General and specific cognitive deficits in schizophrenia

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Biological Psychiatry (Impact Factor: 10.26). 05/2004; 55(8):826-33. DOI: 10.1016/j.biopsych.2003.12.010
Source: PubMed


It is controversial whether the cognitive deficit in schizophrenia is better characterized as generalized or as reflecting relatively independent deficits in different cognitive domains. The issue has implications for assessment practice, intervention design, and the exploration of schizophrenia genetics.
We used a specialized structural equation modeling approach, single common factor analysis, to explore the relative importance of generalized versus independent cognitive deficits in schizophrenia. Eighteen subtest scores from the Wechsler Adult Intelligence Scale-III and the Wechsler Memory Scale-III were included in the analysis. We analyzed these data for 97 schizophrenia or schizoaffective disorder outpatients and 87 healthy control subjects.
Approximately two thirds of the overall effect of a schizophrenia diagnosis on cognitive performance was mediated through a single common factor. The Wechsler subtest scores showed almost uniformly strong relationships with this factor. The independent associations of group status with the subtest scores were smaller in magnitude and only selectively significant.
The relatively greater magnitude of illness effects mediated through the common factor in this analysis, compared with the specific, independent effects, suggests that a generalized cognitive deficit is a core feature of schizophrenia.

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    • "Cognitive impairments in memory, attention and executive functions (Nuechterlein et al., 2004) are critical determinants of functional disability in schizophrenia (Dickinson et al., 2004; Heinrichs and Zakzanis, 1998). Recently, emphasis has been placed on sensory and perceptual impairments , which are also critical in schizophrenia (Nelson et al., 2014; Postmes et al., 2014), and several types of sensory remediation have been proposed (Adcock et al., 2009; Fisher et al., 2009). "
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    ABSTRACT: Metabolic syndrome is more prevalent in schizophrenia than in the general population and is associated with an increased rate of morbidity. It has been associated with cognitive impairments in schizophrenia, which are a core deficit in patients with chronic schizophrenia. Sensory gating deficit is also a core deficit in schizophrenia. The principal objective of this study was to investigate the relationship between sensory gating deficit and metabolic syndrome in patients with schizophrenia, after adjusting for key confounding factors. We hypothesized that patients with metabolic syndrome exhibit a higher rate of sensory gating deficit compared to those without metabolic syndrome. This study investigated sensory gating with the auditory event-related potential method by measuring P50 amplitude changes in a double click conditioning-testing procedure in 51 patients with schizophrenia. Patients with metabolic syndrome (n = 14) had a higher rate of sensory gating deficit (P50 suppression < 50%) (p < 0.001) compared to those without metabolic syndrome (n = 37). This result remained significant (B = 2.94, Wald = 8.32, p = 0.004) after taking into account 5 potential confounding factors (age, gender, duration of disorder, Fagerström test, presence of clozapine or olanzapine). In patients without metabolic syndrome, sensory gating deficit was linked to a poorer attentional performance (rho = -0.371, p = 0.05). In patients with metabolic syndrome, sensory gating deficit was linked to poorer memory performance (rho = -0.635, p = 0.02). These findings suggest that metabolic syndrome may be linked to sensory gating deficit in patients with schizophrenia and that the relationship between neurocognitive function and sensory gating deficit could be affected by the metabolic status of the patients. Further studies are needed to address the causal relationship between sensory gating deficit related to schizophrenia, cognitive impairments and metabolic syndrome.
    Psychoneuroendocrinology 04/2015; 57. DOI:10.1016/j.psyneuen.2015.04.005 · 4.94 Impact Factor
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    • "The similarities in COGS-1 and COGS-2 CVLT-II performance, in the context of similar magnitudes of deficit in both learning and in recall performance, along with the Junghee et al. and Gur et al. findings, suggest a significant role for a generalized deficit, in addition to more discrete problems in executive function. This pattern would be consistent with results of studies showing both specific and generalized cognitive deficits in SZ (Dickinson et al., 2004, 2006, 2008; Sheffield et al., 2014 "
