COGNITIVE TEST-PERFORMANCE IN DETECTING, STAGING, AND TRACKING ALZHEIMERS-DISEASE
COGNITIVE TEST-PERFORMANCE IN DETECTING, STAGING, AND TRACKING ALZHEIMERS-DISEASE
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DOI：
10.1001/archneur.1995.00540350081020
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发表时间：
1995-11-01
影响因子：
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通讯作者：
CORKIN, S
中科院分区：
文献类型：
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作者：
LOCASCIO, JJ;GROWDON, JH;CORKIN, S
目的：确定阿尔茨海默病 (AD) 的特定认知缺陷，并确定哪些认知测试或测试组合最适合检测 AD（即区分 AD 患者与正常对照受试者）、AD 分期（即区分不同严重程度的痴呆）和跟踪疾病进展。受试者：年龄、教育程度和性别分布相当的 AD 患者 (n=123) 和正常对照受试者 (n=60)。地点：门诊患者护理措施：记忆、语言、视觉空间能力和推理能力的十项认知测试；设计：AD 患者在长达 5.5 年的时间里每 6 至 24 个月接受一次测试。结果：AD 患者在所有认知测试中均显着低于正常对照受试者。 AD 患者的评分随着时间的推移而恶化。对故事和人物的延迟回忆显示，早期的情况急剧恶化，这与这些测试可以很好地区分轻度 AD 患者和正常对照受试者但在分期方面较差的发现相一致。 AD 患者的对抗命名、语义流畅性和几何图形的即时识别能力随着时间的推移呈现稳定的线性下降，这与这些测试最适合对痴呆严重程度进行分期一致。结论：我们假设延迟回忆障碍的病理基础是胆碱能腹侧前脑神经元萎缩和海马部分传入神经阻滞，这两者都发生在 AD 病程早期。语言和视觉空间能力的恶化可能反映了新皮质神经元及其连接的逐渐丧失。
Objectives: To identify the specific cognitive deficits that characterize Alzheimer's disease (AD) and determine which cognitive tests, or combination of tests, are best for detecting AD (ie, distinguishing patients with AD from normal control subjects), staging AD (ie, distinguishing different severities of dementia), and tracking disease progression.Subjects: Patients with AD (n=123) and normal control subjects (n=60) of comparable age, education, and gender distribution.Setting: Outpatient care.Measures: Ten cognitive tests of memory, language, visuospatial abilities, and reasoning; the Information, Memory and Concentration subtest of the Blessed Dementia Scale,and the total score on an activities of daily living questionnaire.Design: Patients with AD were tested every 6 to 24 months over a span of up to 5.5 years.Results: Patients with AD were significantly inferior to normal control subjects on all cognitive tests. The scores of patients with AD worsened over time. Delayed recall of stories and figures showed sharp deterioration to an early floor, consistent with the finding that these tests discriminated patients with mild AD from normal control subjects well but were poor for staging. Confrontation naming, semantic fluency, and immediate recognition of geometric figures showed steady linear decline across time for patients with AD, consistent with these tests being found best for staging dementia severity.Conclusions: We postulate that the pathologic bases of impairment in delayed recall are atrophy of cholinergic ventral forebrain neurons and partial deafferentation of the hippocampus, both of which occur early in the course of AD. Worsening language and visuospatial abilities likely reflect progressive loss of neocortical neurons and their connections.