Schizophrenia Bulletin (SCHIZOPHRENIA BULL)

Publisher: United States. Alcohol, Drug Abuse, and Mental Health Administration; Center for Studies of Schizophrenia (U.S.); National Clearinghouse for Mental Health Information (U.S.); National Institute of Mental Health (U.S.); National Institute of Mental Health (U.S.). Office of Communications and Public Liaison, Oxford University Press (OUP)

Journal description

Covers current developments relating to all aspects of schizophrenia research.

Current impact factor: 8.45

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 8.45
2013 Impact Factor 8.607
2012 Impact Factor 8.486
2011 Impact Factor 8.8
2010 Impact Factor 8.273
2009 Impact Factor 7.467
2008 Impact Factor 6.592
2007 Impact Factor 5.843
2006 Impact Factor 4.352
2005 Impact Factor 2.871
2004 Impact Factor 2.592
2003 Impact Factor 2.643
2002 Impact Factor 3.207
2001 Impact Factor 4.04
2000 Impact Factor 6.085
1999 Impact Factor 6.579
1998 Impact Factor 4.455
1997 Impact Factor 3.509

Impact factor over time

Impact factor

Additional details

5-year impact 8.69
Cited half-life 6.70
Immediacy index 1.86
Eigenfactor 0.03
Article influence 2.68
Website Schizophrenia Bulletin website
Other titles Schizophrenia bulletin
ISSN 1745-1701
OCLC 1345919
Material type Government publication, National government publication, Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Oxford University Press (OUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Pre-print can only be posted prior to acceptance
    • Pre-print must be accompanied by set statement (see link)
    • Pre-print must not be replaced with post-print, instead a link to published version with amended set statement should be made
    • Pre-print on author's personal website, employer website, free public server or pre-prints in subject area
    • Post-print in Institutional repositories or Central repositories
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • The publisher will deposit in PubMed Central on behalf of NIH authors
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive impairments are one of the main contributors to disability and poor long-term outcome in schizophrenia. Proof-of-concept trials indicate that repetitive transcranial magnetic stimulation (rTMS) applied to the left dorsolateral prefrontal cortex (DLPFC) has the potential to improve cognitive functioning. We analyzed the effects of 10-Hz rTMS to the left DLPFC on cognitive deficits in schizophrenia in a large-scale and multicenter, sham-controlled study. A total of 156 schizophrenia patients with predominant negative symptoms were randomly assigned to a 3-week intervention (10-Hz rTMS, 15 sessions, 1000 stimuli per session) with either active or sham rTMS. The Rey Auditory Verbal Learning Test, Trail Making Test A and B, Wisconsin Card Sorting Test, Digit Span Test, and the Regensburg Word Fluency Test were administered before intervention and at day 21, 45, and 105 follow-up. From the test results, a neuropsychological composite score was computed. Both groups showed no differences in any of the outcome variables before and after intervention. Both groups improved markedly over time, but effect sizes indicate a numeric, but nonsignificant superiority of active rTMS in certain cognitive tests. Active 10-Hz rTMS applied to the left DLPFC for 3 weeks was not superior to sham rTMS in the improvement of various cognitive domains in schizophrenia patients with predominant negative symptoms. This is in contrast to previous preliminary proof-of-concept trials, but highlights the need for more multicenter randomized controlled trials in the field of noninvasive brain stimulation.
    Schizophrenia Bulletin 10/2015; DOI:10.1093/schbul/sbv142
  • Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv138
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    ABSTRACT: The idea that psychiatric diagnoses are not mere descriptors of a symptomatology but create incrementally negative effects in patients has received considerable support in the literature. The flipside to this effect, that calling someone by a psychiatric diagnosis also has an effect on how this person is perceived by others, however, has been less well documented and remains disputed. An experimental study was conducted with a large sample (N = 2265) to ensure statistical power to detect even small effects of such adding a psychiatric diagnosis to a description of symptoms or not. Dependent variables were chosen in an exploratory manner and tests were corrected for alpha inflation. Results show that calling the identical symptomatology schizophrenia (vs not labeling it) led to greater perceptions of aggressiveness, less trustworthiness, more anxiety toward this person, and stronger assumptions this person feels aggression-related emotions. Although stigmatizing attitudes were generally lower for persons with personal experiences with mental illnesses as either a patient or a close relative, such personal involvement did not moderate the effect. Implications of these findings and limitations of the study are discussed.
    Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv137
  • Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv126
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    ABSTRACT: Chronic neurologic infection with Toxoplasma gondii is relatively common in humans and is one of the strongest known risk factors for schizophrenia. Nevertheless, the exact neuropathological mechanisms linking T gondii infection and schizophrenia remain unclear. Here we utilize a mouse model of chronic T gondii infection to identify protein biomarkers that are altered in serum and brain samples at 2 time points during chronic infection. Furthermore, we compare the identified biomarkers to those differing between "postmortem" brain samples from 35 schizophrenia patients and 33 healthy controls. Our findings suggest that T gondii infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients. The overlapping changes include increases in C-reactive protein (CRP), interleukin-1 beta (IL-1β), interferon gamma (IFNγ), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1). Potential roles of these factors in the pathogenesis of schizophrenia and toxoplasmosis are discussed. Identifying a defined set of markers shared within the pathophysiological landscape of these diseases could be a key step towards understanding their specific contributions to pathogenesis.
    Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv134
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    ABSTRACT: Self-disorders (SDs) (from the German Ichstörungen) are alterations of the first-person perspective, long associated with schizophrenia, particularly in early phases. Although psychopathological features of SDs continue to be studied, their neurobiological underpinnings are unknown. This makes it difficult to integrate SDs into contemporary models of psychosis. The present review aims to address this issue, starting from an historical excursus revealing an interconnection between neuroscientific models and the origin of the psychopathological concept of SDs. Subsequently, the more recent neurobiological models related to SDs are discussed, particularly with respect to the onset of schizophrenia.
    Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv123
  • Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv127
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    ABSTRACT: Research findings are particularly important for medication choice for first-episode patients as individual prior medication response to guide treatment decisions is unavailable. We describe the first large-scale double-masked randomized comparison with first-episode patients of aripiprazole and risperidone, 2 commonly used first-episode treatment agents. One hundred ninety-eight participants aged 15-40 years with schizophrenia, schizophreniform disorder, schizoaffective disorder or psychotic disorder Not Otherwise Specified, and who had been treated in their lifetime with antipsychotics for 2 weeks or less were randomly assigned to double-masked aripiprazole (5-30mg/d) or risperidone (1-6mg/d) and followed for 12 weeks. Positive symptom response rates did not differ (62.8% vs 56.8%) nor did time to response. Aripiprazole-treated participants had better negative symptom outcomes but experienced more akathisia. Body mass index change did not differ between treatments but advantages were found for aripiprazole treatment for total and low-density lipoprotein cholesterol, fasting glucose, and prolactin levels. Post hoc analyses suggested advantages for aripiprazole on depressed mood. Overall, if the potential for akathisia is a concern, low-dose risperidone as used in this trial maybe a preferred choice over aripiprazole. Otherwise, aripiprazole would be the preferred choice over risperidone in most situations based upon metabolic outcome advantages and some symptom advantages within the context of similar positive symptom response between medications. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email:
    Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv125
  • [Show abstract] [Hide abstract]
