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调查社区中人格功能、认知偏差与精神病的(非)感知性临床高危症状之间的关联。

Investigating the associations between personality functioning, cognitive biases, and (non-)perceptive clinical high-risk symptoms of psychosis in the community.

作者信息

Rinaldi Giulia, Lerch Stefan, Schultze-Lutter Frauke, Schmidt Stefanie Julia, Cavelti Marialuisa, Kaess Michael, Michel Chantal

机构信息

University Hospital of Child and Adolescent Psychiatry and Psychotherapy, University of Bern, Bern, Switzerland.

Department of Psychiatry and Psychotherapy, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.

出版信息

Eur Psychiatry. 2025 Jan 22;68(1):e13. doi: 10.1192/j.eurpsy.2024.1812.

DOI:10.1192/j.eurpsy.2024.1812
PMID:39838752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11822964/
Abstract

BACKGROUND

Beyond psychosis prediction, clinical high-risk (CHR-P) symptoms show clinical relevance by their association with functional impairments and psychopathology, including personality pathology. Impaired personality functioning is prioritized in recent dimensional personality disorder models (DSM-5, ICD-11), yet underexplored in CHR-P, as are associations with cognitive biases, which early studies indicate as possibly linking CHR-P-symptoms and personality pathology.

METHODS

A community sample ( 444, 17-60 years, 61.8% female) was assessed via clinical telephone interview and online questionnaires. Using zero-inflated Poisson models, we explored associations of personality functioning, cognitive biases, current psychopathology, and psychosocial functioning with likelihood and severity of overall CHR-P, as well as perceptive (per-) and non-perceptive (nonper-)CHR-P-symptoms distinctly.

RESULTS

Higher nonper-CHR-P-symptom likelihood was associated with more impaired personality functioning and psychosocial functioning, while more severe cognitive biases were associated with higher CHR-P- and per-CHR-P-symptom likelihood, alongside higher CHR-P- and nonper-CHR-P-symptom severity. Further, more axis-I diagnoses were linked to higher CHR-P-, per-CHR-P-, and nonper-CHR-P-symptom likelihood, and younger age to higher CHR-P- and per-CHR-P-symptom severity, with CHR-P-symptom severity appearing higher in females. In an exploratory analysis, personality functioning elements identity and self-direction, and cognitive biases dichotomous thinking, emotional reasoning, and catastrophizing, respectively, showed multifaceted associations with nonper-CHR-P-symptom likelihood and overall CHR-P-symptom expression.

CONCLUSIONS

Our study supports the association of CHR-P-symptoms with multiple mental health factors. Findings suggest intricate associations between personality functioning impairments and cognitive biases with CHR-P-symptom expression in non-help-seeking populations, possibly contributing to different per-CHR-P- and nonper-CHR-P-symptom expression patterns. Therefore, they should be targeted in future longitudinal studies, aiming at better understanding CHR-P-manifestations to inform preventive intervention.

摘要

背景

除了预测精神病外,临床高危(CHR-P)症状通过与功能损害和精神病理学(包括人格病理学)的关联显示出临床相关性。在最近的维度人格障碍模型(DSM-5、ICD-11)中,人格功能受损被列为优先事项,但在CHR-P中尚未得到充分研究,与认知偏差的关联也是如此,早期研究表明认知偏差可能将CHR-P症状与人格病理学联系起来。

方法

通过临床电话访谈和在线问卷对一个社区样本(444人,17 - 60岁,61.8%为女性)进行评估。使用零膨胀泊松模型,我们探讨了人格功能、认知偏差、当前精神病理学和心理社会功能与总体CHR-P的可能性和严重程度,以及与感知性(per-)和非感知性(nonper-)CHR-P症状的明显关联。

结果

较高的非感知性CHR-P症状可能性与更受损的人格功能和心理社会功能相关,而更严重的认知偏差与较高的CHR-P和感知性CHR-P症状可能性相关,同时也与较高的CHR-P和非感知性CHR-P症状严重程度相关。此外,更多的轴I诊断与较高的CHR-P、感知性CHR-P和非感知性CHR-P症状可能性相关,年龄较小与较高的CHR-P和感知性CHR-P症状严重程度相关,CHR-P症状严重程度在女性中似乎更高。在一项探索性分析中,人格功能要素身份认同和自我导向,以及认知偏差二分法思维、情绪推理和灾难化思维,分别与非感知性CHR-P症状可能性和总体CHR-P症状表达呈现多方面的关联。

结论

我们的研究支持CHR-P症状与多种心理健康因素的关联。研究结果表明,在未寻求帮助的人群中,人格功能损害和认知偏差与CHR-P症状表达之间存在复杂的关联,这可能导致不同的感知性CHR-P和非感知性CHR-P症状表达模式。因此,在未来的纵向研究中应针对这些因素,旨在更好地理解CHR-P表现,为预防性干预提供信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/81e838426dc8/S0924933824018121_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/1b7381e64f94/S0924933824018121_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/8e6057d375e6/S0924933824018121_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/a6679b7bf4ec/S0924933824018121_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/81e838426dc8/S0924933824018121_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/1b7381e64f94/S0924933824018121_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/8e6057d375e6/S0924933824018121_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/a6679b7bf4ec/S0924933824018121_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2605/11822964/81e838426dc8/S0924933824018121_fig4.jpg

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