血管性帕金森综合征研究进展

血管性帕金森综合征（VP）是由缺血性脑血管疾病引起的继发性帕金森综合征。VP的主要症状为下半身帕金森综合征,表现为双侧对称的步态异常,对多巴反应差,伴有锥体束征、假性球麻痹、大小便失禁等。VP的诊断很大程度上依赖临床特点和影像学检查,尤其是MRI上基底节区梗死灶和弥漫性皮质下白质病变。不断丰富的临床病理发现将促进我们对发病机制的认识。本文就其发病机制、临床特点、影像表现及诊断治疗等方面进行综述。     

血管性帕金森综合征

帕金森综合征(PS)系多病因性疾病,由血管因素作为病因之一是Critchley(1929)首先提出,以后Critchley又经过多年的研究和观察,提出了血管性帕金森综合征(VP)的诊断.并进一步提出VP的主要临床表现为起病隐袭、表现呆滞、动作减少、慌张步态、强直性肌张力增高,而静止性震颤缺如,左旋多巴治疗效果不佳,常合并假性球麻痹、痴呆及痉挛性瘫痪等.     

血管性帕金森综合征33例

目的：探讨血管性帕金森综合征（VP）的临床特点及MRI的改变。方法：对33例住院确诊的VP患者的临床资料及头颅MRI改变进行分析。结果：本组VP患者多发少动-强直为主,特别是双下肢明显,静止性震颤少见,其发病年龄较帕金森病（PD）晚,除有锥体外系症状和体征外,可伴有锥体束征、假性延髓麻痹及记忆、智能障碍。左旋多巴替代治疗效果不明显,给予改善微循环药物效果满意。头颅MRI改变主要表现为额叶白质损害及主要分布在分水岭、基底节区的单发或多发的腔隙性梗死。结论：VP的临床表现、MRI改变不同于PD,可作为一独立的临床综合征而存在。     

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的研究进展

脑血管病变作为帕金森综合征的一种继发因素已得到公认 ,本文综述近年来有关血管性帕金森综合征流行病学、病理、生化改变与发生机制、临床表现、神经影像学、诊断、治疗等方面的研究进展。     

血管性帕金森综合征的临床研究进展

血管性帕金森综合征（vascularparkinsonism,VP）是一种继发性的帕金森综合征。随着我国老龄人口的增加,脑血管疾病患者增多,VP患病率有可能进一步增高。VP的发病机制尚不明确,且临床表现具有较大的异质性,因此有待更深入的研究。本文将对VP的流行病学、临床表现、影像学特征以及治疗等新进展予以总结分析,以期更好地指导临床实践。     

栉风沐雨——直面血管性帕金森综合征

帕金森综合征涵盖多种病因和临床表现,可谓"一病多症、一症多病",大众甚至部分非神经科医学人员所言的"帕金森"更指向于帕金森病(Parkinson's disease,PD),但实际上,患者所患的可能是继发性帕金森综合征或者帕金森叠加综合征.麦穗两岐,在非专科医师眼中,血管性帕金森综合征(vascular parkins...     

血管性帕金森综合征33例

目的 :探讨血管性帕金森综合征 (VP)的临床特点及MRI的改变。方法 :对 33例住院确诊的VP患者的临床资料及头颅MRI改变进行分析。结果 :本组VP患者多以少动 -强直为主 ,特别是双下肢明显 ,静止性震颤少见 ,其发病年龄较帕金森病 (PD)晚 ,除有锥体外系症状和体征外 ,可伴有锥体束征、假性延髓麻痹及记忆、智能障碍。左旋多巴替代治疗效果不明显 ,给予改善微循环药物效果满意。头颅MRI改变主要表现为额叶白质损害及主要分布在分水岭、基底节区的单发或多发的腔隙性梗死。结论 :VP的临床表现、MRI改变不同于PD ,可作为一独立的临床综合征而存在。     

