Evidence map›Paper›PMID 40956029›Full record

ArticleEpilepsia2025

Novel neuropathological observations in an adult with Dravet syndrome.

Danielle M Andrade, Anne S Bassett, Quratulain ZulfiqarAli, Victor S T Lira, Nikolai Gil Reyes, M Carmela Tartaglia, Alfonso Fasano, Gabor G Kovacs

Abstract readCase Reports
In one paragraph

Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Danielle M AndradeAdult Genetic Epilepsy (AGE) Program, Division of Neurology, University of Toronto, Toronto, Ontario, Canada.
Anne S BassettThe Dalglish Family 22q Clinic, Department of Mental Health and Division of Cardiology, and Toronto General Hospital Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Quratulain ZulfiqarAliAdult Genetic Epilepsy (AGE) Program, Division of Neurology, University of Toronto, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0002-3984-5276
Victor S T LiraAdult Genetic Epilepsy (AGE) Program, Division of Neurology, University of Toronto, Toronto, Ontario, Canada.
Nikolai Gil ReyesDivision of Neurology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
M Carmela TartagliaDivision of Neurology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Alfonso FasanoDivision of Neurology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0001-5346-0180
Gabor G KovacsDivision of Neurology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dravet syndrome (DS) is a developmental and epileptic encephalopathy associated with pathogenic variants in the SCN1A gene. The neuropathological features of adult DS remain poorly understood. We report the postmortem findings of a 55-year-old woman with DS due to a confirmed SCN1A pathogenic variant leading to Nav1.1 loss of function. Clinically, she developed pharmacoresistant seizures, intellectual disability, progressive ataxia, parkinsonism, and cognitive decline. Neuropathological examination revealed a striking excess and several layers of corpora amylacea (wasteosomes) covering the whole convexity of the brain. In addition, abundant p62-positive gray matter neuritic profiles were found mostly in limbic regions and in the white matter in neocortical regions. Pericellular TMEM106B-positive deposits and prominent immunoreactivity for aquaporin 4 were also observed. There was severe Purkinje cell loss in some lobes of the cerebellum together with variable neuronal loss in the substantia nigra, neocortex, and hippocampus. No α-synuclein, amyloid-β, or phospho-TDP-43 pathology was present. Immunostaining for phosphorylated tau revealed neurofibrillary pathology consistent with Braak stage I (left) -II (right). In summary, our study reveals pathological alterations suggestive of chronic glymphatic insufficiency, impaired autophagy, and some degree of neuronal loss without currently known misfolded protein deposits. These findings are suggestive of an accelerated aging and neurodegenerative process in this adult with DS.

Indexed as

BrainEpilepsies, MyoclonicFemaleHumansMiddle AgedNAV1.1 Voltage-Gated Sodium ChannelNAV1.1 Voltage-Gated Sodium ChannelSCN1A protein, humanaccelerated agingagingaquaropin 4corpora amylaceaDravet syndromeglymphatic systemneurodegenerationp62SCN1Awasteosome

Identifiers

PMID40956029
PMCPMC12605653

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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.