P型和C型多系统萎缩的急性多巴反应性研究

目的研究P型和C型多系统萎缩（MSA）对左旋多巴的急性反应性。方法对P型MSA患者18例、C型MSA患者13例和帕金森病（PD）患者23例行急性阶梯式左旋多巴试验，药物剂量依次为左旋多巴／苄丝肼50mg／12．5mg、100mg／25mg、150mg／37．5mg、200mg／50mg和300mg／75mg。以UPDRS运动分量表作为评价标准，计算UPDRS运动评分平均最大改善率并比较各组患者的多巴反应性。结果左旋多巴／苄丝肼剂量为。100mg／25mg、150．mg／37．5mg、200mg／50mg和300mg／75mg时，MSA-P型组和MSA—C型组韵UPDRS运动评分平均最大改善率均显著低于PD组，MSA-P型组高于MSA-C型组。MSA-P型组患者随服用左旋多巴／苄丝肼剂量增加UPDRS评分平均最大改善率呈逐渐增高趋势，而MSA-C型不同剂量间UPDRS评分平均最大改善率差异无统计学意义。结论MSA-P型组具有剂量依赖的急性多巴反应性，而MSA-C型组基本无急性多巴反应性。     

新发帕金森病的急性多巴反应性评价

目的：建立急性左旋多巴负荷试验用于鉴别新发帕金森病（PD）与新发帕金森综合征（PDS）患者,并筛选评价指标的临界值。方法：选择89例有PD样表现但未服用过左旋多巴的患者,根据临床诊断分为PD组（n=48）和PDS组（n=41）,进行了急性左旋多巴／卡比多巴（100／25mg）试验。根据两组患者统-PD评分运动分量表（UPDRS—Ⅲ）评分的平均最大改善率进行比较,并建立受试者工作特征（ROC）曲线,以该曲线上最大Youden指数对应的运动评分最大改善率作为临界值。结果：PD组在服用左旋多巴-卡比多巴后的平均UPDRS-Ⅲ评分平均最大改善率高于PDS组,差异有统计学意义（P〈0．01）。建立的ROC曲线在鉴别PD和PDS差异具有统计学意义,ROC曲线下面积为0．827（P〈0．01）,对应上网UPDRS运动评分改善率的最佳临界值为12．45％（Youden指数0．565,敏感度80．9％,特异度75．6％）。结论：急性左旋多巴-卡比多巴试验可作为PD疗效和诊断的一种辅助参考方法。     

多巴反应性肌张力障碍临床分析

目的回顾性分析多巴反应性肌张力障碍患者的临床特点和治疗原则。方法选择2005年3月-2010年7月门诊或住院治疗且诊断明确的多巴反应性肌张力障碍患者,面对面采集临床资料并门诊或电话随访,对其性别、年龄、发病年龄、家族史、首发症状、就诊症状、诊断延误时间及治疗过程进行分析。结果共21例患者人组,男4例、女17例,平均发病年龄（7．19±3．40）岁,平均诊断延误时间（13．76±11.38）年。均以肢体肌张力障碍为首发症状,20例（95．24％）呈现晨轻暮重现象,6例（28．57％）伴帕金森样症状,2例（9．52％）伴痉挛性截瘫;经小剂量左旋多巴,多巴丝肼治疗后症状显著缓解。随访18例患者,仅1例治疗后仍遗留肢体残疾;3例失访。随访期间左旋多巴／多巴丝肼平均维持剂量（175．35±113．51）mg／d,3例患者辅助应用盐酸苯海索（4.6mg／d）治疗。结论多巴反应性肌张力障碍患者多于儿童期以肢体肌张力障碍发病,小剂量左旋多巴／多巴丝肼治疗效果显著。因此,对于儿童肌张力障碍或青年帕金森样症状患者应行小剂量左旋多巴,多巴丝肼诊断性治疗,以降低多巴反应性肌张力障碍的误诊率。     

