Evidence map›Paper›PMID 31911624›Full record

ReviewNPJ schizophrenia2020

The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research.

Steven G Potkin, John M Kane, Christoph U Correll, Jean-Pierre Lindenmayer, Ofer Agid, Stephen R Marder, Mark Olfson, Oliver D Howes

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in NPJ schizophrenia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07408934 (A Randomized Controlled Trial of Group Cognitive Behavioral Therapy), which is not on this map. Cited by 166 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 10 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.

NCT07408934 naenrolling by invitationnot on this mapstarted 2024, after this paper: background citation

A Randomized Controlled Trial of Group Cognitive Behavioral Therapy (the Feeling Safe Programme) for Psychosis

TypeinterventionalSponsorThe Royal Ottawa Mental Health CentreRan2024 to 2027Enrolled50ConditionsSchizophrenia and Schizoaffective DisorderArmsCognitive Behavioral Therapy for Psychosis
3 · Its place in the literature

Who cites it

166 citing papers in PubMed, 10 syntheses or guidelines pooled it.

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106 more citing papers are in PubMed but not listed here.

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

8 authors.

Steven G PotkinUniversity of California at Irvine, Irvine, CA, USA.
John M KaneDonald and Barbara Zucker School of Medicine at Hofstra/Northwell, Department of Psychiatry and Molecular Medicine, Hempstead, NY, USA.
Christoph U CorrellDonald and Barbara Zucker School of Medicine at Hofstra/Northwell, Department of Psychiatry and Molecular Medicine, Hempstead, NY, USA.
Jean-Pierre LindenmayerDepartment of Psychiatry, New York University School of Medicine, New York, NY, USA.
Ofer AgidCentre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, Toronto, ON, Canada.
Stephen R MarderThe Semel Institute for Neuroscience at UCLA, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0003-0288-309X
Mark OlfsonDepartment of Psychiatry, Columbia University Irving Medical Center, New York, NY, USA.
Oliver D HowesKing's College, London, UK. oliver.howes@kcl.ac.uk.

Funding

Medical Research Council G0700995Medical Research Council MC_U120097115Medical Research Council MR/L022176/1Medical Research Council MR/N026063/1Medical Research Council MR/N027078/1
6 · The paper itself

Abstract

Treatment-resistant schizophrenia (TRS), the persistence of positive symptoms despite ≥2 trials of adequate dose and duration of antipsychotic medication with documented adherence, is a serious clinical problem with heterogeneous presentations. TRS can vary in its onset (at the first episode of psychosis or upon relapse), in its severity, and in the response to subsequent therapeutic interventions (i.e., clozapine, electroconvulsive therapy). The heterogeneity of TRS indicates that the underlying neurobiology of TRS may differ not only from treatment-responsive schizophrenia but also among patients with TRS. Several hypotheses have been proposed for the neurobiological mechanisms underlying TRS, including dopamine supersensitivity, hyperdopaminergic and normodopaminergic subtypes, glutamate dysregulation, inflammation and oxidative stress, and serotonin dysregulation. Research supporting these hypotheses is limited in part by variations in the criteria used to define TRS, as well as by the biological and clinical heterogeneity of TRS. Clinical trial designs for new treatments should be informed by this heterogeneity, and further clinical research is needed to more clearly understand the underlying neurobiology of TRS and to optimize treatment for patients with TRS.

Identifiers

PMID31911624
PMCPMC6946650

What Socratic holds

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LicenceCC BY
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Registered trials

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 Socratic graph.