帕金森氏病伴发抑郁的特点及艾司西酞普兰疗效的研究

目的研究帕金森氏病伴发抑郁的特点，观察抗抑郁剂艾司西酞普兰对帕金森氏病伴发抑郁患者康复的影响，为帕金森氏病伴发抑郁的干预提供依据。方法采用临床流行病学调查方法对门诊和住院的198例帕金森氏病患者进行帕金森氏病伴发抑郁及其相关因素的现状调查，运用抑郁自评量表（SDS）、汉密尔顿抑郁量表（HAMD）、日常生活能力量表（ADL）和自制一般情况调查表对帕金森氏病患者进行评定，将帕金森氏病伴发抑郁患者随机分为艾司西酞普兰治疗组和对照组，观察艾司西酞普兰对患者康复的疗效。结果帕金森氏病伴发抑郁的发生率为56．86％，帕金森氏病伴发抑郁的特点为睡眠障碍、绝望、运动阻滞和焦虑等主要表现；帕金森氏病患者HAMD和ADL评分高；口服艾司西酞普兰后治疗组与对照组相比HAMD、HDL减分明显，抗抑郁治疗在缓解抑郁症状的同时，可以改善患者日常生活能力。结论帕金森氏病伴发抑郁发生率较高，以睡眠障碍、绝望、运动阻滞和焦虑等主要表现，抗抑郁剂艾司西酞普兰不仅可以明显改善帕金森氏病伴发抑郁的抑郁症状，还能提高患者的日常生活能力，促进患者的康复。

对帕金森合并抑郁患者进行艾司西酞普兰治疗的临床效果观察

目的研究帕金森合并抑郁患者进行艾司西酞普兰治疗的临床疗效。方法选取2012年7月~2013年8月间在我院接受治疗的帕金森合并抑郁病患者92例,将其随机分为两组,对照组和研究组各有患者46例。给予对照组帕金森合并抑郁病患者帕罗西汀进行治疗,给予研究组帕金森合并抑郁病患者艾司西酞普兰进行治疗。结果两组帕金森合并抑郁病患者接受治疗后的症状都得到了一定的改善,经治疗后两组患者的抑郁测量表SDS评分无明显变化,UPDRS评分研究组帕金森合并抑郁病患者与对照组相比更高,治疗效果更好。结论艾司西酞普兰治疗帕金森合并抑郁病患者有较好的治疗效果,起效快,不良反应发生率低,增强患者的依从性,值得在临床推广。

益肾疏肝法辨治帕金森病与抑郁共病40例临床观察

目的观察益肾疏肝法辨治帕金森病与抑郁共病的临床疗效。方法将符合帕金森病与抑郁诊断标准且24项汉密尔顿抑郁量表(HAMD-24)≥20分的40例患者作为观察对象,随机分为治疗组和对照组,每组20例。2组均维持基础性用药,另外,对照组予养血柔肝法,治疗组予益肾疏肝法,疗程2个月。于治疗前、治疗1个月、2个月各评定1次统一帕金森病评定量表运动检查部分(UPDRS-III)、HAMD-24、抑郁自评量表(SDS)、汉密尔顿焦虑量表(HARS)、焦虑自评量表(SAS)、帕金森病睡眠量表(PDSS)、简易精神状态量表(MMSE)、39项帕金森病生存质量问卷(PDQ-39)评分。结果 2组组内比较HAMD,SDS,SAS,PDQ-39评分均下降(P<0.05);组间比较1个月时,治疗组评分下降程度大于对照组(P<0.05)。2组组内比较HARS评分均下降(P<0.05);组间比较治疗组评分下降程度均大于对照组(P<0.05)。2组组内比较PDSS评分均上升(P<0.05);组间比较1个月时,治疗组评分上升程度大于对照组(P<0.05)。结论益肾疏肝法能改善帕金森病与抑郁共病患者的抑郁、焦虑、睡眠等症状,且显效较快。

针刺对帕金森抑郁大鼠血清及脑组织SP含量的影响

目的:探讨针刺(常规针刺、调神畅志针刺)对帕金森抑郁大鼠血清和脑中SP含量变化影响。方法:采取6-羟基多巴胺(6-OHDA)单侧纹状体双靶点注射法对大鼠进行帕金森(PD)造模并用阿普吗啡(APO)诱导实验检测。成功后,在PD模型基础上结合慢性不可预见温和应激(chronic unpredictable mildstress,CUMS)法进行帕金森抑郁(PDD)模型建立。将造模成功的40只PDD大鼠随机分为药物组、模型组、常规针刺组、调神畅志针刺组,每组10只,并设空白组10只,予相应治疗4周。采用免疫组织化学法和ELISA法对脑组织和血清中神经肽类P物质(SP)含量检测。结果:与空白组比较,模型组大鼠脑及血清SP含量显著升高(P<0.01)。与模型组比较,药物组大鼠脑及血清SP含量无明显变化(P>0.05),常规针刺组、调神畅志针刺组大鼠脑及血清SP含量均明显降低(P<0.05)。与常规针刺组相比,调神畅志针刺组大鼠脑及血清中SP显著降低(P<0.05,P<0.01)。结论:针刺对帕金森抑郁大鼠脑及血清中SP含量均有调节作用,且调神畅志针刺组优于常规针刺组,而美多芭与氟西汀药物对帕金森抑郁模型大鼠脑及血清中SP含量无明显调节作用。

Therapeutic efficacy and mechanism of heat-sensitive moxibustion for adjuvant treatment of depression in Parkinson disease

Objective:To observe the clinical efficacy of heat-sensitive moxibustion for adjuvant treatment of depression in Parkinson disease and explore its mechanism.Methods:A total of 80 patients with Parkinson disease coupled with depression were randomized into an observation group and a control group,with 40 cases in each group.The control group was treated with levodopa and benserazide hydrochloride tablets and paroxetine tablets,while the observation group was treated with heat-sensitive moxibustion on the basis of the medications in the control group.The treatment course was 2 months.The Hamilton depression scale-17(HAMD-17),unified Parkinson's disease rating scale(UPDRS)and Parkinson's disease quality of life questionnaire-39(PDQ-39)were scored before and after the treatment,and the efficacy was evaluated after treatment.Levels of patients'serum dopamine(DA),5-hydroxytryptamine(5-HT),tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)were detected before and after the treatment.Results:After treatment,the total effective rate of the observation group was higher than that of the control group(P<0.05).The HAMD-17 scores in the two groups decreased significantly after treatment(both P<0.05),and the score in the observation group was obviously lower than that in the control group(P<0.05).The component scores and total scores of UPDRS in both groups decreased significantly(all P<0.05),and the scores in the observation group were lower than those in the control group(all P<0.05).The score of PDQ-39 in the observation group decreased significantly(P<0.05),and was lower than that in the control group(P<0.05).After treatment,the serum DA and 5-HT levels in the observation group increased significantly(both P<0.05)and the TNF-αand IL-6 levels decreased significantly(both P<0.05),which were statistically different from those in the control group(all P<0.05).Conclusion:Heat-sensitive moxibustion has certain auxiliary effect in treating depression in Parkinson disease,significantly improving clinical symptoms and the quality of life,which may be related to the up-regulation of DA and 5-HT levels and down-regulation of TNF-αand IL-6 levels.