Cognitive Impairment in Affective Psychoses: A Meta-analysis

Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Alan Gilbert Building NNF Level 3, Carlton 3053, Australia.
Schizophrenia Bulletin (Impact Factor: 8.45). 09/2009; 36(1):112-25. DOI: 10.1093/schbul/sbp093
Source: PubMed

ABSTRACT It has recently been suggested that cognitive impairment should be included in the diagnostic criteria of schizophrenia. One of the main arguments in support of this suggestion has been the hope that cognitive impairment can help distinguish schizophrenia from bipolar disorder (BD). However, recent evidence shows that cognitive deficits occur in BD and persist beyond euthymia. Further, mood disorders with psychotic features might be expected to manifest greater cognitive impairment, which further complicates the potential to differentiate these disorders. The goal of the current meta-analysis was to examine the magnitude and characteristics of cognitive impairments in affective psychoses (AP). A systematic search of the existing literature sourced 27 studies that met the inclusion criteria. These studies compared cognitive performances of 763 patients with AP (550 BD and 213 major depressive disorder) and 1823 healthy controls. Meta-regression and subgroup analyses were used to examine the effects of moderator variables. Meta-analyses of these studies showed that patients with AP were impaired in all 15 cognitive tasks with large effect sizes for most measures. There were no significant differences between the magnitude of impairments between the BD and major depressive disorder groups. The largest effect size was found for symbol coding, stroop task, verbal learning, and category fluency, reflecting impairments in elementary and complex aspects of attentional processing, as well as learning and memory. In general, the pattern of cognitive impairments in AP was similar to reported findings in euthymic patients with BD, but relatively more pronounced.

