Evidence map›Paper›PMID 29194516›Full record

ArticleSchizophrenia bulletin2018

Deficits in Cortical Suppression During Vocalization are Associated With Structural Abnormalities in the Arcuate Fasciculus in Early Illness Schizophrenia and Clinical High Risk for Psychosis.

Thomas J Whitford, Lena K L Oestreich, Judith M Ford, Brian J Roach, Rachel L Loewy, Barbara K Stuart, Daniel H Mathalon

Open access · bronzeAbstract read
In one paragraph

Article in Schizophrenia bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Efference copy/corollary discharge function and targeted cognitive training in patients with schizophrenia.International journal of psychophysiology : official journal of the International Organization of Psychophysiology · 2019
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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 at 3 institutions in 2 countries.

Thomas J WhitfordSchool of Psychology, The University of New South Wales, Sydney, Australia.
Lena K L OestreichQueensland Brain Institute and Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia.
Judith M FordDepartment of Psychiatry, University of California-San Francisco, San Francisco, CA.
Brian J RoachDepartment of Psychiatry, University of California-San Francisco, San Francisco, CA.
Rachel L LoewyDepartment of Psychiatry, University of California-San Francisco, San Francisco, CA.
Barbara K StuartDepartment of Psychiatry, University of California-San Francisco, San Francisco, CA.
Daniel H MathalonDepartment of Psychiatry, University of California-San Francisco, San Francisco, CA.
University of California, San Francisco · USUniversity of Queensland · AUUNSW Sydney · AU

Funding

Functional Brain Abnormalities in the Schizophrenia ProdromeR01MH076989 · NIMH · YALE UNIVERSITY · PI MATHALON, DANIEL H · 2007 to 2014
$2.3M
Neurobiology of response monitoring failure in schizophreniaK02MH067967 · NIMH · YALE UNIVERSITY · PI FORD, JUDITH M · 2003 to 2010
$1.1M
NIMH NIH HHS K02 MH067967NIMH NIH HHS R01 MH076989
6 · The paper itself

Abstract

Self-generated speech produces a smaller N1 amplitude in the auditory-evoked potential than externally generated speech; this phenomenon is known as N1-suppression. Schizophrenia patients show less N1-suppression than healthy controls. This failure to self-suppress may underlie patients' characteristic tendency to misattribute self-generated thoughts and actions to external sources. While the cause of N1-suppression deficits to speech in schizophrenia remains unclear, structural damage to the arcuate fasciculus is a candidate, due to its ostensible role in transmitting the efference copy of the motor plan to speak. Fifty-one patients with early illness schizophrenia (ESZ), 40 individuals at clinical high-risk for psychosis (CHR), and 59 healthy control (HC) participants underwent an electroencephalogram while they spoke and then listened to a recording of their speech. N1-suppression to the spoken sounds was calculated. Participants also underwent a diffusion-tensor imaging (DTI) scan, from which the arcuate fasciculus and pyramidal tract were extracted with deterministic tractography. ESZ patients exhibited significantly less N1-suppression to self-generated speech than HC participants, with CHR participants exhibiting intermediate levels. ESZ patients also exhibited structural abnormalities in the arcuate fasciculus-specifically, reduced fractional anisotropy and increased radial diffusivity-relative to both HC and CHR. There were no between-group differences in the structural integrity of the pyramidal tract. Finally, level of N1-suppression was linearly related to the structural integrity of the arcuate fasciculus, but not the pyramidal tract, across groups. These results suggest that the self-suppression deficits to willed speech consistently observed in schizophrenia patients may be caused, at least in part, by structural damage to the arcuate fasciculus.

Indexed as

Cerebral CortexPsychotic DisordersSchizophreniaWhite MatterAdolescentAdultAuditory PerceptionChildDiffusion Tensor ImagingElectroencephalographyEvoked Potentials, AuditoryFemaleHumansMaleSpeechYoung Adult

Identifiers

PMID29194516
PMCPMC6192501
OpenAlexW2770434151

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.