Parkinsonism & related disorders · 2014
Diffusion tensor imaging comparison of progressive supranuclear palsy and corticobasal syndromes.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Whitwell Jennifer L, Schwarz Christopher G, Reid Robert I, Kantarci Kejal, Jack Clifford R, Josephs Keith A
Аннотация
BACKGROUND: Corticobasal syndrome (CBS) and progressive supranuclear palsy syndrome (PSPS) are atypical parkinsonian syndromes that are both associated with white matter tract degeneration. However, little is known about how patterns of degeneration compare across these two syndromes.
METHODS: Twenty-seven subjects, nine with CBS and eighteen with probable or definite PSPS (9 pathologically confirmed) were prospectively recruited and underwent 3.0 T diffusion tensor imaging. A whole-brain voxel-based analysis was performed on fractional anisotropy (FA) and mean diffusivity (MD) images to compare both groups to each other and to 50 healthy controls.
RESULTS: The two syndromes showed overlapping regions of reduced FA and increased MD in the body of the corpus callosum, middle cingulum bundle, and premotor and prefrontal white matter, with reduced FA also observed in the superior cerebellar peduncles in both syndromes. However, CBS showed a more supratentorial and posterior pattern of degeneration with greater involvement of the splenium of the corpus callosum, premotor, motor and parietal lobes than PSPS. Findings in CBS were also highly asymmetric. Conversely, PSPS showed a more symmetric and infratentorial pattern of degeneration, with greater involvement of the superior cerebellar peduncles and midbrain than CBS.
CONCLUSIONS: CBS and PSPS are both associated with striking white matter tract degeneration. Despite differences in the supratentorial and infratentorial distribution of degeneration, and in asymmetry, both tend to target a common structural network. Measurements of white matter tract diffusion could therefore be useful disease biomarkers in both of these syndromes.
METHODS: Twenty-seven subjects, nine with CBS and eighteen with probable or definite PSPS (9 pathologically confirmed) were prospectively recruited and underwent 3.0 T diffusion tensor imaging. A whole-brain voxel-based analysis was performed on fractional anisotropy (FA) and mean diffusivity (MD) images to compare both groups to each other and to 50 healthy controls.
RESULTS: The two syndromes showed overlapping regions of reduced FA and increased MD in the body of the corpus callosum, middle cingulum bundle, and premotor and prefrontal white matter, with reduced FA also observed in the superior cerebellar peduncles in both syndromes. However, CBS showed a more supratentorial and posterior pattern of degeneration with greater involvement of the splenium of the corpus callosum, premotor, motor and parietal lobes than PSPS. Findings in CBS were also highly asymmetric. Conversely, PSPS showed a more symmetric and infratentorial pattern of degeneration, with greater involvement of the superior cerebellar peduncles and midbrain than CBS.
CONCLUSIONS: CBS and PSPS are both associated with striking white matter tract degeneration. Despite differences in the supratentorial and infratentorial distribution of degeneration, and in asymmetry, both tend to target a common structural network. Measurements of white matter tract diffusion could therefore be useful disease biomarkers in both of these syndromes.