Schizophrenia Research-Cognition最新文献

Background

The role of loneliness and social exclusion in the development of paranoia is largely unexplored. Negative affect may mediate potential associations between these factors. We investigated the temporal relationships of daily-life loneliness, felt social exclusion, negative affect, and paranoia across the psychosis continuum.

Method

Seventy-five participants, including 29 individuals with a diagnosis of non-affective psychosis, 20 first-degree relatives, and 26 controls used an Experience Sampling Method (ESM) app to capture the fluctuations in loneliness, feelings of social exclusion, paranoia, and negative affect across a 1-week period. Data were analysed with multilevel regression analyses.

Results

In all groups, loneliness and feelings of social exclusion were independent predictors of paranoia over time (b = 0.05, p < .001 and b = 0.04, p < .05, respectively). Negative affect predicted paranoia (b = 0.17, p < .001) and partially mediated the associations between loneliness, social exclusion, and paranoia. It also predicted loneliness (b = 0.15, p < .0001), but not social exclusion (b = 0.04, p = .21) over time. Paranoia predicted social exclusion over time, with more pronounced effects in controls (b = 0.43) than patients (b = 0.19; relatives: b = 0.17); but not loneliness (b = 0.08, p = .16).

Conclusion

Paranoia and negative affect worsen in all groups following feelings of loneliness and social exclusion. This highlights the importance of a sense of belonging and being included for mental well-being. Loneliness, feeling socially excluded, and negative affect were independent predictors of paranoid thinking, suggesting they represent useful targets in its treatment.

Background

Sustained attention and vigilance impairments are well documented in people with schizophrenia (PSZ). The processes implicated in this impairment remain unclear. Here we investigated whether vigilance performance varied as a function of working memory load, and also examined the role of attentional lapsing that might arise from a loss of task set resulting in mind wandering.

Method

We examined Continuous Performance Test Identical Pairs (CPT-IP) data from a cumulative sample of 247 (PSZ) and 238 healthy control (HC) participants collected over a series of studies.

Results

PSZ performed more poorly that HC across conditions with signal/noise discrimination (d′) decreasing with increasing working memory load across both groups However, there was a significant interaction of group and load suggesting that performance of PSZ was more negatively impacted by increasing load. We also found that PSZ has a significantly higher rate of attention lapsing than did HC.

Discussion

Our results suggest that difficulties maintaining task set and working memory limitations are implicated in the impairments observed on the Identical Pairs CPT. Difficulties with task set maintenance appear to explain the majority of between-group variance, with a more subtle impact of increasing working memory load.

Objective

In the general population, repeated cognitive testing produces learning effects with potential for improved test performance. It is currently unclear whether the same effect of repeated cognitive testing on cognition pertains to people living with schizophrenia, a condition often associated with significant cognitive impairments. This study aims to evaluate learning ability in people with schizophrenia and—considering the evidence that antipsychotic medication can additionally impair cognitive performance—explore the potential impact of anticholinergic burden on verbal and visual learning.

Method

The study included 86 patients with schizophrenia, treated with clozapine, who had persisting negative symptoms. They were assessed at baseline, weeks 8, 24 and 52 using Positive and Negative Syndrome Scale, Hopkins Verbal Learning Test–Revised (HVLT-R) and Brief Visuospatial Memory Test-R (BVMT-R).

Results

There were no significant improvements in verbal or visual learning across all measurements. Neither the clozapine/norclozapine ratio nor anticholinergic cognitive burden significantly predicted participants' total learning. Premorbid IQ was significantly associated with verbal learning on the HVLT-R.

Conclusions

These findings advance our understanding of cognitive performance in people with schizophrenia and demonstrate limited learning performance in individuals with treatment-refractory schizophrenia.

Patients with schizophrenia often have cognitive impairments that contribute to diminished psychosocial functioning. Cognitive remediation therapy (CRT) has proven efficacy and is recommended by evidence-based treatment guidelines. Important moderators of efficacy include integration of CRT into a psychiatric rehabilitation concept and patient attendance at a sufficient number of therapy sessions. These conditions can probably best be met in an outpatient setting; however, outpatient treatment is prone to higher rates of treatment discontinuation and outpatient settings are not as well protected as inpatient ones and less closely supervised.

The present study investigated the feasibility of outpatient CRT in schizophrenia over a six-month period. Adherence to scheduled sessions and safety parameters were assessed in 177 patients with schizophrenia randomly assigned to one of two matched CRT programs.

Results showed that 58.8 % of participants completed the CRT (>80 % of scheduled sessions) and 72.9 % completed at least half the sessions. Predictor analysis revealed a high verbal intelligence quotient as favorable for good adherence, but this factor had only low general predictive power. During the six-month treatment phase, serious adverse events occurred in 15.8 % (28/177) of the patients, which is a comparable rate to that reported in the literature.

Our findings support the feasibility of six-month outpatient CRT in schizophrenia in terms of adherence to scheduled sessions and safety.

Trial registration number

NCT02678858, DRKS00010033.

