Evidence map›Paper›PMID 28972591›Full record

ArticleTranslational psychiatry2017

Altered activation and connectivity in a hippocampal-basal ganglia-midbrain circuit during salience processing in subjects at ultra high risk for psychosis.

T Winton-Brown, A Schmidt, J P Roiser, O D Howes, A Egerton, P Fusar-Poli, N Bunzeck, A A Grace, E Duzel, S Kapur and 1 more

Erratum issuedAbstract read
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  13. Neural Circuitry of Salience and Reward Processing in Psychosis.Biological psychiatry global open science · 2023
    Review
  14. Hippocampal circuit dysfunction in psychosis.Translational psychiatry · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

T Winton-BrownDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
A SchmidtDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
J P RoiserInstitute of Cognitive Neuroscience, University College London, London, UK.
O D HowesDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
A EgertonDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
P Fusar-PoliEarly Psychosis: Intervention and Clinical-prediction (EPIC) Lab, Department of Psychosis Studies, Institute of Psychology, Psychiatry and Neuroscience, King's College London, London, UK.
N BunzeckInstitute of Psychology, University of Luebeck, Luebeck, Germany.
A A GraceDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.
E DuzelInstitute of Cognitive Neuroscience, University College London, London, UK.
S KapurDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
P McGuireDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.

Funding

Medical Research Council G0700995Medical Research Council MC_U120097115Medical Research Council MR/N026063/1
6 · The paper itself

Abstract

Animal models of psychosis propose that abnormal hippocampal activity drives increased subcortical dopamine function, which is thought to contribute to aberrant salience processing and psychotic symptoms. These effects appear to be mediated through connections between the hippocampus, ventral striatum/pallidum and the midbrain. The aim of the present study was to examine the activity and connectivity in this pathway in people at ultra high risk (UHR) for psychosis. Functional magnetic resonance imaging was used to compare neural responses in a hippocampal-basal ganglia-midbrain network during reward, novelty and aversion processing between 29 UHR subjects and 32 healthy controls. We then investigated whether effective connectivity within this network is perturbed in UHR subjects, using dynamic causal modelling (DCM). Finally, we examined the relationship between alterations in activation and connectivity in the UHR subjects and the severity of their psychotic symptoms. During reward anticipation, UHR subjects showed greater activation than controls in the ventral pallidum bilaterally. There were no differences in activation during novelty or aversion processing. DCM revealed that reward-induced modulation of connectivity from the ventral striatum/pallidum to the midbrain was greater in UHR subjects than controls, and that in UHR subjects, the strength of connectivity in this pathway was correlated with the severity of their abnormal beliefs. In conclusion, ventral striatal/pallidal function is altered in people at UHR for psychosis and this is related to the level of their psychotic symptoms.

Indexed as

RewardAdultAnticipation, PsychologicalBasal GangliaBrain MappingFemaleHippocampusHumansMagnetic Resonance ImagingMaleMesencephalonNeural PathwaysPsychotic DisordersRisk FactorsYoung Adult

Identifiers

PMID28972591
PMCPMC5682600

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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.