Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy: The Shaking Palsy: Past, Present and Future

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.

Related collections

Most cited references 182

Record: found
Abstract: found
Article: not found

Second consensus statement on the diagnosis of multiple system atrophy.

S. Gilman, G. K. Wenning, P A Low … (2008)

A consensus conference on multiple system atrophy (MSA) in 1998 established criteria for diagnosis that have been accepted widely. Since then, clinical, laboratory, neuropathologic, and imaging studies have advanced the field, requiring a fresh evaluation of diagnostic criteria. We held a second consensus conference in 2007 and present the results here. Experts in the clinical, neuropathologic, and imaging aspects of MSA were invited to participate in a 2-day consensus conference. Participants were divided into five groups, consisting of specialists in the parkinsonian, cerebellar, autonomic, neuropathologic, and imaging aspects of the disorder. Each group independently wrote diagnostic criteria for its area of expertise in advance of the meeting. These criteria were discussed and reconciled during the meeting using consensus methodology. The new criteria retain the diagnostic categories of MSA with predominant parkinsonism and MSA with predominant cerebellar ataxia to designate the predominant motor features and also retain the designations of definite, probable, and possible MSA. Definite MSA requires neuropathologic demonstration of CNS alpha-synuclein-positive glial cytoplasmic inclusions with neurodegenerative changes in striatonigral or olivopontocerebellar structures. Probable MSA requires a sporadic, progressive adult-onset disorder including rigorously defined autonomic failure and poorly levodopa-responsive parkinsonism or cerebellar ataxia. Possible MSA requires a sporadic, progressive adult-onset disease including parkinsonism or cerebellar ataxia and at least one feature suggesting autonomic dysfunction plus one other feature that may be a clinical or a neuroimaging abnormality. These new criteria have simplified the previous criteria, have incorporated current knowledge, and are expected to enhance future assessments of the disease.

0 comments Cited 509 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Selective neuronal vulnerability in Parkinson disease

D. James Surmeier, Jose Obeso, Glenda Halliday (2017)

Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal

0 comments Cited 242 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Levodopa and the progression of Parkinson's disease.

Stanley Fahn, David Oakes, Alice Rudolph … (2004)

Despite the known benefit of levodopa in reducing the symptoms of Parkinson's disease, concern has been expressed that its use might hasten neurodegeneration. This study assessed the effect of levodopa on the rate of progression of Parkinson's disease. In this randomized, double-blind, placebo-controlled trial, we evaluated 361 patients with early Parkinson's disease who were assigned to receive carbidopa-levodopa at a daily dose of 37.5 and 150 mg, 75 and 300 mg, or 150 and 600 mg, respectively, or a matching placebo for a period of 40 weeks, and then to undergo withdrawal of treatment for 2 weeks. The primary outcome was a change in scores on the Unified Parkinson's Disease Rating Scale (UPDRS) between baseline and 42 weeks. Neuroimaging studies of 142 subjects were performed at baseline and at week 40 to assess striatal dopamine-transporter density with the use of iodine-123-labeled 2-beta-carboxymethoxy-3-beta-(4-iodophenyl)tropane ([123I]beta-CIT) uptake. The severity of parkinsonism increased more in the placebo group than in all the groups receiving levodopa: the mean difference between the total score on the UPDRS at baseline and at 42 weeks was 7.8 units in the placebo group, 1.9 units in the group receiving levodopa at a dose of 150 mg daily, 1.9 in those receiving 300 mg daily, and -1.4 in those receiving 600 mg daily (P<0.001). In contrast, in a substudy of 116 patients the mean percent decline in the [123I]beta-CIT uptake was significantly greater with levodopa than placebo (-6 percent among those receiving levodopa at 150 mg daily, -4 percent in those receiving it at 300 mg daily, and -7.2 percent among those receiving it at 600 mg daily, as compared with -1.4 percent among those receiving placebo; 19 patients with no dopaminergic deficits on the baseline scans were excluded from the analysis) (P=0.036). The subjects receiving the highest dose of levodopa had significantly more dyskinesia, hypertonia, infection, headache, and nausea than those receiving placebo. The clinical data suggest that levodopa either slows the progression of Parkinson's disease or has a prolonged effect on the symptoms of the disease. In contrast, the neuroimaging data suggest either that levodopa accelerates the loss of nigrostriatal dopamine nerve terminals or that its pharmacologic effects modify the dopamine transporter. The potential long-term effects of levodopa on Parkinson's disease remain uncertain. Copyright 2004 Massachusetts Medical Society.

0 comments Cited 153 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

M. Stamelou: (View ORCID Profile)

G.M. Halliday: (View ORCID Profile)

J.C. Rothwell: (View ORCID Profile)

G. Deuschl: (View ORCID Profile)

M. Rodriguez-Violante: (View ORCID Profile)

D.G. Standaert: (View ORCID Profile)

Journal

Title: Movement Disorders

Abbreviated Title: Mov Disord.

