Correlates of cognitive deficits in first episode schizophrenia

Heydebrand, Gitry; Weiser, M.; Rabinowitz, Jonathan; Hoff, Anne L.; DeLisi, Lynn E.; Csernansky, John G.

doi:10.1016/s0920-9964(03)00097-5

Cited by 168 publications

(81 citation statements)

References 59 publications

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“…Across the adult studies that show a significant relationship between negative symptoms and cognitive dysfunction, the correlations typically are small in magnitude and account for a minor portion of the variance (often 10% to 15%). 45,[52][53][54] Even when the significant correlations of the neurocognitive domains with the CGI and adaptive behaviors obtained in this study are considered, the magnitude of these correlations accounted for only 6% to 14% of the variance, similar to the range reported in adult studies.Finally, from an assessment perspective, our sample seemed to tolerate the measures used in this study. The next step is to determine whether this battery is sensitive to cognitive changes following pharmacological intervention.…”

supporting

confidence: 64%

Neurocognition in Early-Onset Schizophrenia and Schizoaffective Disorders

Hooper¹,

Giuliano²,

Youngstrom³

et al. 2010

Journal of the American Academy of Child & Adolescent Psych

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Objective-We examined the neuropsychological functioning of youth enrolled in the NIMH funded trial, Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS). We compared the baseline neuropsychological functioning of youth with schizophrenia (SZ, n = 79) to those with schizoaffective disorder (SA, n = 40), and examined the relationship of different variables of illness severity and adaptive behavior to neuropsychological functioning. ©2010 American Academy of Child and Adolescent PsychiatryCorrespondence to Dr. Stephen R. Hooper, Center for Development and Learning, CB# 7255, The Carolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7255; Stephen. hooper@cdl.unc.edu. The opinions and assertions contained in this report are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Health and Human Services, the National Institutes of Health, or the National Institute of Mental Health. Disclosure: Dr. Hooper receives or has received research support or served as a speaker/consultant for Eli Lilly and Sanofi-Aventis. Dr. Youngstrom has previously served on the Data Safety and Monitoring Board for Eli Lilly and consulted in the past with Otsuka. Dr. Sikich has a current financial interest and receives research funding or participates in clinical trials with Janssen, Pfizer, Bristol Myers-Squibb, Neuropharm, Curemark, and Seaside Pharmaceuticals. She also received software for a computer intervention in schizophrenia from Posit Science. In the past, Dr. Sikich received research funding from Eli Lilly, Janssen, Pfizer, Otsuka, and Astra Zeneca, and has served as a consultant for Sanofi Aventis and ABT Associates. Dr. Frazier receives or has received research support and acted as a consultant for Bristol-Myers Squibb Company, Eli Lilly, GlaxoSmithKline, Johnson & Johnson, Neuropharm, Otsuka America Pharmaceutical, and Pfizer. Dr. Findling receives or has received research support, acted as a consultant, and/or served on a speaker's bureau for Abbott, Addrenex, AstraZeneca, Biovail, Bristol-Myers Squibb, Forest, GlaxoSmithKline, Johnson & Johnson, KemPharm, Eli Lilly, Lundbeck, Neuropharm, Novartis, Organon, Otsuka, Pfizer, Sanofi-Aventis, Sepracore, Shire, Solvay, Supernus Pharmaceuticals, Validus, and Wyeth. Dr. McClellan has had past research support from Pfizer. Dr. Hamer has served as a consultant or advisor for Acadia, Cenerx, Corcept, Epix, Johnson & Johnson, NeuroPharmaBoost, Pepper-Hamil-ton, PureTechVentures, SanofiAventis, and Takeda. He has served on the advisory board for Enabled MD, Novartis, and Wyeth. He has served on a Data Safety Monitoring Board (DSMB) for Allergan, Eli Lilly & Company, Pfizer, Schwartz, and Solvey. He has served on a Mock Advisory Panel for Alpharma. He has served as a statistician on a University of North Carolina contract for a clinical trial with AstraZeneca. He has taught several seminars for SAS Institute. He has served as an expert...

