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Parkinson Disease: HELP
Articles from Montreal
Based on 286 articles published since 2008

These are the 286 published articles about Parkinson Disease that originated from Montreal during 2008-2019.
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12
1 Editorial 5-HT 2018

Huot, Philippe. ·Neurodegenerative Disease Group, Montreal Neurological Institute, Montreal, QC H3A 2B4, Canada. · Department of Neuroscience, McGill University, Montreal, QC H3A 2B4, Canada. · Division of Neurology, McGill University Health Centre, Montreal, QC H3A 2B4, Canada. ·Neurodegener Dis Manag · Pubmed #30451579.

ABSTRACT: -- No abstract --

2 Editorial Sleep Disorders and RBD: What Would James Parkinson Think? 2017

Postuma, Ronald B. ·Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. ·Mov Disord · Pubmed #28513080.

ABSTRACT: -- No abstract --

3 Editorial Voice changes in prodromal Parkinson's disease: Is a new biomarker within earshot? 2016

Postuma, Ronald B. ·Department of Neurology, McGill University, Montreal General Hospital, L7-305, 1650 Cedar Ave., Montreal, Quebec, Canada H3G1A4. Electronic address: ron.postuma@mcgill.ca. ·Sleep Med · Pubmed #26825009.

ABSTRACT: -- No abstract --

4 Editorial Serotonin/dopamine transporter ratio as a predictor of L-dopa-induced dyskinesia. 2015

Huot, Philippe / Hutchison, William D. ·From the Department of Pharmacology (P.H.), Faculty of Medicine, University of Montreal, Quebec, Canada · Division of Neurology (P.H.), Centre Hospitalier de l'Université de Montréal, Quebec, Canada · Departments of Surgery and Physiology (W.D.H.), University of Toronto, Ontario, Canada · and Division of Neurosurgery (W.D.H.), Toronto Western Hospital MP11-308 and Toronto Western Research Institute, Ontario, Canada. ·Neurology · Pubmed #26253446.

ABSTRACT: -- No abstract --

5 Editorial Placebo: from belief to movement. 2014

Postuma, Ronald B / Albin, Roger L. ·From the Department of Neurology (R.B.P.), McGill University, Montreal General Hospital, Canada · Neurology Service & GRECC (R.L.A.), VAAAHS · Department of Neurology (R.L.A.), University of Michigan · and Michigan Alzheimer's Disease Center (R.L.A.), Ann Arbor. ·Neurology · Pubmed #24658928.

ABSTRACT: -- No abstract --

6 Editorial Diagnosing REM sleep behavior disorder in Parkinson's disease-can we avoid the polysomnogram? 2014

Postuma, Ronald B. ·Department of Neurology, McGill University, Montreal General Hospital, Montreal, Quebec, Canada; Centre d'Études Avancées en Médecine du Sommeil, Hôpital du Sacré Cœur de Montréal, Montréal, Québec, Canada. ·Mov Disord · Pubmed #24619856.

ABSTRACT: -- No abstract --

7 Review Molecular Imaging of the Noradrenergic System in Idiopathic Parkinson's Disease. 2018

Nahimi, Adjmal / Kinnerup, Martin B / Sommerauer, Michael / Gjedde, Albert / Borghammer, Per. ·Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus, Denmark; Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark. Electronic address: anah@clin.au.dk. · Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Aarhus, Denmark. · Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark; Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark; Department of Radiology and Radiological Science, Johns Hopkins University, Baltimore, MD, United States; Department of Neurology, McGill University, Montreal, QC, Canada. ·Int Rev Neurobiol · Pubmed #30314598.

