舞动治疗在帕金森病康复中的应用

帕金森病是一种常见的中枢神经系统退行性疾病。舞动帕金森病项目通过舞蹈课程改善帕金森病患者的情感、身体机能、认知和人际关系。舞动帕金森病项目可以改善帕金森病患者肢体的协调能力,改善其步态和行动流畅性,并且提高帕金森病患者的平衡能力、认知能力和自我效能感。2001年,美国纽约布鲁克林帕金森病组织和马克·莫里斯舞团共同创建了舞动帕金森病项目,将音乐和舞蹈融入帕金森病的治疗中。本文阐述了舞动帕金森病项目在帕金森病康复治疗中的作用,并介绍其在国内外的发展现状。     

帕金森病患者瞬目反射分析

目的 通过观察帕金森病患者的瞬目反射,为帕金森病患者的诊断及分期治疗提供客观依据.方法 对帕金森病患者及对照组行瞬目反射检查,早期帕金森病组与中晚期帕金森病组瞬目反射结果.结果 帕金森病组和对照组比较,帕金森病组瞬目反射R2波潜伏期较对照组延长(P<0.01);中晚期帕金森病组较早期帕金森病组瞬目反射R2波潜伏期延长(...     

帕金森病和快速眼球运动睡眠期行为障碍的共同发病机制研究进展

帕金森病是中老年人高发的一种神经退行性疾病, 其前驱期可持续数年至数十年, 疾病前驱期标志物是早期识别或诊断帕金森病的重要依据。快速眼球运动睡眠期行为障碍(RBD)是帕金森病的特征性临床前驱症状, 且与帕金森病具有一些相同的发病机制, 部分机制在RBD转化为帕金森病的过程中进行性发展, 可能成为有价值的帕金森病前驱期标志物。文中对帕金森病与RBD的共同发病机制进行综述, 以期为帕金森病的临床早期诊断和治疗提供一些思路。     

帕金森病200年史话

James Parkinson医生于1817年首次描述帕金森病的概念、病程和特征性临床症状,直至1877年Jean-Martin Charcot医生方命名其为帕金森病并广为熟知。Frederic Henry Lewy于1912年在帕金森病患者神经元中检出一种特殊的异常蛋白小体,至1919年Konstantin Tretiakoff将其命名为路易小体,认为帕金森病的主要病变部位是黑质,医学界方对帕金森病的病理学特征有所了解。1867年Leopold Ordenstein医生发现帕金森病患者存在流涎等副交感神经兴奋症状,并予颠茄生物碱治疗,开创药物治疗帕金森病的先河。20世纪50年代以后,研究者们陆续发现帕金森病患者黑质、蓝斑等神经核团存在路易小体,逐渐明确帕金森病的病理学特征。Arvid Carlsson和Isamu Sano发现帕金森病患者脑组织多巴胺缺乏,从而研发出左旋多巴药物。帕金森病的历史已近200年,以此为基础,我们期待很快能够看到帕金森病相关研究的新进展。     

帕金森病视网膜病变的研究进展

帕金森病视网膜病变是帕金森病非运动症状的研究热点之一。帕金森病视功能障碍可能是帕金森病早期特异性较高的生物标记物,视觉电生理的改变可能与多巴胺水平相关。视网膜内层变薄,黄斑处血管变化以及磷酸化α-突触核蛋白沉积于视网膜内层进一步佐证了帕金森病视网膜病变。文中就帕金森病视网膜病变的相关研究作综述。     

吸烟与帕金森病嗅觉障碍

帕金森病是临床常见的神经变性病,根据临床症状可以分为运动症状和非运动症状,嗅觉障碍作为帕金森病最常见的非运动症状越来越受到重视。既往研究显示,尼古丁可能降低帕金森病发病风险,而有吸烟史的帕金森病患者嗅觉障碍轻微,因此吸烟可能通过嗅觉系统对帕金森病产生保护作用。吸烟对帕金森病患者嗅觉功能的影响可能有助于我们更全面地了解帕金森病发病过程。     

