帕金森病患者血浆肿瘤坏死因子-α和白介素-6与非运动症状的相关性分析

目的探讨帕金森病(PD)患者血浆TNF-α和IL-6水平与非运动症状的相关性。方法采用ELISA法测定41例原发性PD患者(PD组)和37名健康对照者(正常对照组)血浆TNF-α和IL-6的水平。采用Hoehn-Yahr分期(H-Y分期)、统一PD评定量表第Ⅱ部分(UPDRSⅡ)、统一PD评定量表第Ⅲ部分(UPDRSⅢ)、非运动症状量表(NMSS)评价PD患者关期时的运动和非运动症状。结果与正常对照组比较,PD组TNF-α和IL-6水平显著降低(均P0.05)。PD组TNF-α水平与H-Y分期、UPDRSⅡ、UPDRSⅢ和NMSS评分无相关性(r=0.093,P=0.562;r=-0.024,P=0.882;r=0.131,P=0.415;r=-0.109,P=0.499)。PD组IL-6水平与H-Y分期、UPDRSⅡ、NMSS评分呈显著负相关(r=-0.411,P=0.008;r=-0.321,P=0.041;r=-0.324,P=0.039),与UPDRSⅢ评分无相关性(r=-0.126,P=0.431)。结论 PD患者可能存在免疫功能异常,且免疫炎症机制的异常可能参与PD非运动症状的致病过程。     

血清YKL-40、RANTES、SSA水平和帕金森病患者MoCA评分的关系

目的 探讨血清人软骨糖蛋白39(YKL-40)、活化T细胞趋化因子(RANTES)、淀粉样蛋白A(SSA)水平和帕金森病患者MoCA评分的关系。方法 选择2017年1月-2018年11月本院接诊的80例帕金森病患者作为观察组,并选择同期于本院接受体检的健康体检者60例作为对照组,比较2组血清YKL-40、RANTES、SSA水平、蒙特利尔认知评估量表(MoCA)评分,记录观察组帕金森病统一评分量表(UPDRS)评分,分析血清YKL-40、RANTES、SSA水平和MoCA评分、UPDRS评分的相关性。结果 观察组血清YKL-40、RANTES、SSA水平均明显比对照组高,MoCA评分明显低于对照组(P<0.05); 经Spearman 相关分析显示,血清YKL-40、RANTES、SSA水平和UPDRS Ⅰ评分均无明显相关性(P>0.05); 血清YKL-40、RANTES、SSA水平和MoCA评分均呈负相关(r=-0.743,-0.812,-0.786,P<0.05),和UPDRS Ⅱ(r=0.832,0.673,0.753)、UPDRS Ⅲ(r=0.698,0.739,0.791)评分均呈正相关(P<0.05)。结论 血清YKL-40、RANTES、SSA水平在帕金森病患者中呈明显升高趋势,且和患者MoCA评分具有密切联系,也为早期发现、防治疾病提供了一定理论基础。     

帕金森病患者纹状体多巴胺转运体显像与帕金森病临床量表评分的相关性

目的研究帕金森病(PD)患者纹状体多巴胺转运体(DAT)显像与PD临床量表评分的相关性。方法以99mTcTRODAT1为显像剂,用单光子发射断层扫描(SPECT)对29例PD患者进行纹状体DAT显像;应用统一PD评定量表(UPDRS)对患者的运动功能进行评分。将UPDRSⅡ(日常生活活动)、Ⅲ(运动评分)和Ⅴ(病情分期)的评分、患者年龄及病程分别与起病肢体同侧、对侧及两侧纹状体的DAT摄取值进行相关性分析。结果纹状体DAT摄取值与UPDRSⅡ、Ⅲ和Ⅴ评分、病程呈负相关(r分别为-0.70、-0.80、-0.49及-0.54,均P<0.01),与年龄无相关性(r=-0.018,P>0.05);纹状体DAT摄取值与UPDRSⅢ的肌僵直和运动迟缓评分呈负相关(r=-0.782、-0.83,均P<0.01),与震颤评分不相关。结论纹状体DAT显像是反映PD严重程度的客观指标,其与PD临床量表部分项目评分有相关性。     