    ABSTRACT: The Mental Health Centers for Intervention Development and Applied Research (CIDAR) program prioritized research to provide an evidence base for biomarker development. At the Zucker Hillside Hospital (ZHH), our CIDAR grant supported research on a comprehensive investigation of treatment response and outcome in first episode schizophrenia. Results provide evidence that baseline neuroimaging, neurocognitive, and genetic measures are significantly associated with clinical response to treatment, and that our currently available interventions can effectively treat aspects of psychotic illness, as well as potentially reduce comorbidity associated with illness. Future research may include combining modalities to more robustly predict response and identify treatment targets, as well as to further develop more effective intervention strategies for these devastating and disabling disorders. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center.
    Schizophrenia Bulletin 09/2015; DOI:10.1093/schbul/sbv117
  • Schizophrenia Bulletin 09/2015; 41(5). DOI:10.1093/schbul/sbv081
  • [Show abstract] [Hide abstract]
    ABSTRACT: It is not well established whether the incident outcomes of the clinical high-risk (CHR) syndrome for psychosis are diagnostically specific for psychosis or whether CHR patients also are at elevated risk for a variety of nonpsychotic disorders. We collected 2 samples (NAPLS-1, PREDICT) that contained CHR patients and a control group who responded to CHR recruitment efforts but did not meet CHR criteria on interview (help-seeking comparison patients [HSC]). Incident diagnostic outcomes were defined as the occurrence of a SIPS-defined psychosis or a structured interview diagnosis from 1 of 3 nonpsychotic Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) groups (anxiety, bipolar, or nonbipolar mood disorder), when no diagnosis in that group was present at baseline. Logistic regression revealed that the CHR vs HSC effect did not vary significantly across study for any emergent diagnostic outcome; data from the 2 studies were therefore combined. CHR (n = 271) vs HSC (n = 171) emergent outcomes were: psychosis 19.6% vs 1.8%, bipolar disorders 1.1% vs 1.2%, nonbipolar mood disorders 4.4% vs 5.3%, and anxiety disorders 5.2% vs 5.3%. The main effect of CHR vs HSC was statistically significant (OR = 13.8, 95% CI 4.2-45.0, df = 1, P < .001) for emergent psychosis but not for any emergent nonpsychotic disorder. Sensitivity analyses confirmed these findings. Within the CHR group emergent psychosis was significantly more likely than each nonpsychotic DSM-IV emergent disorder, and within the HSC group emergent psychosis was significantly less likely than most emergent nonpsychotic disorders. The CHR syndrome is specific as a marker for research on predictors and mechanisms of developing psychosis. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email:
    Schizophrenia Bulletin 09/2015; 41(5). DOI:10.1093/schbul/sbv091
  • [Show abstract] [Hide abstract]
    ABSTRACT: Findings from the Psychiatric Genomics Consortium genome-wide association study (GWAS) showed that variation at the DRD2 locus is associated with schizophrenia risk. However, the functional significance of rs2514218, the top DRD2 single nucleotide polymorphism in the GWAS, is unknown. Dopamine D2 receptor binding is a common mechanism of action for all antipsychotic drugs, and DRD2 variants were related to antipsychotic response in previous studies. The present study examined whether rs2514218 genotype could predict antipsychotic response, including efficacy and adverse events, in a cohort of patients with first episode of psychosis treated with either risperidone or aripiprazole for 12 weeks. Subjects were genotyped using the Illumina Infinium HumanOmniExpressExome array platform. After standard quality control, data from 100 subjects (49 randomly assigned to treatment with aripiprazole and 51 assigned to risperidone) was available for analysis. Subjects were assessed for psychotic symptomatology and medication-related adverse events weekly for 4 weeks, then biweekly for 8 weeks. Linear mixed model analysis revealed that the homozygotes for the risk (C) allele at rs2514218 had significantly greater reduction in positive symptoms during 12 weeks of treatment compared to the T allele carriers. In the aripiprazole group, C/C homozygotes also reported more akathisia than the T allele carriers, while in the risperidone group, male T allele carriers demonstrated greater prolactin elevations compared to male C/C homozygotes. These findings suggest that the schizophrenia risk variant at the DRD2 locus (or another variant in close proximity) is associated with observable differences in response to treatments which reduce striatal dopamine signaling. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email:
    Schizophrenia Bulletin 08/2015; DOI:10.1093/schbul/sbv116