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: 8.61

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
Year

Additional details

5-year impact 8.86
Cited half-life 6.20
Immediacy index 1.66
Eigenfactor 0.03
Article influence 2.97
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

  • Mirella Ruggeri, Chiara Bonetto, Antonio Lasalvia, Angelo Fioritti, Giovanni de Girolamo, Paolo Santonastaso, Francesca Pileggi, Giovanni Neri, Daniela Ghigi, Franco Giubilini, [...], Katia De Santi, Sarah Bissoli, Sara Poli, Elisa Ira, Silvia Zoppei, Paola Rucci, Laura Bislenghi, Giovanni Patelli, Doriana Cristofalo, Anna Meneghelli
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    ABSTRACT: Integrated multi-element psychosocial interventions have been suggested to improve the outcomes of first-episode psychosis (FEP) patients, but they have been studied primarily in experimental settings and in nonepidemiologically representative samples. Thus, we performed a cluster-randomized controlled trial, comparing an integrated multi-element psychosocial intervention, comprising cognitive behavioral therapy, family intervention, and case management, with treatment as usual (TAU) for FEP patients in 117 community mental health centers (CMHCs) in a large area of northern Italy (10 million inhabitants). The randomized units (clusters) were the CMHCs, and the units of observation the patients (and, when available, their family members). The primary hypotheses were that add-on multicomponent intervention: (1) results in greater improvements in symptoms, as assessed with positive and negative syndrome scale and (2) reduces in-hospital stay, based on days of hospitalization over the 9-month follow-up. Four hundred and forty-four FEP patients received the intervention or TAU and were assessed at baseline and 9 months. Based on the retention rates of patients (and families) in the experimental arm, multi-element psychosocial interventions can be implemented in routine mental health services. Regarding primary outcomes, patients in the experimental arm showed greater reductions in overall symptom severity, while no difference could be found for days of hospitalization. Among the secondary outcomes, greater improvements were detected in the experimental arm for global functioning, emotional well-being, and subjective burden of delusions. No difference could be found for service disengagement and subjective burden of auditory hallucinations. These findings support feasibility and effectiveness of early interventions for psychosis in generalist mental health services. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv058
  • Steve Colori
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv066
  • Davide Rivolta, Tonio Heidegger, Bertram Scheller, Andreas Sauer, Michael Schaum, Katharina Birkner, Wolf Singer, Michael Wibral, Peter J Uhlhaas
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    ABSTRACT: Hypofunctioning of the N-methyl-D-aspartate receptor (NMDA-R) has been prominently implicated in the pathophysiology of schizophrenia (ScZ). The current study tested the effects of ketamine, a dissociative anesthetic and NMDA-R antagonist, on resting-state activity recorded with magnetoencephalography (MEG) in healthy volunteers. In a single-blind cross-over design, each participant (n = 12) received, on 2 different sessions, a subanesthetic dose of S-ketamine (0.006mg/Kg) and saline injection. MEG-data were analyzed at sensor- and source-level in the beta (13-30 Hz) and gamma (30-90 Hz) frequency ranges. In addition, connectivity analysis at source-level was performed using transfer entropy (TE). Ketamine increased gamma-power while beta-band activity was decreased. Specifically, elevated 30-90 Hz activity was pronounced in subcortical (thalamus and hippocampus) and cortical (frontal and temporal cortex) regions, whilst reductions in beta-band power were localized to the precuneus, cerebellum, anterior cingulate, temporal and visual cortex. TE analysis demonstrated increased information transfer in a thalamo-cortical network after ketamine administration. The findings are consistent with the pronounced dysregulation of high-frequency oscillations following the inhibition of NMDA-R in animal models of ScZ as well as with evidence from electroencephalogram-data in ScZ-patients and increased functional connectivity during early illness stages. Moreover, our data highlight the potential contribution of thalamo-cortical connectivity patterns towards ketamine-induced neuronal dysregulation, which may be relevant for the understanding of ScZ as a disorder of disinhibition of neural circuits. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv051