不同性别帕金森病患者血尿酸水平的相关性研究

目的研究不同性别帕金森病(PD)患者血尿酸水平的相关影响因素。方法收集72例男性PD患者及56例女性PD患者的临床资料。采取高效液相色谱法检测患者血尿酸水平,分析血尿酸水平与临床资料的相关性。结果相关性分析显示,女性PD患者血尿酸水平与患者年龄、起病年龄呈正相关(r=0.283,P=0.034;r=0.295,P=0.027),与病程、Hoehn-Yahr(H-Y)分级、统一帕金森病评分量表(UPDRS)评分,以及汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、MMSE、非运动症状问卷(NMS-Quest)评分间无明显相关性(均P0.05);男性PD患者血尿酸水平与UPDRSⅣ评分、HAMD呈负相关(r=-0.249,P=0.035;r=-0.279,P=0.017),与年龄、起病年龄、病程、H-Y分级、UPDRSⅡ、UPDRSⅢ、UPDRS总分,以及HAMA、MMSE、NMS-Quest评分无明显相关性(均P0.05)。男性和女性患者血尿酸水平与左旋多巴等效剂量(LED)及左旋多巴剂量均呈负相关(均P0.05),与多巴胺受体激动剂剂量无关(均P0.05)。结论女性PD患者年龄越大、起病越晚,血尿酸水平越高;男性PD患者治疗并发症越多、抑郁越重,血尿酸水平越低。PD患者血尿酸水平与患者左旋多巴服用剂量呈反比。     

帕金森病相关性疼痛的相关因素及其对生活质量的影响

目的探讨帕金森病(PD)相关性疼痛的相关因素及其对生活质量的影响。方法根据是否伴有疼痛将120例PD患者分为疼痛组(49例)和非疼痛组(71例)。采用PD统一评分量表(UPDRS)和Hoehn-Yahr(H-Y)分级评估患者的严重程度,采用PD生活质量量表-39(PDQ-39)测评其生活质量,用数字评分法(NRS)评估疼痛组患者疼痛程度。采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)和MMSE评价患者的焦虑、抑郁及认知情况。结果与无疼痛组比较,疼痛组H-Y分期及UPDRSⅠ、UPDRSⅢ服药后(med-on)、UPDRSⅢ服药前(med-off)、PDQ-39、HAMA、HAMD评分均显著升高(P0.05～0.01)。Spearman相关分析显示,NRS评分与H-Y分级及UPDRSⅠ、UPDRSⅢmed-off、UPDRSⅢmed-on、PDQ-39、HAMA、HAMD评分呈正相关(P0.05～0.01),与年龄、发病年龄、病程、受教育年限及UPDRSⅡ、MMSE评分无相关性(均P0.05)。线性回归分析显示,UPDRSⅡ、HAMA、NRS评分对PDQ-39有显著性影响(均P0.01)。结论 PD相关性疼痛可能与精神活动、运动症状、焦虑抑郁相关。PD相关性疼痛是影响PD患者生活质量的独立预测因子。     