Publisher: Wiley

ISSN: 08853185

Publication date Created: September 2017

Publication date (Print): September 2017

Publication date (Electronic): September 09 2017

Volume: 32

Issue: 9

Pages: 1264-1310

Affiliations

[1 ]HM CINAC; Hospital Universitario HM Puerta del Sur, Mostoles; Madrid Spain

[2 ]Universidad CEU San Pablo; Madrid Spain

[3 ]CIBERNED; Madrid Spain

[4 ]Department of Neurology; Philipps University; Marburg Germany

[5 ]Parkinson's Disease and Movement Disorders Department, HYGEIA Hospital and Attikon Hospital; University of Athens; Athens Greece

[6 ]Department of Neurological Sciences; Rush University Medical Center; Chicago Illinois USA

[7 ]Department of Neurology; Medical University Innsbruck; Innsbruck Austria

[8 ]Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J Safra Program in Parkinson's Disease; Toronto Western Hospital; Toronto Canada

[9 ]Department of Medicine; University of Toronto; Toronto Canada

[10 ]Department of Psychiatry; Perelman School of Medicine at the University of Pennsylvania; Philadelphia Pennsylvania USA

[11 ]Parkinson's Disease and Mental Illness Research, Education and Clinical Centers (PADRECC and MIRECC); Corporal Michael J. Crescenz Veteran's Affairs Medical Center; Philadelphia Pennsylvania USA

[12 ]Medical Sciences; Newcastle University; Newcastle UK

[13 ]Brain and Mind Centre, Sydney Medical School; The University of Sydney; Sydney Australia

[14 ]School of Medical Sciences; University of New South Wales and Neuroscience Research Australia; Sydney Australia

[15 ]Université de Bordeaux; Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives; Bordeaux France

[16 ]China Academy of Medical Sciences; Institute of Lab Animal Sciences; Beijing China

[17 ]Departments of Neurology, Pathology, and Cell Biology, the Center for Motor Neuron Biology and Disease; Columbia University; New York New York USA

[18 ]Columbia Translational Neuroscience Initiative; Columbia University; New York New York USA

[19 ]Institut du Cerveau et de la Moelle épinière - ICM, Centre de NeuroImagerie de Recherche - CENIR; Sorbonne Universités; UPMC Univ Paris 06, Inserm U1127, CNRS UMR 7225 Paris France

[20 ]Groupe Hospitalier Pitié-Salpêtrière; Paris France

[21 ]Clinical Sciences Department; Newcastle University; Newcastle UK

[22 ]Department of Nuclear Medicine; Aarhus University; Aarhus Denmark

[23 ]Human Neurophysiology, Sobell Department; UCL Institute of Neurology; London UK

[24 ]Human Motor Control Section, National Institute of Neurological Disorders and Stroke; National Institutes of Health; Bethesda Maryland USA

[25 ]Department of Neurology; Emory University School of Medicine; Atlanta Georgia USA

[26 ]Morton and Gloria Shulman Movement Disorders Centre and the Edmond J Safra Program in Parkinson's disease, Toronto Western Hospital; University of Toronto; Toronto Canada

[27 ]Movement Disorders and Neuromodulation Center, Department of Neurology; University of California-San Francisco; San Francisco California USA

[28 ]Parkinson's Disease Research, Education and Clinical Center; San Francisco Veterans Affairs Medical Center; San Francisco California USA

[29 ]Veterans Affairs Pacific Islands Health Care System; Honolulu Hawaii USA

[30 ]Parkinson's Institute; Sunnyvale California USA

[31 ]Institute of Neurogenetics; University of Luebeck; Luebeck Germany

[32 ]Department of Clinical Genetics; Erasmus University Medical Center; Rotterdam The Netherlands

[33 ]Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology; Baylor College of Medicine; Houston Texas USA

[34 ]Department of Neurosurgery; Toronto Western Hospital; University of Toronto Toronto Canada

[35 ]Department of Neurology, Universitätsklinikum Schleswig-Holstein; Christian Albrechts University Kiel; Kiel Germany

[36 ]Department of Medical Neurobiology; Institute of Medical Research Israel-Canada; Jerusalem Israel

[37 ]Edmond and Lily Safra Center for Brain Sciences; The Hebrew University; Jerusalem Israel

[38 ]Department of Neurosurgery; Hadassah University Hospital; Jerusalem Israel

[39 ]Parkinson's Disease and Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències; Hospital Clínic de Barcelona; Barcelona Spain

[40 ]Department of Medicine; Universitat de Barcelona; IDIBAPS, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Barcelona Spain

[41 ]Movement Disorders Clinic; Clinical Neurodegenerative Research Unit; Mexico City Mexico

[42 ]Instituto Nacional de Neurología y Neurocirugía; Mexico City Mexico

[43 ]Department of Neurology; Columbia University Medical Center; New York New York USA

[44 ]Department of Neurology, McGill University; Montreal General Hospital; Montreal Quebec Canada

[45 ]Klinik für Neurologie, UKSH, Campus Kiel; Christian-Albrechts-Universität; Kiel Germany

[46 ]Institute for Neurodegenerative Disorders; New Haven Connecticut USA

[47 ]Department of Neurology; University of Alabama at Birmingham; Birmingham Alabama USA

[48 ]Department of Physiology, Feinberg School of Medicine; Northwestern University; Chicago Illinois USA

[49 ]Departments of Neurology and Neuroscience; Mount Sinai School of Medicine; New York New York USA

[50 ]Research Center for Brain Repair; Rush University Medical Center; Chicago Illinois USA

[51 ]Neuroscience Graduate Program; Rush University Medical Center; Chicago Illinois USA

[52 ]Neurological Clinic, Department of Medicine, Hospital Santa Maria della Misericordia; University of Perugia; Perugia Italy

[53 ]Laboratory of Neurophysiology; Santa Lucia Foundation, IRCCS; Rome Italy

[54 ]University Department of Clinical Neurosciences, UCL Institute of Neurology; University College London; London UK

[55 ]Pacific Parkinson's Research Centre, Division of Neurology & Djavadf Mowafaghian Centre for Brain Health; University of British Columbia; British Columbia Canada

[56 ]Vancouver Coastal Health; Vancouver British Columbia Canada