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
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  • 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

Publications in this journal

  • Matthijs Vink · Max de Leeuw · Jurjen J Luykx · Kristel R van Eijk · Hanna E van den Munkhof · Mariët van Buuren · René S Kahn ·
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    ABSTRACT: A recent Genome-Wide Association Study showed that the rs2514218 single nucleotide polymorphism (SNP) in close proximity to dopamine receptor D2 is strongly associated with schizophrenia. Further, an in silico experiment showed that rs2514218 has a cis expression quantitative trait locus effect in the basal ganglia. To date, however, the functional consequence of this SNP is unknown. Here, we used functional Magnetic resonance imaging to investigate the impact of this risk allele on striatal activation during proactive and reactive response inhibition in 45 unaffected siblings of schizophrenia patients. We included siblings to circumvent the illness specific confounds affecting striatal functioning independent from gene effects. Behavioral analyses revealed no differences between the carriers (n = 21) and noncarriers (n = 24). Risk allele carriers showed a diminished striatal response to increasing proactive inhibitory control demands, whereas overall level of striatal activation in carriers was elevated compared to noncarriers. Finally, risk allele carriers showed a blunted striatal response during successful reactive inhibition compared to the noncarriers. These data are consistent with earlier reports showing similar deficits in schizophrenia patients, and point to a failure to flexibly engage the striatum in response to contextual cues. This is the first study to demonstrate an association between impaired striatal functioning and the rs2514218 polymorphism. We take our findings to indicate that striatal functioning is impaired in carriers of the DRD2 risk allele, likely due to dopamine dysregulation at the DRD2 location.
    Schizophrenia Bulletin 11/2015; DOI:10.1093/schbul/sbv166
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    ABSTRACT: Background: Physical exercise may be valuable for patients with schizophrenia spectrum disorders as it may have beneficial effect on clinical symptoms, quality of life and cognition. Methods: A systematic search was performed using PubMed (Medline), Embase, PsychInfo, and Cochrane Database of Systematic Reviews. Controlled and uncontrolled studies investigating the effect of any type of physical exercise interventions in schizophrenia spectrum disorders were included. Outcome measures were clinical symptoms, quality of life, global functioning, depression or cognition. Meta-analyses were performed using Comprehensive Meta-Analysis software. A random effects model was used to compute overall weighted effect sizes in Hedges' g. Results: Twenty-nine studies were included, examining 1109 patients. Exercise was superior to control conditions in improving total symptom severity (k = 14, n = 719: Hedges' g = .39, P < .001), positive (k = 15, n = 715: Hedges' g = .32, P < .01), negative (k = 18, n = 854: Hedges' g = .49, P < .001), and general (k = 10, n = 475: Hedges' g = .27, P < .05) symptoms, quality of life (k = 11, n = 770: Hedges' g = .55, P < .001), global functioning (k = 5, n = 342: Hedges' g = .32, P < .01), and depressive symptoms (k = 7, n = 337: Hedges' g = .71, P < .001). Yoga, specifically, improved the cognitive subdomain long-term memory (k = 2, n = 184: Hedges' g = .32, P < .05), while exercise in general or in any other form had no effect on cognition. Conclusion: Physical exercise is a robust add-on treatment for improving clinical symptoms, quality of life, global functioning, and depressive symptoms in patients with schizophrenia. The effect on cognition is not demonstrated, but may be present for yoga.
    Schizophrenia Bulletin 11/2015; DOI:10.1093/schbul/sbv164

  • Schizophrenia Bulletin 11/2015; DOI:10.1093/schbul/sbv156
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    ABSTRACT: Background: Face perception impairment in schizophrenia has long been recognized. However, brain mechanisms underlying this socially important perceptual deficit are not well understood. Previous magnetic resonance imaging (MRI) studies have shown that patients have altered structure in brain regions responsible for processing face information, but functional properties of these brain regions are not clearly determined. A key functional property of the face-processing system-face selectivity-has yet to be evaluated in schizophrenia. Methods: We used functional MRI (fMRI) to examine face selectivity of 3 core face-processing regions-fusiform face area (FFA), occipital face area (OFA), and superior temporal sulcus (STS)-in schizophrenia patients (n = 24) and healthy controls (n = 23). To disassociate face-specific processing from general perceptual processing, we compared cortical activations during performance of perceptually equated face and tree detection tasks. Results: Activation levels of the 3 putative face-processing regions during face detection did not differ between patients and controls, being similar for FFA and OFA and absent for STS. However, face selectivity, indexed by the difference in cortical activation between face and tree detection, was significantly reduced in patients for FFA, especially for low-contrast stimuli. FFA activation and perceptual performance during face detection were associated in patients. Conclusions: These results show a lack of face-specific processing in the schizophrenic brain region presumably subserving face perception. This finding suggests boosting visual salience of face images as a potential therapeutic venue for improving face perception in this psychiatric disorder.
    Schizophrenia Bulletin 10/2015; DOI:10.1093/schbul/sbv140
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    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: People with schizophrenia typically experience auditory hallucinations or delusions during acute episodes. Although effective drug treatments are available, many have intractable symptoms that do not recover between acute episodes. One proposed alternative to drug treatments is transcranial magnetic stimulation (TMS). To date, many research trials to assess effectiveness of TMS for people with symptoms of schizophrenia have been conducted worldwide. However, there is a lack of consensus on whether TMS should be recommended to be adopted in routine clinical practice. We conducted a systematic review of the literature for all relevant randomized controlled trials (RCTs) comparing TMS with sham or standard treatment. Forty-one trials (1473 participants) survived eligibility criteria and had extractable data. We found significant differences in favor of temporoparietal TMS compared with sham TMS for global state (7 RCTs, n = 224, MD: -0.5, 95% CI: -0.76 to -0.23) and for positive symptoms measured on the Positive and Negative Syndrome Scale (5 RCTs, n = 127, MD: -6.09, 95% CI: -10.95 to -1.22). However, we also found that the quality of trial reporting was frequently suboptimal and the risks of bias were strong or unascertainable for many trial aspects; this led to many results being graded as very low-quality evidence. On that basis, we were unable to definitively support or refute the routine use of TMS in clinical practice. Future definitive trials of TMS with rigorous processes and high-quality reporting are needed.
    Schizophrenia Bulletin 09/2015; 41(6):1220-1222. DOI:10.1093/schbul/sbv121