治疗帕金森病的不同药物对基底节多巴胺能系统的影响

目的:应用99mTc -TRODAT 1SPECT显像多巴胺转运体(DAT)和13 1I -epideprideSPECT显像多巴胺D2 受体,研究早期帕金森(PD)病人中用不同药物单一治疗14个月的随访情况。方法:72例早期(Hoehn&YahrⅠ～Ⅱ级)PD患者双盲、区组随机化方法分为4组,分别给予苯海索6mg·d-1(n =15 ) ;L 多巴制剂(美多巴2 5 0’,每天2 .5片) (n =2 2 ) ;L deprenyl(司来吉兰7.5mg·d-1) (n =2 2 ) ;多巴胺受体激动剂培高利特0 .5mg·d-1(n =13 )并随访14个月。分别在基线,随访7和14个月时,进行临床评分,同时以99mTc -TRODAT 1和13 1I -epidepride为配体,应用SPECT功能显像各组患者基底节区DAT和多巴胺D2 受体,比较不同治疗方案对基底节多巴胺能系统的影响情况。结果:99mTc -TRODAT 1SPECT显像结果显示,苯海索组和多巴制剂治疗组在治疗14个月后,基底节DAT均显著降低(P <0 .0 5 ) ,司来吉兰治疗组和多巴受体激动剂组在治疗7和14个月后,基底节区DAT虽有降低,但与基线比较无统计学意义(P >0 .0 5 )。随访14个月时,与对照组(苯海索组)比,仅受体激动剂组患者基底节区DAT值较高(P <0 .0 5 ) ,即减少程度最小。13 1I- epideprideSPECT显像结果显示,随访7和14个月时各组和基线比较均无显著差异,各组间亦无明显差异。结论:早期PD患者中,用多巴     

帕金森病患者血脂、胱抑素C及同型半胱氨酸水平分析

目的探讨帕金森病(PD)患者的血脂、胱抑素C(CysC)及同型半胱氨酸(Hcy)水平变化及其在PD不同分型之间的差异及临床相关性。方法选取165例PD患者为PD组,103例健康体检者为对照组。PD组再根据H-Y分期评估结果分为PD早期亚组(39例)、PD中期亚组(51例)和PD晚期亚组(75例)。再根据UPDRS评分中的震颤项目(16,20,21)和强直少动项目(13~15,29,30)的平均评分比值将PD组分为震颤型PD亚组(TD亚组,123例)和姿势不稳步态障碍型PD亚组(PIGD亚组,42例),依据是否应用左旋多巴分为左旋多巴亚组和非左旋多巴亚组。检测所有研究对象血脂、血清CysC及Hcy水平,分析各组间各项指标的差异及临床相关性。结果 PD组三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白-胆固醇(LDL-C)、高密度脂蛋白-胆固醇(HDL-C)和载脂蛋白B(Apo B)水平均明显低于对照组(均P0.05),Cys C、Hcy水平均显著高于对照组(均P0.01);Cys C和Hcy水平在PD早、中、晚期亚组中逐渐升高(均P0.05)。PIGD亚组HDL-C水平明显高于TD亚组(P0.05)。PD左旋多巴亚组TG水平明显低于非左旋多巴亚组(P0.05),PD左旋多巴亚组Cys C和Hcy水平均明显高于非左旋多巴亚组(均P0.05)。相关分析提示,PD组TG水平与病程(r=-0.188)、左旋多巴每日等效剂量(r=-0.253)呈负相关,Apo B与年龄(r=-0.194)呈正相关,CysC水平与病程(r=0.194)、H-Y分期(r=0.281)、年龄(r=0.270)呈正相关(均P0.05);Hcy水平与H-Y分期(r=0.238)、年龄(r=0.166)呈正相关(均P0.05)。结论血脂、CysC和Hcy水平在PD患者中存在异常,均参与了PD进程,对PD的疾病进展和病情严重程度具有一定的预测作用。     

46例血管性帕金森综合征临床分析

目的探讨血管性帕金森综合征(VP)的临床与影像学特点,并与原发性帕金森病(PD)相鉴别。方法对46例VP患者的临床表现及影像学结果进行回顾性分析,并与31例PD患者的临床资料进行对比。结果VP发病年龄大于PD;病前绝大多数患者有高血压、脑卒中及糖尿病病史;急性或亚急性起病多见;最早以步行困难、运动迟缓起病;临床表现以肌强直-运动迟缓为主、静止性震颤少见;多伴有锥体束损害、智能障碍及尿失禁等;影像学改变以皮质下白质、基底节多发腔隙性梗死为主。结论VP发病年龄较高;急性或亚急性起病多见;最早以步行困难、运动迟缓起病;临床表现以肌强直-运动迟缓为主,静止性震颤少见;影像学改变主要以皮质下白质、基底节多发腔隙性梗死为主。     