帕金森病患者血清EGF和BDNF水平变化与认知障碍的关系

目的探讨帕金森病(PD)患者血清表皮生长因子(EGF)和脑源性神经营养因子(BDNF)的变化及其与认知功能的关系。方法入选PD患者76例和年龄、性别相匹配的40例健康对照组,记录PD患者的性别、年龄、病程、受教育年限、HoehnYahr(H-Y)分级,采用蒙特利尔认知评估量表(Mo CA)对所有研究对象认知功能进行评估,采用酶联免疫吸附法(ELISA)检测血清EGF和BDNF水平,并对结果进行分析。结果 PD组血清EGF、BDNF水平明显低于健康对照组[(745±148)ng·L~(-1)比(952±157)ng·L~(-1),P0.05;(5.1±3.1)μg·L~(-1)比(6.8±3.9)μg·L~(-1),P0.05];早期PD组与中晚期PD组血清EGF和BDNF水平无差异(P0.05);但合并轻度认知功能障碍(MCI)的PD组血清EGF水平低于无MCI的PD组[(713±146)ng·L~(-1)比(865±189)ng·L~(-1),P0.01];PD患者Mo CA评分与受教育年限(β=0.611,P0.01)、血清EGF水平(β=0.513,P0.01)呈正相关,与病程(β=-0.373,P0.05)、H-Y分级(β=-0.264,P0.05)呈负相关。结论 EGF和BDNF水平的改变可能参与了PD患者的发病机制;血清EGF水平的下降可能与PD患者的MCI具有相关性,其可能为PD患者合并认知功能障碍的潜在早期预测指标。     

脑梗死后认知障碍与血清视锥蛋白样蛋白-1水平及神经功能缺损关系的研究

目的探讨脑梗死后认知障碍与血清视锥蛋白样蛋白-1(VILIP-1)水平及神经功能缺损的相关性。方法收集120例急性脑梗死患者,根据蒙特利尔认知评估量表(Mo CA)测评结果分为认知障碍组和认知正常组,比较两组患者入院时和发病1年时血清VILIP-1水平、美国国立卫生研究院卒中量表(NIHSS)评分、Barthel指数(BI)评分,分析Mo CA分值与血清VILIP-1水平、NIHSS评分和BI评分的相关性。结果两组患者发病1年时NIHSS评分均低于入院时(P0.01);BI评分均高于入院时(P0.01)。认知障碍组入院时及发病1年时血清VILIP-1水平高于认知正常组(P0.01);NIHSS评分高于认知正常组(P0.01);BI评分低于认知正常组(P0.01)。入院时及发病1年时所有患者Mo CA分值与血清VILIP-1水平呈负相关(r=-0.736,P=0.000;r=-0.450,P=0.000);与NIHSS评分呈负相关(r=-0.575,P=0.000;r=-0.377,P=0.001);与BI评分呈正相关(r=0.431,P=0.000;r=0.483,P=0.000)。结论脑梗死后认知障碍与血清VILIP-1水平及神经功能的康复有重要相关性。     

帕金森病患者血清脂联素水平与运动症状及非运动症状的相关性

目的 探讨帕金森病(PD)患者血清脂联素水平与运动症状以及非运动症状的相关性.方法 选取94例PD患者以及90名健康对照者,利用ELISA法检测PD患者及健康对照者血清脂联素水平,并记录PD患者的年龄、多巴丝肼片剂量,并对所有PD患者行帕金森病评价量表第三部分评分(UPDRSⅢ)、Hoehn-Yahr分期、ADL、Webster、疲劳严重度量表(FSS)、匹茨堡睡眠质量指数(PSQI)、自主神经功能量表(SCOPA-AUT)、汉密尔顿抑郁量表(HAMD)评估.结果 PD患者血清脂联素水平为(8.2士2.6)mg/L,明显低于健康对照组的(17.5±7.1)mg/L,且差异有统计学意义(t=-4.12,P＜0.01).脂联素水平与PD患者的UPDRSⅢ评分、H-Y分期、Webster评分、ADL评分及PSQI评分均呈负相关(r分别为-0.71,-0.82,-0.77,-0.64,-0.69;P＜ 0.05).结论 PD患者血清脂联素水平降低,且与PD患者的运动症状及非运动症状均有关.     

