scholarly journals The role of cognitive functioning in the outcome of those at clinical high risk for developing psychosis

2012 ◽  
Vol 21 (4) ◽  
pp. 335-342 ◽  
Author(s):  
J. Addington ◽  
M. Barbato

Although it is well established that cognitive impairment is a common feature of schizophrenia, only recently has cognitive functioning been prospectively studied in individuals at clinical high risk (CHR) for developing psychosis. To date, both cross-sectional and longitudinal studies have been conducted in the CHR population and in the context of later conversion to psychosis. A comprehensive review of the literature suggests that CHR individuals have general and specific baseline cognitive deficits compared to healthy controls. As a group, their cognitive course, tends to remain stable over time and in this way does not differ from healthy controls. For those who go on to develop a full-blown psychotic illness compared to those who do not convert, there appeared to be minimal differences at baseline with respect to cognition, although over time the converters may show deterioration in certain cognitive abilities compared to the non-converters. However, for many cognitive domains results are mixed, and may result from methodological limitations.

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000012598
Author(s):  
Willem S. Eikelboom ◽  
Esther van den Berg ◽  
Ellen H. Singleton ◽  
Sara J. Baart ◽  
Michiel Coesmans ◽  
...  

Objective:To investigate the prevalence and trajectories of neuropsychiatric symptoms (NPS) in relation to cognitive functioning in a cohort of amyloid-β positive individuals across the Alzheimer’s disease (AD) clinical spectrum.Methods:In this single-center observational study, we included all individuals who visited the Alzheimer Center Amsterdam and had 1) a clinical diagnosis of subjective cognitive decline (SCD), mild cognitive impairment (MCI), or probable AD dementia, and 2) were amyloid-β positive (A+). We measured NPS with the Neuropsychiatric Inventory (NPI), examining total scores and the presence of specific NPI domains. Cognition was assessed across five cognitive domains and with the MMSE. We examined trajectories including model based trends for NPS and cognitive functioning over time. We used linear mixed models to relate baseline NPI scores to cognitive functioning at baseline (whole-sample) and longitudinal time-points (subsample n=520, Mean=1.8 [SD=0.7] years follow-up).Results:We included 1,524 amyloid-β positive individuals from the Amsterdam Dementia Cohort with A+ SCD (n=113), A+ MCI (n=321), or A+ AD dementia (n=1,090). NPS were prevalent across all clinical AD stages (≥1 NPS 81.4% in SCD, 81.2% in MCI, 88.7% in dementia; ≥1 clinically relevant NPS 54.0% in SCD, 50.5% in MCI, 66.0% in dementia). Cognitive functioning showed an uniform gradual decline; while in contrast, large intra-individual heterogeneity of NPS was observed over time across all AD groups. At baseline, we found associations between NPS and cognition in dementia that were most pronounced for NPI total scores and MMSE (range β=0.18 to 0.11, FDR-adjusted p<0.05), while there were no cross-sectional relationships in SCD and MCI (range β=-0.32 to 0.36, all FDR-adjusted p>0.05). There were no associations between baseline NPS and cognitive functioning over time in any clinical stage (range β=-0.13 to 0.44, all FDR-adjusted p>0.05).Conclusion:NPS and cognitive symptoms are both prevalent across the AD continuum, but show a different evolution during the course of the disease.


2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S64-S64
Author(s):  
Raktima Datta ◽  
Gregory Strauss ◽  
Nina Kraguljac ◽  
Sydney Howie ◽  
Adrienne Lahti

Abstract Background Prior studies indicate that chronic schizophrenia (SZ) is associated with a specific profile of reinforcement learning abnormalities. These impairments are characterized by: 1) reductions in learning rate, and 2) impaired Go learning and intact NoGo learning. Furthermore, each of these deficits are associated with greater severity of negative symptoms, consistent with theoretical perspectives positing that avolition and anhedonia are associated with deficits in generating, updating, and maintaining mental representations of reward value hat are needed to guide decision-making. However, it is unclear whether these deficits extend to earlier phases of psychotic illness and when individuals are unmedicated. Methods Two studies were conducted to examine reinforcement learning deficits in earlier phases of psychosis. In study 1, participants included 35 participants with first episode psychosis (FEP) and 25 healthy controls (HC). Study 2 included 17 antipsychotic naïve individuals who met criteria for attenuated psychosis syndrome (APS) (i.e., those with a prodromal syndrome) and 18 matched healthy controls (HC). In both studies, participants completed the Temporal Utility Integration Task, a measure of probabilistic reinforcement learning that contained Go and NoGo learning blocks. Participants in the clinical groups also completed neuropsychological testing and standard clinical interviews designed to determine symptom severity and diagnosis. Results FEP displayed impaired Go learning and intact NoGo learning. In contrast, APS did not display impairments in Go or NoGo learning at the group level. Negative symptoms were not significantly associated with reinforcement learning in APS participants. However, greater impairments in Go learning were associated with increased cross-sectional risk for conversion on the NAPLS risk calculator score in the APS group. Discussion Findings provide new evidence for areas of spared and impaired reinforcement learning in early phases of psychosis. Similar to chronic SZ, FEP was associated with impaired Go learning, and intact NoGo learning. Reinforcement learning is more spared in those at clinical high-risk, except those at greatest risk for conversion, where Go learning deficits are more pronounced. These findings suggest that reinforcement learning deficits may emerge early among those who are at clinical high risk for developing psychosis and that they are already pronounced by illness onset in the first episode. Importantly, these reinforcement learning deficits do not appear to be a byproduct of illness chronicity or antipsychotic medication use, but rather a consequence of the illness itself.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Lorna Staines ◽  
Ruchika Gajwani ◽  
Joachim Gross ◽  
Andrew I. Gumley ◽  
Stephen M. Lawrie ◽  
...  