ABSTRACT: Noradrenergic neurons in both the peripheral nervous system and in the central nervous system (CNS) undergo severe degeneration in patients with Parkinson's disease (PD). This loss of noradrenaline may play essential roles in the occurrence of a wide range of prevalent non-motor symptoms and can further complicate the lives of PD patients. In vivo molecular imaging of noradrenaline may provide insights into to the extent of degeneration of noradrenergic neurons and subsequent depletion of noradrenergic projections. Molecular imaging methods exist to quantify the noradrenergic deficiency in peripheral autonomic terminals, such as [

8 Review The effects of exercise on cognition and gait in Parkinson's disease: A scoping review. 2018

Intzandt, Brittany / Beck, Eric N / Silveira, Carolina R A. ·PERFORM Centre, Concordia University, 7200 rue Sherbrooke O, Montreal, H4B 1R6, Canada. Electronic address: brittany.intzandt@mail.concordia.ca. · School of Medicine, Trinity College Dublin, University of Dublin, College Green, Dublin, 2, Ireland. Electronic address: becke@tcd.ie. · Lawson Health Research Institute, 750 Base Line Rd E, London, N6C 2R5, Canada. Electronic address: carolina.silveira@sjhc.london.on.ca. ·Neurosci Biobehav Rev · Pubmed #30291852.

ABSTRACT: Cognitive and gait deficits are two debilitating symptoms that occur in Parkinson's disease (PD). Importantly, a relationship between cognitive and gait deficits exists in PD, suggesting reliance on cognition is increased to compensate for gait deficits and/or deterioration of cognition and gait may share common mechanisms. Rehabilitation strategies targeting one factor could lead to the improvement of the other, presenting a unique opportunity to treat both simultaneously. Gold-standard pharmaceuticals partially alleviate these deficits with significant side effects, highlighting the importance of investigating adjunct therapies like exercise. We critically reviewed the influence of three exercise modalities (aerobic, resistance, and goal-based) on cognition and/or gait in PD. Most studies showed improvements in cognition or gait, yet, a limited number investigated them concurrently. This is the first review examining exercise for cognition and gait in PD. Key gaps in the literature are identified; potential exercise-driven mechanisms for enhancements in cognition and gait proposed, and suggestions for the design of future studies investigating the effects of exercise on cognition and gait in PD.

9 Review New insights into the structure of PINK1 and the mechanism of ubiquitin phosphorylation. 2018

Rasool, Shafqat / Trempe, Jean-François. ·a Department of Biochemistry , McGill University , Montréal , Canada. · b Groupe de Recherche Axé sur la Structure des Protéines (GRASP) , Montréal , Canada. · c Department of Pharmacology & Therapeutics , McGill University , Montréal , Canada. ·Crit Rev Biochem Mol Biol · Pubmed #30238821.

ABSTRACT: Mutations in PINK1 cause early-onset recessive Parkinson's disease. This gene encodes a protein kinase implicated in mitochondrial quality control via ubiquitin phosphorylation and activation of the E3 ubiquitin ligase Parkin. Here, we review and analyze functional features emerging from recent crystallographic, nuclear magnetic resonance (NMR) and mass spectrometry studies of PINK1. We compare the apo and ubiquitin-bound PINK1 structures and reveal an allosteric switch, regulated by autophosphorylation, which modulates substrate recognition. We critically assess the conformational changes taking place in ubiquitin and the Parkin ubiquitin-like domain in relation to its binding to PINK1. Finally, we discuss the implications of these biophysical findings in our understanding of the role of PINK1 in mitochondrial function, and analyze the potential for structure-based drug design.

10 Review Sleep disorders and Parkinson disease; lessons from genetics. 2018

Gan-Or, Ziv / Alcalay, Roy N / Rouleau, Guy A / Postuma, Ronald B. ·Montreal Neurological Institute, McGill University, Montréal, QC, Canada; Department of Human Genetics, McGill University, Montréal, QC, Canada; Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. Electronic address: ziv.gan-or@mail.mcgill.ca. · Department of Neurology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, NY, USA. · Montreal Neurological Institute, McGill University, Montréal, QC, Canada; Department of Human Genetics, McGill University, Montréal, QC, Canada; Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. · Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. ·Sleep Med Rev · Pubmed #29449121.

