帕金森病的抑郁症状

了解帕金森病 (ＰＤ)患者伴发抑郁症状的情况。1　对象与方法ＰＤ组为本院神经内科病人 ,按 1984年全国锥体外系疾病研讨会制定的诊断标准[1] 。共 39例 ,男 2 3例 ,女 16例 ;年龄 5 8～ 86岁 ,平均 6 3 5岁 ;病程 0 5～ 11年。对照组为同期我院老年病科体检的无神经精神及躯体疾病的老年人 ,共32例 ,男 19例 ,女 13例 ;年龄 5 5～ 82岁 ,平均 6 2 9岁。两组的性别、年龄和文化程度差异均无显著性。以汉密尔顿抑郁量表 (ＨＡＭＤ)及症状自评量表 (ＳＣＬ 90 )评分。对伴抑郁的患者 (ＨＡＭＤ >2 0分 )在治疗帕金森病同时用帕罗西汀 2 0ｍ…     

帕金森病伴抑郁的治疗研究进展

帕金森病(PD)抑郁是帕金森病最常见的非运动症状之一,然而在PD早期抑郁常常被忽略,未能及时得到治疗。随着疾病的进展,抑郁症状表现更为突出,严重时患者有自杀的倾向,严重降低患者的生活质量。目前,临床针对PD伴抑郁的治疗方法虽较多,但其临床效果尚不明确,迄今仍缺乏有效的治疗干预手段。本文总结归纳了国内外较为常见的治疗手段,以期为PD伴抑郁患者制定个体化的治疗方案提供参考。     

帕金森病患者的抑郁及其相关因素

目的：探讨帕金森病（PD）患者的抑郁发生及相关因素。方法：对50例PD和40例糖尿病（对照组）患者,用汉密顿抑郁量表（HAMD）调查抑郁的发生情况及症状特点。结果：PD组抑郁发生率（485）明显高于对照组（10％）（P＜0．005）,PD组轻度抑郁占58％,中－重度抑郁占42％,抑郁病人病情统一评级标准（UPDS）平均分值57．14;无抑郁病人为35．47（P＜0．01）,Hoehn-YahrⅢ期以上发生抑郁占645;病程＞5年的抑郁发生率为69％,病程＜5年的抑制发生率为11％（P＜0．001）。结论PD患者中有较高的抑郁发生率,其与PD症状严重程度密切相关,病程长者发生率更高。     

帕金森病伴发抑郁的影像学研究进展

帕金森病（PD ）是一种发生于中老年人的慢性神经系统退行性疾病,主要病理改变为中脑黑质多巴胺（D A ）神经元变性、坏死和胞质路易小体形成,其运动症状包括静止性震颤、肌强直、运动迟缓和姿势步态异常等。近年来,PD的非运动症状日益受到关注,包括抑郁、情感淡漠、睡眠紊乱、嗅觉障碍和认知功能下降等。其中 PD伴发抑郁（PDD ）是 PD最常见的非运动症状之一,其发生率高达52％［1］。抑郁可加重PD患者的认知障碍和运动症状,是PD患者的致残因素之一,严重影响患者的生活质量及预后,增加照料者负担。因此,探讨 PDD 的发病机制,进行早期预防、早期诊断和早期治疗对于改善PD患者的生活质量及减轻社会负担意义重大。PDD的发病机制尚存在争议,主流观点认为,内源性的生物学因素起主导作用,外源性的心理社会因素也参与致病。随着医学影像学技术的飞速发展,已经有很多研究报道了PDD的影像学改变,对深入了解PDD的发病机制提供了更多帮助,现对PDD的影像学研究进展作一综述。     

帕金森病抑郁的研究进展

抑郁是帕金森病(PD)其最常见的神经精神症状,约有50%的PD患者受其影响.它是PD的一个原发症状,且与PD患者的疾病严重性、运动功能、日常生活能力及认知功能损害等密切相关,严重影响患者的生活质量.目前其发病机制仍不明确.对所有PD患者医生都应该常规、仔细地观察其有无抑郁的表现,一旦明确诊断为抑郁,应及早给予合理的治疗干预.     