首诊帕金森病患者血清miR-128的水平测定及其相关研究

目的研究首诊帕金森病(PD)患者血清miR-128治疗前后的变化,及血清miR-128与统一PD评定量表(UPDRS)和炎性因子的相关性,为进一步探讨miR-128在PD中的诊断价值和发病机制提供帮助。方法检测54例首诊PD患者(首诊PD组)治疗前后的血清miR-128水平,并与50名健康对照者(健康对照组)比较。评定患者的UPDRS评分,检测血清IL-1β、TNF-α水平,并对结果进行分析。结果首诊PD组患者血清miR-128相对表达量明显低于健康对照组(t=8.87,P0.01)。首诊PD组患者治疗2个月后血清miR-128相对表达量明显高于治疗前(t=-5.13,P0.01);UPDRS评分明显低于治疗前(t=9.67,P0.01)。首诊PD组患者血清miR-128水平分别与UPDRS评分、IL-1β和TNF-α水平呈负相关(r=-0.763,r=-0.656,r=-0.674;均P0.01)。血清miR-128相对表达量的受试者工作特征曲线下面积为0.882(95%CI:0.776～0.952,P0.01),其诊断PD的灵敏度72.0%,特异度88.9%。结论首发PD患者血清miR-128水平表达异常,可作为评估PD病情和辅助诊断的较优的外周血指标,在PD发病机制中起到重要作用。     

帕金森病患者临床量表UPDRS与^18F-FP-CIT PET-DAT功能显像相关性的研究

目的研究临床中普遍应用的UPDRS量表中第Ⅱ、Ⅲ和Ⅴ部分评分与多巴胺转运体(Dopamine transporter,DAT)PET功能显像的相关性,推断这些评分在帕金森病(Parkinson disease,PD)临床应用的可靠性.方法以18F标记的FP-CIT为特异性配体,应用PET检测了31例原发性PD患者双侧基底节区(包括尾状核、前壳核和后壳核)DAT数量.将这些患者的UPDRS中第Ⅱ、Ⅲ和Ⅴ部分的临床评分与双侧基底节不同区域DAT均值进行相关性分析.结果UPDRSⅡ、Ⅲ、Ⅴ评分与尾状核、前壳核和后壳核DAT呈显著负相关.它们与后壳核DAT的相关系数r分别为-0.363,-0.473及-0.532.在UPDRS Ⅲ中的PD主要症状评分中,肌强直评分与上述3个基底节不同区域DAT均呈显著负相关,动作迟缓评分仅与后壳核DAT呈显著负相关,而震颤评分与这3个区域中的任何区域DAT均无相关性.结论UPDRS Ⅱ、Ⅲ、Ⅴ评分均能客观反映PD患者的严重程度,其中UPDRS Ⅲ相对更全面可靠.PD患者震颤发生的机制可能与黑质纹状体通路障碍无关.     

Classical Parkinson disease versus Parkinson complex – Reflections against staging and in favour of heterogeneity

Pathological studies have prompted the idea that Parkinson disease (PD) is a multisystem disorder, which starts far away from the nigrostriatal dopamine system and it goes through a long pre-clinical period. Evidence from epidemiological research, functional imaging, olfaction and sleep studies provides support to this hypothesis. Accordingly, PD is seen as an homogeneous disease which sequentially affects different neural structures leading to a well-defined clinical picture. This concept, recently named PD complex, has deep theoretical and practical implications which raise some concerns. This report shows the concept of classical PD as opposed to PD complex. Although the relevance of the central argument concerning the PD complex concept is admitted, it needs to be fully proved before premature conclusions are drawn. In contrast, the notion of classical and clinically significant PD can explain many of the well-characterized pathological and clinical features of the disease and it gives support to the idea that the magic word in PD is variability.     