进展期帕金森病的识别与治疗策略

帕金森病是一种常见的神经退行性疾病,呈慢性进展性病程。随着疾病进展及口服治疗时间的延长,帕金森病并发症的出现使临床诊治变得棘手。为了对帕金森病患者进行有效的长期治疗和管理,国际专家们对帕金森病进行新的分期,提出进展期帕金森病的概念,并针对进展期帕金森病的特点,研发出新剂型的药物治疗方式和装置辅助治疗手段。本文就进展期帕金森病的有效识别和治疗策略做一评述。     

应重视帕金森病认知功能障碍

认知功能障碍是帕金森病常见的非运动症状,影响患者生活质量、增加家属负担。帕金森病认知功能障碍包括帕金森病轻度认知损害和帕金森病痴呆。本文拟对国内外帕金森病认知功能障碍发病机制、临床表现、诊断标准和药物治疗研究进展进行概述。     

帕金森病不同亚型睡眠质量及相关影响因素分析

目的分析帕金森病不同亚型睡眠质量及相关影响因素。方法 2009-01—2013-03于我院住院治疗的原发性帕金森病患者83例,根据临床表现不同分为强直少动组47例,震颤组36例,分析震颤型帕金森病患者与强直少动型帕金森病患者的UPDRSⅢ评分、MMSE评分、HAMDS评分、每日左旋多巴的使用剂量、睡眠量表评分及帕金森病患者合并睡眠障碍的危险因素。结果强直少动型帕金森病患者UPDRSⅢ总分、HAMDS评分及每日使用左旋多巴剂量均显著高于震颤型帕金森病患者,而MMSE评分低于震颤型帕金森病患者(P0.05);震颤型帕金森病患者与强直少动型帕金森病患者的PDSS-1、PDSS-2、PDSS-3、PDSS-8以及PDSS-12差异有统计学意义(P0.05),而其他评分差异无统计学意义(P0.05);强直少动型帕金森病患者睡眠功能障碍与抑郁评分、UPDRSⅢ以及每日使用左旋多巴剂量相关,而与H-Y分期、MMSE评分无关;震颤型帕金森病患者睡眠功能障碍只与H-Y分期和MMSE评分相关。结论睡眠障碍严重程度与帕金森病临床亚型相关,强直少动型帕金森病患者睡眠障碍较震颤型帕金森病患者更严重。     

帕金森病轻度认知损害

认知功能障碍是帕金森病较为常见的非运动症状,影响帕金森病患者生活质量、增加照料者负担。帕金森病认知功能障碍可以表现为轻度认知损害,也可以表现为痴呆。帕金森病轻度认知损害见于疾病早期,随着病情进展发病率逐渐升高,可进展为帕金森病痴呆。帕金森病轻度认知损害的诊断标准包括纳入标准、排除标准和损害水平判断。非药物治疗如运动锻炼和认知行为疗法可以改善帕金森病轻度认知损害症状,其药物治疗尚待进一步研究。     

MPTP-induced parkinsonism as a model for Parkinson's disease

Abstract– It is now well recognized that 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) can induce a syndrome in human and non-human primates similar to Parkinson's disease. This highly selective neurotoxin, which affects specific catecholaminergic nuclei in the brainstem, has provided an important new tool for the study of Parkinson's disease. In this article we review several specific areas related to current research on MPTP, including the question of disease progression, issues regarding the validity of the animal model induced by MPTP, the role of aging in regard to its neurotoxicity and Parkinson's disease, and new therapeutic strategies that have evolved from basic research with the compound. We conclude that both clinical and basic research stemming from the discovery of MPTP have provided valuable insights regarding both the cause and treatment of Parkinson's disease.     