Individuals with schizophrenia spectrum disorders (SSD) have significantly lower life-expectancy than healthy people. Previously, we have identified baseline neurocognitive function in general and verbal memory and executive function in particular as related to mortality nearly two decades later. In this study, we aim to replicate these findings with a larger and age-matched sample. The patient group consisted of 252 individuals, 44 of whom were deceased and 206 alive. Neurocognition was assessed with a comprehensive battery. Results showed that the deceased group, compared to the living group, had significantly more severe neurocognitive deficits across nearly all domains. There were no differences in sex, remission status, psychosis symptoms, or function level between the groups. Immediate verbal memory and executive function were the strongest predictors of survival status. These results were nearly identical to our previous studies, and we conclude that baseline neurocognitive function is an important predictor for mortality in SSD. Clinicians should be mindful of this relationship in patients with significant cognitive deficits.

Increasing evidence of a common neurodevelopmental etiology between schizophrenia and developmental dyslexia suggests that neurocognitive functions, such as reading, may be similarly disrupted. However, direct comparisons of reading performance in these disorders have yet to be conducted. To address this gap in the literature, we employed a gaze-contingent moving window paradigm to examine sentence-level reading fluency and perceptual span (breadth of parafoveal processing) in adults with schizophrenia (dataset from Whitford et al., 2013) and psychiatrically healthy adults with dyslexia (newly collected dataset). We found that the schizophrenia and dyslexia groups exhibited similar reductions in sentence-level reading fluency (e.g., slower reading rates, more regressions) compared to matched controls. Similar reductions were also found for standardized language/reading and executive functioning measures. However, despite these reductions, the dyslexia group exhibited a larger perceptual span (greater parafoveal processing) than the schizophrenia group, potentially reflecting a disruption in normal foveal-parafoveal processing dynamics. Taken together, our findings suggest that reading and reading-related functions are largely similarly disrupted in schizophrenia and dyslexia, providing additional support for a common neurodevelopmental etiology.

Introduction

Neurocognitive impairment (NCI) is commonly exhibited among patients experiencing their first episode of psychosis. However, there are few resources in many low-income countries, such as Uganda, that allow for the administration of extensive neurocognitive test batteries for the detection of NCI. NeuroScreen is a brief tablet-based neurocognitive assessment battery that can be administered by all levels of healthcare staff. We examined the validity of NeuroScreen to assess neurocognition and detect NCI in first-episode psychosis (FEP) patients in Uganda.

Methods

We enrolled 112 participants FEP patients and matched controls at Butabika Mental Referral Hospital. Each participant completed NeuroScreen and a traditionally administered neurocognitive battery: the MATRIC Consensus Cognitive Battery (MCCB). We examined correlations between participant performance on NeuroScreen and the MCCB. A ROC curve determined sensitivity and specificity of NeuroScreen to detect NCI as determined by MCCB criterion.

Results

There was a large, statistically significant correlation between overall performance on NeuroScreen and the MCCB [r(112) = 0.64, p < .001]. Small to large correlations were found between tests in the MCCB and NeuroScreen batteries. The ROC curve of NeuroScreen performance to detect MCCB-defined NCI had an area under curve of 0.80 and optimal sensitivity and specificity of 83 % and 60 %, respectively.

Conclusion

There was a moderate positive correlation between overall performance on both batteries. NeuroScreen shows promise as a valid assessment battery to assess neurocognition and detect NCI in FEP patients in Uganda. Further studies of NeuroScreen in healthy individuals and in a range of mental disorders are recommended.

Cognitive impairment is one of the core clinical symptom domains of schizophrenia. Research shows that cognitive deficits in this neuropsychiatric syndrome is associated with neurodevelopmental pathology affecting multiple brain regions such as the dorsolateral prefrontal cortex, the hippocampus and the parietal lobe. The insula is a relatively small structure that is highly connected with several brain regions as well as multiple brain networks. A large number of studies have reported the involvement of the insula in many of the psychotic and nonpsychotic manifestations of schizophrenia. Here we review the role of the insula as a hub across key neurocircuits which have been implicated in the various cognitive pathologies in schizophrenia. Structural and functional abnormalities in the right and left insulae may serve as a biomarker for susceptibility to schizophrenia.

Working memory (WM) impairments are well recognized in schizophrenia patients (PSZ) and contribute to poor psycho-social outcomes in this population. Distinct neural networks underlay the ability to encode and recall visual and spatial information raising the possibility that profile of visual working memory performance may help pinpoint dysfunctional neural correlates in schizophrenia. This study assessed the resolution and associative aspects of visual working memory deficits in schizophrenia and whether these deficits arise during encoding or maintenance processes. A total of 60 participants (30 PSZ and 30 healthy controls) matched in age, gender and education assessed on a modified object in place (OiPT), a delayed non-match-to-sample (DNMST) and a delayed spatial estimation (DSET) task. Patients demonstrated lower accuracy than controls in binding visual features of the same object and recognizing novel objects as well as lower precision recalling the location of a memorized target. Moreover, response choice set size affected recognition accuracy more in PSZ than controls. However, delay duration affected spatial recall precisions, binding, and recognition accuracy equally in the two groups. Our results suggest that visual working memory (vWM) impairments in schizophrenia predominantly reflect spatial and non-spatial binding deficits, with largely preserved discrete feature information. Moreover, these impairments likely arise more during encoding than during maintenance. These binding deficits may reflect impaired effective neural functional connectivity observed in schizophrenia.