Abstract

Objective: To investigate the alterations of the volumes and 3D shapes of fifteen subcortical nucleus in patients with post-stroke depression (PSD) and to explore the pathogenesis regularity and mechanism of early PSD. Methods: From 2015 to 2017, a total of 28 patients with PSD and 18 stroke patients without depression (PSND), 13 patients with depression (De) and 11 cases of healthy volunteers (NC) were enrolled to perform 3.0 T high resolution MRI.Computer automatic segmentation and vertex analysis were used to segment and measure the volume of bilateral nucleus accumbens, caudate nucleus, putamen, globus pallidus, thalamus, hippocampus, mygdale and brainstem. Results: The volume of bilateral nucleus accumbens and bilateral thalamus, left pallidum were different among groups with statistical difference (P<0.05). The nucleus volume of the PSD group was (415±128) mm(3) (L-Nac)/(303±90) mm(3) (R-Nac), (7 590±867) mm(3) (L-Th)/(7 459±905) mm(3) (R-Th), (1 675±328) mm(3) (L-Pa), which was smaller than that of PSND group (433±100) mm(3) /(307±88) mm(3), (7 999±961) mm(3) /(7 753± 955) mm(3), (1 790±286) mm(3) and other groups.The nuclei with significantly statistical differences between inter-group were found in following: between PSD group and NC group, right accumbens and bilateral thalamus (P<0.01); between PSD group and De group, right accumbens and right thalamus (P<0.001), left accumbens, left pallidum and left thalamus (P<0.01); between PSND group and NC group, right accumbens (P<0.05); between PSND group and De group, right accumbens (P<0.001), left accumbens and right thalamus (P<0.05). Significant differences in morphology changes of nuclei (P<0.05) by F test mainly located on the top and tail of right accumbens, the anterior and middle body of right caudate nucleus, the most part of bilateral thalamus, the ventromedial body of bilateral hippocampus, the anterior and body of left caudate nucleus, especially in left thalamus. Conclusion: PSD has abnormal volume and morphological structure of subcortical nuclei, which supports the role of subcortical structures changes in the pathophysiology and pathogenesis of early PSD.

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