Evidence map›Paper›PMID 22717193›Full record

SynthesisPsychological medicine2013

Prenatal maternal infection, neurodevelopment and adult schizophrenia: a systematic review of population-based studies.

G M Khandaker, J Zimbron, G Lewis, P B Jones

Open access · greenAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Psychological medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 6 pooled it
7.0field-weighted citation impact, top 2% 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

218 citing papers in PubMed, 6 syntheses or guidelines pooled it, 470 citations in OpenAlex.

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158 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

4 authors at 3 institutions in 1 country.

G M KhandakerDepartment of Psychiatry, University of Cambridge, UK. gmk24@medschl.cam.ac.uk
J Zimbron
G Lewis
P B Jones
University of Cambridge · GBCambridgeshire and Peterborough NHS Foundation Trust · GBUniversity of Bristol · GB

Funding

Medical Research Council G0001354Medical Research Council G1000183Wellcome Trust 088869/Z/09/ZWellcome Trust 094790/Z/10/ZWellcome Trust 095844Wellcome Trust 095844/Z/11/Z
6 · The paper itself

Abstract

backgroundDisruption of foetal development by prenatal maternal infection is consistent with a neurodevelopmental model of schizophrenia. Whether specific prenatal infections are involved, their timing and the mechanisms of any effect are all unknown. We addressed these questions through a systematic review of population-based studies.

methodElectronic and manual searches and rigorous quality assessment yielded 21 studies that included an objective assessment of individual-level prenatal maternal infection and standardized psychotic diagnoses in adult offspring. Methodological differences between studies necessitated a descriptive review.

resultsResults for prenatal maternal non-specific bacterial, respiratory or genital and reproductive infection differed between studies, which reported up to a two- to fivefold increased risk of schizophrenia. Evidence for herpes simplex virus type 2 (HSV-2) and Toxoplasma gondii was mixed; some studies reported up to a doubling of schizophrenia risk. Prenatal HSV-1 or cytomegalovirus (CMV) infections were not associated with increased risk. Exposure to influenza or other infections during early pregnancy may be more harmful than later exposure. Increased proinflammatory cytokines during pregnancy were also associated with risk. Prenatal infection was associated with structural and functional brain abnormalities relevant to schizophrenia.

conclusionsPrenatal exposure to a range of infections and inflammatory responses may be associated with risk of adult schizophrenia. Larger samples, mediation and animal models should be used to investigate whether there is a 'sensitive period' during development, and the effects of prenatal infections on neurodevelopment. Inclusion of genetic and immunological information should help to elucidate to what extent genetic vulnerability to schizophrenia may be explained by vulnerability to infection.

Indexed as

Prenatal Exposure Delayed EffectsAdultAnimalsAutoimmunityBrainConfounding Factors, EpidemiologicCytokinesDatabases, BibliographicDisease Models, AnimalFemaleGenetic Predisposition to DiseaseHumansPregnancyPregnancy Complications, InfectiousPregnancy TrimestersRisk FactorsCytokines

Identifiers

PMID22717193
PMCPMC3479084
OpenAlexW2125343575

What OpenQuestion holds

Textmetadata
LicenceTDM
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.