Gold James M, Hahn Britta, Zhang Wei Wei, Robinson Benjamin M, Kappenman Emily S, Beck Valerie M, Luck Steven J
Maryland Psychiatric Research Center, Baltimore, MD 21228, USA.
Arch Gen Psychiatry. 2010 Jun;67(6):570-7. doi: 10.1001/archgenpsychiatry.2010.65.
Working memory deficits are considered a core feature of schizophrenia. Several recent integrative articles have offered mechanistic computational and neurobiological models of the origins of this cognitive deficit.
To test predictions of these models using a new experimental paradigm from the basic science literature that makes it possible to determine whether patients with schizophrenia show (1) deficits in working memory storage capacity, (2) deficits in the precision of working memory representations, and (3) an amplification of these deficits as the retention interval increases.
Case-control design. All subjects performed a color working memory test in which they were asked to recall 3 or 4 items after a 1- or 4-second delay. All subjects also received a standard measure of intelligence and the Matrics Consensus Cognitive Battery.
A tertiary care research outpatient clinic. Patients A total of 31 clinically stable patients with a DSM-IV diagnosis of schizophrenia or schizoaffective disorder and 26 healthy volunteers participated. The 2 groups were similar in age, sex, and ethnicity distribution.
(1) The number of items stored in working memory and (2) the precision of the working memory representations.
Patients showed a clear reduction in the number of items stored in working memory. Patients did not differ from controls in the precision of their working memory representations. There was no evidence of delay-related amplification of impairment in either capacity or precision.
Patients do not show the type of imprecision or delay-dependent amplification of impairment that is predicted on the basis of current models of the neurobiology of schizophrenia. The models need to be revised to account for a pure reduction in the number of items that patients are able to store in working memory.
工作记忆缺陷被认为是精神分裂症的核心特征。最近有几篇综合性文章提出了关于这种认知缺陷起源的机制性计算和神经生物学模型。
使用基础科学文献中的一种新实验范式来检验这些模型的预测,该范式能够确定精神分裂症患者是否表现出:(1)工作记忆存储容量缺陷;(2)工作记忆表征精度缺陷;以及(3)随着延迟间隔增加这些缺陷的放大。
病例对照设计。所有受试者都进行了一项颜色工作记忆测试,要求他们在1秒或4秒延迟后回忆3或4个项目。所有受试者还接受了智力标准测量和矩阵共识认知电池测试。
三级护理研究门诊诊所。患者共有31名临床稳定的DSM-IV诊断为精神分裂症或分裂情感性障碍的患者以及26名健康志愿者参与。两组在年龄、性别和种族分布上相似。
(1)工作记忆中存储的项目数量;(2)工作记忆表征的精度。
患者在工作记忆中存储的项目数量明显减少。患者与对照组在工作记忆表征精度方面没有差异。没有证据表明在能力或精度方面存在与延迟相关的损伤放大。
患者并未表现出基于当前精神分裂症神经生物学模型所预测的那种不精确或延迟依赖性损伤放大类型。这些模型需要修订,以解释患者在工作记忆中能够存储的项目数量单纯减少的情况。