ABSTRACT: Parkinson disease is a common, age-related neurodegenerative disorder, projected to afflict millions of individuals in the near future. Understanding its etiology and identifying clinical, genetic or biological markers for Parkinson disease onset and progression is therefore of major importance. Various sleep-related disorders are the most common group of non-motor symptoms in advanced Parkinson disease, but they can also occur during its prodromal phase. However, with the exception of REM sleep behavior disorder, it is unclear whether they are part of the early pathological process of Parkinson disease, or if they develop as Parkinson disease advances because of treatments and neurodegeneration progression. The advancements in genetic studies in the past two decades have generated a wealth of information, and recent genetic studies offer new insight on the association of sleep-related disorders with Parkinson disease. More specifically, comparing genetic data between Parkinson disease and sleep-related disorders can clarify their association, which may assist in determining whether they can serve as clinical markers for Parkinson disease risk or progression. In this review, we discuss the current knowledge on the genetics of sleep-related disorders in Parkinson disease context, and the potential implications on research, diagnosis, counseling and treatment.

11 Review Chronic pain and pain processing in Parkinson's disease. 2018

Blanchet, Pierre J / Brefel-Courbon, Christine. ·Department of Stomatology, Faculty of Dental Medicine, Université de Montréal; Montréal, QC, Canada; Service de neurologie, CHU Montréal, Montréal, QC, Canada. Electronic address: pierre.j.blanchet@umontreal.ca. · Service de Pharmacologie Clinique, Faculty of Medicine, University Hospital, Toulouse, France; Service de neurologie B8, Pierre Paul Riquet Hospital, University Hospital, Toulouse, France. Electronic address: christine.brefel-courbon@univ-tlse3.fr. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #29031913.

ABSTRACT: Pain is experienced by the vast majority of patients living with Parkinson's disease. It is most often of nociceptive origin, but may also be ascribed to neuropathic (radicular or central) or miscellaneous sources. The recently validated King's Parkinson's Disease Pain Scale is based on 7 domains including musculoskeletal pain, chronic body pain (central or visceral), fluctuation-related pain, nocturnal pain, oro-facial pain, pain with discolouration/oedema/swelling, and radicular pain. The basal ganglia integrate incoming nociceptive information and contribute to coordinated motor responses in pain avoidance and nocifensive behaviors. In Parkinson's disease, nigral and extra-nigral pathology, involving cortical areas, brainstem nuclei, and spinal cord, may contribute to abnormal central nociceptive processing in patients experiencing pain or not. The dopamine deficit lowers multimodal pain thresholds that are amenable to correction following levodopa dosing. Functional brain imaging with positron emission tomography following administration of H

12 Review Assessment of sexual function in women with neurological disorders: A review. 2018

Courtois, Frédérique / Gérard, Marina / Charvier, Kathleen / Vodušek, David B / Amarenco, Gérard. ·Université du Québec, department of sexology, CP 8888 Succursale-centre-ville, H3C 3P8 Montreal, Quebec, Canada. Electronic address: courtois.frederique@uqam.ca. · Université du Québec, department of psychology, H3C 3P8 Montreal, Quebec, Canada. · Hospices civils de Lyon, 69230 Saint-Genis-Laval, France. · Division of neurology, university medical centre, 7, Zaloška cesta, 1525 Ljubljana, Slovenia. · GRC-UPMC 01, GREEN (group of clinical research in neuro-urology), university Pierre-et-Marie-Curie), 75005 Paris, France; Department of neuro-urology, Tenon hospital, Assistance publique-Hôpitaux de Paris, 75020 Paris, France. ·Ann Phys Rehabil Med · Pubmed #28713038.

ABSTRACT: BACKGROUND: Although the rehabilitation of sexual function has been identified as a top priority among women presenting neurological conditions, sexual function is rarely assessed in this clinical group. OBJECTIVES: To review published assessment tools of sexual dysfunction in women with neurological conditions including multiple sclerosis (MS), spinal cord injury (SCI), Parkinson disease, stroke, traumatic brain injury. METHODS: A systematic literature review was conducted with Medline via PubMed, PubMed Central, and Medline databases. RESULTS: There are three reliable methods to assess sexual dysfunctions in women with neurological conditions: physiological assessments of reflexes and perineal sensitivity testing, self-reporting questionnaires on sexual function and sexual satisfaction, and electrophysiological assessments. Physiological assessments of sacral and thoracolumbar reflexes have mainly been conducted among women with SCI. When performed, they reveal the existence of a psychogenic and/or reflex sexual potential in those women. Other forms of physiological assessments include vulvar sensitivity testing in women with SCI, quantitative sensory testing and pudendal somatosensory evoked potentials in MS populations. A few validated self-reporting measures are also available to assess sexual potential and sexual satisfaction, although mostly in women with SCI and MS. CONCLUSION: Despite high prevalence rates and important clinical implications, sexual dysfunction is not systematically assessed in women presenting various neurological conditions. Several well-validated tools exist for such assessments, which could be used for sexual rehabilitation in these patients. The implementation of systematic assessments of sexual potential is feasible and renewed efforts should be made to do so in clinical practice.