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    ABSTRACT: The "Kraepelinian dichotomy" between schizophrenia (SZ) and bipolar disorder (BD) has been a dominant force in our thinking on the classification of these mental disorders. Emerging evidence indicates that these 2 disorders overlap significantly with regard to epidemiology, clinical presentation, genetic susceptibility, structural neuroanatomy, and treatment. Prenatal infection and immunologic dysfunction appear to be risk factors for both SZ and BD; some of these gestational exposures are present in both disorders while others may be specific to 1 or the other of the 2 syndromes. In this paper, we shall review prior studies of prenatal infections and immunologic insults in schizophrenia and BD, including exposures which overlap and which differ between these disorders, discuss the potential utility of maternal infection as one strategy toward developing a more biologically meaningful diagnostic classification system, and propose new recommendations for future research aimed at dissecting these 2 disorders from one another at the etiologic level. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv063
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    ABSTRACT: The default-mode network (DMN) is vital in the neurobiology of schizophrenia, and the cerebellum participates in the high-order cognitive network such as the DMN. However, the specific contribution of the cerebellum to the DMN abnormalities remains unclear in unaffected siblings of schizophrenia patients. Forty-six unaffected siblings of schizophrenia patients and 46 healthy controls were recruited for a resting-state scan. The images were analyzed using the functional connectivity (FC) method. The siblings showed significantly increased FCs between the left Crus I and the left superior medial prefrontal cortex (MPFC), as well as between the lobule IX and the bilateral MPFC (orbital part) and right superior MPFC compared with the controls. No significantly decreased FC was observed in the siblings relative to the controls. The analyses were replicated in 49 first-episode, drug-naive patients with schizophrenia, and the results showed that the siblings and the patients shared increased FCs between the left Crus I and the left superior MPFC, as well as between the lobule IX and the left MPFC (orbital part) compared with the controls. These findings suggest that increased cerebellar-DMN connectivities emerge earlier than illness onset, which highlight the contribution of the cerebellum to the DMN alterations in unaffected siblings. The shared increased cerebellar-DMN connectivities between the patients and the siblings may be used as candidate endophenotypes for schizophrenia. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv062
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    ABSTRACT: Endophenotypes are disease-associated phenotypes that are thought to reflect the neurobiological or other mechanisms that underlie the more overt symptoms of a psychiatric illness. Endophenotypes have been critical in understanding the genetics, neurobiology, and treatment of schizophrenia. Because psychiatric illnesses have multiple causes, including both genetic and nongenetic risk factors, an endophenotype linked to one of the mechanisms may be expressed more frequently than the disease itself. However, in schizophrenia research, endophenotypes have almost exclusively been studied in older adolescents or adults who have entered or passed through the age of risk for the disorder. Yet, schizophrenia is a neurodevelopmental disorder where prenatal development starts a cascade of brain changes across the lifespan. Endophenotypes have only minimally been utilized to explore the perinatal development of vulnerability. One major impediment to the development of perinatally-useful endophenotypes has been the established validity criteria. For example, the criterion that the endophenotype be more frequently present in those with disease than those without is difficult to demonstrate when there can be a decades-long period between endophenotype measurement and the age of greatest risk for onset of the disorder. This article proposes changes to the endophenotype validity criteria appropriate to perinatal research and reviews how application of these modified criteria helped identify a perinatally-usable phenotype of risk for schizophrenia, P50 sensory gating, which was then used to propose a novel perinatal primary prevention intervention. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv054