Analysis of PARK genes in a Korean cohort of early-onset Parkinson disease

Mutations in five PARK genes (SNCA, PARKIN, DJ-1, PINK1, and LRRK2) are well-established genetic causes of Parkinson disease (PD). Recently, G2385R substitution in LRRK2 has been determined as a susceptibility allele in Asian PD. The objective of this study is to determine the frequency of mutations in these PARK genes in a Korean early-onset Parkinson disease (EOPD) cohort. The authors sequenced 35 exons in SNCA, PARKIN, DJ-1, PINK1, and LRRK2 in 72 unrelated EOPD (age-at-onset ≤50) recruited from ten movement disorders clinics in South Korea. Gene dosage change of the aforementioned genes was studied using multiple ligation-dependent probe amplification. We found four patients with PARKIN mutations, which were homozygous deletion of exon 4, compound heterozygous deletion of exon 2 and exon 4, heterozygous deletion of exon 4, and heterozygous nonsense mutation (Q40X). Four patients had PINK1 mutations; a compound heterozygous mutation (N367S and K520RfsX522) and three heterozygous mutations (G32R, R279H, and F385L). A missense mutation of SNCA (A53T) was found in a familial PD with autosomal dominant inheritance. Nine patients (12.5%) had heterozygous G2385R polymorphism of LRRK2, whereas none had G2019S mutation. However, no mutations were detected in DJ-1 and UCHL1 in our series. We identified genetic variants in PARKIN, PINK1, LRRK2, and SNCA as a cause or genetic risk factors for PD in 25% of Korean EOPD, and mutation of PARKIN was the most common genetic cause. Jung Mi Choi and Myoung Soo Woo equally contributed to this work.     

The hypothalamus in Parkinson Disease

It is currently believed that Parkinson disease (PD) is due to a degenerative process that independently damages multiple areas of the central and peripheral nervous system. Loss of nigrostriatal dopamine is now widely recognized as being directly related to the motor symptoms in Parkinson's disease. Parkinsonian patients also exhibit symptoms and signs suggestive of hypothalamic dysfunction (e.g. dysautonomia, impaired heat tolerance). The latter clinical features are supported by pathological, biochemical and endocrinological findings. Lewy body formation has been demonstrated in every nucleus of the hypothalamus, specifically the tuberomamillary and posterior hypothalamic. Preferential involvement of the hypothalamus was also noted in patients after post-encephalitic parkinsonism. Loss of dopamine (30–40%) in the hypothalamus of affected patients has been shown in recent studies, and is compatible with the reported abnormalities of growth hormone release in response to L-dopa administration, elevated plasma levels of MSH, and reduced CSF levels of somatostatin and beta-endorphins in these patients. Deranged immunological mechanisms have been found in PD patients including the presence of autoantibodies against sympathetic ganglia neurons, adrenal medulla and caudate nucleus. On the evidence of on pathological studies demonstrating the early vulnerability of the hypothalamus in aging and PD, and the known role of the hypoth lamus in immune modulation, we expect that it will be shown that primary damage ot the hypothalamus leads to subsequent secondary degeneration of structures receiving direct projections from the hypothalamus. Within this framework, the dopaminergic systems may be damaged, since striatal dopamine synthesis and receptor sensitivity have been shown to be regulated by ACTH and alpha-MSH through direct arcuate nucleus-striatal projections. We also demonstrate that virtually all other areas well known to be impacted upon in Parkinson disease receive significant hypothalamic peptidergic projections.