Parkinson's disease with dementia, lewy-body disorders and alpha-synuclein: recent advances and a case report

The advance in research on the dementia syndrome associated with Parkinson's disease recently gains momentum in part because Parkinson's disease inevitably causes declined cognition and then lead to poor quality of life. More importantly, dementia of Lewy bodies, now known as the second most common neurodegenerative disorder, shares the common neuropathological hallmark with Parkinson's disease and yet exhibits a unique clinical syndrome. Recent genetic, neurochemical and neuropsychological experiments robustly confirm a link between dementia associated with Parkinson's disease and dementia with Lewy bodies. Meanwhile, controversial issues regarding diagnostic criteria and proper treatments remain unresolved. Here I review milestone research conclusions and report a typical case with pathological data in order to clarify different aspects of these two dementia disorders.     

Changing epidemiology of Parkinson's disease: Predicted effects of levodopa treatment

Recent studies suggest that levodopa treatment reduces the excess mortality due to Parkinson's disease, found to be three times that expected in the general population. This will affect the equilibrium state of the epidemiology of Parkinson's disease. The predicted increase in prevalence of Parkinson's disease was calculated according to two mortality patterns, one the same as expected in the general population and the other 1.5 times that expected; the proportional increase in prevalence is 1.8 and 1.4, respectively. The predicted increase in the duration of the disease is 6.3 or 3.2 years. As a consequence, there will be an increase of patients with longterm levodopa treatment difficulties and with Parkinson's disease symptoms not treatable with levodopa, e. g. dementia. This seriously warrants the research of new approaches in the treatment of Parkinson's disease.     

Depression and Parkinson's disease: a review.

OBJECTIVE: The purpose of this review is to provide an update of the research regarding depression in Parkinson's disease and to synthesize the information into a neurobiological model relating the structural and biochemical changes in this disorder to the behavioral manifestations. METHOD: The author used a computer-based search of the literature, augmented by extensive bibliography-guided article reviews, to find information on depression and Parkinson's disease. FINDINGS: Depression occurs in approximately 40% of patients with Parkinson's disease; depression in Parkinson's disease is distinguished from other depressive disorders by greater anxiety and less self-punitive ideation. Lower CSF levels of 5-hydroxyindoleacetic acid, a past history of depression, and greater functional disability are associated with a greater risk of depression in Parkinson's disease. Female gender, early age at onset of Parkinson's disease, and greater left brain involvement may also be risk factors. Approximately half of depressed patients with Parkinson's disease meet criteria for major depressive episodes; half have dysthymia. Depression is more common in Parkinson's disease with prominent bradykinesia and gait instability than in tremor-dominant syndromes. Depressed patients with Parkinson's disease have greater frontal lobe dysfunction and greater involvement of dopaminergic and noradrenergic systems than nondepressed patients with the disease. Mood changes in Parkinson's disease respond to treatment with conventional tricyclic antidepressants or ECT. CONCLUSIONS: Neurobiological investigations suggest that depression in Parkinson's disease may be mediated by dysfunction in mesocortical/prefrontal reward, motivational, and stress-response systems. Neuropsychological, metabolic, clinical, pharmacological, and anatomical studies support the involvement of frontal dopaminergic projections in patients with Parkinson's disease and depression.     

Changing epidemiology of Parkinson's disease: predicted effects of levodopa treatment.

Recent studies suggest that levodopa treatment reduces the excess mortality due to Parkinson's disease, found to be three times that expected in the general population. This will affect the equilibrium state of the epidemiology of Parkinson's disease. The predicted increase in prevalence of Parkinson's disease was calculated according to two mortality patterns, one the same as expected in the general population and the other 1.5 times that expected; the proportional increase in prevalence is 1.8 and 1.4, respectively. The predicted increase in the duration of the disease if 6.3 or 3.2 years. As a consequence, there will be an increase of patients with long-term levodopa treatment difficulties, and with Parkinson's disease symptoms not treatable with levodopa, e.g. dementia. This seriously warrants the research of new approaches in the treatment of Parkinson's disease.     

Epidemiology of Parkinson's disease—An overview

Summary Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future.Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing.Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful.Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.     

