Postural instability and gait difficulty (PIGD) is a debilitating subtype in patients with Parkinson’s disease (PD). Gait performance under dual-task (DT) may reveal subtle impairments. This exploratory retrospective cross-sectional study aimed to investigate whether gait performance under DT differs between PD motor subtypes and to generate hypotheses for future confirmatory studies. This study enrolled 66 PD patients (mean age 64.64 ± 8.36 years). Motor subtypes [tremor-dominant (TD), PIGD and intermediate type (IT)] were classified by MDS-UPDRS-derived ratios. Gait parameters under single-task (ST) and DT were assessed by wearable G-Walk system. Binary logistic regression examined the association between gait parameters and PIGD subtype, adjusting for age, sex and H-Y staging and gait parameters (primary analysis). A sensitivity analysis excluded the IT subtype. Receiver operating characteristic (ROC) analysis evaluated the discriminatory ability of gait parameters. In the primary analysis, cadence under DT was associated with the PIGD subtype after adjusting for age, sex and H-Y staging (OR = 1.056, 95

BackgroundCerebral small vessel disease (CSVD) may worsen motor and cognitive impairment in Parkinson’s disease (PD), yet whether peripheral metabolic inflammation mediates this link remains unclear. The triglyceride-glucose (TyG) index, a surrogate for insulin resistance, has been associated with CSVD and neurodegeneration. This study examined whether the TyG index statistically accounts for the association between CSVD burden and motor or cognitive deficits in PD.MethodsThis retrospective cross-sectional study enrolled 362 PD patients. The 4-point scale assessed CSVD burden. Movement Disorder Society Unified Parkinson’s Disease Rating Scale part III (MDS-UPDRS III) and Montreal Cognitive Assessment (MoCA) evaluated motor and cognitive function, separately. Spearman correlation and mediation analyses were performed, adjusting for age, sex, education, hypertension, diabetes, and daily dose equivalent of levodopa. Sensitivity analyses were conducted to assess the robustness and specificity of the findings.ResultsCSVD burden was positively associated with MDS-UPDRS III (total effect = 2.309, 95% CI [0.463, 4.155, p = 0.014]) and negatively associated with TyG index (a = −0.067, p = 0.025). TyG index was negatively associated with MDS-UPDRS III (b = −6.561, p < 0.001). The indirect effect was 0.441 (95% CI [0.048, 0.958]), accounting for 19.1% of the total effect. This mediation was specific to TyG, as four alternative inflammatory indices showed no significant effects. Additional analyses adjusting for disease duration and Hoehn-Yahr staging confirmed robustness [indirect effect = 0.288, 95% CI (0.019, 0.687)]. Neither fasting triglycerides nor glucose alone mediated the effect. No mediation was found for cognition.ConclusionThe TyG index statistically accounts for part of the association between CSVD and motor function in PD via a negative-to-negative pathway, suggesting a hypothesis-generating metabolic target that warrants prospective investigation.

Abstract Background Gait impairment is a common and disabling motor symptom in Parkinson’s disease (PD), deteriorated gait parameters have showed in both single-task (ST) and dual-task (DT) conditions. The aim of this study was to investigate the effects of different motor-cognitive and motor-motor DTs on gait and the correlation between gait speed and clinical features in PD patients. Methods Fifty-six individuals with PD completed two motor-cognitive DTs (serial-7 subtractionand digit backward) and one motor-motor DT (button pressing). Spatiotemporal gait parameters were evaluated by wearable sensors. DT effects (DTEs) of gait parameters were calculated. Clinical variables recorded including Hoehn & Yahr (H-Y) staging, Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) part I, II and III, New Freezing of Gait Questionnaire (NFOG-Q), Montreal Cognitive Assessment (MoCA), Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD), 39-item Parkinson’s Disease Questionnaire (PDQ-39) and Nonmotor Symptom Scale (NMSS). Results Gait parameters including gait speed, cadence, stride length, gait cycle duration, double support phase deteriorated under the motor-cognitive DT conditions by Paired-sample t test and Wilcoxon signed-rank test (p＜0.01, p＜0.05). The motor-motor DT had no significant effect on gait performance except for gait speed (p＞0.05). The serial-7 subtraction DT paradigm had similar effect on gait with the digit backward DT. Gait speed was negatively correlated with MDS-UPDRS I, II, HAMA, HAMD, NMSS and PDQ-39 scores in PD patients under both ST and DT conditions (p＜0.01, p＜0.05). Conclusion Effects of DT conditions on gait deficits were independent of the types of cognitive tasks. Gait speed was influenced by clinical features of PD under both ST and DT conditions. Whatever the types, motor-cognitive DT training should be used to improve gait performance under DT conditions, which is required to provide more therapeutic support of PD patients in the future.