13 Review Domperidone for Hypotension in Parkinson's Disease: A Systematic Review. 2017

Bacchi, Stephen / Chim, Ivana / Kramer, Philippe / Postuma, Ronald B. ·University of Adelaide, Adelaide, SA, Australia. · McGill University, Montreal, QC, Canada. ·J Parkinsons Dis · Pubmed #29103053.

ABSTRACT: BACKGROUND: Domperidone is a proposed treatment of orthostatic hypotension (OH) in Parkinson's disease (PD). However, domperidone use in PD is tempered by concerns regarding QT prolongation and ventricular tachyarrhythmia and sudden cardiac death (VT/SCD). OBJECTIVE: The aim is to identify peer-reviewed studies in which either (1) the effect of domperidone on blood pressure in patients with PD, or (2) the adverse effects associated with domperidone use in PD patients has been reported. METHODS: PubMed, EMBASE, Medline and Scopus were searched using the terms Parkinson's disease and domperidone. RESULTS: Twenty-two articles fulfilled the inclusion criteria. One study was a randomized placebo-controlled trial with domperidone administration independent of the commencement of dopaminergic medications. This study identified a non-statistically significant trend that domperidone may be beneficial for OH in PD. Several studies identified statistically significant differences in BP with domperidone in the setting of initiating dopaminergic medication. There is currently the most evidence to support domperidone use with apomorphine commencement. Studies reporting domperidone adverse effects in PD patients were largely retrospective or cross-sectional. The identified studies demonstrated that domperidone may cause QT prolongation and is associated with increased risk of VT/SCD in PD patients with preexisting cardiac disease. CONCLUSIONS: Domperidone may help to ameliorate OH associated with dopaminergic medications in PD, namely when used in conjunction with apomorphine. When considering whether to use domperidone in PD, factors that should be taken into account include pre-existing heart disease and drug interactions, as well as the impact of OH on mobility, cognition and quality of life.