---

Sommario Si ritiene correntemente che la malattia di Parkinson (P.D.) sia dovuta ad un processo degenerativo che danneggia numerose zone del sistema nervoso centrale e di quello periferico. Si sa che la carenza di dopomine nigrostriale è certamente correlata ai disturbi motori in questa malattia. Ma i parkinsoniani hanno anche sintomi e segni suggestivi per un interessamento ipotalamico (disautonomia e ridotta tolleranza al calore). Questi aspetti clinici sono dovuti a fattori patologici sia biochimici che endocrinologici. è stata dimostrata la formazione di corpi Lewy in ogni nucleo dell'ipotolamo specialmente in quelli tubero mamillare e posteriori e un interessamento preferenziale, dell'ipotolamo è stato segnalato in pazienti affetti da parkinsonismo postencefalitico. Una perdita di dopamina del 30/40% nell'ipotalamo è stata vista in recenti ricerche ed è compatibile con la anormalità di formazione dell'ormone della crescita in risposta all'L-dopa e livelli ridotti di somatostatina e di beta-endorfina nel liquor. Meccanismi di sregolazione immunologica sono stati trovati in pazienti parkinsoniani quale la presenza di autoanticorpi contro neuroni dei gangli simpatici e del nucleo candato. Poiché sappiamo che vi è una precoce vulnerabilità dell'ipotalamo nella vecchiaia e nel morbo di Parkinson e conosciamo il ruolo delliipotalamo nell'immunamodulazione ci attendiamo che un danno primitivo dell'ipotalamo posti a una secondaria degenerazione delle strutture che ricevono una diretta proiezione dell'ipotalamo. All'interno di questa struttura i sistemi dopasinergici possono essere danneggiati del momento che la sintesi di dopamina e la sensibilità dei recettori sono regolata dall'ACTH e dell'ormone stimolante le alpha-melanoiti attraverso la proiezione arcate nucleostristriatali. Noi dimostriamo inoltre che virtualmente tutte le altre aree interessate nel morbo di Parkinson ricevono importanti proiezioni ipotalamiche peptidergiche.

     

帕金森病患者线粒体功能缺陷的研究

目的　探讨帕金森病 (PD)患者线粒体功能缺陷类型及其基因突变基础。方法　用溴化乙啶抑制人食管癌细胞系的线粒体DNA复制 ,制备出无线粒体DNA细胞系。将 2 0例PD患者组及2 0名正常对照组血小板与之融合 ,用选择性培养液挑选出融合细胞 ,大量培养后用极谱法测定线粒体酶复合体活性及抗氰呼吸。结果　以苹果酸和谷氨酸为底物时患者组 ( 1.2 5± 0 .0 8)明显低于正常对照组 ( 1.75± 0 .0 8) ,降低 2 8.6% ;以琥珀酸、维生素C和TMPD为底物时患者组与正常对照组差别无统计学意义。这些结果表明 ,线粒体酶复合体II～Ⅴ活性正常 ,以苹果酸和谷氨酸为底物的氧耗率的降低来源于酶复合体I活性受损。由于融合细胞核背景一致 ,其线粒体功能仅受mtDNA影响 ,因此本试验发现的患者酶复合体I缺陷来源于mtDNA的突变。抗氰呼吸PD患者组平均为 ( 8.76±0 .2 5 ) % ,正常对照组平均为 ( 6.2 0± 0 .10 ) % ,差异有显著意义 (P <0 .0 5 )。结论　PD患者线粒体酶复合体I活性降低 ,来源于线粒体DNA突变 ,可能导致自由基增多 ,在PD神经元变性中起重要作用。     

当归注射液对帕金森病模型大鼠的作用及其机制的研究

目的 观察当归注射液对6-羟多巴胺(6-OHDA)致帕金森病(PD)大鼠模型的影响探讨当归注射液可能的作用机制. 方法 成年雄性Wistar大鼠采用随机数字表法分为模型组、小剂量当归注射液(12.5%)治疗组和大剂量当归注射液(25%)治疗组、空白对照组、生理盐水组,每组8只:采用6-羟多巴胺6-OHDA右侧中脑黑质注射制作大鼠帕金森病PD模型,模型成功后小剂量治疗组及大剂量治疗组每日1次腹腔注射当归注射液.生理盐水组注射等量生理盐水,空白对照组不做任何处理.旋转实验采用阿朴吗啡大鼠背部正中皮下注射后记录其每分钟旋转数,每周一次;治疗4周后采用SABC法行CD40、黑质酪氨酸羟化酶TH免疫组织化学染色. 结果 与模型组比较,大剂量当归注射液治疗组于治疗3周后旋转减慢差异统计学意义(P<0.05),治疗4周后明显减慢差异统计学意义.治疗4周后,大剂量当归注射液治疗组右侧(注射侧)黑质TH、CD40阳性神经元数量较小剂量当归注射液治疗组及模型组明显增多差异统计学意义(P<0.01);空白对照组及生理盐水组右侧黑质未见CD40阳性小胶质细胞;模型组与治疗组右侧黑质CD40阳性小胶质细胞计数差异无统计学意义. 结论 当归注射液对PD大鼠有治疗作用.能明显减少黑质多巴胺神经元的丢失:当归注射液可能通过特定信号通路增加CD40在神经元的表达从而发挥其作用.     