Introduction Emerging evidence has suggested that lipid metabolism is correlated with Parkinson's disease ( PD) onset and progression. However, the effect of lipid metabolism on motor performance in PD patients is still unknown. This study estimated the association between lipid profiles and the severity of motor performance in PD. Methods This cross-sectional study enrolled 279 idiopathic PD patients from the Department of Neurology of Beijing Tiantan Hospital from May 2016 to August 2018. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL- C), apolipoprotein A1 (Apo-A1), and apolipoprotein B (Apo-B) levels were detected in fast serum samples. Motor performance was assessed by Movement Disorder Society-Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS III) total scores and subscores in these patients. The associations of lipid profiles with motor performance were analyzed using multivariable linear regression models. Results Compared to males, females with PD exhibited significantly higher serum TC, LDL-C, HDL-C, Apo-A1, and Apo-B levels. When accounting for covariates, lower serum TG levels were significantly associated with higher MDS-UPDRS III total scores and gait/postural instability subscores. Additionally, the univariate linear regression model showed that in males with PD, serum HDL-C or Apo-A1 levels were significantly associated with tremor subscores. Conclusion Lower serum TG levels were associated with more severe motor performance in patients with PD and TG may be a potential predictive biomarker for motor performance in PD patients.

Emerging evidence suggests that cerebral small vessel disease (CSVD) may worsen cognitive functions in Parkinson’s disease (PD). However, the effect of microbleeds on cognitive function in patients with PD remains unknown. This study explored the association between the presence, number and location of microbleeds with dementia in PD patients. This cross-sectional study included 431 patients with PD from Beijing Tiantan Hospital from May 2016 to August 2019. Cognition assessments (MMSE, MoCA) were performed for these patients. MRI imaging sequences were obtained and reviewed independently by two well-trained readers who were blind to all clinical data. Spearman’s correlation analysis and logistic regression model analysis were further used for the assessments. An association between cerebral microbleeds with cognitive ability and dementia in PD patients was revealed. A significance was observed between the total number of microbleeds and two widely used scores of cognitive assessments (Spearman R = − 0.120 to MMSE with a p = 0.016, and − 0.117 to MoCA with a p = 0.020). In detail, infratentorial microbleeds were associated with the level of cognition in PD patients (Spearman R = − 0.099 to MMSE with a p = 0.049, and − 0.116 to MoCA with a p = 0.021). Furthermore, logistic regression analysis results also confirmed such correlations between the number of microbleeds and cognitive ability after adjusting for age, cholesterol level, Hamilton Anxiety Scale, Hamilton Depression Scale, and white matter hyperintensity Fazekas score (OR 3.28, p = 0.035, 95

Objective Whether perivascular space (PVS) visible on magnetic resonance imaging (MRI) represents glymphatic dysfunction and whether this imaging marker is pathologic in Parkinson's disease (PD) have been controversial. The objective was to determine whether PVS visible on MRI is independently associated with cognitive decline in patients with PD, and to test whether pathologic proteins in the CSF (such as Aβ42) mediate the pathologic role of PVS. Methods A total of 341 patients with Parkinson's disease from Parkinson's Progression Marker Initiative (PPMI) cohort was included in the present study. PVS in the basal ganglia (BG-PVS) and centrum semiovale were evaluated with a semiquantitative scale. Changes in the Montreal Cognitive Assessment (MoCA) score and the absolute MoCA score at the 3-year assessment were considered the main cognitive outcome. A multivariable linear regression model was used to test the association between PVS and cognitive decline. A mixed linear model and path analysis were used to test the interaction among PVS, CSF biomarkers and cognitive decline. Results BG-PVS was associated with cognitive decline in patients with PD at the 3-year follow-up independent of age, baseline cognition, motor and nonmotor function, presynaptic dopaminergic deficiency, and CSF biomarkers. The interaction between BG-PVS and Aβ42/tTau, Aβ42/pTau, and Aβ42 levels was significantly predictive of 3-year cognitive decline. Path analysis confirmed that CSF Aβ42/tTau levels partially mediated the pathologic effect of BG-PVS on cognitive outcome in PD. Conclusions BG-PVS is independently associated with cognitive decline in PD, and this association may be partially mediated by toxic CSF proteins.

