Longitudinal study of symptoms and cognitive function in chronic schizophrenia

Hughes, Christopher R.; Kumari, Veena; Soni, William; Das, M.B.; Binneman, Brendon; Drozd, Sonia; O'Neil, Shaun; Mathew, V. M.; Sharma, Tonmoy

doi:10.1016/s0920-9964(01)00393-0

Cited by 180 publications

(104 citation statements)

References 27 publications

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“…These discordant deficits in the clinical and cognitive domains of schizophrenics also were consistent with a previous study (Hughes et al, 2003). Similarly, these sex differences in cognitive domains are consistent with previous studies (Antonova et al, 2004;Halari et al, 2006;Sota and Heinrichs, 2003), and have been suggested as due to differences in brain structure for the two sexes and to differences in neural lateralization (Antonova et al, 2004).…”

Section: Discussionsupporting

confidence: 91%

“…Several studies have focused on gender differences in the cognitive deficits of schizophrenia and showed gender differences in cognitive domains in both schizophrenia and healthy populations (Goldstein et al, 2002;Halari et al, 2006;Phillips and Silverman, 1997;Ragland et al, 1999;Wisner et al, 2011). Furthermore, gender differences in schizophrenia' cognitive deficits are evident in the prodromal symptoms, acute psychotic episodes, illness course, and clinical response to antipsychotic treatment (Grigoriadis and Seeman, 2002;Hughes et al, 2003;Rubin et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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Gender differences in cognitive function of patients with chronic schizophrenia

Han¹,

Huang²,

Chen³

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

122

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Schizophrenic patients have cognitive impairments, but gender differences in these cognitive deficits have had limited study. This study assessed cognitive functioning in 471 subjects including 122 male and 78 female schizophrenic patients and 141 male and 130 female healthy controls. We found that immediate memory, language, delayed memory and total RBANS scores were significantly decreased in schizophrenia compared with healthy controls for both genders. Male patients had significant lower immediate memory, delayed memory and total RBANS scores than female patients, and healthy controls showed a similar gender difference. The RBANS showed modest correlations with PANSS scores, duration of illness and antipsychotic dose (chlorpromazine equivalents). Almost all RBANS scores in the schizophrenics and healthy controls showed significant positive correlations with education. Thus, patients of both sexes with schizophrenia experienced more deteriorated performance than healthy controls on cognitive domains of immediate memory, language and delayed memory. Furthermore, male schizophrenic patients had more serious cognitive deficits than female patients in immediate and delayed memory, but not in language, visuospatial and attention indices. AbstractSchizophrenic patients have cognitive impairments, but gender differences in these cognitive deficits have had limited study. This study assessed cognitive functioning in 471 subjects including 172 male and 78 female schizophrenic patients and 141 male and 130 female healthy controls. We found that immediate memory, language, delayed memory and total RBANS scores were significantly decreased in schizophrenia compared with healthy controls for both genders. Male patients had significant lower immediate memory, delayed memory and total RBANS scores than female patients, and healthy controls showed a similar gender difference. The RBANS showed modest correlations with PANSS scores, duration of illness and antipsychotic dose (chlorpromazine equivalents). Almost all RBANS scores in the schizophrenics and healthy controls showed significant positive correlations with education. Thus, patients of both sexes with schizophrenia experienced more deteriorated performance than healthy controls on cognitive domains of immediate memory, language and delayed memory.Furthermore, male schizophrenic patients had more serious cognitive deficits than female patients in immediate and delayed memory, but not in language, visuospatial and attention indices.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Gender differences in cognitive function of patients with chronic schizophrenia

Han¹,

Huang²,

Chen³

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

122

View full text Add to dashboard Cite

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“…In addition, the correlations between neurocognitive deficits and general symptoms were also low, ruling out the notion that neurocognitive deficits can be ascribed to symptoms such as mood and anxiety. As expected, however, the correlations with negative symptoms were in the small to medium range, consistent with previous studies (Addington et al, 1991;Buchanan et al, 1997;Hughes et al, 2003;Tamlyn et al, 1992;Bilder et al, 2000). While most evidence suggests that the relationship between negative symptoms and neurocognitive deficits is not causal (Harvey et al, 1996), the data from this study clearly indicate that in the general population of patients with schizophrenia, neurocognitive deficits are certainly not caused by positive symptoms, as they are completely uncorrelated.…”

Section: Discussionsupporting

confidence: 91%

“…The magnitude of the correlations between cognition and clinical symptoms in schizophrenia has been inconsistent, but generally small (Goldberg et al, 1993;Addington et al, 1991;Hughes et al, 2003;Strauss, 1993;Mohamed et al, 1999;Bilder et al, 2000;Gladsjo et al, 2004). This finding, which may contradict clinicians' impressions, could potentially be explained by the possibility that patients who agree to participate in research studies do not reflect the general population of patients with schizophrenia, especially for those studies with extensive and demanding neurocognitive batteries.…”

Section: Discussionmentioning

confidence: 99%

Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

Keefe

Bilder²,

Harvey

et al. 2006

Neuropsychopharmacol

422

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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“…Amelioration of cognitive deficits was correlated with reduced negative but not with reduced positive symptoms across the duration of the trial. The independence of cognitive deficits from positive symptoms has been shown in previous studies (Breier et al, 1991;Green, 1996;Hughes et al, 2003). The improvement in negative symptoms and in cognitive deficits may partly be mediated by common underlying mechanisms, presumably dopaminergic, that are pharmacologically influenced by both atypical drugs studied here.…”

Section: Cognitive Improvement In Schizophrenic Patientssupporting

confidence: 79%

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

Wagner

Quednow

Westheide

et al. 2004

Neuropsychopharmacol

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Combined serotonin-2A (5-HT 2A ) and dopamine-2 (D 2 ) receptor blockade has been proposed as a candidate mechanism by which second-generation antipsychotics (SGAs) improve both cognition and negative symptoms in schizophrenic patients, in contrast to antipsychotics of the first generation. The SGA amisulpride, however, only binds to D 2 /D 3 receptors, which makes it an interesting tool to test this assumption. In a randomized controlled trial, 52 schizophrenic patients were allocated to treatment with either olanzapine (10-20 mg/day) or amisulpride (400-800 mg/day). A comprehensive neuropsychological test battery and clinical ratings were used to assess participants at inclusion and after 4 and 8 weeks. Cognitive improvements of moderate size were observed, with effect sizes similar to those obtained in previous studies on the cognitive effects of SGAs. Importantly, amisulpride was not inferior to olanzapine for any cognitive domain. Combined 5-HT 2A /D 2 receptor blockade is probably not necessary for cognitive improvement by SGAs.

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Longitudinal study of symptoms and cognitive function in chronic schizophrenia

Cited by 180 publications

References 27 publications

Gender differences in cognitive function of patients with chronic schizophrenia

Gender differences in cognitive function of patients with chronic schizophrenia

Baseline Neurocognitive Deficits in the CATIE Schizophrenia Trial

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

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