帕金森病合并高血压病患者认知功能障碍进展及其与皮层下微结构损害的关系研究

A study on the progression of cognitive impairment in patients with Parkinson’s disease combined with high blood pressure and its correlation with damage to subcortical microstructure

目的 探讨帕金森病(PD)合并高血压病(HBP)患者认知功能障碍进展及其与皮层下微结构损害的关系。方法 选取40例PD患者,剔除因未进行磁共振成像(MRI)扫描或扫描影像质量差患者3例,最终37例患者纳入研究,根据是否合并HBP分为PD-HBP组(11例)及PD-NHBP组(26例)。两组患者均进行脑结构MRI扫描。比较两组患者的一般资料与临床特征、血管周围间隙扩大(EPVS)特征、基底节和中脑微结构。结果 随访1年后, PD-HBP组患者蒙特利尔认知评估量表(MoCA)评分20(11, 26)分低于PD-NHBP组的24(12, 28)分,差异有统计学意义(P<0.05)。PD-HBP组患者全脑的中位EPVS数量多于PD-NHBP组,直径大于PD-NHBP组,差异具有统计学意义(P<0.05)。两组患者皮层下白质的中位EPVS数量比较差异无统计学意义(P>0.05);PD-HBP组患者基底节区和中脑的中位EPVS数量多于PD-NHBP组,差异具有统计学意义(P<0.05)。PD-HBP组双侧黑质、壳核、苍白球、尾状核的平均峰度(MK)值高于PD-NHBP组,差异具有统计学意义(P<0.05)。两组患者双侧黑质、壳核、苍白球和尾状核的轴向峰度(AK)、径向峰度(RK)、峰度部分各向异性(Kfa)、轴向弥散(AD)、径向弥散(RD)、部分各向异性(FA)和平均弥散(MD)值比较差异无统计学意义(P>0.05)。结论 HBP可能通过损害PD-HBP患者皮层下微结构引起认知障碍进展,这为寻找临床认知障碍进展特异性指标提供了线索。

Objective To discuss the progression of cognitive impairment in patients with Parkinson’s disease(PD) combined with high blood pressure(HBP) and its correlation with damage to subcortical microstructure. Methods 40 patients with PD were selected, and three patients were excluded because they did not undergo magnetic resonance imaging(MRI) scans or had poor quality scans. 37 patients were finally included in the study and were divided into the PD-HBP group(11 patients) and the PD-NHBP group(26 patients)according to whether they had HBP in combination. All subjects underwent MRI scanning of brain structure. The general data, clinical features, enlarged perivascular spaces(EPVS) features, and basal ganglia and midbrain microstructure of the two groups were compared. Results After 1 year of follow-up, patients in the PD-HBP group had lower Montreal Cognitive Assessment Scale(MoCA) scores of 20(11, 26) compared with 24(12, 28) in the PD-NHBP group, and the difference was statistically significant(P<0.05). Patients in the PD-HBP group had more median EPVS in the whole brain than in the PD-NHBP group and larger diameter than in the PD-NHBP group, and the difference was statistically significant(P<0.05). There was no statistically significant difference in the median number of EPVS in the subcortical white matter between the two groups(P>0.05). The median number of EPVS in the basal ganglia and midbrain in the PD-HBP group was significantly higher than that in the PDNHBP group, and the difference was statistically significant(P<0.05). The mean kurtosis(MK) values of bilateral substantia nigra, putamen, globus pallidus, and caudate nucleus in PD-HBP group were higher than those in PD-NHBP group, and the difference was statistically significant(P<0.05). The differences in axial kurtosis(AK),radial kurtosis(RK), kurtosis fractional anisotropy(Kfa), axial dispersion(AD), radial dispersion(RD), fractional anisotropy(FA) and mean dispersion(MD) values were not statistically significant(P>0.05) when comparing the bilateral substantia nigra, putamen, globus pallidus, and caudate nucleus in the two groups. Conclusion HBP may cause progression of cognitive impairment by impairing subcortical microstructure in patients with PD-HBP,which provides clues for finding specific indicators of clinical cognitive impairment progression.