帕金森病伴发抑郁研究进展

对帕金森病伴发抑郁的流行病学特征、神经生化发病机制及药物治疗研究进展进行概述。     

帕金森病伴发抑郁的机制

抑郁是帕金森病(Parkinson disease, PD)常见的伴发症状之一,发生率高达40%～50%[1].PD患者出现抑郁的时间分别在起病和病重阶段各有一高峰[2].抑郁与PD本身症状相互重叠,易被忽略,不能得到及时的治疗.     

帕金森病性抑郁的研究进展

抑郁是帕金森病最常合并的一种精神障碍,严重影响患者生活质量.对其发病率、发病机制、诊断和治疗等方面进行深入研究,将有利于临床早期、准确地识别和及时、有效的干预抑郁,从而造福患者.现将这方面的研究综述如下.     

帕金森病伴发的抑郁

目的：探讨帕金森病伴发抑郁的特点。方法：将门诊及住院的帕金森病患者进行抑郁自评量表（ＳＤＳ）筛查，对伴或不伴抑郁的病人进行比较。结果：６４例病人中出现抑郁症状２１例，占３２．８％，这些病人具有年轻、文化程度高的特点；同时还发现以肌强直为主的病人伴发抑郁的机率明显高于以震颤为主的病人。结论：抑郁在帕金森病中具有较高的发病率，应引起足够的重视。     

帕金森病患者亚抑郁的研究

目的研究131例门诊帕金森病（Parkinson’s disease,PD）患者中亚抑郁的发病率及其临床特点。方法采用统一PD评定量表（Unified Parkinson＇s Disease Rating Scale,UPDRS）,Hoehn-Yahr（H＆Y）分级和简易智力状态检查（Mini-Mental State Examimation,MMSE）对患者进行评估和分级,根据汉密顿抑郁量表（Hamilton Rating Scale for Depression,HRSD）得分情况将患者分为非抑郁组、亚抑郁组和抑郁组,研究亚抑郁与临床特征间关系及其症状特点。结果27例（20.6%）患者被纳入抑郁组,71例（54.2%）患者被纳入亚抑郁组,33例（25.2%）患者被纳入非抑郁组。年龄、性别和震颤评分在各组间无差异（P〉0.05）,亚抑郁组与抑郁组类似,在PD病程、UPDRS总分、强直评分和H＆Y分级上与非抑郁组有明显差异（P〈0.05）,且这些指标的强度从亚抑郁到抑郁呈递增趋势。亚抑郁组的常见症状为兴趣缺失、能力减退感、睡眠障碍、胃肠道症状和抑郁情绪,但其同样为抑郁组和非抑郁组的常见症状。结论亚抑郁与抑郁一样是PD的一种常见并发症,与PD的各种特征有类似的联系,并可能伴随PD的进一步进展而发展为抑郁。由于PD伴随症状与亚抑郁症状之间的重叠性,进一步的研究需要针对这些症状来制订更为详尽的亚抑郁诊断评分标准。     

经脑间质给药治疗帕金森病的研究新进展

帕金森病（PD）是一种常见的神经系统变性疾病，其致病因素除细胞功能紊乱及有毒物质 作用外，细胞外微环境异常也逐渐受到关注，与此相关的前沿治疗方法主要包括对流增强给药和简单 扩散给药，尤其后者的高效性及安全性已在多项研究中得到证实。现以脑间质治疗手段为基础，重点 介绍国内学者研发的简单扩散给药在PD治疗领域的全新应用。     

帕金森病早期生物学标记物研究新进展

帕金森病(PD)是中老年人常见的中枢神经系统变性疾病,≥65岁人群患病率约为1%.以黑质多巴胺能神经元变性缺失和残存神经元出现特征性包涵体--路易小体(LB)为主要病理改变.     

Antidepressants in the treatment of psychosis with comorbid depression in Parkinson disease

Psychotic symptoms are commonly associated with Parkinson disease and can be a source of significant morbidity. Depression has been reported as a comorbidity in patients with psychosis. We describe a patient with Parkinson disease with psychotic symptoms and comorbid depression whose treatment refractory delusions and hallucinations improved markedly only after antidepressant monotherapy was initiated. The phenomenology of the delusions was atypical for those found in Parkinson or in depression. Psychotic symptoms refractory or only partially responsive to conventional treatment should prompt a search for potential underlying psychiatric comorbidities. Given case reports of exacerbation of psychotic symptoms with antidepressants, we emphasize careful identification and active follow up of the comorbid depressive disorders in PD patients with psychosis. Potential mechanisms implicated in the response of psychosis to antidepressants are discussed.     