Impaired gait is observed in patients with Parkinson’s disease (PD) in both single-task (ST) and dual-task (DT) conditions. Non-motor symptoms (NMSs), another vital symptom future experienced along the PD disease trajectory, contribute to gait performance in PD. However, whether DT gait performance is indicative of NMS burden (NMSB) remains unknown. This study investigated correlation between NMS and DT gait performance and whether NMSB is reflected in the DT effects (DTEs) of gait parameters in PD. Thirty-three idiopathic PD participants were enrolled in this study; the median H-Y staging was 2.5. NMSB was assessed by Non-motor Symptoms Scale (NMSS). Spatiotemporal gait parameters under ST and DT conditions were evaluated by wearable sensors. Gait parameters under ST and DT conditions and DTEs of gait parameters were compared across NMSB groups. The associations between NMS and DTEs of gait parameters were analyzed by correlation analysis and linear regression models. Compared to PD patients with mild-moderate NMSB, the severe-very severe NMSB group showed slower gait speed and shorter stride length under both ST and DT conditions (p < 0.05). DT had significantly negative effect on gait parameters in PD patients, including gait speed, stride length, and gait cycle duration (p < 0.05). PD patients with mild-moderate NMSB showed larger DTEs of cadence and bilateral gait cycle duration (p < 0.05). DTEs of bilateral gait cycle duration and swing phase on the more affected (MA) side were significantly correlated with NMSS scores (∣rSp∣ ≥ 0.3, p < 0.05). Gait cycle duration on the less affected (LA) side explained 43

Purpose: Lacunae are imaging biomarkers of cerebral small vessel disease (CSVD) and are correlated with the degree of gait instability in Parkinson's disease (PD). The wearing-off phenomenon (WO) occurs more frequently in PD patients as disease progresses. The present study aimed to investigate the overall impact of the quantity and location of lacunae on the WO in PD. Patients and Methods: This retrospective, single-center study included 315 consecutive eligible patients with PD from Beijing Tiantan Hospital from May 2016 to August 2018. We collected data on demographics and clinical features, assessed lacunae and examined the presence of the WO. The association between lacunae and the WO was assessed using a binary logistic regression model. Results: The number of lacunae was significantly associated with the WO in patients with PD according to a model adjusted for age at onset, disease duration, Hoehn-Yahr (H-Y) staging, Movement Disorder Society-Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS III) total score and levodopa equivalent daily dosage (LEED) (P=0.037, OR 1.156, 95% CI 1.009, 1.325) and to a model further adjusted for other CSVD imaging biomarkers (P=0.046, OR 1.172, 95% CI 1.003, 1.369). Following additional adjustment for other potential confounders, the association remained significant (P=0.043, OR 1.195, 95% CI 1.005, 1.421). Lacunae in subcortical areas (P=0.004, OR 0.498, 95% CI 0.308, 0.803) and basal ganglia (P=0.046, OR 1.616, 95% CI 1.009, 2.587), especially in the caudate nuclei (P=0.023, OR 1.104, 95% CI 0.185, 0.881), were significantly associated with the WO in PD patients. Conclusion: Our finding highlights the significant association between lacune and the WO, and lacunae may be an independent contributor to the WO in PD patients. Promoting neurovascular health may prevent the progression of the WO in PD patients.

1Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, People’s Republic of China; 2China National Clinical Research Center for Neurological Diseases (NCRC-ND), Beijing, People’s Republic of China; 3Department of Neurology, Beijing Hospital, National Center of Gerontology, Beijing, People’s Republic of China; 4Department of Rehabilitation, Beijing Tiantan Hospital, Capital Medical University, Beijing, People’s Republic of China Purpose: Lacunae are imaging biomarkers of cerebral small vessel disease (CSVD) and are correlated with the degree of gait instability in Parkinson’s disease (PD). The wearing-off phenomenon (WO) occurs more frequently in PD patients as disease progresses. The present study aimed to investigate the overall impact of the quantity and location of lacunae on the WO in PD. Patients and Methods: This retrospective, single-center study included 315 consecutive eligible patients with PD from Beijing Tiantan Hospital from May 2016 to August 2018. We collected data on demographics and clinical features, assessed lacunae and examined the presence of the WO. The association between lacunae and the WO was assessed using a binary logistic regression model. Results: The number of lacunae was significantly associated with the WO in patients with PD according to a model adjusted for age at onset, disease duration, Hoehn–Yahr (H-Y) staging, Movement Disorder Society-Unified Parkinson’s Disease Rating Scale part III (MDS-UPDRS III) total score and levodopa equivalent daily dosage (LEED) (P=0.037, OR 1.156, 95% CI 1.009, 1.325) and to a model further adjusted for other CSVD imaging biomarkers (P=0.046, OR 1.172, 95% CI 1.003, 1.369). Following additional adjustment for other potential confounders, the association remained significant (P=0.043, OR 1.195, 95% CI 1.005, 1.421). Lacunae in subcortical areas (P=0.004, OR 0.498, 95% CI 0.308, 0.803) and basal ganglia (P=0.046, OR 1.616, 95% CI 1.009, 2.587), especially in the caudate nuclei (P=0.023, OR 1.104, 95% CI 0.185, 0.881), were significantly associated with the WO in PD patients. Conclusion: Our finding highlights the significant association between lacune and the WO, and lacunae may be an independent contributor to the WO in PD patients. Promoting neurovascular health may prevent the progression of the WO in PD patients.

路易体痴呆(dementia with Lewy bodies,DLB)是一种神经变性性痴呆,以细胞内路易体(Lewy bodies,LB)沉积为病理特点,临床表现为波动性认知功能障碍、视幻觉和帕金森综合征.这一疾病由Lewy等[1]于1912年首次报道.由于帕金森病(Parkinson disease,PD)患者晚期可发展为帕金森病痴呆(Parkinson's disease with dementia,PDD),且PDD患者中脑内也存在LB,故区别二者十分困难.有学者制定了1年原则,即若患者发生痴呆在锥体外系症状1年后则倾向于诊断为PDD,反之,痴呆发生于锥体外系症状前或者后1年内则倾向于诊断为DLB[2].近期也有学者提出DLB与PDD是同种疾病的不同进展形式[3].此外,有研究在DLB患者发现老年斑(senile plaque,SP)和神经元纤维缠结(neurofibrillary tangles,NFT)沉积,提示DLB与阿尔兹海默病(Alzheimer disease,AD)存在相似性和联系[4].

INTRODUCTION:Emerging evidence has suggested that cerebral small vessel disease (CSVD) may worsen motor function and cognition in Parkinson's disease (PD). However, the effect of CSVD on anxiety and depression in patients with PD remains unknown. This study explored the multi-dimensional effects of CSVD on PD outcomes (motor, cognition, and depression/anxiety).METHODS:This cross-sectional study included 431 patients with PD from Beijing Tiantan Hospital from May 2016 to August 2019. CSVD imaging markers were assessed and the four-point CSVD burden score was calculated. Motor function (MDS-UPDRS III score and subscores), cognition (MMSE, MoCA), anxiety (HAMA), and depression (HAMD) were assessed in these patients. The associations of CSVD with these outcomes were analyzed using the Spearman's correlation and multivariable linear regression models.RESULTS:Motor dysfunction, cognitive impairment, depression, and anxiety were significantly worse in patients with severe CSVD than in those with mild CSVD. Multivariable linear regression showed that CSVD burden was significantly associated with motor dysfunction (MDS-UPDRS III score and rigidity and bradykinesia subscores), impaired cognition, and high levels of depression and anxiety. A marginally significant association was observed between CSVD burden and gait/postural instability in multivariable regression analysis. Among the CSVD imaging markers, white matter hyperintensity, number of lacunes, and microbleeds were positively correlated with the severity of motor, cognitive, and emotional impairments, while the perivascular space in the basal ganglia was only correlated with cognitive impairments.CONCLUSIONS:Comorbid CSVD may affect multiple functional domains in patients with PD. Management of cerebrovascular disease may improve PD outcomes.

