Trevor F Williams, James M Gold, James A Waltz, Jason Schiffman, Lauren M Ellman, Gregory P Strauss, Elaine F Walker, Scott W Woods, Albert R Powers, Joshua Kenney, Minerva K Pappu, Philip R Corlett, Tanya Tran, Steven M Silverstein, Richard E Zinbarg, Vijay A Mittal
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Participants (N = 621) were recruited from clinics and the community as part of the Computerized Assessment of Psychosis Risk (CAPR) consortium study. Structured clinical interviews, a dimensional risk calculator, and behavioral tasks were administered. Clinical interviews identified the following groups: (a) CHR-P (n = 273), (b) non-CHR-P individuals with limited psychosis like experiences (PLEs; n = 120), (c) participants with mental disorders and no PLEs (CLN; n = 82), and (d) healthy controls (HC; n = 146). Multinomial logistic regression indicated that the task battery differentiated groups (p < 0.001), with utility for identifying CHR-P individuals (Sensitivity = 0.87, PPV = 0.51, NPV = 0.77), though with high false positives that varied based on comparison group (Specificity = 0.21-0.43). Tasks also predicted psychosis risk calculator scores (Adjusted R<sup>2</sup> = 0.12), with the two unique predictors being positive symptom task variables associated with updating beliefs regarding environmental volatility. Overall, symptom mechanism tasks differentiated CHR-P individuals from control groups, suggesting their potential as novel screening tools. 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引用次数: 0
摘要
临床精神病高危人群(chrp)对了解疾病进展和治疗具有重要意义;然而,识别chrp个体的标准方法既昂贵又费力。关注个体精神病症状(阳性、阴性和紊乱)背后的神经认知机制可能会改善筛查和识别。本研究探讨了行为任务组是否可以通过分析症状机制来识别chrp个体并预测风险严重程度。参与者(N = 621)从诊所和社区招募,作为精神病风险计算机化评估(CAPR)联合研究的一部分。采用结构化临床访谈、维度风险计算器和行为任务。临床访谈确定了以下组:(a) chrp - p (n = 273), (b)有有限精神病样经历的非chrp个体(ple, n = 120), (c)有精神障碍但无ple的参与者(CLN, n = 82),以及(d)健康对照组(HC, n = 146)。多项逻辑回归表明,任务组区分组(p 2 = 0.12),两个独特的预测因子是与更新有关环境波动的信念相关的积极症状任务变量。总体而言,症状机制任务将chrp个体与对照组区分开来,表明它们有可能成为新的筛查工具。使用任务更有效地识别chrp个体(例如,丰富样本),可以降低障碍并识别可能被遗漏的个体。
Identifying individuals at clinical high risk for psychosis using a battery of tasks sensitive to symptom mechanisms.
The clinical high risk for psychosis (CHR-P) population is important for understanding disease progression and treatment; however, standard approaches to identifying CHR-P individuals are expensive and labor-intensive. Focusing on neurocognitive mechanisms that underlie individual psychosis symptoms (positive, negative, and disorganization) may improve screening and identification. The present study examines whether a behavioral task battery that assays symptom mechanisms can identify CHR-P individuals and predict risk severity. Participants (N = 621) were recruited from clinics and the community as part of the Computerized Assessment of Psychosis Risk (CAPR) consortium study. Structured clinical interviews, a dimensional risk calculator, and behavioral tasks were administered. Clinical interviews identified the following groups: (a) CHR-P (n = 273), (b) non-CHR-P individuals with limited psychosis like experiences (PLEs; n = 120), (c) participants with mental disorders and no PLEs (CLN; n = 82), and (d) healthy controls (HC; n = 146). Multinomial logistic regression indicated that the task battery differentiated groups (p < 0.001), with utility for identifying CHR-P individuals (Sensitivity = 0.87, PPV = 0.51, NPV = 0.77), though with high false positives that varied based on comparison group (Specificity = 0.21-0.43). Tasks also predicted psychosis risk calculator scores (Adjusted R2 = 0.12), with the two unique predictors being positive symptom task variables associated with updating beliefs regarding environmental volatility. Overall, symptom mechanism tasks differentiated CHR-P individuals from control groups, suggesting their potential as novel screening tools. Using tasks to more efficiently identify CHR-P individuals (e.g., enrich samples), may lower barriers and identify individuals that may otherwise be missed.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.