Pseudopheochromocytoma in Parkinson disease and depression

We report the case of a 62-year-old woman with parkinson's disease and depression. Her symptoms included episodes of flushing, palpitations and hypertension, giving rise to the suspicion of the existence of a phaeochromocytoma. The levels of adrenaline and vanillymandelic acid in the urine were moderately elevated, the noradrenaline level was high-normal. Upon further examination, there was no evidence of a phaeochromocytoma or a carcinoid tumor. In the literature, there are reports of pseudophaeochromocytoma in patients receiving levodopa. Elevated levels of catecholamins and their metabolites can be caused by the metabolic process of levodopa and levodopa can influence the outcome of laboratory tests. The patient's depression resolved and the flushing disappeared after treatment with antidepressants and after changing the Parkinson regime.     

Seeking progress in disease modification in Parkinson disease

ObjectiveDisease modification in Parkinson disease (PD) has remained an elusive goal, in spite of large investments over several decades. Following a large meeting of experts, this review article discusses the state of the science, possible reasons for past PD trials’ failures to demonstrate disease-modifying benefit, and potential solutions.MethodsThe National Institute of Neurological Disorders and Stroke (NINDS) convened a meeting including leaders in the field and representatives of key stakeholder groups to discuss drug therapy with the goal of disease modification in PD.ResultsImportant lessons can be learned from previous attempts, as well as from other fields. The selection process for therapeutic targets and agents differs among various organizations committed to therapeutic development. The areas identified as critical to target in future research include the development of relevant biomarkers, refinements of the targeted patient populations, considerations of novel trial designs, and improving collaborations between all stakeholders.ConclusionsWe identify potential barriers to progress in disease modification for Parkinson's and propose a set of research priorities that may improve the likelihood of success.     

帕金森病相关外泌体研究进展

帕金森病（Parkinson disease, PD）是一种神经变性疾病,具有不可逆性、高发病率和高致 残率的特点,早期识别和干预对改善PD 意义重大。然而,目前临床上对PD 的诊断缺乏客观的实验室 检测指标,药物疗法对早期疾病修饰的证据尚不充分。外泌体是细胞产生、释放到胞外环境的囊泡,内 含丰富的生物活性分子。中枢神经系统起源的外泌体,其中PD标志性蛋白质,如α-突触核蛋白、DJ-1 和RNA 分子水平的变化反映了机体病理生理状态的改变,是筛选疾病诊断、鉴别诊断、分期、预后等标 志物的重要来源。间充质干细胞来源的外泌体具有与母细胞类似的组织修复、神经保护效应,而一些 活性分子（如过氧化物酶、多巴胺、小干扰RNAs等）也可以外泌体为载体靶向运输到脑组织,针对PD 不 同的致病通路发挥作用。现综述外泌体在PD 发生发展、诊断和治疗中的研究进展,探讨当前所面临的 问题和未来可能的研究方向。     

Treatment of depression in Parkinson’s disease

Depression is one of the most common nonmotor features observed in Parkinson’s disease (PD), affecting approximately 40% of patients. Depression in Parkinson’s disease (dPD) significantly affects quality of life of both patients and their families and has been shown to be more predictive of distress than motor disability. Depression frequently goes unrecognized in this population, however, in part because the diagnosis is often complicated by the overlap of psychiatric and PD symptoms. The etiology of dPD is unclear; dopaminergic, serotonergic, and noradrenergic systems may be implicated. Options for managing dPD include antidepressant medication; cognitive-behavioral therapy; behavioral lifestyle interventions such as exercise; and, in refractory cases, noninvasive brain stimulation (electroconvulsive therapy, transcranial magnetic stimulation). Randomized controlled trials are needed to evaluate the efficacy of interventional approaches for dPD; several trials are currently underway.