Abstract Introduction Duration of risk symptoms (DUR) in people at clinical high risk for psychosis (CHR-P) has been related to poorer clinical outcomes, such as reduced functioning, but it is currently unclear how different symptoms emerge as well as their link with cognitive deficits. To address these questions, we examined the duration of basic symptoms (BS) and attenuated psychotic symptoms (APS) in a sample of CHR-P participants to test the hypothesis that BS precede the manifestation of APS. As a secondary objective, we investigated the relationship between DUR, functioning and neuropsychological deficits. Methods Data from 134 CHR-P participants were assessed with the Comprehensive Assessment of At-Risk Mental State and the Schizophrenia Proneness Interview, Adult Version. Global, role and social functioning and neurocognition were assessed and compared to a sample of healthy controls (n = 57). Results In CHR-P participants who reported both APS and BS, onset of BS and APS was not significantly related. When divided into short and long BS duration (</> 8 years), CHR-P participants with a longer duration of BS showed evidence for an onset of BS preceding APS (n = 8, p = 0.003). However, in the short BS duration group, APS showed evidence of preceding BS (n = 56, p = 0.020). Finally, there were no significant effects of DUR on cognition or functioning measures. Conclusion The present findings do not support the view that APS constitute a secondary phenomenon to BS. Moreover, our data could also not confirm that DUR has a significant effect on functioning and cognitive deficits. These findings are discussed in the context of current theories regarding emerging psychosis and the importance of DUR.


2015 ◽  
Vol 44 (2) ◽  
pp. 203-213 ◽  
Author(s):  
Jacqueline Stowkowy ◽  
Lu Liu ◽  
Kristin S. Cadenhead ◽  
Tyrone D. Cannon ◽  
Barbara A. Cornblatt ◽  
...  

Background: Schema Theory proposes that the development of maladaptive schemas are based on a combination of memories, emotions and cognitions regarding oneself and one's relationship to others. A cognitive model of psychosis suggests that schemas are crucial to the development and persistence of psychosis. Little is known about the impact that schemas may have on those considered to be at clinical high risk (CHR) of developing psychosis. Aims: To investigate schemas over time in a large sample of CHR individuals and healthy controls. Method: Sample included 765 CHR participants and 280 healthy controls. Schemas were assessed at baseline, 6 and 12 months using the Brief Core Schema Scale (BCSS). Baseline schemas were compared to 2-year clinical outcome. Results: CHR participants evidenced stable and more maladaptive schemas over time compared to controls. Schemas at initial contact did not vary amongst the different clinical outcome groups at 2 years although all CHR outcome groups evidenced significantly worse schemas than healthy controls. Although there were no differences on baseline schemas between those who later transitioned to psychosis compared to those who did not, those who transitioned to psychosis had more maladaptive negative self-schemas at the time of transition. Associations between negative schemas were positively correlated with earlier abuse and bullying. Conclusions: These findings demonstrate a need for interventions that aim to improve maladaptive schemas among the CHR population. Therapies targeting self-esteem, as well as schema therapy may be important work for future studies.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1232.1-1232
Author(s):  
M. Di Battista ◽  
S. Barsotti ◽  
A. Della Rossa ◽  
M. Mosca

Background:Cardiovascular (CV) diseases, namely myocardial infarction and stroke, are not among the most known and frequent complications of systemic sclerosis (SSc), but there is growing evidence that SSc patients have a higher prevalence of CV diseases than the general population [1].Objectives:To compare two algorithms for CV risk estimation in a cohort of patients with SSc, finding any correlation with clinical characteristics of the disease.Methods:SSc patients without previous myocardial infarction or stroke were enrolled. Traditional CV risk factors, SSc-specific characteristics and ongoing therapies were assessed. Framingham and QRISK3 algorithms were then used to estimate the risk of develop a CV disease over the next 10 years.Results:Fifty-six SSc patients were enrolled. Framingham reported a median risk score of 9.6% (IQR 8.5), classifying 24 (42.9%) subjects at high risk, with a two-fold increase of the mean relative risk in comparison to general population. QRISK3 showed a median risk score of 15.8% (IQR 19.4), with 36 (64.3%) patients considered at high-risk. Both algorithms revealed a significant role of some traditional risk factors and a noteworthy potential protective role of endothelin receptor antagonists (p=0.003). QRISK3 was also significantly influenced by some SSc-specific characteristics, as limited cutaneous subset (p=0.01), interstitial lung disease (p=0.04) and non-ischemic heart involvement (p=0.03), with the first two that maintain statistically significance in the multivariate analysis (p=0.02 for both).Conclusion:QRISK3 classifies more SSc patients at high-risk to develop CV diseases than Framingham, and it seems to be influenced by some SSc-specific characteristics. If its predictive accuracy were prospectively verified, the use of QRISK3 as a tool in the early detection of SSc patients at high CV risk should be recommended.References:[1]Ngian GS, Sahhar J, Proudman SM, Stevens W, Wicks IP, Van Doornum S. Prevalence of coronary heart disease and cardiovascular risk factors in a national cross-sectional cohort study of systemic sclerosis. Ann Rheum Dis. 2012;71:1980-3.Disclosure of Interests:None declared