帕金森病与QTc间期的关系

目的：观察帕金森病（PD）与QTc间期的关系。方法：分析了37例PD患者及37例健康对照组的QTc间期,并比较PD病病情与QTc间期的关系,结果：PD组QTc间期明显超过对照组（P＝0．001）,PD病情的轻重可影响QTc间期。结论：对QTc间期的监测有助于发现PD患者自主神经功能障碍,同时可作了为解病情轻重的一个参考指标。     

Multicenter trial of L-Deprenylin Parkinson disease

A multicenter trial was conducted at 9 Neurology Departements to evaluate the action of L-Deprenyl, a specific monoamine oxidase-B inhibitor, combined with L-Dopa in the treatment of Parkinson disease. In all, 76 patients were treated, 33 women and 43 men, on stable treatment with L-Dopa+aromatic decarboxylase inhibitors (DI) for at least 6 months. After a 50% reduction of the L-Dopa dose, all received L-Deprenyl 5 mg twice daily for 35 day. The combined treatment resulted in a definite improvement in rigidity, bradykinesia and, most of all, tremor. Further, at the end of treatment fewer patients had depressive symptoms and the total daily number of hours of wellbeing and normal movement increased. 12 patients presented modest side effects, in no case serious enough to warrant suspension of treatment. The trial shows that with the L-Deprenyl+L-Dopa combination the dose of L-Dopa needed to control the disease can be drastically reduced.

---

Sommario È stato condotto uno studio multicentrico in 9 Centri di Neurologia per valutare l'azione del L-Deprenyl, inibitore specifico delle monoaminoossidasi (MAO) di tipo B, in associazione a L-Dopa nel trattamento del Morbo di Parkinson.Sono stati trattati complessivamente 76 pazienti, 33 donne e 43 uomini, in trattamento stabile con L-Dopa +DI da almeno 6 mesi. A tutti, dopo una riduzione del 50% della dose di L-Dopa, sono stati somministrati 5 mg di L-Deprenyl due volte algiorno per 35 giorni.Il trattamento continuato di L-Dopa e L-Deprenyl ha determinato un evidente miglioramento della rigidità, della bradicinesia ed in particolare del tremore.Sono stati inoltre riscontrati al termine del trattamento una riduzione del numero di pazienti con sintomatologia depressiva ed un aumento delle ore complessive giornaliere di benessere e di normale motilità. 12 pazienti hanno presentato effetti collaterali di modesta entità che in nessun caso hanno richiesto la sospensione del trattamento.Lo studio evidenzia che il trattamento associato L-Deprenyl+L-Dopa consente una considerevole riduzione del dosaggio di L-Dopa necessario al controllo della malattia.

     

帕金森病定向术后影像学分析

目的:总结立体定向丘脑毁损术治疗128例帕金森病的影像学改变及影响疗效的因素分析。方法:128例帕金森病病人均采用温控射频热凝制造丘脑腹外侧核毁损灶。结果:本组病例症状完全控制95例(74.21％),症状控制伴有肢体麻木、情感、智能障碍27例(21.09％),无效5例(3.90％),恶化1例(0.78％)。结论:经统计学处理显示CT定位靶点法与脑室造影定位法对疗效影响无显著性差异。靶点定位、毁损灶大小与手术疗效、并发症密切相关。