随着人口老龄化的加重,老年期痴呆的发生率呈逐年上升趋势.目前全球至少有5000万痴呆患者,其中约1200万在中国[1].阿尔茨海默病(Alzheimer's disease,AD)是导致老年期痴呆的主要原因,也是21世纪老年保健面临的重大挑战之一.AD为进行性神经系统退行性疾病,以记忆力下降和行为减退为主要临床表现,病理改变表现为β淀粉样蛋白(amyloid β-protein,Aβ)沉积和tau 蛋白形成的神经纤维缠结,同时伴有神经元及其突触的变性、胶质细胞激活和神经紊乱 [2].然而,到目前为止并未发现具有AD疾病修饰作用的药物.

Levodopa is widely used to treat Parkinson’s disease (PD), and its long-term therapy may induce dyskinesia in a dose-dependent manner. However, the threshold dose with a relatively low risk for dyskinesia has not been determined. Demographic, clinical profiles and detailed information of dopaminergic drugs were recorded for 403 PD patients in treatment with levodopa. Variables were compared between dyskinesia and non-dyskinesia groups. Logistic regression analysis was used to assess the association between levodopa dose–related variables and dyskinesia. Receiver operating characteristic curve and decision tree classification model were used to investigate the cut-off value of levodopa dose to best separate the dyskinesia group from the non-dyskinesia group. Patients with dyskinesia tended to have a lower weight and age at onset, higher percentage of female and wearing-off, longer duration of disease and levodopa treatment, higher H-Y stage and MDS-UPDRS Part III score, and higher levodopa dose and levodopa equivalent dose than those without dyskinesia. After adjusted for demographical and clinical variables, levodopa dose–related factors (daily dose, cumulative dose, and weight-adjusted dose) were still associated with dyskinesia. Both the receiver operating characteristic and decision tree classification analysis indicated that patients who have taken levodopa dose ≤ 400 mg per day may be associated with a reduced risk for dyskinesia. In conclusion, we evaluated the thresholds of levodopa treatment with a relatively low risk for dyskinesia. These data should be considered for prevention and management of dyskinesia in patients with PD.

帕金森病(Parkinson's disease,PD)是常见神经系统退行性疾病之一,除典型运动症状外,非运动症状也不容忽视.轻度认知障碍(mild cognitive impairment,MCI)是PD早期出现的主要非运动症状,随着病程进展逐渐加重并最终发展为帕金森痴呆(PDD).随访研究发现,1/3的MCI患者最终可发展为PDD,80％的PD患者15?20年后发展为PDD[1].PD与路易体痴呆(DLB)同属于α突触核蛋白(α-syn)病,二者具有相似的临床症状和病理改变.除α-syn沉积外,研究还发现PDD患者存在老年斑、神经纤维缠结等阿尔茨海默病(AD)的病理改变[2].这些大大增加了PDD的早期诊断及鉴别诊断难度.因此,可靠标志物对PDD的诊断和鉴别诊断异常重要,同时有助于疾病的早期干预以及发现疾病进展的潜在病理生理机制.因此,本综述将对目前PDD相关的生物标志物和影像标志物研究进展进行总结,为PDD的早期诊断、进展、预后及早期干预治疗提供依据.

额颞叶变性是一组以人格改变和言语功能障碍为主要临床特征的神经退行性疾病,病理表现为局限性额叶和/或颞叶萎缩.此病病因尚未明确,30％～50％的额颞叶变性患者有家族聚集倾向,提示遗传相关性.额颞叶变性按临床表现可分为行为变异型额颞叶痴呆、进行性非流利性失语及语义性痴呆3型.本文从额颞叶变性的遗传学、病理学、临床表现和治疗进展4方面进行综述.

Deposition of intracellular misfolded α-synuclein (α-syn) in the central nervous system and peripheral nervous system leads to Parkinson′s disease, dementia with Lewy body, multiple system atrophy and other synucleinopathies. But the pathological mechanism of the transmission is not fully understood. Recent studies have shown that intercellular transmission of neurotoxic oligomer α-syn is the main mode of disease transmission between brain regions. This article reviews the existing evidence for different modes of cell secretion and uptake of oligomer α-syn, including direct intercellular transmission, prion-like transmission, exosomes and endocytosis, tunneling nanotubes and microglia-mediated, to provide a more detailed understanding of the patterns of synucleinopathy throughout the brain and to provide new targets for the treatment of disease.

