A longitudinal diffusion tensor imaging study in symptomatic Huntington's disease

Sritharan, Anusha; Egan, Gary F.; Johnston, Leigh A.; Horne, Malcolm; Bradshaw, John L.; Bohanna, India; Asadi, Hamed; Cunnington, Ross; Churchyard, Andrew; Chua, Phyllis; Farrow, Maree; Georgiou‐Karistianis, Nellie

doi:10.1136/jnnp.2007.142786

Cited by 61 publications

(45 citation statements)

References 30 publications

(45 reference statements)

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“…Abnormalities in WM microstructure have been reported in postmortem studies of humans with HD (de la Monte et al 1988;Halliday et al 1998). This research was confirmed by in vivo studies with magnetic resonance imaging (MRI), which reported extensive WM volume loss (Aylward et al 1998, 2012Thieben et al 2002;Rosas et al 2003;Fennema-Notestine et al 2004;Beglinger et al 2005;Ciarmiello et al 2006;Paulsen et al 2006;Jech et al 2007;Squitieri et al 2009;Tabrizi et al 2009Tabrizi et al , 2011Tabrizi et al , 2012Tabrizi et al , 2013) and changes in WM microstructure (Mascalchi et al 2004;Reading et al 2005;Rosas et al 2006;Bartzokis et al 2007;Sritharan et al 2010;Stoffers et al 2010;Dumas et al 2012;Matsui et al 2014). Nevertheless, these previous macro-and microstructural studies focused on wholebrain WM or Region of Interest analyses.…”

Section: Introductionmentioning

confidence: 54%

The Corticospinal Tract in Huntington's Disease

Phillips¹,

Squitieri

Sánchez-Castañeda

et al. 2014

Cereb. Cortex

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Huntington's disease (HD) is characterized by progressive motor impairment. Therefore, the connectivity of the corticospinal tract (CST), which is the main white matter (WM) pathway that conducts motor impulses from the primary motor cortex to the spinal cord, merits particular attention. WM abnormalities have already been shown in presymptomatic (Pre-HD) and symptomatic HD subjects using magnetic resonance imaging (MRI). In the present study, we examined CST microstructure using diffusion tensor imaging (DTI)-based tractography in 30-direction DTI data collected from 100 subjects: Pre-HD subjects (n = 25), HD patients (n = 25) and control subjects (n = 50), and T 2 *-weighted (iron sensitive) imaging. Results show decreased fractional anisotropy (FA) and increased axial (AD), and radial diffusivity (RD) in the bilateral CST of HD patients. Pre-HD subjects had elevated iron in the left CST, regionally localized between the brainstem and thalamus. CAG repeat length in conjunction with age, as well as motor (UHDRS) assessment were correlated with CST FA, AD, and RD both in Pre-HD and HD. In the presymptomatic phase, increased iron in the inferior portion supports the "dying back" hypothesis that axonal damage advances in a retrograde fashion. Furthermore, early iron alteration may cause a high level of toxicity, which may contribute to further damage.

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Section: Introductionmentioning

confidence: 54%

The Corticospinal Tract in Huntington's Disease

Phillips¹,

Squitieri

Sánchez-Castañeda

et al. 2014

Cereb. Cortex

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“…Previous studies have primarily relied on scalar maps (e.g., FA) derived from the diffusion tensor to perform independent registrations to a standard template (Weaver et al, 2009), and have generally failed to differentiate longitudinal changes in HD from controls (Sritharan et al, 2010;Weaver et al, 2009). Registration of DTI data using full tensor information improves both specificity and precision for detecting longitudinal changes compared to standard scalar approaches (Keihaninejad et al, 2013).…”

Section: Discussionmentioning

confidence: 98%

Longitudinal change in white matter microstructure in Huntington's disease: The IMAGE-HD study

Poudel

Stout

Domínguez

et al. 2015

Neurobiology of Disease

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“…Although prior studies have suggested that DTI measurement is a valuable bio-marker to assess HD severity in human, limited longitudinal study has been performed to evaluate progressive changes 25–31 . In this study, DTI was performed on HD monkeys and age-matched control monkeys starting at six-months and at every 6-months interval up to 48 months of age to assess changes in the integrity of the white matter across development.…”

Section: Introductionmentioning

confidence: 99%

Developmental Whole Brain White Matter Alterations in Transgenic Huntington’s Disease Monkey

Meng

Jiang

Bachevalier

et al. 2017

Sci Rep

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Transgenic Huntington’s disease monkey (HD monkey) model provides great opportunity for studying disease progression that could lead to new insight for developing biomarker, early intervention and novel therapeutics. Whole brain white matter integrity of HD-monkeys was examined longitudinally from 6 to 48 months using diffusion tensor imaging (DTI) and tract-based spatial statistics (TBSS). Progressive developmental white matter alterations in HD monkeys were widespread and were observed not only in fiber bundles connecting cortical areas to the striatum (e.g. striatal bundle and external capsule), but also in long association fiber pathways, commissural fibers, and subcortical fiber bundle. In all fiber tracts, the data indicate an arrest in white matter development around 23 months followed by slight decline until adulthood in HD monkeys. The microstructural changes parallel the progressive motor, memory and cognitive decline previously reported as HD monkeys aged. The findings revealed the widespread progressive temporal-spatial microstructural changes in HD monkey brains from infancy to adulthood, suggesting differentiated degenerations across different brain areas during brain development.

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A longitudinal diffusion tensor imaging study in symptomatic Huntington's disease

Cited by 61 publications

References 30 publications

The Corticospinal Tract in Huntington's Disease

The Corticospinal Tract in Huntington's Disease

Longitudinal change in white matter microstructure in Huntington's disease: The IMAGE-HD study

Developmental Whole Brain White Matter Alterations in Transgenic Huntington’s Disease Monkey

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