2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Roberta da Silva Filha ◽  
Sérgio Veloso Brant Pinheiro ◽  
Thiago Macedo e Cordeiro ◽  
Victor Feracin ◽  
Érica Leandro Marciano Vieira ◽  
...  

AbstractIntroduction: Renin angiotensin system (RAS) plays a role in idiopathic nephrotic syndrome (INS). Most studies investigated only the classical RAS axis. Therefore, the aims of the present study were to evaluate urinary levels of RAS molecules related to classical and to counter-regulatory axes in pediatric patients with INS, to compare the measurements with levels in healthy controls and to search for associations with inflammatory molecules, proteinuria and disease treatment. Subjects and methods: This cross-sectional study included 31 patients with INS and 19 healthy controls, matched for age and sex. Patients and controls were submitted to urine collection for measurement of RAS molecules [Ang II, Ang-(1-7), ACE and ACE2] by enzyme immunoassay and cytokines by Cytometric Bead Array. Findings in INS patients were compared according to proteinuria: absent (<150 mg/dl, n = 15) and present (≥150 mg/dl, n = 16). Results: In comparison to controls, INS patients had increased Ang II, Ang-(1-7) and ACE, levels while ACE2 was reduced. INS patients with proteinuria had lower levels of ACE2 than those without proteinuria. ACE2 levels were negatively correlated with 24-h-proteinuria. Urinary concentrations of MCP-1/CCL2 were significantly higher in INS patients, positively correlated with Ang II and negatively with Ang-(1-7). ACE2 concentrations were negatively correlated with IP-10/CXCL-10 levels, which, in turn, were positively correlated with 24-h-proteinuria. Conclusion: INS patients exhibited changes in RAS molecules and in chemokines. Proteinuria was associated with low levels of ACE2 and high levels of inflammatory molecules.


BJPsych Open ◽  
2021 ◽  
Vol 7 (4) ◽  
Author(s):  
Timea Sparding ◽  
Erik Joas ◽  
Caitlin Clements ◽  
Carl M. Sellgren ◽  
Erik Pålsson ◽  
...  

Background Cross-sectional studies have found impaired cognitive functioning in patients with bipolar disorder, but long-term longitudinal studies are scarce. Aims The aims of this study were to examine the 6-year longitudinal course of cognitive functioning in patients with bipolar disorder and healthy controls. Subsets of patients were examined to investigate possible differences in cognitive trajectories. Method Patients with bipolar I disorder (n = 44) or bipolar II disorder (n = 28) and healthy controls (n = 59) were tested with a comprehensive cognitive test battery at baseline and retested after 6 years. We conducted repeated measures ANCOVAs with group as a between-subject factor and tested the significance of group and time interaction. Results By and large, the change in cognitive functioning between baseline and follow-up did not differ significantly between participants with bipolar disorder and healthy controls. Comparing subsets of patients, for example those with bipolar I and II disorder and those with and without manic episodes during follow-up, did not reveal subgroups more vulnerable to cognitive decline. Conclusions Cognitive performance remained stable in patients with bipolar disorder over a 6-year period and evolved similarly to healthy controls. These findings argue against the notion of a general progressive decline in cognitive functioning in bipolar disorder.


2014 ◽  
Vol 29 (2) ◽  
pp. 144-154 ◽  
Author(s):  
C Bois ◽  
HC Whalley ◽  
AM McIntosh ◽  
SM Lawrie

There is a growing consensus that a symptomatology as complex and heterogeneous as schizophrenia is likely to be produced by widespread perturbations of brain structure, as opposed to isolated deficits in specific brain regions. Structural brain-imaging studies have shown that several features of the brain, such as grey matter, white matter integrity and the morphology of the cortex differ in individuals at high risk of the disorder compared to controls, but to a lesser extent than in patients, suggesting that structural abnormalities may form markers of vulnerability to the disorder. Research has had some success in delineating abnormalities specific to those individuals that transition to psychosis, compared to those at high risk that do not, suggesting that a general risk for the disorder can be distinguished from alterations specific to frank psychosis. In this paper, we review cross-sectional and longitudinal studies of individuals at familial or clinical high risk of the disorder. We conclude that the search for reliable markers of schizophrenia is likely to be enhanced by methods which amalgamate structural neuroimaging data into a coherent framework that takes into account the widespread distribution of brain alterations, and relates this to leading hypotheses of schizophrenia.


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