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Available from: Murat Yucel, Sep 29, 2015
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    • "Abnormalities have also been observed when more complex processing is required (MacDonald et al., 2005; Cannon et al., 2005; Tan et al., 2007; Kim et al., 2004). In recent years working memory impairments have come into focus as a cognitive feature in bipolar disorder with psychosis (Bora et al., 2010; Glahn et al., 2006; Brandt et al., 2014), suggesting that impairment in this RDoC domain extends across disorders. Yet, the relative magnitude of impairments across psychotic disorders and the extent to which these impairments are familial (Schulze et al., 2011; Bora et al., 2008) remains unclear. "
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    ABSTRACT: Working memory impairment is well established in psychotic disorders. However, the relative magnitude, diagnostic specificity, familiality pattern, and degree of independence from generalized cognitive deficits across psychotic disorders remain unclear. Participants from the Bipolar and Schizophrenia Network on Intermediate Phenotypes (B-SNIP) study included probands with schizophrenia (N=289), psychotic bipolar disorder (N=227), schizoaffective disorder (N=165), their first-degree relatives (N=315, N=259, N=193, respectively), and healthy controls (N=289). All were administered the WMS-III Spatial Span working memory test and the Brief Assessment of Cognition in Schizophrenia (BACS) battery. All proband groups displayed significant deficits for both forward and backward span compared to controls. However, after covarying for generalized cognitive impairments (BACS composite), all proband groups showed a 74% or greater effect size reduction with only schizoaffective probands showing residual backward span deficits compared to controls. Significant familiality was seen in schizophrenia and bipolar pedigrees. In relatives, both forward and backward span deficits were again attenuated after covarying BACS scores and residual backward span deficits were seen in relatives of schizophrenia patients. Overall, both probands and relatives showed a similar pattern of robust working memory deficits that were largely attenuated when controlling for generalized cognitive deficits. Copyright © 2015. Published by Elsevier B.V.
    Schizophrenia Research 05/2015; 166(1-3). DOI:10.1016/j.schres.2015.05.018 · 3.92 Impact Factor
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    • "Specifically, if subclinical psychosis represents a milder manifestation of the psychotic symptoms observed in disorders such as SZ, we might expect to see cognitive impairment in the individuals exhibiting high levels of subclinical psychotic symptoms similar to, albeit less severe than, those observed in SZ. Indeed, it has generally been found that cognitive deficits consistently accompany clinically significant psychotic symptoms (Bora et al., 2010; Lewandowski et al., 2011; Simonsen et al., 2011 "
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    ABSTRACT: Considerable data support the phenomenological and temporal continuity between subclinical psychosis and psychotic disorders. In recent years, neurocognitive deficits have increasingly been recognized as a core feature of psychotic illness but there are few data seeking to elucidate the relationship between subclinical psychosis and neurocogntive deficits in non-clinical samples. The goal of the present study was to examine the relationship between subclinical positive and negative symptoms, as measured by the Community Assessment of Psychic Experiences (CAPE) and performance on the MATRICS Consensus Cognitive Battery (MCCB) in a large (n=303) and demographically diverse non-clinical sample. We found that compared to participants with low levels of subclinical positive symptoms, participants with high levels of subclinical positive symptoms performed significantly better in the domains of working memory (p<.001), verbal learning (p=.007) and visual learning (p=.014). Although comparison of participants with high and low levels of subclinical negative symptoms revealed no differences in MCCB performance, we found that individuals with high levels of subclinical negative symptoms performed significantly better on a measure of estimated IQ (WRAT-3 Reading subtest; p=.02) than those with low levels of subclinical negative symptoms. These results are at odds with prior reports that have generally shown a negative relationship between neurocognitive functioning and severity of subclinical psychotic symptoms, and suggest some potential discontinuities between clinically significant psychotic symptoms and sub-syndromal manifestations of psychosis.
    Schizophrenia Research: Cognition 12/2014; 1(4):175-179. DOI:10.1016/j.scog.2014.09.002
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    • "It is known that cognitive impairment is not restricted to symptomatic phases, but that it also accompanies euthymia in a substantial number of bipolar patients, even though the published evidence is heterogeneous with regard to the specific functions affected, degree of impairment, and the degree of variability explained by the disorder itself compared to that attributed to moderating and mediating variables (Jamrozinski 2010). There seems to be a correlation between the duration of illness (DOI) as well as the number of illness episodes (especially depressive ones) and the degree of impairment (Bearden et al. 2001, Bora et al. 2010). Data on the latter, however, are discordant and even the causal direction is not yet clear (Martino et al. 2014). "
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    ABSTRACT: Cognitive impairment in patients with bipolar disorder (BD) is not restricted to symptomatic phases. It is also present in euthymia. There is evidence of differences in the brain's structure between bipolar patients and healthy individuals, as well as changes over time in patients. Lithium constitutes the gold standard in long-term prophylactic treatment. Appropriate therapy that prevents new episodes improves the disease's course and reduces the frequency of harmful outcomes. Interestingly, preclinical data suggest that lithium has a (additional) neuroprotective effect. There is limited data on its related effects in humans and even less on its long-term application. In this multi-center cross-sectional study from the International Group for the Study of Lithium-treated Patients (IGSLi), we compared three groups: bipolar patients without long-term lithium treatment (non-Li group; <3 months cumulative lithium exposure, ≥24 months ago), bipolar patients with long-term lithium treatment (Li group, ongoing treatment ≥24 months), and healthy subjects (controls). Strict inclusion and exclusion criteria were defined; the inclusion criteria for patients were diagnosis of BD types I or II, duration of illness ≥10 years, ≥5 episodes in patient's history and a euthymic mood state. Neurocognitive functioning was assessed using the Wechsler Adult Intelligence Scale-Revised (WAIS-R), the California Verbal Learning Test (CVLT), and a visual backward masking (VBM) task. A total of 142 subjects were included, 31 in the non-Li and 58 in the Li group, as well as 53 healthy controls. Treated patients with long-standing BD and controls did not differ significantly in overall cognitive functioning and verbal learning, recall, and recognition; regardless of whether lithium had been part of the treatment. Patients, however, demonstrated poorer early visual information processing than healthy controls, with the lithium-treated patients performing worse than those without. Our data suggest that bipolar patients with a long illness history and effective prophylactic treatment do not reveal significantly impaired general cognitive functioning or verbal learning and memory. However, they are worse at processing early visual information. Accompanying volumetric and spectroscopic data suggest cell loss in patients not treated with lithium that may be counterbalanced by long-term lithium treatment.
    12/2014; 2(1):1. DOI:10.1186/s40345-014-0016-7
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