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    ABSTRACT: Measurement of social cognition in treatment trials remains problematic due to poor and limited psychometric data for many tasks. As part of the Social Cognition Psychometric Evaluation (SCOPE) study, the psychometric properties of 8 tasks were assessed. One hundred and seventy-nine stable outpatients with schizophrenia and 104 healthy controls completed the battery at baseline and a 2-4-week retest period at 2 sites. Tasks included the Ambiguous Intentions Hostility Questionnaire (AIHQ), Bell Lysaker Emotion Recognition Task (BLERT), Penn Emotion Recognition Task (ER-40), Relationships Across Domains (RAD), Reading the Mind in the Eyes Task (Eyes), The Awareness of Social Inferences Test (TASIT), Hinting Task, and Trustworthiness Task. Tasks were evaluated on: (i) test-retest reliability, (ii) utility as a repeated measure, (iii) relationship to functional outcome, (iv) practicality and tolerability, (v) sensitivity to group differences, and (vi) internal consistency. The BLERT and Hinting task showed the strongest psychometric properties across all evaluation criteria and are recommended for use in clinical trials. The ER-40, Eyes Task, and TASIT showed somewhat weaker psychometric properties and require further study. The AIHQ, RAD, and Trustworthiness Task showed poorer psychometric properties that suggest caution for their use in clinical trials. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv056
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    ABSTRACT: Schizophrenia is a severe mental disorder associated with derogated function across various domains, including perception, language, motor, emotional, and social behavior. Due to its complex symptomatology, schizophrenia is often regarded a disorder of cognitive processes. Yet due to the frequent involvement of sensory and perceptual symptoms, it has been hypothesized that functional disintegration between sensory and cognitive processes mediates the heterogeneous and comprehensive schizophrenia symptomatology. Here, using resting-state functional magnetic resonance imaging in 71 patients and 196 healthy controls, we characterized the standard deviation in BOLD (blood-oxygen-level-dependent) signal amplitude and the functional connectivity across a range of functional brain networks. We investigated connectivity on the edge and node level using network modeling based on independent component analysis and utilized the brain network features in cross-validated classification procedures. Both amplitude and connectivity were significantly altered in patients, largely involving sensory networks. Reduced standard deviation in amplitude was observed in a range of visual, sensorimotor, and auditory nodes in patients. The strongest differences in connectivity implicated within-sensorimotor and sensorimotor-thalamic connections. Furthermore, sensory nodes displayed widespread alterations in the connectivity with higher-order nodes. We demonstrated robustness of effects across subjects by significantly classifying diagnostic group on the individual level based on cross-validated multivariate connectivity features. Taken together, the findings support the hypothesis of disintegrated sensory and cognitive processes in schizophrenia, and the foci of effects emphasize that targeting the sensory and perceptual domains may be key to enhance our understanding of schizophrenia pathophysiology. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 05/2015; DOI:10.1093/schbul/sbv060
  • Schizophrenia Bulletin 05/2015; 41(3):535-541. DOI:10.1093/schbul/sbv029
  • Schizophrenia Bulletin 05/2015; 41(3):546-548. DOI:10.1093/schbul/sbv026
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    ABSTRACT: A number of influences have converged that make this Special Theme Issue timely: "A New Direction: Considering Developmentally Sensitive Targets for Very Early Intervention in Schizophrenia". These factors include: 1. the substantial knowledge about premorbid developmental vulnerabilities to psychosis, especially regarding schizophrenia; 2. the promising results emerging from interventions during the clinical high-risk (CHR) phase of psychosis and; 3. the recognition that the CHR period is a relatively late phase of developmental derailment. These factors have together led to a perspective that even earlier intervention is warranted. This paper briefly summarizes the articles comprising the Special Theme including new data on early neurocognitive development, proposed potential targets for psychosocial and psychopharmacological interventions during the premorbid period as early as pregnancy, and ethical challenges. These thought experiments must be empirically tested, and the ethical challenges overcome as posed by the various interventions, which range from relatively low risk, supportive, psychosocial to higher risk, experimental, pharmacological interventions. All of the interventions proposed require careful study of ethics, safety, potential stigma, feasibility, efficacy and tolerability, and the meaning to the people involved. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv050
  • Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv049
  • Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv053