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supporting

confidence: 64%

Neurocognition in Early-Onset Schizophrenia and Schizoaffective Disorders

Hooper¹,

Giuliano²,

Youngstrom³

et al. 2010

Journal of the American Academy of Child & Adolescent Psych

View full text Add to dashboard Cite

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“…These items included positive and negative formal thought disorder, "incoherent," "speech difficult to understand," and "information not credible." Consistent with this interpretation is the correlation of negative symptoms and cognitive dysfunction found both in patients with first-episode schizophrenia (35) and in patients with chronic schizophrenia (36). Furthermore, patients with high levels of negative symptoms perform worse on cognitive tasks subserved by the prefrontal cortex, such as spatial working memory (37).…”

Section: Relationship Between High-risk Haplotype and Clinical Featuresmentioning

confidence: 76%

Relationship Between a High-Risk Haplotype in the DTNBP1 (Dysbindin) Gene and Clinical Features of Schizophrenia

Fanous¹,

Oord²,

Riley³

et al. 2005

AJP

148

103

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Objective: The purpose of this study was to determine whether a haplotype in the dystrobrevin binding protein 1 (DTNBP1) gene previously associated with schizophrenia not only increases the susceptibility to psychotic illness but also to a more or less clinically specific form of psychotic illness. Method:In the Irish Study of High-Density Schizophrenia Families, subjects with psychotic illness (N=755) were given lifetime ratings of clinical features according to the Operational Criteria Checklist for Psychotic Illness. Exploratory and confirmatory factor analyses were used to extract five factors-hallucinations, delusions, negative, manic, and depressive symptoms-and to create factor-derived scores. The family-based transmission disequilibrium test operationalized in the program TRANSMIT was used to determine whether a high-risk haplotype in the DTNBP1 gene was overtransmitted to subjects in the upper 20th and 40th percentiles for each factor score. These results were compared to baseline overtransmission by examining the empirical distribution of chi-square statistics in groups of 5,000 replicates in which 20% and 40% of ill subjects were randomly selected. This analysis was done for both narrow and broad definitions of psychotic illness.Results: Subjects in the upper 40th percentile for the negative symptom factorin both the narrowly (p=0.004) and broadly (p=0.01) defined illness groupswere more likely to inherit the high-risk haplotype than would be expected by chance. No other significant relationships between clinical features and high-risk haplotype transmission were observed. Conclusions:The etiologically relevant variation in DTNBP1, which is in presumptive linkage disequilibrium with the highrisk haplotype, may predispose individuals to a form of psychotic illness associated with high levels of negative symptoms. This finding supports previous evidence suggesting that genetic factors influence the clinical heterogeneity of schizophrenia.

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“…A clinical high-risk status for psychosis (at risk mental state, ARMS) is associated with a set of neurofunctional abnormalities that are qualitatively similar to those observed in patients with the disorder [66]. As these findings are not attributable to chronic psychotic symptoms [67] and antipsychotic treatment, they may represent markers of increased vulnerability to psychotic disorders. Structural MRI studies of non-medicated patients in a prodromal phase of psychosis or ARMS demonstrated that neuroanatomical abnormalities are already evident in the very early phase of psychosis.…”

Section: Effects Of Antipsychotic Medication On Structural Neuroimagimentioning

confidence: 97%

The Effects of Antipsychotics on the Brain: What Have We Learnt from Structural Imaging of Schizophrenia? – A Systematic Review

Smieskova

Fusar‐Poli²,

Allen³

et al. 2009

CPD

186

131

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Abstract:Despite a large number of neuroimaging studies in schizophrenia reporting subtle brain abnormalities, we do not know to what extent such abnormalities reflect the effects of antipsychotic treatment on brain structure. We therefore systematically reviewed cross-sectional and follow-up structural brain imaging studies of patients with schizophrenia treated with antipsychotics. 30 magnetic resonance imaging (MRI) studies were identified, 24 of them being longitudinal and six cross-sectional structural imaging studies. In patients with schizophrenia treated with antipsychotics, reduced gray matter volume was described, particularly in the frontal and temporal lobes. Structural neuroimaging studies indicate that treatment with typical as well as atypical antipsychotics may affect regional gray matter (GM) volume. In particular, typical antipsychotics led to increased gray matter volume of the basal ganglia, while atypical antipsychotics reversed this effect after switching. Atypical antipsychotics, however, seem to have no effect on basal ganglia structure.

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Correlates of cognitive deficits in first episode schizophrenia

Cited by 168 publications

References 59 publications

Neurocognition in Early-Onset Schizophrenia and Schizoaffective Disorders

Neurocognition in Early-Onset Schizophrenia and Schizoaffective Disorders

Relationship Between a High-Risk Haplotype in the DTNBP1 (Dysbindin) Gene and Clinical Features of Schizophrenia

The Effects of Antipsychotics on the Brain: What Have We Learnt from Structural Imaging of Schizophrenia? – A Systematic Review

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