14 Review Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy. 2017

Obeso, J A / Stamelou, M / Goetz, C G / Poewe, W / Lang, A E / Weintraub, D / Burn, D / Halliday, G M / Bezard, E / Przedborski, S / Lehericy, S / Brooks, D J / Rothwell, J C / Hallett, M / DeLong, M R / Marras, C / Tanner, C M / Ross, G W / Langston, J W / Klein, C / Bonifati, V / Jankovic, J / Lozano, A M / Deuschl, G / Bergman, H / Tolosa, E / Rodriguez-Violante, M / Fahn, S / Postuma, R B / Berg, D / Marek, K / Standaert, D G / Surmeier, D J / Olanow, C W / Kordower, J H / Calabresi, P / Schapira, A H V / Stoessl, A J. ·HM CINAC, Hospital Universitario HM Puerta del Sur, Mostoles, Madrid, Spain. · Universidad CEU San Pablo, Madrid, Spain. · CIBERNED, Madrid, Spain. · Department of Neurology, Philipps University, Marburg, Germany. · Parkinson's Disease and Movement Disorders Department, HYGEIA Hospital and Attikon Hospital, University of Athens, Athens, Greece. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA. · Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. · Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Canada. · Department of Medicine, University of Toronto, Toronto, Canada. · Department of Psychiatry, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA. · 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. · Medical Sciences, Newcastle University, Newcastle, UK. · Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, Australia. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney, Australia. · Université de Bordeaux, Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives, Bordeaux, France. · China Academy of Medical Sciences, Institute of Lab Animal Sciences, Beijing, China. · Departments of Neurology, Pathology, and Cell Biology, the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York, USA. · Columbia Translational Neuroscience Initiative, Columbia University, New York, New York, USA. · 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. · Groupe Hospitalier Pitié-Salpêtrière, Paris, France. · Clinical Sciences Department, Newcastle University, Newcastle, UK. · Department of Nuclear Medicine, Aarhus University, Aarhus, Denmark. · Human Neurophysiology, Sobell Department, UCL Institute of Neurology, London, UK. · Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. · Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, USA. · 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. · Movement Disorders and Neuromodulation Center, Department of Neurology, University of California-San Francisco, San Francisco, California, USA. · Parkinson's Disease Research, Education and Clinical Center, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA. · Veterans Affairs Pacific Islands Health Care System, Honolulu, Hawaii, USA. · Parkinson's Institute, Sunnyvale, California, USA. · Institute of Neurogenetics, University of Luebeck, Luebeck, Germany. · Department of Clinical Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA. · Department of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Department of Neurology, Universitätsklinikum Schleswig-Holstein, Christian Albrechts University Kiel, Kiel, Germany. · Department of Medical Neurobiology, Institute of Medical Research Israel-Canada, Jerusalem, Israel. · Edmond and Lily Safra Center for Brain Sciences, The Hebrew University, Jerusalem, Israel. · Department of Neurosurgery, Hadassah University Hospital, Jerusalem, Israel. · Parkinson's Disease and Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències, Hospital Clínic de Barcelona, Barcelona, Spain. · Department of Medicine, Universitat de Barcelona, IDIBAPS, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Barcelona, Spain. · Movement Disorders Clinic, Clinical Neurodegenerative Research Unit, Mexico City, Mexico. · Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico. · Department of Neurology, Columbia University Medical Center, New York, New York, USA. · Department of Neurology, McGill University, Montreal General Hospital, Montreal, Quebec, Canada. · Klinik für Neurologie, UKSH, Campus Kiel, Christian-Albrechts-Universität, Kiel, Germany. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. · Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York, USA. · Research Center for Brain Repair, Rush University Medical Center, Chicago, Illinois, USA. · Neuroscience Graduate Program, Rush University Medical Center, Chicago, Illinois, USA. · Neurological Clinic, Department of Medicine, Hospital Santa Maria della Misericordia, University of Perugia, Perugia, Italy. · Laboratory of Neurophysiology, Santa Lucia Foundation, IRCCS, Rome, Italy. · University Department of Clinical Neurosciences, UCL Institute of Neurology, University College London, London, UK. · Pacific Parkinson's Research Centre, Division of Neurology & Djavadf Mowafaghian Centre for Brain Health, University of British Columbia, British Columbia, Canada. · Vancouver Coastal Health, Vancouver, British Columbia, Canada. ·Mov Disord · Pubmed #28887905.

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.

15 Review Alpha-synuclein oligomers: a new hope. 2017

Bengoa-Vergniory, Nora / Roberts, Rosalind F / Wade-Martins, Richard / Alegre-Abarrategui, Javier. ·Department of Physiology, Anatomy and Genetics, Oxford Parkinson's Disease Centre, University of Oxford, South Parks Road, Oxford, OX1 3QT, UK. · Montreal Neurological Institute, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. · Department of Physiology, Anatomy and Genetics, Oxford Parkinson's Disease Centre, University of Oxford, South Parks Road, Oxford, OX1 3QT, UK. Richard.wade-martins@dpag.ox.ac.uk. · Department of Physiology, Anatomy and Genetics, Oxford Parkinson's Disease Centre, University of Oxford, South Parks Road, Oxford, OX1 3QT, UK. Javier.alegre@dpag.ox.ac.uk. ·Acta Neuropathol · Pubmed #28803412.

