Van Os Jim, Delespaul Philippe
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, European Graduate School of Neuroscience, Maastricht University, The Netherlands.
Dialogues Clin Neurosci. 2005;7(1):53-67. doi: 10.31887/DCNS.2005.7.1/jvanos.
Screening for preschizophrenia in the general population with the aim of preventing transition to full-blown illness is an epidemiological impossibility because a rare disease cannot be predicted. The lack of specificity resulting in abundance of false-positives can be remedied in part by using much more restrictive screening criteria that combine several indicators of risk for transition to schizophrenia. Raising the specificity (reducing the false-positives), however, can only be done at the expense of sensitivity (increasing the false-negatives). The most commonly used strategy to raise specificity is the sample enrichment strategy. This involves the creation of samples enriched with schizophrenia risk by selectively filtering at-risk people out over a range of consecutive referral processes starting in the general population, through to general practioners, mental health services, and the early detection clinic. However, improvements in specificity obtained by the sample enrichment strategy should not be attributed to the use of some predictive instrument that supposedly identifies high-risk individuals. The epidemiologically and ethically most viable way for screening and early detection is to selectively increase the permeability of the filters on the pathway to mental health care. This will occasion samples of help-seekers enriched with schizophrenia risk at the level of mental health services (thus reducing false-positives), while at the same time making an attempt to "attract" as many detectable schizophrenia prodromes as possible through the filters along the pathway to mental health care (thus reducing false-negatives). Early psychosis research has yielded some useful suggestions in that it is becoming increasingly clear that it is not just psychosis itself, but rather the clinical context of the psychotic experience that determines risk for transition to schizophrenia. Thus, risk for transition to full-blown psychotic disorder is to a large degree determined by size of psychosis "load," comorbid distress and depression, cannabis use, cognitive ability, and subjective reports of impairment and coping. Making a diagnosis of psychotic disorder is not an exact science: it involves an arbitrary cutoff imposed on dimensional variation of psychopathology and need for care over time. Gaining insight into the cognitive and biological factors that drive the dimensional variation, including therapeutic interventions, is arguably more useful than sterile dichotomous prediction models.
在普通人群中筛查精神分裂症前期以预防其发展为全面发作的疾病，从流行病学角度来看是不可能的，因为罕见疾病无法预测。通过使用更为严格的筛查标准（结合多种向精神分裂症转变的风险指标），可以部分弥补因缺乏特异性而导致大量假阳性的问题。然而，提高特异性（减少假阳性）只能以牺牲敏感性（增加假阴性）为代价。提高特异性最常用的策略是样本富集策略。这包括通过在一系列连续的转诊过程中进行选择性筛选，从普通人群开始，经过全科医生、心理健康服务机构，直至早期检测诊所，来创建富含精神分裂症风险的样本。然而，样本富集策略所带来的特异性提高不应归因于使用了某种据称能识别高危个体的预测工具。从流行病学和伦理角度来看，筛查和早期检测最可行的方法是有选择地提高通往精神卫生保健途径上各环节的筛选标准的通透性。这将在心理健康服务层面产生富含精神分裂症风险的求助者样本（从而减少假阳性），同时试图通过通往精神卫生保健途径上的各环节筛选标准“吸引”尽可能多的可检测到的精神分裂症前驱症状者（从而减少假阴性）。早期精神病研究已经给出了一些有用的建议，因为越来越清楚的是，不仅仅是精神病本身，而是精神病体验的临床背景决定了向精神分裂症转变的风险。因此，向全面发作的精神障碍转变的风险在很大程度上取决于精神病“负荷”的大小、共病的痛苦和抑郁、大麻使用情况、认知能力以及功能损害和应对的主观报告。做出精神病性障碍的诊断并非一门精确的科学：它涉及对精神病理学维度变化所设定的任意界限以及对一段时间内护理需求的考量。深入了解驱动维度变化的认知和生物学因素，包括治疗干预，可能比无意义的二分法预测模型更有用。