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    ABSTRACT: Individuals who develop schizophrenia in adulthood exhibit, on average, deficits in childhood cognition relative to healthy controls. However, it remains unclear when in childhood such deficits emerge and whether they are stable across childhood or change (increase or decrease) across development. Importantly, whether the trajectory of childhood cognition differs among youth who later develop affective psychoses (AP) vs schizophrenia as adults remains unresolved. Subjects in the Collaborative Perinatal Project were administered the Stanford-Binet IQ test at age 4 and the Wechsler Intelligence Scale for Children at age 7. A total of 9809 (54.7%) participants in the New England Study sites were tested at both ages, including 37 who later developed schizophrenia spectrum psychoses (SSP) and 39 who later developed AP. Logistic regression models examined the association of level of and change in childhood IQ and later SSP or AP. Lower overall childhood IQ was associated with higher risk of SSP. Additionally, there was a small mean increase in IQ in the SSP group relative to a mean decrease in the control group from age 4 to 7 such that positive change in IQ was significantly associated with a higher risk of SSP. Neither overall level nor change in IQ was associated with risk of AP. The results are consistent with neurocognitive impairment throughout early childhood specifically for children who later develop schizophrenia, affirming the theory of atypical neurodevelopment in premorbid schizophrenia. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv027
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    ABSTRACT: Neuropsychological impairment is heterogeneous in psychosis. The association of intracranial volume (ICV) and total brain volume (TBV) with cognition suggests brain structure abnormalities in psychosis will covary with the severity of cognitive impairment. We tested the following hypotheses: (1) brain structure abnormalities will be more extensive in neuropsychologically impaired psychosis patients; (2) psychosis patients with premorbid cognitive limitations will show evidence of hypoplasia (ie, smaller ICV); and (3) psychosis patients with evidence of cognitive decline will demonstrate atrophy (ie, smaller TBV, but normal ICV). One hundred thirty-one individuals with psychosis and 97 healthy subjects underwent structural magnetic resonance imaging and neuropsychological testing. Patients were divided into neuropsychologically normal and impaired groups. Impaired patients were further subdivided into deteriorated and compromised groups if estimated premorbid intellect was average or below average, respectively. ICV and TBV were compared across groups. Localized brain volumes were qualitatively examined using voxel-based morphometry. Compared to healthy subjects, neuropsychologically impaired patients exhibited smaller TBV, reduced grey matter volume in frontal, temporal, and subcortical brain regions, and widespread white matter volume loss. Neuropsychologically compromised patients had smaller ICV relative to healthy subjects, and neuropsychologically normal and deteriorated patient groups, but relatively normal TBV. Deteriorated patients exhibited smaller TBV compared to healthy subjects, but relatively normal ICV. Unexpectedly, TBV, adjusted for ICV, was reduced in neuropsychologically normal patients. Patients with long-standing cognitive limitations exhibit evidence of early cerebral hypoplasia, whereas neuropsychologically normal and deteriorated patients show evidence of brain tissue loss consistent with progression or later cerebral dysmaturation. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv048
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    ABSTRACT: A number of recent articles, many appearing in Schizophrenia Bulletin, signal a renewed interest in phenomenological approaches to our understanding of schizophrenia. These approaches conceptualize schizophrenia as a disorder of altered self-awareness and decreased prereflective social attunement, which may manifest as an impaired understanding of self, others, and the physical world. Phenomenological approaches to psychopathology are sometimes construed as being incompatible with the reductionistic methodology of contemporary neuroscience. In this article, we re-examine findings from the phenomenological investigation of schizophrenia in light of an influential neurocomputational account of mindreading, which postulates that understanding of others is subserved by coherent internal self-models. We argue that the phenomenological approach to schizophrenia is not incompatible with a neurocomputational account of mindreading, and that the 2 approaches should instead be viewed as existing in a relationship of mutual constraint and enlightenment. Our hypothesis, while speculative, is an attempt to marry the phenomenological and neuronal realities of schizophrenia. Furthermore, it has implications for psychotherapeutic interventions and future research. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Schizophrenia Bulletin 04/2015; DOI:10.1093/schbul/sbv035