ABSTRACT: Alpha-synuclein is a protein implicated in Parkinson's disease and thought to be one of the main pathological drivers in the disease, although it remains unclear how this protein elicits its neurotoxic effects. Recent findings indicate that the assembly of toxic oligomeric species of alpha-synuclein may be one of the key processes for the pathology and spread of the disease. The absence of a sensitive in situ detection method has hindered the study of these oligomeric species and the role they play in the human brain until recently. In this review, we assess the evidence for the toxicity and prion-like activity of oligomeric forms of alpha-synuclein and discuss the advances in our understanding of the role of alpha-synuclein in Parkinson's disease that may be brought about by the specific and sensitive detection of distinct oligomeric species in post-mortem patient brain. Finally, we discuss current approaches being taken to therapeutically target alpha-synuclein oligomers and their implications.

16 Review Nonmotor Aspects of Parkinson's Disease-How Do They Help Diagnosis? 2017

Postuma, Ronald B. ·Montreal General Hospital, Montreal, QC, Canada. Electronic address: ron.postuma@mcgill.ca. ·Int Rev Neurobiol · Pubmed #28802931.

ABSTRACT: Not only are nonmotor aspects of Parkinson's disease important because of their impact, they also can help diagnose Parkinson's. This chapter summarizes the ways in which recognition of the nonmotor profile of Parkinson's can help in clinical diagnosis. It also emphasizes the essential role that nonmotor Parkinson's disease plays in the diagnosis of prodromal stages of disease.

17 Review Contribution of language studies to the understanding of cognitive impairment and its progression over time in Parkinson's disease. 2017

Auclair-Ouellet, Noémie / Lieberman, Philip / Monchi, Oury. ·Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. Electronic address: noemie.auclairouellet@mcgill.ca. · Department of Cognitive, Linguistic & Psychological Sciences, Brown University, United States. · Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. ·Neurosci Biobehav Rev · Pubmed #28782623.

ABSTRACT: Parkinson's disease is a frequent neurodegenerative disease that is mostly known for its motor symptoms. However, cognitive impairment is now recognised as an important part of the disease. Studies of cognitive impairment in Parkinson's disease reveal considerable heterogeneity in terms of which cognitive domains are impaired, and of how cognitive impairment progresses over time. In parallel, a growing body of research reports language difficulties in Parkinson's disease, more specifically in the domains of sentence processing and lexical-semantic processing. In this review, the performance of patients with Parkinson's disease in these domains of language will be reviewed with a focus on the links that they have with the rest of cognition and on how they could contribute to the earlier and more precise characterization and prediction of cognitive impairment in Parkinson's disease. More specifically, the potential for modulation of complexity and sensitivity of language tasks to mild deficits and difficulties that are predictive of further decline will be emphasized. Other motivations for studying language difficulties in this disease will also be discussed.

18 Review Hyperechogenicity of substantia nigra for differential diagnosis of Parkinson's disease: A meta-analysis. 2017

Shafieesabet, Azin / Fereshtehnejad, Seyed-Mohammad / Shafieesabet, Azadeh / Delbari, Ahmad / Baradaran, Hamid Reza / Postuma, Ronald B / Lökk, Johan. ·Medical Student Research Committee (MSRC), Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: azin.sh68@gmail.com. · Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada; Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institute, Stockholm, Sweden. Electronic address: sm.fereshtehnejad@mail.mcgill.ca. · Department of Rehabilitation Medicine, New York University Langone Medical Center, New York, NY, United States. Electronic address: a.shafieesabet@gmail.com. · Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institute, Stockholm, Sweden; Iranian Research Center on Aging, University of Social Welfare and Rehabilitation, Tehran, Iran. Electronic address: ahmad_1128@yahoo.com. · Endocrine Research Center, Institute of Endocrinology and Metabolism, Iran University of Medical Sciences, Tehran, Iran. Electronic address: baradaran.hr@iums.ac.ir. · Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada; Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Coeur de Montréal, Montreal, QC, Canada. Electronic address: ron.postuma@mcgill.ca. · Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institute, Stockholm, Sweden; Department of Geriatric Medicine, Karolinska University Hospital, Stockholm, Sweden. Electronic address: johan.lokk@karolinska.se. ·Parkinsonism Relat Disord · Pubmed #28647434.

