Tractography of the corpus callosum in Huntington's disease.
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Tractography results showed decreased fractional anisotropy (FA) and increased radial diffusivity (RD) across broad regions of the CC in Pre-HD subjects.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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PubMed Central - PubMed
Affiliation: Clinical and Behavioural Neurology Department, Istituto di Ricovero e Cura a Carattere Scientifico Santa Lucia Foundation, Rome, Italy.
ABSTRACT
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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. Related in: MedlinePlus |
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pone-0073280-g002: Significant Correlations between Corpus Callosum FA, RD and CAG Repeat Length, Disease Burden, UDRS1 & UDRS2. Mentions: Correlations between callosal measures, clinical scores and genetic value within Pre-HD subjects and HD patients were significant for CAG Repeat length, Disease Burden, UHDRSI, and UHDRS2. Scatterplots in Figure 2 display correlations between the whole CC FA and RD and CAG repeats, Disease Burden, UHDRSI and UHDRS2. |
View Article: PubMed Central - PubMed
Affiliation: Clinical and Behavioural Neurology Department, Istituto di Ricovero e Cura a Carattere Scientifico Santa Lucia Foundation, Rome, Italy.