Identification of separable cognitive factors in schizophrenia

Nuechterlein, Keith H.; Deanna, M; Gold, James M.; Goldberg, Terry E.; Green, Michael F.; Heaton, Robert K.

doi:10.1016/j.schres.2004.09.007

Cited by 1,110 publications

(800 citation statements)

References 48 publications

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“…CFA suggested that a singlefactor model of five domain scores, designed to estimate the domain scores following the model forwarded by the MATRICS Neurocognition Committee (Green et al, 2004b) based on a review of factor analytic studies (Nuechterlein et al, 2004), provided the best fit. A five-factor model also fit the data.…”

Section: Discussionmentioning

confidence: 99%

“…Composite scores were calculated in two different ways: a domain-based approach and an empirical approach using PCA. The domain-based composite score was the standardized average of the five domain summary scores, following the MATRICS 7-factor model (Nuechterlein et al, 2004) with the exception of visual memory, for which there was no assessment, and social cognition, for which the data were unacceptably skewed. The PCA composite score was created by applying the weights generated from the PCA to the standardized variables and then standardizing the mean.…”

Section: Social Cognitionmentioning

confidence: 99%

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Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

Keefe

Bilder²,

Harvey

et al. 2006

Neuropsychopharmacol

412

293

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Neurocognition is moderately to severely impaired in patients with schizophrenia. However, the factor structure of the various neurocognitive deficits, the relationship with symptoms and other variables, and the minimum amount of testing required to determine an adequate composite score has not been determined in typical patients with schizophrenia. An 'all-comer' approach to cognition is needed, as provided by the baseline assessment of an unprecedented number of patients in the CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness) schizophrenia trial. From academic sites and treatment providers representative of the community, 1493 patients with chronic schizophrenia were entered into the study, including those with medical comorbidity and substance abuse. Eleven neurocognitive tests were administered, resulting in 24 individual scores reduced to nine neurocognitive outcome measures, five domain scores and a composite score. Despite minimal screening procedures, 91.2% of patients provided meaningful neurocognitive data. Exploratory principal components analysis yielded one factor accounting for 45% of the test variance. Confirmatory factor analysis showed that a single-factor model comprised of five domain scores was the best fit. The correlations among the factors were medium to high, and scores on individual factors were very highly correlated with the single composite score. Neurocognitive deficits were modestly correlated with negative symptom severity (r ¼ 0.13-0.27), but correlations with positive symptom severity were near zero (ro0.08). Even in an 'all-comer' clinical trial, neurocognitive deficits can be assessed in the overwhelming majority of patients, and the severity of impairment is similar to meta-analytic estimates. Multiple analyses suggested that a broad cognitive deficit characterizes this sample. These deficits are modestly related to negative symptoms and essentially independent of positive symptom severity.

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Section: Discussionmentioning

confidence: 99%

Section: Social Cognitionmentioning

confidence: 99%

Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

Keefe

Bilder²,

Harvey

et al. 2006

Neuropsychopharmacol

412

293

View full text Add to dashboard Cite

show abstract

“…First, the Neurocognition Committee identified the primary domains of cognitive deficits that characterize patients with schizophrenia: working memory; attention/vigilance; verbal learning and memory; visual learning and memory; speed of processing; reasoning and problemsolving; and social cognition (Nuechterlein et al, 2004). Second, the Neuropharmacology Committee identified the most promising molecular targets, existing compounds, human test measures, and potentially useful animal models for use in the discovery of treatments that target basic mechanisms related to complex cognitive operations (Geyer and Tamminga, 2004).…”

Section: The Matrics Consensus Processmentioning

confidence: 99%

The family of sensorimotor gating disorders: Comorbidities or diagnostic overlaps?

2006

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Prepulse inhibition (PPI) of startle is an operational measure of the pre-attentive filtering process known as sensorimotor gating. Originally identified in patients with schizophrenia, PPI deficits have been observed in multiple but not all psychiatric disorders. Thus, as with most signs and symptoms of psychiatric disorders, deficits in PPI cut across diagnostic categories. It remains unclear whether the diversity of disorders exhibiting deficient PPI bespeaks diagnostic overlaps or comorbidities. Given the recent focus on treatments for cognitive deficits of schizophrenia independently of treating psychosis, the relationship of PPI deficits to cognitive deficits becomes of interest. Although PPI cannot be considered to be a cognitive process per se, abnormalities in pre-attentive information processing may be predictive of or lead to complex cognitive deficits. Animal models of PPI deficits produced by dopamine agonists reliably predict existing antipsychotics. Nevertheless, since neither PPI nor cognitive deficits in schizophrenia are ameliorated by standard antipsychotics, current research is exploring the predictive value of non-dopaminergic PPI models in identifying treatments for gating disturbances independently of their relevance to specific disorders. Both PPI and cognitive deficits in schizophrenia patients are not reversed by first generation antipsychotics but may be attenuated by clozapine. Similarly, effects of glutamate antagonists on symptoms in patients and PPI in animals appear to be reduced by clozapine. Hence, treatment-induced reversals of deficits in PPI produced by glutamate antagonists may provide animal, and human, models to aid in the discovery of treatments of cognitive deficits in patients already treated with existing antipsychotics.

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“…Impairments in executive function have long been considered a core feature of schizophrenia [17,43,54] as highlighted by the MATRICS initiative [44]. Novel antipsychotics are required to improve cognition as the CATIE study revealed that atypical antipsychotics, such as clozapine, show little efficacy against cognitive symptoms [38].…”

Section: Introductionmentioning

confidence: 99%

A preliminary investigation into the effects of antipsychotics on sub-chronic phencyclidine-induced deficits in attentional set-shifting in female rats

McLean

Beck

Woolley

et al. 2008

Behavioural Brain Research

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Rationale: The NMDA receptor antagonist, phencyclidine (PCP), has been shown to induce symptoms characteristic of schizophrenia. A loss in executive function and the ability to shift attention between stimulus dimensions is impaired in schizophrenia; this can be assessed in rodents by the perceptual attentional set-shifting task. Objective: The aim of this study was to investigate whether the deficits induced by sub-chronic PCP in attentional set-shifting could be reversed by sub-chronic administration of clozapine, risperidone or haloperidol. Methods: Adult female hooded-Lister rats received subchronic PCP (2 mg/kg) or vehicle (1 ml/kg) i.p. twice daily for seven days, followed by a seven-day washout period. PCP-treated rats then received clozapine, risperidone, haloperidol or vehicle once daily for seven days and were then tested in the perceptual set-shifting task. Results: PCP significantly (p<0.01) increased the number of trials to reach criterion in the EDS phase when compared to vehicle and this deficit was significantly (p<0.01) attenuated by sub-chronic clozapine (2.5 mg/kg) and risperidone (0.2 mg/kg), but not by sub-chronic haloperidol treatment (0.05 mg/kg). Conclusions:These data show that sub-chronic PCP produced a robust deficit within the EDS phase in the attentional set-shifting task, in female rats. Atypical antipsychotics, clozapine and risperidone, but not the classical agent, haloperidol, significantly improved the PCPinduced cognitive deficit.

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Identification of separable cognitive factors in schizophrenia

Cited by 1,110 publications

References 48 publications

Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

The family of sensorimotor gating disorders: Comorbidities or diagnostic overlaps?

A preliminary investigation into the effects of antipsychotics on sub-chronic phencyclidine-induced deficits in attentional set-shifting in female rats

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