目的 探讨脑白质高信号(WMH)对帕金森病(PD)运动症状和认知损害的影响.方法 回顾性纳入315例PD患者,根据Fazekas量表评分分为轻度WMH组191例,中度WMH组74例,重度WMH组50例.收集脑血管病相关危险因素,Hoehn-Yahr(H-Y)分级、世界运动障碍协会统一帕金森病评定量表第三部分(MDS-UPDRSⅢ)总分及震颤、强直、运动迟缓、步态姿势异常评分评估运动症状,用简易智能状态检查量表(MMSE)、蒙特利尔认知评估量表(MoCA)评估认知功能,用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)评估情绪,用3T MRI及Fazekas量表评估WMH程度,用Spearman相关和多元线性回归分析.结果 3组年龄、起病年龄、病程、MMSE和MoCA评分比较,有统计学差异(P＜0.05,P＜0.01).3组H-Y分级、MDS-UPDRSⅢ总分、震颤、强直、运动迟缓、步态姿势异常、HAMA、HAMD评分及体位性低血压比例比较,无统计学差异(P＞0.05).多元线性回归分析校正年龄、病程、起病年龄、MoCA、同型半胱氨酸、缺血性脑卒中、高血压、吸烟、性别、体质量指数和心脏病等因素后,WMH与MMSE仍显著相关(β=-0.183,95％CI:-0.134～-0.007,P=0.029).脑室旁WMH(r=-0.246,P=0.000;r=-0.235,P=0.000)和深部WMH(r=-0.192,P=0.001;r=-0.187,P=0.001)与MMSE和MoCA呈显著负相关.WMH与PD运动症状不相关(P＞0.05).结论 WMH对PD认知损害影响明显,临床需警惕PD伴发WMH,脑血管病二级预防可能对PD患者认知减退有潜在预防作用.

Parkinson's disease (PD) is a common neurodegenerative disorder. To date, the diagnosis of PD relies mainly on clinical manifestations whereas neuropathological confirmation of the brain is only possible with postmortem studies. Neuronal loss in the substantia nigra pars compacta (SNc) associated with Lewy bodies/neurites is the pathological hallmark feature of PD. The major component of Lewy pathology (LP) is misfolded alpha-synuclein (α-SYN). There is evidence that the distribution of LP is not only limited to the brain but extends to peripheral tissues, including gastrointestinal tract, salivary glands, olfactory mucosa, skin, retina, adrenal gland, and heart. Sensitivity and specificity of α-SYN detection in PD vary greatly among studies due to methodological heterogeneity, such as sampling sites and size, tissue preparation, staining techniques, and antibodies used. Of note, α-SYN has also been found in preclinical and prodromal PD. Further in vivo studies focusing on favorable biopsy sites and standard techniques are needed to get better understanding of α-SYN deposits in preclinical, prodromal, and clinical PD.

目的 探讨帕金森病(Parkinson's disease,PD)患者既往服用左旋多巴情况与异动症风险的相关性,并基于数据驱动方法分析PD患者左旋多巴每日最高安全剂量以及累积安全剂量.方法 选择于2017年3～12月于我院住院的PD患者142例,将伴发异动症患者41例作为异动组,不伴异动症患者101例作为非异动组.logistic回归分析PD患者服用左旋多巴情况与异动症风险的相关性;利用分类决策树模型计算左旋多巴安全剂量.结果 异动组病程、服用药物时间明显高于非异动组,发病年龄和体质量明显低于非异动组.异动组左旋多巴累积剂量和峰日剂量明显高于非异动组[(949.10±750.39)g vs (510.77±428.36)g,P＜0.01;(639.81±363.87)mg/d vs (381.93±169.89)mg/d,P＜0.01].logistic回归分析显示,左旋多巴累积剂量和峰日剂量与PD异动症风险均具有相关性(OR=1.002,P=0.002;OR=1.006,P=0.000).分类决策树模型预测提示,左旋多巴峰日剂量400.00mg/d、左旋多巴累积剂量609.75 g为区分异动症与非异动症的安全剂量.结论 左旋多巴峰日剂量和累积剂量与PD异动风险可能具有相关性.