血管性帕金森综合征临床病例对照研究

目的 探讨脑血管病及其危险因素在帕金森综合征发病中的作用,分析血管性帕金森综合征（VP）与帕金森病（PD）的临床特点。方法 收集在我科住院的86例帕金森综合征及PD,根据有无高血压病、动脉硬化或脑卒中病史,分为VP组和PD组,并对两组的临床特点进行回顾性对比分析。结果 脑血管病及其危险因素在两组间的发生率有显著性差异（P＜0.001),与PD组比较,VP组病人发病年龄偏大（P＜0.01）,临床表现以少动－四肢强直为主,而静止性震颤少见（P＜0.05）,常伴发假性延髓麻痹、尿失禁（P＜0.01）、智能障碍（P＜0.001）等,头颅MRI以基底节区腔隙性脑梗死多见。且左旋多巴的治疗效果多不满意（P＜0.05）。结论 VP是病因、发病机理及临床特征不同于PD的一种帕金森综合征。     

卡比多巴-左旋多巴控释片治疗帕金森病合并睡眠障碍的疗效观察

目的探讨卡比多巴-左旋多巴控释片对治疗帕金森病(Parkinson′s disease,PD)合并睡眠障碍患者睡眠障碍的疗效。方法选取符合英国脑库原发性帕金森病临床诊断标准确诊为原发性帕金森病的患者96例,并随机分成卡比多巴-左旋多巴控释片及左旋多巴组各48例,分别进行3个月药物治疗后,通过睡眠量表(PDSS)、匹兹堡睡眠质量指数(PSQI),及用ESS评分评价2组睡眠质量。结果与左旋多巴组比较,卡比多巴-左旋多巴控释片治疗后能明显改善患者的PDSS量表在PDSS-1、3、4、5、6、8、10、11、13、15项目上得分明显增高(P0.05);卡比多巴-左旋多巴控释片组患者较左旋多巴组能明显降低PSQI及ESS评分(P0.05);同时,多导睡眠图监测实验显示患者卧床时间、总睡眠时间、睡眠效率明显升高、觉醒次数明显下降,差异有统计学意义(P0.05)。结论与左旋多巴比较,卡比多巴-左旋多巴控释片在改善PD合并睡眠障碍患者的睡眠状况方面有更好的优势。     

脑微出血对帕金森病认知功能的影响

目的探讨合并脑微出血(CMBs)以及不同部位CMBs帕金森病(PD)患者的临床特点以及CMBs对PD患者认知功能的影响。方法收集2016-09—2018-03于苏州高新区人民医院、南京医科大学附属苏州医院就诊的PD患者112例,根据是否合并CMBs病灶分为PD合并CMBs组和PD不合并CMBs组。进一步根据CMBs所处的分布区域分为单纯脑叶CMBs和非单纯脑叶CMBs亚组。比较各组患者临床特征、统一帕金森病评分量表(UPDRS)评分、Hoehn-Yahr(H-Y)分级、蒙特利尔认知评估量表(MoCA)等差异。采用非条件Logistics回归分析影响PD认知功能障碍的相关因素。结果与PD未合并CMBs组(n=81)比较,PD合并CMBs组(n=31)患者MoCA评分更低、服用左旋多巴等效剂量更大,侧脑室周围白质病(periventricular white matter hyperintensity,PWMH)和深部白质病变(deep white matter hyperintensity,DWPH)的Fazekas得分均更高(均P0.05)。与单纯脑叶CMBs亚组(n=10)比较,非单纯脑叶CMBs组患者MocA评分以及视空间与执行、语言项目评分升高(P0.05或P0.01),非单纯脑叶CMBs组体位性低血压比例升高(P0.05)。非条件多因素Logistic回归分析显示,CMBs是PD患者认知障碍的重要影响因素之一。结论合并CMBs的PD患者认知功能更差,对药物反应性越差,脑白质病变和腔隙性脑梗死的程度越重。CMBs对PD患者的认知功能产生一定影响,且CMBs的分布区域不同,认知损害的领域及程度也有所不同。     