ABSTRACT: Studies have suggested that the majority of patients with Parkinson's disease have abnormal ultrasound hyperechogenicity of the substantia nigra, and that this may be useful in diagnosis. We performed a systematic review and meta-analysis to evaluate diagnostic value of substantia nigra ultrasound to differentiate Parkinson's disease from atypical parkinsonism and from essential tremor. We systematically searched PubMed and EMBASE for relevant studies published until November 2016. Eligible articles were screened, data were extracted and study quality was scored by two independent reviewers. We applied random effect models to calculate pooled estimates for the prevalence of hyperechogenicity in each condition. For final meta-analysis, 71 articles with a total number of 5730 participants (idiopathic Parkinson's disease: 4494, atypical parkinsonism: 594, essential tremor: 642) were included. The pooled prevalence rate of hyperechogenicity was 84% (95 %CI 80-87%) in idiopathic Parkinson's disease, 28% (95% CI 20-36%) in atypical parkinsonism and 15% (95% CI 7-23%) in essential tremor. Based on our meta-analysis, substantia nigra hyperechogenecity has 75% (95% CI: 60-86%) sensitivity and 70% (95% CI: 55-81%) specificity to differentiate idiopathic Parkinson's disease from atypical parkinsonism. Sensitivity and specificity to distinguish idiopathic Parkinson's disease from essential tremor was calculated as 78% (95% CI: 69-85%) and 85% (95% CI: 77-91%), respectively. Findings from our meta-analysis showed that transcranial sonography can provide useful information to differentiate idiopathic Parkinson's disease from mimicking movement disorders, although sensitivity and specificity are suboptimal, particularly for differentiating from atypical parkinsonism.

19 Review Multimodal PET Imaging of Amyloid and Tau Pathology in Alzheimer Disease and Non-Alzheimer Disease Dementias. 2017

Xia, Chenjie / Dickerson, Bradford C. ·Department of Neurology, Jewish General Hospital, McGill University, 3755 Chemin de la Côte-Sainte-Catherine Road, Suite E-005, Montreal, QC H3T 1E2, Canada. · Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital, Harvard University, 149 13th Street, Suite 2691, Charlestown, Boston, MA 02129, USA. Electronic address: brad.dickerson@mgh.harvard.edu. ·PET Clin · Pubmed #28576172.

ABSTRACT: Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments. Amyloid PET imaging is an integral part of the diagnostic assessment of Alzheimer disease. Its use has also deepened understanding of the role of amyloid pathology in Lewy body disorders and aging. Tau PET imaging is an imaging biomarker that will likely play an important role in the diagnosis, monitoring, and treatment in dementias. Using tau PET imaging to examine how tau pathology relates to amyloid and other markers of neurodegeneration will serve to better understand the pathophysiologic cascade that leads to dementia.

20 Review The New Diagnostic Criteria for Parkinson's Disease. 2017

Postuma, Ronald B / Berg, Daniela. ·L7-305 Montreal General Hospital, Montreal, Canada. Electronic address: ron.postuma@mcgill.ca. · Christian-Albrechts-University of Kiel, Kiel, Germany. ·Int Rev Neurobiol · Pubmed #28554421.

ABSTRACT: This chapter summarizes the advances in diagnosis of Parkinson's disease (PD) that were encapsulated in new International Parkinson Disease and Movement Disorders Society diagnostic criteria for PD. Numerous changes in our understanding of PD have occurred, including our understanding of the nonmotor profile of disease, the recognition of PD as a synucleinopathy, identification of genetic causes, novel hypotheses about spread of disease, etc. These have been reflected in a new definition of PD, which includes a clinicogenetic subtype of PD, removes dementia with Lewy Bodies as an exclusion criterion against PD, and recognizes multiple stages of early disease. The Clinical Diagnostic Criteria for PD reflect these changes and offer a new standardized diagnostic method for use in clinical research and even clinical practice. The criteria for prodromal PD use a method not seen in previous diagnostic criteria; they rely upon published studies of PD predictors to calculate the probability that any individual will develop PD. The field of PD is constantly advancing, and our methods of diagnosis need to advance with it; one hopes for a future filled with constant revisions and updates in our diagnostic methodology.

