Evidence map›Paper›PMID 32217468›Full record

ArticleNeuroImage. Clinical2020

Patients with mutations of the Thyroid hormone beta-receptor show an ADHD-like phenotype for performance monitoring: an electrophysiological study.

Jan Uter, Marcus Heldmann, Berenike Rogge, Martina Obst, Julia Steinhardt, Georg Brabant, Carla Moran, Krishna Chatterjee, Thomas F Münte

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NeuroImage. Clinical, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Guideline
  2. Observational
  3. Review
  4. Article
  5. Review
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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

9 authors at 2 institutions in 2 countries.

Jan UterDepartment of Neurology, University of Lübeck, Lübeck, Germany.
Marcus HeldmannDepartment of Neurology, University of Lübeck, Lübeck, Germany; Department of Psychology II, University of Lübeck, Lübeck, Germany.
Berenike RoggeDepartment of Neurology, University of Lübeck, Lübeck, Germany.
Martina ObstDepartment of Neurology, University of Lübeck, Lübeck, Germany.
Julia SteinhardtDepartment of Neurology, University of Lübeck, Lübeck, Germany.
Georg BrabantDepartment of Internal Medicine I, University of Lübeck, Lübeck, Germany.
Carla MoranDepartment of Endocrinology, University of Cambridge, Cambridge, UK.
Krishna ChatterjeeDepartment of Endocrinology, University of Cambridge, Cambridge, UK.
Thomas F MünteDepartment of Neurology, University of Lübeck, Lübeck, Germany; Department of Psychology II, University of Lübeck, Lübeck, Germany. Electronic address: thomas.muente@neuro.uni-luebeck.de.
University of Lübeck · DEUniversity of Cambridge · GB

Funding

Department of HealthWellcome TrustWellcome Trust 210755/Z/18/Z
6 · The paper itself

Abstract

Resistance to thyroid hormone beta (RTHβ) is a syndrome of reduced responsiveness of peripheral tissue to thyroid hormone, caused by mutations in the thyroid hormone receptor beta (THRB). Its cognitive phenotype has been reported to be similar to attention deficit hyperactivity disorder (ADHD). This study used electrophysiological biomarkers of performance monitoring in RTHβ to contribute further evidence on its phenotypical similarity to ADHD. Twenty-one participants with RTHβ aged 18-67 years and 21 matched healthy controls performed a modified flanker task during EEG recording. The RTHβ and control groups were compared on behavioural measures and components of event related potentials (ERPs), i.e. the error related negativity (ERN), the error positivity (Pe) and P3 component. There were no significant group differences with regard to behaviour. RTHβ subjects displayed significantly reduced ERN and Pe amplitudes compared to the controls in the response-locked ERPs. In addition, we observed reduced P3 amplitudes in both congruent and incongruent trials, as well as prolonged P3 latencies in RTHβ subjects in the stimulus-locked ERPs. Our findings reveal alterations in error detection and performance monitoring of RTHβ patients, likely indicating reduced error awareness. The electrophysiological phenotype of RTHß subjects with regard to action monitoring is indistinguishable from ADHD.

Indexed as

AdolescentAdultAgedAttention Deficit Disorder with HyperactivityElectroencephalographyEvoked PotentialsFemaleHumansMaleMiddle AgedMutationPhenotypeThyroid Hormone Receptors betaThyroid Hormone Resistance SyndromeYoung AdultThyroid Hormone Receptors betaAction monitoringADHD-like symptomsEvent-related potentialsResistance to thyroid hormonesTH beta receptorThyroid hormones (TH)

Identifiers

PMID32217468
PMCPMC7109456
OpenAlexW3011275255

What OpenQuestion holds

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Registered trials

None linked

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.