Evidence map›Paper›PMID 32991786›Full record

ArticleAnnals of clinical and translational neurology2020

White matter and neurite morphology differ in psychogenic nonepileptic seizures.

Adam M Goodman, Jane B Allendorfer, Andrew S Blum, Mark S Bolding, Stephen Correia, Lawrence W Ver Hoef, Tyler E Gaston, Leslie E Grayson, Nina V Kraguljac, Adrienne C Lahti and 7 more

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

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  13. Recent Advances in Neuroimaging of Epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
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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

17 authors at 3 institutions in 1 country.

Adam M GoodmanDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-7550-679X
Jane B AllendorferDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Andrew S BlumDepartment of Neurology, Rhode Island Hospital, Providence, Rhode Island, USA.ORCID 0000-0003-0868-6257
Mark S BoldingDepartment of Radiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-7684-4125
Stephen CorreiaBrown University, Providence, Rhode Island, USA.
Lawrence W Ver HoefDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-1026-550X
Tyler E GastonDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-6525-789X
Leslie E GraysonDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Nina V KraguljacDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Adrienne C LahtiDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Amber N MartinDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
William S MonroeDepartment of Research Computing, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Noah S PhilipBrown University, Providence, Rhode Island, USA.ORCID 0000-0002-4889-8775
Krista ToccoDepartment of Neurology, Rhode Island Hospital, Providence, Rhode Island, USA.
Valerie VogelDepartment of Neurology, Rhode Island Hospital, Providence, Rhode Island, USA.
W Curt LaFranceCenter for Neurorestoration and Neurotechnology, Providence VA Medical Center, Providence, Rhode Island, USA.ORCID 0000-0002-4901-3852
Jerzy P SzaflarskiDepartment of Neurology and the UAB Epilepsy Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-5936-6627
University of Alabama at Birmingham · USBrown University · USChildren's of Alabama · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo further evaluate the relationship between the clinical profiles and limbic and motor brain regions and their connecting pathways in psychogenic nonepileptic seizures (PNES). Neurite Orientation Dispersion and Density Indices (NODDI) multicompartment modeling was used to test the relationships between tissue alterations in patients with traumatic brain injury (TBI) and multiple psychiatric symptoms.

methodsThe sample included participants with prior TBI (TBI; N = 37) but no PNES, and with TBI and PNES (TBI + PNES; N = 34). Participants completed 3T Siemens Prisma MRI high angular resolution imaging diffusion protocol. Statistical maps, including fractional anisotropy (FA), mean diffusivity (MD), neurite dispersion [orientation dispersion index (ODI)] and density [intracellular volume fraction (ICVF), and free water (i.e., isotropic) volume fraction (V-ISO)] signal intensity, were generated for each participant. Linear mixed-effects models identified clusters of between-group differences in indices of white matter changes. Pearson's r correlation tests assessed any relationship between signal intensity and psychiatric symptoms.

resultsCompared to TBI, TBI + PNES revealed decreases in FA, ICVF, and V-ISO and increases in MD for clusters within cingulum bundle, uncinate fasciculus, fornix/stria terminalis, and corticospinal tract pathways (cluster threshold α = 0.05). Indices of white matter changes for these clusters correlated with depressive, anxiety, PTSD, psychoticism, and somatization symptom severity (FDR threshold α = 0.05). A follow-up within-group analysis revealed that these correlations failed to reach the criteria for significance in the TBI + PNES group alone.

interpretationThe results expand support for the hypothesis that alterations in pathways comprising the specific PNES network correspond to patient profiles. These findings implicate myelin-specific changes as possible contributors to PNES, thus introducing novel potential treatment targets.

Indexed as

AnisotropyMagnetic Resonance ImagingAdultBrain Injuries, TraumaticDiffusion Magnetic Resonance ImagingDiffusion Tensor ImagingFemaleHumansMaleMiddle AgedMyelin SheathNerve NetNeuritesSeizuresWhite Matter

Identifiers

PMID32991786
PMCPMC7545605
OpenAlexW3090823852

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.