A quantitative meta-analysis of population-based studies of premorbid intelligence and schizophrenia.
A quantitative meta-analysis of population-based studies of premorbid intelligence and schizophrenia.
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DOI：
10.1016/j.schres.2011.06.017
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发表时间：
2011-11
影响因子：
4.5
通讯作者：
Jones, Peter B.
中科院分区：
文献类型：
--
作者：
Khandaker, Golam M.;Barnett, Jennifer H.;White, Ian R.;Jones, Peter B.
病前智商缺陷支持精神分裂症的发展维度及其认知方面，这些方面对功能结果至关重要。更好地描述病前智商和疾病之间的联系，可能会进一步深入了解其起源和病因。我们的目标是通过对纵向的、基于人群的研究进行系统回顾和荟萃分析来量化精神分裂症病前的认知功能，并在病前智商的整个范围内表征精神分裂症的风险。电子和手动搜索确定了一般的基于人群的队列或嵌套病例对照研究，这些研究使用标准的心理测量学测试来衡量精神分裂症精神病发作前的智力，并使用同期的ICD或DSM来确定病例。Meta分析探索了病前认知缺陷(使用全量表、言语和操作智商)与精神分裂症风险之间的剂量-反应关系。Meta回归分析探索了与发病年龄、病前智力随时间的变化以及性别差异的关系。来自12项独立研究的4,396例病例和超过745,000名对照的荟萃分析证实，在未来的病例中，病前智商(效应大小−(0.43))显著降低。精神分裂症的风险表现为一致的剂量-反应效应，智商每下降一分，精神分裂症的风险就会增加3.7%(p<0.0001)。语言和非语言措施同样受到影响。病前智商下降程度越大，发病时间越早(P<0.0001)。没有证据表明，在疾病发作前的一段时间内，赤字逐渐增加。病前智商与精神分裂症风险和发病年龄之间的强烈关联证明，神经发育对精神分裂症的广泛贡献贯穿于整个智力范围。这也表明，高智商可能通过增加主动认知储备对精神分裂症起到保护作用。
A premorbid IQ deficit supports a developmental dimension to schizophrenia and its cognitive aspects that are crucial to functional outcome. Better characterisation of the association between premorbid IQ and the disorder may provide further insight into its origin and etiology. We aimed to quantify premorbid cognitive function in schizophrenia through systematic review and meta-analysis of longitudinal, population-based studies, and to characterize the risk of schizophrenia across the entire range of premorbid IQ. Electronic and manual searches identified general population-based cohort or nested case–control studies that measured intelligence before onset of schizophrenic psychosis using standard psychometric tests, and that defined cases using contemporaneous ICD or DSM. Meta-analyses explored dose–response relationships between premorbid cognitive deficit (using full-scale, verbal and performance IQ) and risk of schizophrenia. Meta-regression analyses explored relationships with age of illness onset, change in premorbid intelligence over time and gender differences. Meta-analysis of 4396 cases and over 745 000 controls from 12 independent studies confirmed significant decrements in premorbid IQ (effect size − 0.43) among future cases. Risk of schizophrenia operated as a consistent dose–response effect, increasing by 3.7% for every point decrease in IQ (p < 0.0001). Verbal and nonverbal measures were equally affected. Greater premorbid IQ decrement was associated with earlier illness onset (p < 0.0001). There was no evidence of a progressively increasing deficit during the premorbid period toward illness onset. Strong associations between premorbid IQ and risk for schizophrenia, and age of illness onset argue for a widespread neurodevelopmental contribution to schizophrenia that operates across the entire range of intellectual ability. This also suggests higher IQ may be protective in schizophrenia, perhaps by increasing active cognitive reserve.
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