左旋多巴治疗帕金森病发生剂末现象的相关因素

目的探讨左旋多巴治疗帕金森病发生剂末现象的相关因素。方法收集帕金森病患者临床资料,通过统计学分析对比分析剂末现象发生的相关因素。结果剂末现象的发生与性别、年龄、教育年限、体重、毒药物接触史、吸烟史、饮酒史、高蛋白饮食、脑血管病史无关(P 0. 05)。发生剂末现象的患者发病年龄早,病程长,左旋多巴起始、终点剂量高,左旋多巴用药时间长,疾病进展阶段(HY分期)高,统一帕金森病评分量表第三部分(UPDRSⅢ)评分高,汉密尔顿焦虑评分(HAMA)评分高(P 0. 05)。其中发病年龄、左旋多巴起始剂量、HY分期、焦虑是发生剂末现象的独立影响因素(P 0. 05);独立预测因素分别为HY分期、HAMA评分、发病年龄、左旋多巴起始剂量(P 0. 05)。HY分期具有较好的敏感度和特异度(80. 9%)。随治疗时间的增长,中晚期患者剂末现象发生风险高(P 0. 05)。结论多种因素影响左旋多巴临床治疗中发生剂末现象。     

左旋多巴诱导的帕金森病患者剂末现象发生的预测因素

目的研究左旋多巴(LD)诱导的帕金森病(PD)患者剂末现象(WO)发生的预测因素。方法收集使用LD治疗的原发性PD患者113例,记录性别、年龄、起病年龄、病程、LD日剂量、LD疗程、使用的其他抗PD药物、WO的发生时间等资料,H-Y分级和UPDRS运动部分(UPDRS PartⅢ)评分用于评估疾病的严重程度。结果 113例PD患者中出现WO患者43例(38.3%),与未发生WO的患者相比,发生WO的患者起病年龄早(P<0.042),病程长(P<0.001),LD起始剂量较高(P<0.001),起病至首次使用DA治疗的间隔时间较长(P<0.001),UPDRS运动部分评分及H-Y分级较高(P<0.001),以DA启动治疗的患者较LD启动治疗后再添加DA的患者WO发生率低(P=0.002)。起病年龄、病程、LD起始剂量、UPDRS运动部分(UPDRS PartⅢ)评分是WO发展的独立影响因素。结论较早的起病年龄、较长的病程、较高的LD起始剂量、较长的LD使用时间、较晚的DA起始治疗时间、较高的UPDRS PartⅢ评分及H-Y分级是WO发展的预测因素。     

帕金森病剂末现象的危险因素

目的探讨帕金森病剂末现象(WO)的危险因素。方法采用剂末现象-9项问卷(WOQ-9)评价149例PD患者有无WO。根据临床WO定义将WOQ-9(+)患者分为临床WO(+)组和临床WO(-)组。详细记录患者的一般情况(性别,发病年龄)、疾病概况(评估时疾病持续时间、疾病严重程度)及药物治疗概况[发病至启动左旋多巴(LD)的时间、LD治疗时间、LD起初剂量、LD终末剂量、是否联合应用多巴胺受体激动剂]。结果与临床WO(-)组相比,临床WO(+)组发病年龄显著降低,疾病持续时间、统一帕金森病评定量表Ⅲ(UPDRSⅢ)评分、LD治疗时间、LD初始剂量及终末剂量均显著升高(均P0.01)。两组患者性别、发病至启动LD的时间、使用多巴胺受体激动剂比率差异均无统计学意义(均P0.05)。多因素Logistic回归分析显示,发病年龄、LD终末剂量、UPDRSⅢ评分为WO的独立危险因素(均P0.01)。ROC曲线分析显示,UPDRSⅢ评分、LD终末剂量可较好预测WO的发生。UPDRSⅢ评分的准确性(曲线下面积0.913)及灵敏性(85.5%)最高,起病年龄的特异最高(97.7%)。随着LD治疗时间的延长,WO发生的风险随之增加(P=0.008)。发病年龄的早晚(分为早发型50岁、晚发型≥50岁)与WO关联不大(P=0.565),而每日接受LD治疗剂量超过400 mg的PD患者WO发生风险显著增加(P0.001)。结论在临床中应警惕发病年龄较低、UPDRSⅢ分值及LD终末剂量偏高的患者发生WO,根据个体特征进行个性化治疗则是降低运动并发症的最佳选择。     

