Haishan Qiu1, Jing Zhao1, Manshi Hu1, Mengzhu Wang2, and Jianping Chu1
1Sun Yat-sen University, Guangzhou, China, 2Simens Healthcare, Guangzhou, China
1Sun Yat-sen University, Guangzhou, China, 2Simens Healthcare, Guangzhou, China
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gene confirmed SCA3 patients, including 37 symptomatic and 15 presymptomatic,
and 35 health controls were prospectively included, and VBM and TBSS were used to
investigate the differences of GM and WM. Our study
indicates that there is an evolving history of structural images with SCA3
patients in different disease stages. The WM damage starts with the impairment
of ICP and goes through SCP extends to the midbrain, then widespread to the
whole brain. The alteration of GMV does not occur until the arise of ataxia
symptom, then began to involve the medulla, cerebellum, and pons, and developed
to involve basal ganglion, after the decompensation of bilateral dorsal
thalamus, finally affect the cortical cortex. The impairment of WM tracts
precedes the GM atrophy and, irrespective of the patients with or without
clinical manifestation, the identified WM damage was significantly correlated
with SARA.
Tract-based statistical analysis of DKT/DTI
metrics between symptomatic SCA3 patients and health controls.
Red-yellow highlights show areas of decreased DKI/DTI metrics values in symptomatic SCA3. Blue highlights show areas of increased MD value in symptomatic SCA3.(P＜0.05, TFCE correction)
Tract-based statistical analysis of DKT/DTI
metrics between symptomatic SCA3 patients and health controls.
Red-yellow highlights show areas of decreased DKI/DTI metrics values in symptomatic SCA3. Blue highlights show areas of increased MD value in symptomatic SCA3.(P＜0.05, TFCE correction)