Evidence map›Paper›PMID 37344172›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2023

Morphometry and network-based atrophy patterns in SCN1A-related Dravet syndrome.

Matteo Lenge, Simona Balestrini, Davide Mei, Letizia Macconi, Maria Eugenia Caligiuri, Valeria Cuccarini, Domenico Aquino, Federica Mazzi, Ludovico d'Incerti, Francesca Darra and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2023. 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
1.6field-weighted citation impact, top 18% of its field
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, 7 citations in OpenAlex.

  1. Article
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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

12 authors at 4 institutions in 1 country.

Matteo LengeNeuroscience Department, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.ORCID 0000-0003-2848-621X
Simona BalestriniNeuroscience Department, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.
Davide MeiNeuroscience Department, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.
Letizia MacconiNeuroradiology Unit, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.
Maria Eugenia CaligiuriNeuroscience Research Center, Department of Medical and Surgical Sciences, Magna Grecia University, 88100, Catanzaro, Italy.
Valeria CuccariniNeuroradiology Unit, Fondazione IRCCS Neurologico Carlo Besta, 20100, Milan, Italy.
Domenico AquinoNeuroradiology Unit, Fondazione IRCCS Neurologico Carlo Besta, 20100, Milan, Italy.
Federica MazziNeuroradiology Unit, Fondazione IRCCS Neurologico Carlo Besta, 20100, Milan, Italy.
Ludovico d'IncertiNeuroradiology Unit, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.
Francesca DarraChild Neuropsychiatry Unit, Department of Engineering for Innovation Medicine University of Verona, 37100, Verona, Italy.
Bernardo Dalla BernardinaChild Neuropsychiatry Unit, Department of Engineering for Innovation Medicine University of Verona, 37100, Verona, Italy.
Renzo GuerriniNeuroscience Department, Meyer Children's Hospital IRCCS, 50139, Florence, Italy.
Meyer Children's Hospital · ITFondazione IRCCS Istituto Neurologico Carlo Besta · ITUniversity of Verona · ITMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations of the voltage-gated sodium channel SCN1A gene (MIM#182389) are among the most clinically relevant epilepsy-related genetic mutations and present variable phenotypes, from the milder genetic epilepsy with febrile seizures plus to Dravet syndrome, a severe developmental and epileptic encephalopathy. Qualitative neuroimaging studies have identified malformations of cortical development in some patients and mild atrophic changes, partially confirmed by quantitative studies. Precise correlations between MRI findings and clinical variables have not been addressed. We used morphometric methods and network-based models to detect abnormal brain structural patterns in 34 patients with SCN1A-related epilepsy, including 22 with Dravet syndrome. By measuring the morphometric characteristics of the cortical mantle and volume of subcortical structures, we found bilateral atrophic changes in the hippocampus, amygdala, and the temporo-limbic cortex (P-value < 0.05). By correlating atrophic patterns with brain connectivity profiles, we found the region of the hippocampal formation as the epicenter of the structural changes. We also observed that Dravet syndrome was associated with more severe atrophy patterns with respect to the genetic epilepsy with febrile seizures plus phenotype (r = -0.0613, P-value = 0.03), thus suggesting that both the underlying mutation and seizure severity contribute to determine atrophic changes.

Indexed as

Epilepsies, MyoclonicEpilepsySeizures, FebrileHumansMutationNAV1.1 Voltage-Gated Sodium ChannelPhenotypeNAV1.1 Voltage-Gated Sodium ChannelSCN1A protein, humanDravet syndromeepilepsyhippocampuslimbic formationSCN1A mutation

Identifiers

PMID37344172
PMCPMC10431750
OpenAlexW4381598141

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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.