吡贝地尔对早期帕金森病非运动症状的影响

目的:观察复方左旋多巴和吡贝地尔单用和联合应用对早期帕金森病(PD)患者非运动症状的影响。方法:早期PD患者67例,分为单用吡贝地尔组(25例),复方左旋多巴与吡贝地尔联合用药组(20例),单用复方左旋多巴组(22例)。采用UPDRS-Ⅰ、Ⅱ,PD生活质量评定量表,Hamilton抑郁量表和PD睡眠评分量表对患者进行基线评定,并在治疗后1、3和6个月进行跟踪随访。结果:联合用药组UPDRS-Ⅰ、Ⅱ、抑郁情绪评分、睡眠质量评分以及生活质量评分在各个随访点均较用药前有显著改善;吡贝地尔组Hamilton抑郁评分在各观察窗内均较用药前降低;复方左旋多巴组在第6个月出现睡眠状况的恶化。结论:吡贝地尔单用或联合复方旋多巴应用,吡贝地尔可以较好地改善早期PD患者的精神、情绪和睡眠等非运动症状;早期联合应用吡贝地尔可显著提高患者生活质量。     

[123I] FP‐CIT spect study in vascular parkinsonism and Parkinson's disease

There is substantial evidence to support a role for small vessel disease (SVD) as a cause for vascular parkinsonism (VP). Using [¹²³I] FP‐CIT SPECT (single photon emission computed tomography), we have tried to determine whether VP patients have pre‐synaptic dopaminergic function similar to PD patients, and whether the severity of parkinsonian symptoms as well as the levodopa response in VP patients are correlated with pre‐synaptic dopaminergic dysfunction. Thirteen patients fulfilling operational clinical criteria for VP had [¹²³I] FP‐CIT scans. Mean [¹²³I] FP‐CIT uptake in the basal ganglia was significantly lower in VP patients than in healthy controls, and the asymmetry index was not significantly different between these groups. In contrast, compared with the PD group, only the mean asymmetry index was significantly lower in VP patients. None of the parameters measured was significantly different between VP patients who had an insidious onset of parkinsonism (VPi) and those who had an acute onset (VPa). There was a significant correlation between the bilateral basal ganglia FP‐CIT uptake reduction in the VP patients and UPDRS motor scores, but not with the mean % reduction in motor UPDRS after levodopa. We suggest that in the majority of VP patients, pre‐synaptic dopaminergic function is reduced. The presence of a rather symmetrical FP‐CIT uptake in the basal ganglia may help to distinguish VP from PD and could therefore be used as a criterion for the clinical diagnosis of VP. © 2007 Movement Disorder Society     

Levodopa-induced sleepiness in the Parkinson variant of multiple system atrophy.

Recent observations suggest that levodopa can induce irresistible sleep onset in multiple system atrophy (MSA). Therefore, we assessed sleepiness during a levodopa challenge in 17 MSA compared with 23 Parkinson's disease (PD) patients using the Stanford Sleepiness Scale (SSS). SSS scores during the levodopa challenge compared with baseline were significantly increased in the MSA compared with the PD group. These findings suggest greater potential of levodopa to induce sleepiness in MSA compared with PD, which may be related to differences in basal ganglia and brainstem pathology between the two disorders.     

Vascular parkinsonism: a distinct, heterogeneous clinical entity

OBJECTIVES: The aim of this study was to define the symptoms and signs of suspected vascular parkinsonism (VP) which is still a debatable concept. MATERIAL AND METHODS: Patients with parkinsonism were grouped into patients with suspected VP and Parkinson's disease (PD) after other causes for secondary parkinsonism, and parkinsonism-plus syndromes were excluded. The clinical features of 16 patients with suspected VP to those of 50 diagnosed with PD were compared. All patients were assessed using unified Parkinson's disease rating scale (UPDRS) and all had cerebral MRIs. RESULTS: Patients with VP had significantly older onset age and shorter duration of disease with gait disorder as the most frequent initial symptom. All PD patients had satisfactory response to levodopa treatment, whereas only 38% VP patients had satisfactory response to levodopa treatment. Vascular risk factors were more common in VP (81%) than PD (32%). Postural instability, freezing, gait disturbance, pyramidal signs, and postural tremor were significantly more prevalent in patients with VP than in PD. In VP patients these features were more prominent in the lower limbs. Twenty-five percent had acute onset VP. All patients with VP had ischemic lesions, mainly in subcortical white matter, to a lesser extent basal ganglia and brainstem, in their cerebral MRIs, while 70% of PD patients had normal MRIs. CONCLUSION: The differences in the clinical features support the concept that VP is a distinct clinical entity with heterogeneous clinical, MRI, and possibly pathophysiological features.     

White matter hyperintensities rather than lacunar infarcts are associated with depressive symptoms in older people: the LADIS study.

OBJECTIVE: Both white matter hyperintensities (WMH) and lacunar infarcts have been associated with the development of depression in older subjects, although the relative importance of the two and the influence of lesion location and concomitant vascular disease are unclear. This study investigates the relationship between location and burden of WMH and lacunes on depressive features in older people. METHOD: In a pan-European multicenter study of 626 older subjects, the authors examined the relationship between regional magnetic resonance imaging white matter hyperintensities, number of lacunar infarcts, depressive symptoms as assessed by the 15-item geriatric depression scale (GDS), cognitive status (Mini-Mental Status Examination), hypertension, and self-perceived health quality of life (QoL). RESULTS: The authors found depressive symptoms to be correlated with WMH rating in the frontal (N=626; Spearman's rho=0.161, p <0.001) and temporal (rho=0.14, p <0.001) but not occipitoparietal region (rho=0.07, p=0.07). Basal ganglia lacunes were only weakly correlated with GDS (rho=0.09, p=0.03), and lacunes in other regions showed no association. In a ordinal logistic regression model (controlling for QoL, Mini-Mental Status Examination, age, and with an interaction between WMH and hypertension), temporal WMH in the absence of hypertension independently predicted GDS, whereas neither history of stroke nor number of lacunar infarcts did. The authors compared left- versus right-sided WMH and found no effect of laterality on depressive symptoms. CONCLUSIONS: The results suggest that in this population of nondisabled older people, WMH have a greater influence on depressive symptoms than infarcts.     

What features improve the accuracy of the clinical diagnosis of progressive supranuclear palsy‐parkinsonism (PSP‐P)?

Progressive supranuclear palsy‐parkinsonism (PSP‐P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson's disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation. The aim of this study was to identify particular clinical features (green flags) that may be helpful in differentiating PSP‐P from these other disorders. We identified 37 patients with PSP‐P from 726 patients archived at the Queen Square Brain Bank. Using a retrospective case notes review the clinical features were compared between the PSP‐P group and Lewy body associated parkinsonism (PD, n = 444 and dementia with Lewy bodies (DLB), n = 46), MSA (n = 90), and VP (n = 19), using the χ²‐test for proportions for a two‐by‐two contingency table. The sensitivity, specificity, and positive predictive values (PPV) and negative predictive values (NPV) were calculated for individual clinical features. A specificity of >0.85 or a PPV of >0.85 were considered reliable discriminators. No clinical features were predictive of PSP‐P, but late drug induced dyskinesias (specificity 0.92, PPV 0.99), late autonomic dysfunction (specificity 0.94, PPV 0.99) and any visual hallucinations (specificity 0.94, PPV 0.99) were better in distinguishing PD and PSP‐P than predicted using operational diagnostic criteria for PD. PSP‐P shares many clinical features with PD and DLB, MSA and VP, but visual hallucinations, drug induced dyskinesias and autonomic dysfunction are very uncommon and may be helpful exclusion criteria. © 2010 Movement Disorder Society     

脑小血管病MRI表现对痴呆的预测作用

随着全球老龄化,痴呆发病率快速上升,而且痴呆具有不可逆性、缺乏有效治疗措施,故 探索预测痴呆发生的有效指标成为关键。脑小血管病（cerebral small vessel disease,CSVD）被认为与 痴呆密切相关,其颅脑磁共振成像（magnetic resonance imaging,MRI）可表现为腔隙（lacunes）、新发皮 层下小梗死（recent small subcortical infarcts）、脑白质高信号（white matter hyperintensities,WMH）、扩 大的血管周围间隙（enlarged perivascular spaces,EPVS）及脑微出血（cerebral microbleeds,CMB）等。本文 通过综述CSVD颅脑MRI表现与痴呆相关性的研究进展,发现多发静息性或位于基底节区的腔隙性梗死 （lacunar infarction,LI）或腔隙、重度WMH、多脑叶分布性脑叶微出血（lobar microbleeds,LMB）,均可作 为预测痴呆发生的有效指标。     

The relationship between cerebral vascular disease and parkinsonism: The VADO study

BackgroundThe observation of gait abnormalities, parkinsonism and vascular lesions in elderly patients is often reported as vascular parkinsonism (VP). However the status of striatal dopamine transporter (DAT) and the effects of brain vascular lesions on motor features and levodopa responsiveness are poorly defined.MethodsWe recorded clinical features, chronic response to levodopa and vascular risk factors in a cross-sectional cohort of consecutive elderly patients with possible Parkinson's disease (PD) or VP recruited in 20 centers in Italy.ResultsWe included a total of 158 patients. Onset of motor symptoms was asymmetric in 93 (59%) and symmetric in 65 patients (41%). Symmetric motor onset was associated with greater disease severity. Chronic levodopa response was positive in 75 (47.8%) and negative in 82 patients (52.2%). A negative response to levodopa was associated with greater frequency of symmetric onset of motor symptoms, worst disease severity, absence of dyskinesia and greater number of vascular risk factors. Frontal lobe showed largest vascular load. Striatal DAT was normal in 48 (30.4%) and abnormal in 110 (69.6%) patients. Patients with normal DAT binding showed higher vascular load at MRI. Significant predictive factors of worst disease severity and negative response to levodopa were hypertension, vascular lesions in basal ganglia/periventricular regions, and normal DAT uptake.ConclusionsMultiple cerebral vascular lesions modify clinical presentation and severity in patients with parkinsonism and this is underlined by specific risk factors primarily hypertension. Striatal DAT assessment is helpful in identifying patients where therapy benefit is less likely.     

Motor subtype and cognitive decline in Parkinson's disease, Parkinson's disease with dementia, and dementia with Lewy bodies

BACKGROUND: A previous cross sectional study found over-representation of a postural instability gait difficulty (PIGD) motor subtype in Parkinson's disease patients with dementia (PDD) and dementia with Lewy bodies (DLB), compared with Parkinson's disease (PD). AIMS: (1) To examine rates of cognitive and motor decline over two years in PD (n=40), PDD (n=42) and DLB (n=41) subjects, compared with age matched controls (n=41), (2) to record whether motor phenotypes of PD, PDD, and DLB subjects changed during the study, (3) to find out if cognitive and motor decline in PD was associated with baseline motor subtype, and (4) to report the incidence of dementia in PD patients in relation to baseline motor subtype. RESULTS: Most of PDD and DLB participants were PIGD subtype at baseline assessment. In the non-demented PD group, tremor dominant (TD) and PIGD subtypes were more evenly represented. Cognitive decline over two years was greater in PDD and DLB groups (mean decline in MMSE -4.5 and -3.9, respectively), compared with PD (-0.2) and controls (-0.3). There was an association between PIGD subtype and increased rate of cognitive decline within the PD group. Of 40 PD patients, 25% of the 16 PIGD subtype developed dementia over two years, compared with none of the 18 TD or six indeterminate phenotype cases (chi2=6.7, Fisher's exact test p<0.05). CONCLUSION: A PIGD motor subtype is associated with a faster rate of cognitive decline in PD and may be considered a risk factor for incident dementia in PD.     

Different clinical and evolutional patterns in late idiopathic and vascular parkinsonism

Objective The aim of this study was to examine the clinical picture of Parkinson’s disease (PD) and vascular parkinsonism (VP) in the elderly, in an attempt to differentiate the clinical history, symptoms, signs and response to therapy. Material and methods Thirty–two elderly patients with late onset PD and 45 with VP were enrolled and the clinical features of two groups were compared. All patients underwent brain MRI and were scored using the Unified Parkinson’s Disease Rating Scales (UPDRS) –II, –III. Results Patients with PD had a younger age at onset and a longer duration of the disease as compared to patients with VP. Nearly all PD patients showed a good response to levodopa therapy, while only 29% of patients with VP were responsive to levodopa treatment. Vascular risk factors as well as postural tremor, gait disorders and pyramidal signs with lower body predominance, were more frequent in patients with VP. Ninety–three % of PD patients had normal MRI, whereas all patients with VP had cerebral vascular lesions. UPDRS–II, –III scores at baseline were higher in VP than in PD patients and their increases throughout the follow–up period were more marked in VP than in PD patients. Conclusions Clinical history, symptoms, signs, response to therapy, and brain imaging help to differentiate PD and VP as two clinical entities with different clinical, prognostic and therapeutic implications, even if the coexistence of PD and a cerebral vascular disease in elderly patients is not infrequent and can make the diagnosis difficult.