Boxer Adam L, Garbutt Siobhan, Seeley William W, Jafari Aria, Heuer Hilary W, Mirsky Jacob, Hellmuth Joanna, Trojanowski John Q, Huang Erik, DeArmond Steven, Neuhaus John, Miller Bruce L
Memory and Aging Center, Department of Neurology, University of California-San Francisco, CA 94143-1207, USA.
Arch Neurol. 2012 Apr;69(4):509-17. doi: 10.1001/archneurol.2011.1021.
Deficits in the generation and control of saccades have been described in clinically defined frontotemporal dementia (FTD) and Alzheimer disease (AD).
To determine the saccade abnormalities associated with autopsy-defined cases of frontotemporal lobar degeneration (FTLD) and of AD, because clinical FTD syndromes can correspond to a number of different underlying neuropathologic FTD and non-FTD diagnoses.
An infrared eye tracker was used to record visually guided saccades to 10° targets and antisaccades in subjects with autopsy-confirmed FTD and subjects with autopsy-confirmed AD, a mean (SE) of 35.6 (10.0) months prior to death, and age-matched normal controls. Twelve subjects with FTD had an FTLD-TAR DNA-binding protein 43 pathology, 15 had an FTLD-tau pathology, and 1 subject showed an FTLD-fused in sarcoma protein pathology. Receiver operating curve statistics were used to determine the diagnostic value of the oculomotor variables. Neuroanatomical correlates of oculomotor abnormalities were investigated using voxel-based morphometry.
Memory and Aging Center, Department of Neurology, University of California, San Francisco.
A total of 28 subjects with autopsy-confirmed FTD, 10 subjects with autopsy-confirmed AD, and 27 age-matched normal controls.
All subjects with FTD or AD were impaired relative to normal controls on the antisaccade task. However, only FTLD-tau and AD cases displayed reflexive visually guided saccade abnormalities. The AD cases displayed prominent increases in horizontal saccade latency that differentiated them from the FTD cases. Impairments in velocity and gain were most severe in individuals with progressive supranuclear palsy but were also present in other tauopathies. By using vertical and horizontal saccade velocity and gain as our measures, we were able to differentiate patients with progressive supranuclear palsy from other patients. Vertical saccade velocity was strongly correlated with dorsal midbrain volume.
Decreased visually guided saccade velocity and gain are suggestive of underlying tau pathology in FTD, with vertical saccade abnormalities most diagnostic of progressive supranuclear palsy.
临床诊断的额颞叶痴呆（FTD）和阿尔茨海默病（AD）患者已被描述存在扫视的产生和控制缺陷。
确定与经尸检确诊的额颞叶变性（FTLD）和AD病例相关的扫视异常，因为临床FTD综合征可能对应多种不同的潜在神经病理学FTD和非FTD诊断。
使用红外眼动仪记录经尸检确诊的FTD患者、经尸检确诊的AD患者（死亡前平均（SE）35.6（10.0）个月）以及年龄匹配的正常对照者对10°目标的视觉引导扫视和反扫视。12例FTD患者存在FTLD - TAR DNA结合蛋白43病理学改变，15例存在FTLD - tau病理学改变，1例显示FTLD - 肉瘤融合蛋白病理学改变。采用受试者工作特征曲线统计来确定眼动变量的诊断价值。使用基于体素的形态学方法研究眼动异常的神经解剖学相关性。
加利福尼亚大学旧金山分校神经学系记忆与衰老中心。
共有28例经尸检确诊的FTD患者、10例经尸检确诊的AD患者以及27例年龄匹配的正常对照者。
所有FTD或AD患者在反扫视任务中相对于正常对照者均有损害。然而，只有FTLD - tau和AD病例表现出反射性视觉引导扫视异常。AD病例水平扫视潜伏期显著增加，使其与FTD病例区分开来。速度和增益受损在进行性核上性麻痹患者中最为严重，但在其他tau蛋白病中也存在。以垂直和水平扫视速度及增益作为测量指标，我们能够将进行性核上性麻痹患者与其他患者区分开来。垂直扫视速度与中脑背侧体积密切相关。
视觉引导扫视速度和增益降低提示FTD存在潜在的tau蛋白病理学改变，垂直扫视异常对进行性核上性麻痹最具诊断意义。
