Longitudinal MRI in progressive supranuclear palsy and multiple system atrophy: rates and regions of atrophy
Longitudinal MRI in progressive supranuclear palsy and multiple system atrophy: rates and regions of atrophy
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DOI：
10.1093/brain/awl021
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发表时间：
2006-04-01
期刊：
影响因子：
14.5
通讯作者：
Fox, NC
中科院分区：
文献类型：
--
作者：
Paviour, DC;Price, SL;Fox, NC
进行性核上性麻痹（PSP）和多系统萎缩（MSA）的脑萎缩率及其与临床疾病进展的关系尚不清楚。24例PSP患者，11例MSA-P患者（帕金森变异型），12名帕金森病患者和18名健康对照受试者被招募进行连续MRI扫描，临床评估和正式的神经心理学评估，以测量PSP和MSA-P患者生活中的脑萎缩及其与疾病进展的相关性。边界位移积分通过局部配准感兴趣区域，计算脑干（中脑和脑桥）、小脑、侧脑室和第三脑室以及额叶和后下脑区域的萎缩率，以获得局部边界位移积分（BSI）。82%的受试者完成了连续MRI扫描（17例PSP，9例MSA-P，9例帕金森病患者和18例健康对照）。PSP组全脑萎缩的平均（SD）年发生率最高：1.2%（1.0%），是对照组的3倍。PSP的平均（SD）中脑萎缩率为2.2%（1.5%），是健康对照组的7倍。在MSA-P中，脑桥萎缩率最高：4.5%（3.2%），是对照组的20倍以上，是PSP脑桥萎缩率的3倍。帕金森病患者的萎缩率与对照组的萎缩率没有显著差异。当使用BSI而不是手动测量计算时，萎缩率的变异性较低。PSP中运动功能障碍的加重与中脑萎缩有关，而MSA-P中的脑桥小脑萎缩与执行功能障碍的加重与PSP中额叶萎缩率的增加有关。小脑萎缩率是比横截面体积更好的鉴别MSA-P的指标。我们证实，序列MRI可以应用于测量全脑和区域萎缩率PSP和MSA-P。区域，而不是全脑萎缩率更好地区分PSP和MSA-P从健康对照组。临床-放射学相关性表明，这些局部萎缩率有可能作为新疗法试验中疾病进展的标志物。
The rate of brain atrophy and its relationship to clinical disease progression in progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) is not clear. Twenty-four patients with PSP, 11 with MSA-P (Parkinsonian variant), 12 with Parkinson's disease, and 18 healthy control subjects were recruited for serial MRI scans, clinical assessments and formal neuropsychological evaluations in order to measure brain atrophy during life and its association with disease progression in PSP and MSA-P. Serial scans were registered and rates of whole brain atrophy calculated from the brain-boundary shift integral. Regional rates of atrophy were calculated in the brainstem (midbrain and pons), the cerebellum, the lateral and third ventricles as well as frontal and posterior inferior brain regions, by locally registering to a region of interest in order to derive a local boundary shift integral (BSI). 82% of recruited subjects completed serial MRI scans (17 PSP, 9 MSA-P, 9 Parkinson's disease patients and 18 healthy controls). Mean (SD) annualized rates of whole-brain atrophy were greatest in PSP: 1.2% (1.0%), three times that in controls. Mean (SD) midbrain atrophy rates in PSP, 2.2% (1.5%), were seven times greater than in healthy controls. In MSA-P, atrophy rates were greatest in the pons: 4.5% (3.2%), over 20 times that in controls and three times the rate of pontine atrophy in PSP. Atrophy rates in Parkinson's disease were not significantly different from control rates of atrophy. Variability in the atrophy rates was lower when calculated using the BSI rather than manual measurements. Worsening motor deficit was associated with midbrain atrophy in PSP, and ponto-cerebellar atrophy in MSA-P. Worsening executive dysfunction was associated with increased rates of frontal atrophy in PSP. Cerebellar atrophy rates were better discriminators of MSA-P than cross-sectional volumes. We confirm that serial MRI can be applied to measure whole brain and regional atrophy rates in PSP and MSA-P. Regional rather than whole-brain atrophy rates better discriminate PSP and MSA-P from healthy controls. Clinico-radiological associations suggest these regional atrophy rates have potential as markers of disease progression in trials of novel therapies.