Cognitive impairment in patients with Parkinson's disease: diagnosis, biomarkers, and treatment

Dementia is one of the most common and important aspects of Parkinson's disease and has consequences for patients and caregivers, and has health-related costs. Mild cognitive impairment is also common and frequently progresses to dementia. The underlying mechanisms of dementia associated with Parkinson's disease are only partly known and no mechanism-based treatments are available. Both dysmetabolism of α-synuclein and amyloid-protein and cholinergic deficits contribute to cognitive impairment in Parkinson's disease, and preliminary findings show that imaging and neurophysiological and peripheral biomarkers could be useful in diagnosis and prognosis. Rivastigmine is the only licensed treatment for dementia in Parkinson's disease, but emerging evidence suggests that memantine might also be useful. Whether these or other treatments can delay the progression from mild cognitive impairment to dementia in Parkinson's disease is a key research question.     

Potential therapeutic effects of polyphenols in Parkinson's disease: in vivo and in vitro pre-clinical studies

Parkinson's disease is a neurodegenerative disorder characterized by a combination of severe motor and non-motor symptoms. Over the years, several factors have been discovered to play a role in the pathogenesis of this disease, in particular, neuroinflammation and oxidative stress. To date, the pharmacological treatments used in Parkinson's disease are exclusively symptomatic. For this reason, in recent years, the research has been directed towards the discovery and study of new natural molecules to develop potential neuroprotective therapies against Parkinson's disease. In this context, natural polyphenols have raised much attention for their important anti-inflammatory and antioxidant properties, but also for their ability to modulate protein misfolding. In this review, we propose to summarize the relevant in vivo and in vitro studies concerning the potential therapeutic role of natural polyphenols in Parkinson's disease.     

Genetic and environmental factors of Parkinson's disease

We present a review on the genetic and environmental factors implicated in the aetiology of Parkinson's disease. The environmental hypothesis was strongly suggested about 20 years ago after the report of a parkinsonian syndrome in young adults that were intoxicated by a neurotoxin called MPTP which selectively destroys nigrostriatal dopaminergic neurons. Several chemical products used in herbicides and pesticides are similar structurally to MPTP, including paraquat, diquat and rotenone. Epidemiological studies have revealed an increased risk for Parkinson's disease with the use of pesticides and herbicides or the consumption of well water in rural areas of industrialised countries. However, it has not been possible to identify any causative environmental chemical agent in the aetiology of Parkinson's disease despite intensive research. Comparatively, the genetic hypothesis of Parkinson's disease has gained considerable interest during the last decade. Epidemiological studies reveal a family history in 10-25 p. cent Parkinson's disease patients. Several large kindreds with autosomal dominant Parkinson's disease associated with mutations of alpha-synuclein gene (PARK 1) were recently described. alpha-synuclein is a constituant of Lewy bodies, the hallmark of idiopathic Parkinson's disease. However, alpha-synuclein gene mutations are rare as opposed to parkin gene mutations (PARK 2), which are frequently found in autosomal recessive and sporadic young onset Parkinson's disease patients. Other genes or locus are implicated in autosomal dominant familial cases (PARK 3, 4 and 5). Nevertheless, a pure genetic origin can be demonstrated only in a minority of Parkinson's disease patients. Investigation of the possible interaction between genes and environment and of several candidate genes gave contradictory results, notably concerning the association between allelic variants of CYP2D6 gene and the occurrence of Parkinson's disease. In conclusion, the aetiology of Parkinson's disease remains unknown. There are probably several types or causes of Parkinson's disease. In most cases, this heterogeneity could be attributed both to genetic and environmental factors.     

Intervening in the neuropsychiatric features of Parkinson's disease

Although Parkinson's disease is considered a movement disorder, it has a wide range and high prevalence of affective, psychotic, cognitive, behavioral and sleep-related features. To treat such features, agents including antidepressants, anxiolytics, antipsychotics and cognition-enhancing agents are commonly prescribed, although the targeted syndromes are often incompletely understood and controlled studies demonstrating a treatment's efficacy and tolerability in Parkinson's disease patients are often lacking. Nevertheless, the available information does suggest the outlines of management methods, pending expanded research to identify optimal strategies specific to Parkinson's disease.