应重视帕金森病治疗中剂末现象的识别与防治

<正> 目前帕金森病(PD)的治疗仍以多巴胺能药物(包括左旋多巴制剂及多巴胺受体激动剂)为主,对PD的强直、少动及震颤症状有明显疗效。但随着药物的使用,患者逐渐出现剂末现象及异动症等运动波动。这些远期运动并发症与多巴胺能药物的长期使用有关,但其发生率文献报道并不一致。一般认为,左旋多巴使用5～10年约50%～80%的患者发生运动波动,近年研究报道在服用左旋多巴平均2年时,剂末现象的发生率达65.2%。剂末现象是最常见的远期并发症。尽管临床对剂末现象比较关注,但因其表现多种多样,不仅表现     

帕金森病左旋多巴剂峰异动症的治疗

帕金森病(PD)是一种神经系统退行性疾病,左旋多巴仍是治疗PD的金标准用药,但是随着疾病的发展,长期服用左旋多巴会出现左旋多巴诱发异动症(LID),LID是常见的运动并发症。文中主要讨论LID的临床表现及治疗问题。     

电针刺激联合左旋多巴治疗帕金森病的疗效观察

目的观察电针刺激联合左旋多巴(L-dopar)治疗帕金森病(PD)的临床疗效。方法将40例PD患者随机分为治疗组20例,患者在口服L-dopar进行常规治疗的基础上,使用电针刺激风府穴、脑户穴、百会穴、印堂穴、水沟五穴,1次/d;对照组20例,患者按照常规剂量口服L-dopar,2组连续治疗30d,试验终点时间第30天。第30天分别比较治疗前后改良Webster量表评分和统一帕金森评分量表(UPDRS)评分。结果 2组患者均在改善震颤、强直、运动障碍等临床症状较治疗前效果明显(P0.01);改良Webster量表评分显示治疗后2组差异无统计学意义(P0.05),但2组改良Webster量表总分减分率方面,治疗组在改善便秘、多汗、肌强直方面优于对照组(P0.05);治疗后UPDRS评分显示治疗组优于对照组(P0.05)。结论电针联合L-dopar治疗PD疗效肯定,且无不良反应,是治疗PD安全有效的辅助疗法。     

定振汤治疗帕金森病的临床观察

目的 观察定振汤治疗帕金森病(PD)的临床疗效.方法 选择2006年3月～2008年9月我院PD患者65例,将其随机分为治疗组和对照组,对照组根据"国际帕金森病治疗指南"用药原则进行治疗,治疗组在此基础上予以定振汤,连续服用6月.在治疗前、治疗后3月和6月分别进行帕金森病统一评分量表(UPDRS)评分、观察两组在治疗前、治疗后3月及6月自主神经症状发生率.结果 治疗后两组患者UPDRS评分均呈上升趋势,治疗组较对照组UPDRS评分上升明显减慢,在治疗后第6月时,两组UPDRS评分比较差异有显著性(P＜0.05).治疗后3月时,治疗组便秘的发生率明显低于对照组(P＜0.05),治疗6月时,治疗组泌尿障碍的发生率明显低于对照组(P＜0.05).结论 定振汤能有效减慢PD患者的UPDRS评分的上升速度,延缓病情进展,改善便秘、泌尿障碍等自主神经症状.     

普拉克索治疗帕金森病的临床疗效观察

目的 观察普拉克索治疗帕金森病的临床疗效.方法 对40例帕金森病病人进行统一评分量表(UPDRS)评分,其中6例病人未服用任何抗帕金森药物即予普拉克索治疗,其余病人在原药基础上加服普拉克索.用药12周后再次应用UDPRS量表进行评分.比较普拉克索治疗前后UDPRS量表分值的差异.部分帕金森病人采用2周,4周,8周,12周随访,对病情进行评分,来观察疗效.结果 40例病人经普拉克索治疗后,有效35例,有效率87.5%.治疗前后,大部分帕金森患者在UDPRS总评分、日常活动、运动功能、震颤、肌僵直、精神症状、开关现象等方面的评分改善均有统计学意义.而且对部分门诊病人的随访评分中发现,病人的各方面病情也有很大的好转.结论 普拉克索可有效改善帕金森病人的临床症状,是一种使用安全、疗效理想的抗帕金森病药物.     

