Anterior-medial thalamic lesions in dementia: frequent, and volume dependently associated with sudden cognitive decline

Anterior-medial thalamic lesions in dementia: frequent, and volume dependently associated with sudden cognitive decline
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DOI:
10.1136/jnnp.2006.091561
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发表时间:
2006-12-01
影响因子:
11
通讯作者:
Black, S. E.
Black, S. E.
中科院分区:
医学1区
文献类型:
--
作者:
Swartz, R. H.;Black, S. E.

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背景:与记忆处理相关的前内侧丘脑 (AMT) 受到阿尔茨海默病病理学的严重影响,当受损时,可能是痴呆的唯一原因。目的:评估影响 AMT 的磁共振成像 (MRI) 高信号频率及其与突然认知能力下降的关系。方法:来自大学认知神经病学诊所的 205 名连续参与者接受了临床评估、神经心理学测试和定量 MRI。结果:AMT 34 名正常对照中的 0 名出现> 5 mm(3) 的高信号,但在 30 名患有认知障碍但无痴呆 (CIND) 的参与者中发现了 5 名 (17%),在 109 名可能患有阿尔茨海默病的患者中发现了 9 名 (8%),在 17 名患有混合疾病的患者中发现了 7 名 (41%),在 15 名可能患有血管性痴呆 (VaD) 的患者中发现了 8 名 (53%)。逐步下降的参与者比缓慢进展的参与者更容易出现 AMT 高信号 (chi(2) = 31.7;p < 0.001)。在 29 名 AMT 高信号患者中,进展缓慢的患者内侧颞叶宽度较小 (p < 0.001),丘脑前内侧高信号较小 (p < 0.001)。在逻辑回归模型中,两个变量均显着,并且 86% 的样本中的下降模式被正确分类(Cox 和 Snell R-2 = 0.56;p < 0.001)。无论内侧颞叶宽度如何,AMT 高信号> 55 mm(3) 的患者认知功能可能会逐步下降;相比之下,那些 AMT 高信号较小的患者仅在没有内侧颞叶萎缩的情况下才表现出逐步下降。所有 VaD 患者均有左侧 AMT 高信号,而 CIND 患者则有右侧 AMT 高信号。结论:AMT 高信号 > 55 mm(3) 可能会导致症状下降,而较小的病变可能会被临床医生和放射科医生忽视。只有一半 AMT 高信号患者诊断为 VaD 或混合疾病;其他 AMT 高信号发生在诊断患有阿尔茨海默病或 CIND 的患者中。然而,这些无症状的高信号可能会导致认知功能障碍。 AMT 高信号可能是导致认知障碍的一个主要且未被充分认识的因素。
Background: The anterior-medial thalamus (AMT), which is associated with memory processing, is severely affected by Alzheimer's disease pathology and, when damaged, can be the sole cause of dementia.Objective: To assess the frequency of magnetic resonance imaging (MRI) hyperintensities affecting the AMT, and their relationship with sudden cognitive decline.Methods: 205 consecutive participants from a university cognitive neurology clinic underwent clinical evaluation, neuropsychological testing and quantitative MRI.Results: AMT hyperintensities > 5 mm(3) occurred in 0 of 34 normal controls but were found in 5 of 30 (17%) participants with cognitive impairment with no dementia (CIND), 9 of 109 (8%) patients with probable Alzheimer's disease, 7 of 17 (41%) with mixed disease and 8 of 15 (53%) with probable vascular dementia (VaD). AMT hyperintensities occurred more often in participants with stepwise decline than in those with slow progression (chi(2) = 31.7; p < 0.001). Of the 29 people with AMT hyperintensities, those with slow progression had smaller medial temporal width (p < 0.001) and smaller anterior-medial thalamic hyperintensities (p < 0.001). In a logistic regression model, both variables were significant, and the pattern of decline was correctly classified in 86% of the sample (Cox and Snell R-2 = 0.56; p < 0.001). Those with AMT hyperintensities > 55 mm(3) were likely to have stepwise decline in cognitive function regardless of medial temporal lobe width; in contrast, those with smaller AMT hyperintensities showed a stepwise decline only in the absence of medial temporal lobe atrophy. All patients with VaD had left-sided AMT hyperintensities, whereas those with CIND had right-sided AMT hyperintensities.Conclusions: AMT hyperintensities > 55 mm(3) probably result in symptomatic decline, whereas smaller lesions may go unrecognised by clinicians and radiologists. Only half of those with AMT hyperintensities had diagnoses of VaD or mixed disease; the other AMT hyperintensities occurred in patients diagnosed with Alzheimer's disease or CIND. These silent hyperintensities may nevertheless contribute to cognitive dysfunction. AMT hyperintensities may represent a major and under-recognised contributor to cognitive impairment.