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    ABSTRACT: The first phase of the Consortium on the Genetics of Schizophrenia (COGS-1) showed performance deficits in learning and memory on the California Verbal Learning Test, Second Edition (CVLT-II) in individuals with schizophrenia (SZ), compared to healthy comparison subjects (HCS). A question is whether the COGS-1 study, which used a family study design (i.e. studying relatively intact families), yielded "milder" SZ phenotypes than those acquired subsequently in the COGS-2 case-control design that did not recruit unaffected family members. CVLT-II performance was compared for the COGS-1 and COGS-2 samples. Analyses focused on learning, recall and recognition variables, with age, gender and education as covariates. Analyses of COGS-2 data explored effects of additional covariates and moderating factors in CVLT-II performance. 324 SZ subjects and 510 HCS had complete CVLT-II and covariate data in COGS-1, while 1356 SZ and 1036 HCS had complete data in COGS-2. Except for recognition memory, analysis of covariance showed significantly worse performance in COGS-2 on all CVLT-II variables for SZ and HCS, and remained significant in the presence of the covariates. Performance in each of the 5 learning trials differed significantly. However, effect sizes comparing cases and controls were comparable across the two studies. COGS-2 analyses confirmed SZ performance deficits despite effects of multiple significant covariates and moderating factors. CVLT-II performance was worse in COGS-2 than in COGS-1 for both the SZ and the HCS in this large cohort, likely due to cohort effects. Demographically corrected data yield a consistent pattern of performance across the two studies in SZ. Copyright © 2014. Published by Elsevier B.V.
    Schizophrenia Research 12/2014; 163(1-3). DOI:10.1016/j.schres.2014.10.029 · 3.92 Impact Factor
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    • "Cognitive impairments in memory, attention, and executive functions (Nuechterlein et al., 2004) are critical determinants of functional disability in schizophrenia (Dickinson et al., 2004; Heinrichs and Zakzanis, 1998), even after successful treatment and reduction of psychotic symptoms (McGurk et al., 2004; Nuechterlein et al., 2012). Because first and second generation antipsychotics have limited benefits on these impairments (Keefe et al., 2007), understanding the neurobiological mechanisms affecting cognition in schizophrenia may serve to develop new approaches (Gold, 2004). "
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    ABSTRACT: Objective We aimed to investigate the brain functional substrate underlying relationships between metabolic syndrome (MetS) and cognitive impairment in schizophrenia. Methods In this cross-sectional study, we collected socio-demographic, clinical, anthropometric, blood, and cognition data and performed brain 99mTc-ECD-SPECT imaging of cerebral blood flow in patients with schizophrenia. Patients were grouped according to the absence or presence of MetS. Whole-brain perfusion SPECTs were compared at voxel level between these two groups, and voxel-wise interregional correlation was performed to compare functional connectivity (voxel level significance of p < 0.005, uncorrected; p < 0.05 for the cluster, uncorrected; using SPM8). A structural equation model (SEM) was applied to examine the relationships between brain perfusion, connectivity between brain areas, and cognition. Results Of the 55 patients, 17 had MetS. They performed significantly worse than patients without MetS on tests of executive functions (processing speed p = 0.005 for TMT-A; and reactive flexibility p = 0.014 for TMT-B), attention (D2 attention task p = 0.007), and memory (California Verbal Learning Test p = 0.039). In comparison to patients without MetS, those with MetS exhibited significant hypoperfusion within the left orbital prefrontal cortex and greater functional connectivity from this left frontal cluster within the left insula and middle/superior frontal gyrus. SEM confirmed the effect on executive functions of brain hypoperfusion and of increased connectivity, suggesting possible compensatory networks in patients with MetS. Conclusion Our study identifies the brain functional impact of MetS on cognition, with orbital prefrontal impairment and possible compensatory networks.
    Psychoneuroendocrinology 12/2014; 50:95–105. DOI:10.1016/j.psyneuen.2014.07.019 · 4.94 Impact Factor
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