依达拉奉治疗帕金森病的疗效观察

目的 探讨依达拉奉治疗帕金森病(PD)的临床疗效.方法 对18例早期PD(病程≤3.5年)和12例晚期PD(病程≥4年)患者,应用依达拉奉30 mg加入生理盐水中静脉滴注,每天2次,连续14 d.在治疗前和治疗后14 d、1个月、3个月进行PD统一评分量表(UPDRS)评分,并观察治疗期间的不良反应.结果 早期PD组在治疗后14 d、1个月、3个月精神活动、行为和精神评分、日常生活活动评分和运动检查评分较治疗前有显著降低(P<0.05～0.01);晚期PD组治疗前后UPDRS评分的差异无统计学意义(均P＞0.05).1例出现轻度恶心、食欲下降;1例出现天冬氨酸转氨酶升高;无其他不良反应.结论 依达拉奉能改善早期PD患者的病情,对晚期PD患者无明显效果.     

对左旋多巴长期治疗帕金森病的评价

很多研究证明长期应用左旋多巴(L-dopa)治疗帕金森病(PD),可明显改善PD患者的症状,而且应该在PD的早期应用适量的左旋多巴进行治疗,以改善患者的早期症状。长期应用左旋多巴治疗PD与长期应用多巴胺受体激动剂对疾病导致的病死率相同。长期应用多巴胺受体激动剂治疗PD的疗效与长期应用左旋多巴相同,前者并未显示出优越性。     

Voice abnormalities and their relation with motor dysfunction in Parkinson's disease

Objective – To evaluate changes in perceptual and several acoustic parameters of voice in patients with Parkinson’s disease (PD) and to find out any relation with these parameters and motor components of Unified Parkinson’s Disease Rating Scale (UPDRS) in this patient group. Materials and methods – Twenty patients with PD (12 male and 8 female) were given objective and subjective voice tests and results were compared with those of 20 age‐ and sex‐matched controls. Patient's perceptual voice analysis was assessed using GRBAS scale including Grade of Dysphonia, Roughness, Breathiness, Asthenia and Strain items. Measurements for objective voice analysis, acoustic assessment tests including frequency perturbation [jitter (jitt)%], intensity perturbation [shimmer (shim)%], noise to harmonic ratio (NHR), fundamental frequency (F0), variability of fundamental frequency (vF0), diadochokinetic rate (DDK) and maximum phonation time (MPT) were used. An assessment of disability caused by voice disorders was scored according to the Voice Handicap Index (VHI) by the patient. All subjects also underwent videolaryngostroboscopic (VLS) examination. Motor components of UPDRS and acoustic parameters of voice were investigated for any correlations. Results – Compared with controls, roughness (P = 0.15), breathiness (P = 0.004) and asthenia (P = 0.031) values of males and breathiness (P = 0.043) and asthenia (P = 0.023) values of females were higher in patients with PD. Mean VHI scores of patients with PD were higher for both male and female patients (P = 0.0001 for male, P = 0.002 for female). The mean values for MPT (P = 0.02) and DDK (P = 0.025) were shorter in patients with PD. Jitt%, shim% and mean F0 values were similar among the two groups. But mean vF0 values were significantly higher in male patients with PD (P = 0.05). On VLS examination, non‐closure glottic pattern was found to be more frequent in the PD group. Conclusion – Although it is well known that pathophysiological changes in PD affect the voice, the present study found only few significant correlations between motor component of UPDRS and voice parameters.     