血管性帕金森综合征临床研究进展

血管性帕金森综合征(VP)临床表现以肌强直、少动为主,静止性震颤少见,常伴有智能障碍、假性球麻痹、尿失禁等,多数患者有高血压、动脉粥样硬化及脑卒中史,影像学以基底节区和脑室周围多发性腔隙性脑梗死为主,常伴脑萎缩、白质疏松。VP患者临床特点有锥体系和锥体束损害的表现,影像学有脑缺血的改变,嗅觉功能无异常。VP与帕金森病在神经病理学、症状学神经影像都有所不同,本文就该病的病理、影像与临床特征进行综述。     

血管性帕金森综合征53例临床分析

目的　探讨血管性帕金森综合征 (VP)的临床诊断。方法　对 5 3例 VP患者的临床特点、MMSE、HDS、FAQ、HIS量表及 MRI检查资料进行分析。结果　本组 VP患者中 2次以上脑卒中者 31例(5 8.5 % ) ;病程呈阶梯样进展 ,有局限性神经系统定位体征 ,多无静止性震颤 ,智能障碍 32例 (6 0 .4% ) ;MMSE、HDS2 4.6± 2 .1分 2 8例 (5 2 .8% ) ,MMSE、HDS15 .1± 1.7分 4例 (7.5 % ) ,FAQ≥ 7分 16例(30 .2 % ) ,HIS>6分 5 3例 (10 0 % ) ;MRI均可见局限性或普遍性脑萎缩 ,多发性脑梗死 (MCI) 36例 (6 7.9% ) ,脑白质疏松 9例 (17% )。结论　 VP的发生与脑血管病发生次数及 MCI有关 ,临床诊断应结合其临床特征、智能障碍及影像学改变进行综合分析。     

血管性帕金森综合征的临床与头部MRI研究

目的探讨血管性帕金森综合征(Vascular Parkinsonism,VP)患者的临床表现、MRI的特征及发病机制。方法对42例VP患者的临床表现及MRI结果进行回顾性分析。结果本研究中多数患者有脑血管病危险因素及卒中史;临床表现以细碎步态、运动减少、肌强直为主,无4~6Hz静止性震颤;多有局灶性神经定位体征,伴有智能障碍、假性球麻痹、尿失禁等;对左旋多巴制剂疗效欠佳。MRI以基底节区、脑室周围多发性腔隙性脑梗死为主,可伴脑白质疏松或脑萎缩。结论VP的临床诊断应结合病史、临床表现、影像学改变及对多巴胺制剂的疗效进行综合分析。     

Effects of vitamin D analogs on the expression of plasminogen activator inhibitor-1 in human vascular cells

INTRODUCTION: Vitamin D analogs such as paricalcitol and calcitriol have been shown to provide survival benefit for Stage 5 chronic kidney disease (CKD) patients, possibly due to their positive impact on the cardiovascular system. Plasminogen activator inhibitor-1 (PAI-1) is one of the risk markers for coronary artery disease. MATERIALS AND METHODS: Human coronary artery smooth muscle cells (SMC) and endothelial cells (CAEC) were treated with vitamin D analogs to assess the effects of the drugs on the expression of PAI-1 mRNA and protein. RESULTS: In SMC, both paricalcitol and calcitriol down-regulated the expression of PAI-1 mRNA and protein in a dose-dependent manner. The EC(50) values of paricalcitol and calcitriol on suppressing PAI-1 mRNA were 3.0 and 2.8 nM, respectively. Interestingly, these two drugs had no significant effect on the expression of PAI-1 protein or mRNA in CAEC. Further analysis showed that CAEC did not express functional vitamin D receptor (VDR) and paricalcitol failed to induce the expression of 25-hydroxyvitamin D-24-hydroxylase (CYP24A1) mRNA, a gene known to be regulated by VDR. As a comparison, SMC expressed VDR and paricalcitol induced CYP24A1 mRNA in SMC (>150-fold at 10 nM) dose-dependently. The effect of paricalcitol on suppressing PAI-1 in SMC was blocked by cycloheximide, suggesting that protein synthesis was involved. CONCLUSION: These results demonstrate that vitamin D analogs suppress PAI-1 in SMC, but not in CAEC. Suppression of PAI-1 in SMC may be one of the factors contributing to the survival benefits of vitamin D analog therapy in CKD patients.     

