Evidence map›Paper›PMID 27776562›Full record

ArticlePsychological medicine2017

Clinical anxiety promotes excessive response inhibition.

C Grillon, O J Robinson, K O'Connell, A Davis, G Alvarez, D S Pine, M Ernst

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Psychological medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

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  12. The Posterior Cingulate Cortex Reflects the Impact of Anxiety on Drift Rates During Cognitive Processing.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2023
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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

7 authors.

C GrillonSection on Neurobiology of Fear and Anxiety,National Institute of Mental Health,National Institutes of Health,Bethesda,MD,USA.
O J RobinsonInstitute of Cognitive Neuroscience,University College London,London,UK.
K O'ConnellSection on Neurobiology of Fear and Anxiety,National Institute of Mental Health,National Institutes of Health,Bethesda,MD,USA.
A DavisSection on Neurobiology of Fear and Anxiety,National Institute of Mental Health,National Institutes of Health,Bethesda,MD,USA.
G AlvarezSection on Neurobiology of Fear and Anxiety,National Institute of Mental Health,National Institutes of Health,Bethesda,MD,USA.
D S PineSection on Development and Affective Neuroscience,National Institute of Mental Health,Bethesda,MD,USA.
M ErnstSection on Neurobiology of Fear and Anxiety,National Institute of Mental Health,National Institutes of Health,Bethesda,MD,USA.

Funding

The Psychophysiology Of Fear And AnxietyZIAMH002798 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI GRILLON, CHRISTIAN · 2009 to 2022
$29.0M
The Psychophysiology Of Fear And AnxietyZ01MH002798 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI GRILLON, CHRISTIAN · 2002 to 2008
$3.8M
Intramural NIH HHS Z01 MH002798Intramural NIH HHS ZIA MH002798Medical Research Council MR/K024280/1
6 · The paper itself

Abstract

backgroundLaboratory tasks to delineate anxiety disorder features are used to refine classification and inform our understanding of etiological mechanisms. The present study examines laboratory measures of response inhibition, specifically the inhibition of a pre-potent motor response, in clinical anxiety. Data on associations between anxiety and response inhibition remain inconsistent, perhaps because of dissociable effects of clinical anxiety and experimentally manipulated state anxiety. Few studies directly assess the independent and interacting effects of these two anxiety types (state v. disorder) on response inhibition. The current study accomplished this goal, by manipulating state anxiety in healthy and clinically anxious individuals while they complete a response inhibition task.

methodThe study employs the threat-of-shock paradigm, one of the best-established manipulations for robustly increasing state anxiety. Participants included 82 adults (41 healthy; 41 patients with an anxiety disorder). A go/nogo task with highly frequent go trials was administered during alternating periods of safety and shock threat. Signal detection theory was used to quantify response bias and signal-detection sensitivity.

resultsThere were independent effects of anxiety and clinical anxiety on response inhibition. In both groups, heightened anxiety facilitated response inhibition, leading to reduced nogo commission errors. Compared with the healthy group, clinical anxiety was associated with excessive response inhibition and increased go omission errors in both the safe and threat conditions.

conclusionsResponse inhibition and its impact on go omission errors appear to be a promising behavioral marker of clinical anxiety. These results have implications for a dimensional view of clinical anxiety.

Indexed as

Inhibition, PsychologicalAdultAnxiety DisordersBiomarkersFearFemaleHumansMalePsychomotor PerformanceSignal Detection, PsychologicalYoung AdultBiomarkersAnxietyanxiety disordersbehavioral inhibitiongo/nogothreat of shock

Identifiers

PMID27776562
PMCPMC6100803

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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.