Specific impairment of visual spatial covert attention mechanisms in Parkinson's disease

Visual deficits in early and high level processing nodes have been documented in Parkinson's disease (PD). Non-motor high level visual integration deficits in PD seem to have a cortical basis independently of a low level retinal contribution. It is however an open question whether sensory and visual attention deficits can be separated in PD. Here, we have explicitly separated visual and attentional disease related patterns of performance, by using bias free staircase procedures measuring psychophysical contrast sensitivity across visual space under covert attention conditions with distinct types of cues (valid, neutral and invalid). This further enabled the analysis of patterns of dorsal-ventral (up-down) and physiological inter-hemispheric asymmetries. We have found that under these carefully controlled covert attention conditions PD subjects show impaired psychophysical performance enhancement by valid attentional cues. Interestingly, PD patients also show paradoxically increased visual homogeneity of spatial performance profiles, suggesting flattening of high level modulation of spatial attention. Finally we have found impaired higher level attentional modulation of contrast sensitivity in the visual periphery, where mechanisms of covert attention are at higher demands.These findings demonstrate a specific loss of attentional mechanisms in PD and a pathological redistribution of spatial mechanisms of covert attention.     

Cardiac 123I-MIBG scintigraphy can assess the disease severity and phenotype of PD

Objective: Cardiac ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy studies of patients with idiopathic Parkinson's disease (PD) found decreased uptake. Whether this decrease is associated with clinical severity as assessed by the Unified Parkinson's Disease Rating Scale (UPDRS) and the phenotypes of PD has not been determined. Methods: Cardiac MIBG scintigraphy was performed on 34 patients with PD, 7 with multiple system atrophy (MSA), 4 with dementia with Lewy bodies (DLB), and 11 normal controls (NCs). Early and delayed MIBG heart/mediastinum (H/M) ratios were evaluated. PD severity was assessed by the Hoehn and Yahr (H–Y) stage and UPDRS. Patients were grouped in two phenotypes, tremor and postural instability gait difficulty (PIGD)-dominant groups based on UPDRS components. Associations between MIBG uptake and age at onset, UPDRS, and disease phenotype were analyzed in each group. Results: The early H/M ratio was significantly lower in patients with PD (1.45±0.207) than in the NCs (2.08±0.231), and in those with MSA (1.99±0.284), but not in those with DLB (1.29±0.0435). The delayed H/M ratio for PD (1.33±0.276) also was significantly decreased as compared to the ratios for NCs (2.17±0.286) and MSA (2.16±0.414) but not DLB (1.16±0.0949). The early H/M ratio was significantly correlated with both UPDRS score and age at onset, whereas the delayed H/M ratio only was significantly correlated with age at onset. The PIGD-dominant group had significantly higher UPDRS scores and lower H/M ratios than the tremor-dominant group. Conclusion: Cardiac MIBG scintigraphy can be used to differentiate PD from MSA and NC, and to determine the disease severity and phenotypes of PD.     

Recognition of emotional prosody is altered after subthalamic nucleus deep brain stimulation in Parkinson's disease

The recognition of facial emotions is impaired following subthalamic nucleus (STN) deep brain stimulation (DBS) in Parkinson's disease (PD). These changes have been linked to a disturbance in the STN's limbic territory, which is thought to be involved in emotional processing. This was confirmed by a recent PET study where these emotional modifications were correlated with changes in glucose metabolism in different brain regions, including the amygdala and the orbitofrontal regions that are well known for their involvement in emotional processing. Nevertheless, the question as to whether these emotional changes induced by STN DBS in PD are modality-specific has yet to be answered. The objective of this study was therefore to examine the effects of STN DBS in PD on the recognition of emotional prosody.An original emotional prosody paradigm was administered to twenty-one post-operative PD patients, twenty-one pre-operative PD patients and twenty-one matched controls. Results showed that both the pre- and post-operative groups differed from the healthy controls. There was also a significant difference between the pre and post groups. More specifically, an analysis of their continuous judgments revealed that the performance of the post-operative group compared with that of the other two groups was characterized by a systematic emotional bias whereby they perceived emotions more strongly.These results suggest that the impaired recognition of emotions may not be specific to the visual modality but may also be present when emotions are expressed through the human voice, implying the involvement of the STN in the brain network underlying the recognition of emotional prosody.     

