Tractography of the Corpus Callosum in Huntington's Disease

被引:48
作者
Phillips, Owen [1 ]
Sanchez-Castaneda, Cristina [2 ]
Elifani, Francesca [3 ]
Maglione, Vittorio [3 ]
Di Pardo, Alba [3 ]
Caltagirone, Carlo [1 ,4 ]
Squitieri, Ferdinando [3 ]
Sabatini, Umberto [2 ]
Di Paola, Margherita [1 ,5 ]
机构
[1] Ist Ricovero & Cura Carattere Sci Santa Lucia Fdn, Clin & Behav Neurol Dept, Rome, Italy
[2] Ist Ricovero & Cura Carattere Sci Santa Lucia Fdn, Dept Radiol, Rome, Italy
[3] Ist Ricovero & Cura Carattere Sci Neuromed, Ctr Neurogenet & Rare Dis, Pozzilli, Italy
[4] Univ Roma Tor Vergata, Neurosci Dept, Rome, Italy
[5] Univ Aquila, Dept Internal Med & Publ Hlth, I-67100 Laquila, Italy
来源
PLOS ONE | 2013年 / 8卷 / 09期
关键词
CEREBRAL WHITE-MATTER; MAGNETIC-RESONANCE; DIFFUSION; BRAIN; MORPHOLOGY; DYSMYELINATION; CONNECTIVITY; EXPRESSION; ANISOTROPY; PATHOLOGY;
D O I
10.1371/journal.pone.0073280
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
White matter abnormalities have been shown in presymptomatic and symptomatic Huntington's disease (HD) subjects using Magnetic Resonance Imaging (MRI) and Diffusion Tensor Imaging (DTI) methods. The largest white matter tract, the corpus callosum (CC), has been shown to be particularly vulnerable; however, little work has been done to investigate the regional specificity of tract abnormalities in the CC. Thus, this study examined the major callosal tracts by applying DTI-based tractography. Using TrackVis, a previously defined region of interest tractography method parcellating CC into seven major tracts based on target region was applied to 30 direction DTI data collected from 100 subjects: presymptomatic HD (Pre-HD) subjects (n = 25), HD patients (n = 25) and healthy control subjects (n = 50). Tractography results showed decreased fractional anisotropy (FA) and increased radial diffusivity (RD) across broad regions of the CC in Pre-HD subjects. Similar though more severe deficits were seen in HD patients. In Pre-HD and HD, callosal FA and RD were correlated with Disease Burden/CAG repeat length as well as motor (UHDRSI) and cognitive (URDRS2) assessments. These results add evidence that CC pathways are compromised prior to disease onset with possible demyelination occurring early in the disease and suggest that CAG repeat length is a contributing factor to connectivity deficits. Furthermore, disruption of these callosal pathways potentially contributes to the disturbances of motor and cognitive processing that characterize HD.
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页数:9
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