维生素E、C在CVD与PD患者中抗氧化作用的临床研究

目的 探讨维生素E（Vit E)与维生素C（Vit C)在脑血管病（CVD）与帕金森病（PD）中的抗氧化作用。方法 检测CVD162例和PD77例共239例患者服用VitE和VitC前后血浆Vit E、Vit C、过氧化脂质（LPO）水平和红细胞超氧化物歧化酶（SOD）活性,并与对照组进行了比较。结果 服药前两组患者血浆Vit E、Vit C水平和红细胞SOD活性明显低于正常对照组;服药后两组患者的Vit E、Vit C水平和SOD活性无明显变化,而CVD组的LPO值升高。结论 CVD和PD患者可能有Vit E、Vit C水平和SOD活性降低,服用Vit E、Vit C后仅见CVD患者的LPO值升高,但匀不能象健康对照组那样提高Vit E、Vit C水平和SOD活性。     

Lisuride in the treatment of Parkinsonism

Lisuride 1.2–4.8 mg daily was given to 10 patients with severe Parkinsonism for up to 9 months. All had been taking bromocriptine and eight had been taking levodopa combined with carbidopa. Total replacement of bromocriptine by lisuride was achieved in every case, but partial or total levodopa replacement was possible only in five patients. Lisuride 1 mg has approximately the same antiparkinsonian activity as bromocriptine 15 mg or levodopa 250–500 mg combined with carbidopa, but the duration of action of each dose is short, and gastro-intestinal and neuropsychiatric side effects are common. However, lisuride i.v. may be of considerable value in the emergency treatment of severe Parkinsonism.     

维生素D治疗抑郁症的增效作用

目的 比较帕罗西汀联合维生素D与帕罗西汀联合安慰剂治疗抑郁症的效果.方法 将50例抑郁症患者随机分成两组,研究组25例给予帕罗西汀联合维生素D,对照组25例给予帕罗西汀和安慰剂,进行为期8周的双盲安慰剂对照的随机分组研究.采用24项汉密尔顿抑郁量表(HAMD)和不良反应量表(TESS)评定临床疗效和不良反应,以电化学发光法测定受试者基础血清维生素D水平.结果 共有48例受试完成试验.治疗8周后,研究组和对照组患者的显效率分别为87.5％(21/24)和75.0％(18/24),差异有统计学意义(X2＝10.71,P＜0.05).治疗后6周和8周时,研究组HAMD评分明显低于对照组,两组间比较差异有统计学意义(P＜0.05).两组TESS评分比较差异无统计学意义(P＞0.05).结论 维生素D能增强帕罗西汀治疗抑郁症的效果.     

Association of serum levels and receptor genes BsmI,TaqI and FokI polymorphisms of vitamin D with the severity of multiple sclerosis

PurposeMultiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease. Vitamin D has a major role in preventing inflammatory disorders. Therefore, any alteration in vitamin D receptor (VDR) might be a genetic risk factor for MS development. This study aimed to evaluate the effect of serum levels and VDR FokI, BsmI, and TaqI gene polymorphisms on the severity of MS.MethodsThis case-control study recruited 160 MS patients (71.9% females, mean age of 34.3 ± 8.3 years) and 162 (66.7% females, mean age 35.4 ± 7.9 year) age, sex, and ethnicity matched healthy controls. FokI (rs2228570), BsmI (rs1544410), and TaqI (rs731236) polymorphisms were carried out using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Demographic, clinical parameters, and the levels of vitamin D were compared between groups.ResultsWe found that the frequency of FokI and TaqI polymorphisms significantly differed between the patients and the controls (p = 0.0127 and p = 0.0236, respectively). The MS patients had low levels of vitamin D compared to the controls (p = 0.011). In addition, TaqI T/C polymorphism significantly decreased the levels of vitamin D in the MS patients (p = 0.002). However, there was no significant association between FokI or BsmI SNPs and the levels of vitamin D in MS patients (p > 0.5).ConclusionOur results suggest that FokI and TaqI polymorphisms of VDR are associated with MS risk and TaqI polymorphism is associated with Vitamin D levels in MS patients. Meanwhile, no difference was observed between VDR gene polymorphisms and any types of MS.