Concurrent validation of the 21-item and 6-item Hamilton Depression Rating Scale versus the DSM-IV diagnostic criteria to assess depression in patients with Parkinson's disease: an exploratory analysis

OBJECTIVE: The concurrent validity of this 6-item version of Hamilton Depression Rating Scale (HDRS-6) compared to the original 21-item tool (HDRS-21), using the DSM-IV criteria for major depression as the gold standard in patients with Parkinson's disease. METHODS: In analytical study were analyzed: Cronbach's alpha (alpha C), item-total correlation, the receiver operating characteristic curve (ROC) and their area under the curve (AUC), Finally, used the Fagan nomogram. RESULTS: The 115-patient sample with mean illness duration of 7.15 years. HDRS-21 achieved an alpha C of 0.83, HDRS-6 a value of 0.68. Eleven of the HDRS-21 items failed to reach a minimum value. HDRS-21 obtained its better AUC capacity of 0.94 (cut/score of 18/19); HDRS-6 got an AUC of 0.92 (cut/score of 7/8). The Fagan nomogram was (89-94% and 83-90%, respectively). CONCLUSIONS: Our results suggest that HDRS-6 is sufficient, valid and has a sound psychometric structure for use with Parkinson's disease patients.     

Impact of belief in neuroprotection on therapeutic intervention in Parkinson's disease

We explored the hypotheses that an investigator's belief in a putative neuroprotective agent might influence the timing of symptomatic intervention and the assessment of signs and symptoms of patients with Parkinson's disease with the Unified Parkinson's Disease Rating Scale (UPDRS). These hypotheses were tested with Cox and general linear modeling, using data from a previously published double‐blind placebo‐controlled futility trial of coenzyme Q₁₀ and GPI‐1485. We found the investigators' level of confidence in these agents had no effect on the time to symptomatic therapy or on the change in UPDRS during 12 months of treatment. © 2010 Movement Disorder Society     

Assessment of depression in Parkinson's disease: The contribution of somatic symptoms to the clinimetric performance of the Hamilton and Montgomery–Åsberg rating scales

Objective

To assess the influence of somatic symptoms of the Hamilton Depression Rating Scale (HAMD) and Montgomery–Åsberg Depression Rating Scale (MADRS) on the clinimetric performance of these scales in patients with Parkinson's disease (PD).

Methods

A total of 224 patients underwent a protocolized mental status examination, consisting of the Structured Clinical Interview for DSM-IV depressive disorder (SCID-D), as well as the HAMD and MADRS. Sensitivity, specificity, positive, and negative predictive values for a range of cut-off scores were calculated for both rating scales and for modified versions of these scales in which all somatic items were eliminated. In addition, receiver operating characteristic (ROC) curves were obtained for both the modified and unmodified scales.

Results

Elimination of the somatic items of depression from the HAMD and MADRS resulted in a reduced specificity of both the HAMD and the MADRS, and an increased sensitivity of the MADRS.

Conclusion

The authors recommend the full version of the HAMD and MADRS if used for diagnostic purposes; for screening purposes, the abbreviated version without somatic items can be used. Additional advantages of using full rating scales, with somatic items included, are that these provide more information on the severity of depression and allow for easier comparison across studies.     

Validity of Hamilton Depression Inventory in Parkinson's disease.

Studies investigating the assessment of depression in Parkinson's disease (PD) are limited. We examined the concurrent validity and the internal consistency of the Hamilton Depression Inventory (HDI) and compared it to the Hamilton and Geriatric Depression Scales. PD patients (n = 79) were recruited from neurology clinics. Diagnosis of depressive disorder was made according to DSM-IV criteria. Receiver operating characteristic curves were used to calculate sensitivity, specificity, and positive and negative predictive values. The HDI exhibited an optimal cutoff for discriminating between depressed and nondepressed PD patients of 13.5/14.0 and is a valid instrument to use in the setting of PD.     

Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease.

The anterior cingulate (AC) gyrus and the presupplementary motor area (pre-SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre-SMA, or posterior cingulate (PC). Forty-four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini-Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid-sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 +/- 8.8 for PD. Pre-SMA NAA/Cr was lower in PD (PD: 1.39 +/- 0.17; control: 1.47 +/- 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre-SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD.