背景:在小儿双相情感障碍(PBD)中已证实认知功能受损。皮质下边缘结构在PBD中起关键作用。然而,皮质下边缘结构的解剖和功能特征及其与PBD神经认知的关系尚不清楚。
方法:三十六个I型PBD(PBD-I)(15.36±0.32岁),纳入20名PBDII型(PBD-II)(14.80±0.32岁)和19名年龄性别匹配的健康对照(HCs)(14.16±0.36岁)。首先,获得了皮质下边缘结构的体积,并评估了体积的差异.然后,这些结构作为感兴趣区域的种子来计算体素的功能连接(FC).之后,在显示显着差异的大脑区域的体积和FC之间完成了相关分析,并进行了神经心理学测试。
结果:与HC相比,PBD-I和PBD-II患者的Stroop颜色词测试(SCWT)和数字跨度向后测试得分均下降.与HC相比,PBD-II患者显示右间隔核体积显著增加,PBD-I患者表现为右伏核和双侧苍白球的FC增加,右基底前脑,右壳核和左苍白球。显著改变的体积和FC均与SCWT评分呈负相关。
结论:该研究揭示了皮质下边缘结构和功能异常在PBD患者认知损害中的作用。这些可能对PBD的病因具有深远的意义,并为PBD亚型的鉴别诊断提供神经影像学线索。
结论:PBD亚型中神经结构和功能的独特特征可能有助于更好地理解PBD的潜在机制。
BACKGROUND: Impaired cognition has been demonstrated in pediatric bipolar disorder (PBD). The subcortical limbic structures play a key role in PBD. However, alternations of anatomical and functional characteristics of subcortical limbic structures and their relationship with neurocognition of PBD remain unclear.
METHODS: Thirty-six PBD type I (PBD-I) (15.36 ± 0.32 years old), twenty PBD type II (PBD-II) (14.80 ± 0.32 years old) and nineteen age-gender matched healthy controls (HCs) (14.16 ± 0.36 years old) were enlisted. Primarily, the volumes of the subcortical limbic structures were obtained and differences in the volumes were evaluated. Then, these structures served as seeds of regions of interest to calculate the voxel-wised functional connectivity (FC). After that, correlation analysis was completed between volumes and FC of brain regions showing significant differences and neuropsychological tests.
RESULTS: Compared to HCs, both PBD-I and PBD-II patients showed a decrease in the Stroop color word test (SCWT) and digit span backward test scores. Compared with HCs, PBD-II patients exhibited a significantly increased volume of right septal nuclei, and PBD-I patients presented increased FC of right nucleus accumbens and bilateral pallidum, of right basal forebrain with right putamen and left pallidum. Both the significantly altered volumes and FC were negatively correlated with SCWT scores.
CONCLUSIONS: The study revealed the role of subcortical limbic structural and functional abnormalities on cognitive impairments in PBD patients. These may have far-reaching significance for the etiology of PBD and provide neuroimaging clues for the differential diagnosis of PBD subtypes.
CONCLUSIONS: Distinctive features of neural structure and function in PBD subtypes may contribute to better comprehending the potential mechanisms of PBD.