Disorders, Hôpital Femme Mère Enfant, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Lyon, France.ORCID https://orcid.org/0000-0002-2076-5006
Matthildi Athina Papathanasiou TerziDepartment of Pediatric Epileptology, Functional Neurology and Sleep Disorders, Hôpital Femme Mère Enfant, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Lyon, France.
Gaëtan LescaDepartment of Medical Genetics, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Université Claude Bernard Lyon 1, Lyon, France.ORCID https://orcid.org/0000-0001-7691-9492
Mateusz BielaDepartment of Pediatrics, Endocrinology, Diabetology and Metabolic Diseases, Medical University of Wroclaw, Wrocław, Poland.
Robert SmigielDepartment of Pediatrics, Endocrinology, Diabetology and Metabolic Diseases, Medical University of Wroclaw, Wrocław, Poland.
Eleni PanagiotakakiDepartment of Pediatric Epileptology, Functional Neurology and Sleep Disorders, Hôpital Femme Mère Enfant, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Lyon, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We report on an 11 year old Polish girl who experienced paroxysmal episodes with decreased consciousness, (hemi)plegia, movement disorders, slurred speech, dysphagia, and abnormal eye movements. An extensive etiological work-up (brain MRI, EEG, EMG, NCS, toxic, metabolic, infectious, and auto-immune screening) was not conclusive. A genetic analysis with whole-exome sequencing demonstrated a de novo heterozygous mutation in the ATP1A3 gene (c.2232C>G, p.Asn744Lys). A 48 h video-EEG monitoring that was conducted in our unit later confirmed the absence of ictal discharge during an episode of hemidystonia, demonstrating its non-epileptic etiology. However, several discharges of generalized spike waves, which were facilitated by intermittent photic stimulation and eyelid closure were recorded, of which a few were associated with eyelid myoclonia. Taken together, these findings are characteristic of epilepsy with eyelid myoclonia. The clinical picture of this patient partially fulfills the diagnostic criteria of relapsing encephalopathy with cerebellar ataxia as well as alternating hemiplegia of childhood. It is increasingly recognized that the distinct syndromes described with ATP1A3 mutations are overlapping and could be identified in the same patients. Certain variations in ATP1A3 have been linked to an increased risk of developing generalized epilepsy syndromes. We hereby present the second case in the literature of a patient with epilepsy with eyelid myoclonia with an ATP1A3-related neurological disorder.

Indexed as

Sodium-Potassium-Exchanging ATPaseCerebellar AtaxiaChildElectroencephalographyEpilepsyFemaleHemiplegiaHumansMyoclonusATP1A3 protein, humanSodium-Potassium-Exchanging ATPasealternating hemiplegia of childhoodATP1A3epilepsy with eyelid MyocloniaEtiology: genetic disorderLocalization: generalizedPhenomenology: myoclonic (eyelids)relapsing encephalopathy with cerebellar ataxiaSyndrome: Jeavons syndrome

Identifiers

PMID39235869
PMCPMC11651374

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.