抑郁障碍与基底节区脑梗死患者早期运动障碍加重的关系

Association Between Depressive Disorders and Early Progressive Motor Deficits Among Patients with Cerebral Infarcts in Basal Ganglia Region

目的探讨抑郁障碍对基底节区脑梗死早期运动障碍加重的影响。方法收集首次发病的基底节区急性脑梗死患者85例,所有患者完善头颅磁共振成像(MRI)+磁共振血管成像(MRA)+弥散加权成像(DWI)检查。入院时通过Hamilton抑郁量表评分,将入选患者分为无抑郁障碍组和抑郁障碍组;入院后依据美国国立卫生脑卒中量表(NIHSS)对早期运动障碍动态评分,将以上每组再分成稳定亚组和进展亚组。比较各组的早期运动障碍进展发生率、梗死灶体积前后比(V2/V1)、大脑中动脉(MCA)病变及血压、血脂、空腹血糖。结果 1.抑郁障碍组早期运动障碍进展率(10/27,37.04%)明显高于无抑郁障碍组(9/58,15.52%)(χ2=4.92,P=0.03);2.基底节区脑梗死存在明显MCA狭窄或闭塞(37/85,43.53%),抑郁障碍组与无抑郁障碍组MCA病变差异无统计学意义(χ2=0.34,P=0.56);3.进展亚组V2/V1大于稳定亚组;在进展亚组中,抑郁障碍组V2/V1与无抑郁障碍组差异有统计学意义(F=167.39,P=0.00);4.收缩压、空腹血糖在病情进展时明显偏高,其中空腹血糖与抑郁障碍存在明显相关性(r=0.425,P=0.000)。结论抑郁障碍能促进基底节区脑梗死早期运动障碍进展。

Objective To explore the impact of depressive disorders on early progressive motor deficits among patients with cerebral infarcts of basal ganglia region. Methods Eighty- five patients with first cerebral infarcts in basal ganglia re- gion were enrolled into this study. All patients were examined with brain magnetic resonance imaging （MRI）, magnetic reso- nance angiography （MRA） and diffusion weighted imaging （DWI）. According to the Hamilton Depression Rating Scale scores on admission, patients were divided into non- depressive disorders group and depressive disorders group. Based on NIHSS scores of early progressive motor deficits, each above- mentioned group was further divided into stable subgroup and progressive subgroup. The occurrence rate of early progressive motor deficits, front- to- back ratio of volume of lesions （Vz/V1）, pathological changes in the middle cerebral artery （MCA）, blcxxi pressure, blood lipids and fasting blood glucose were compared between non- depres- sive disorders and depressive disorders groups. Results The occurrence rate of early progressive motor deficits in depressive disorders group was significantly higher than that of non- depressive disorders group （10/27, 37.04% vs 9]58, 15.52% , X2 = 4.92, P = 0.03）. MCAs were obviously stenosing or occlusive （37/85, 43.53 % ） in cerebral infarcts of basal ganglia region, but no statistically significant difference was found in the pathological changes in the MCA between non- depressive disorders and de- pressive disorders groups （ X2 =0.34, P=0.56）. V2/V1 of progressive subgroups was larger than that of stable subgroups, and V2/VI of depressive disorders groups was significantly different from that of non- depressive disorders in progressive subgroups （ F = 167.39, P = 0.00）. Systolic blood pressure and fasting blood glucose were significantly higher in the progression of the dis- ease, and there was a significantly correlation between fasting blood glucose and depressive disorders （ r = 0. 425, P = 0. 000）. Conclusions Depressive disorders can promote the progression of early motor deficits in cerebral infarcts of basal ganglia region.