21 Review Serotonergic Approaches in Parkinson's Disease: Translational Perspectives, an Update. 2017

Huot, Philippe / Sgambato-Faure, Véronique / Fox, Susan H / McCreary, Andrew C. ·Centre de Recherche du Centre Hospitalier de l'Université de Montréal , Montreal, QC H2X 0A9, Canada. · Department of Pharmacology, Université de Montréal , Montreal, QC H3T 1J4, Canada. · Unité des Troubles du Mouvement André Barbeau, Centre Hospitalier de l'Université de Montréal , Montreal, QC H2L 4M1, Canada. · Division of Neurology, Centre Hospitalier de l'Université de Montréal , Montreal, QC, Canada. · Institute of Cognitive Neuroscience Marc Jeannerod, UMR 5229 CNRS, 69 675 Cedex Bron, France. · University Lyon 1 , 69100 Villeurbanne, France. · Movement Disorder Clinic, Toronto Western Hospital, University of Toronto , Toronto, ON M5T2S8, Canada. · Janssen Vaccines & Prevention B.V. , Archimedesweg 4, 2333 CN Leiden, The Netherlands. ·ACS Chem Neurosci · Pubmed #28460160.

ABSTRACT: Parkinson's disease (PD) has long been seen as a disorder caused by degeneration of the dopaminergic system, leading to the classic motor manifestations of the disease. However, there is now overwhelming evidence that PD is more than a disease merely caused by dopamine depletion. It is well-known that a myriad of other neurotransmitters are affected by the disease process. One such neurotransmitter is serotonin (5-HT). 5-HT has been shown to play a role in several motor and nonmotor manifestations of PD, including tremor, cognition, depression and psychosis. 5-HT also seems to play a critical role in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. A breadth of preclinical studies and clinical trials have been conducted that aimed at modulating the 5-HT system in order to alleviate depression, cognitive deficits, psychosis, and dyskinesia. In this Review, we summarize recent advances in the 5-HT field in PD, but with a translational emphasis. We start by presenting a novel nonhuman primate model of PD that presents with dual dopamine and 5-HT lesions. We then present preclinical and clinical data that introduce new concepts, such as the use of biased and partial agonists, as well as molecules recently introduced to the field of PD, such as eltoprazine, pimavanserin, nelotanserin, and SYN-120, to enhance therapeutic benefit while minimizing adverse events, notably on parkinsonian disability.

22 Review Reward Prediction Errors in Drug Addiction and Parkinson's Disease: from Neurophysiology to Neuroimaging. 2017

García-García, Isabel / Zeighami, Yashar / Dagher, Alain. ·Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. isabel.garciagarcia@mail.mcgill.ca. · Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. ·Curr Neurol Neurosci Rep · Pubmed #28417291.

ABSTRACT: PURPOSE OF REVIEW: Surprises are important sources of learning. Cognitive scientists often refer to surprises as "reward prediction errors," a parameter that captures discrepancies between expectations and actual outcomes. Here, we integrate neurophysiological and functional magnetic resonance imaging (fMRI) results addressing the processing of reward prediction errors and how they might be altered in drug addiction and Parkinson's disease. RECENT FINDINGS: By increasing phasic dopamine responses, drugs might accentuate prediction error signals, causing increases in fMRI activity in mesolimbic areas in response to drugs. Chronic substance dependence, by contrast, has been linked with compromised dopaminergic function, which might be associated with blunted fMRI responses to pleasant non-drug stimuli in mesocorticolimbic areas. In Parkinson's disease, dopamine replacement therapies seem to induce impairments in learning from negative outcomes. The present review provides a holistic overview of reward prediction errors across different pathologies and might inform future clinical strategies targeting impulsive/compulsive disorders.

23 Review Subtypes of Parkinson's Disease: What Do They Tell Us About Disease Progression? 2017

Fereshtehnejad, Seyed-Mohammad / Postuma, Ronald B. ·Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. · Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden. · Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. ron.postuma@mcgill.ca. · Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Coeur de Montréal, Montreal, QC, Canada. ron.postuma@mcgill.ca. · Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC, H3G 1A4, Canada. ron.postuma@mcgill.ca. ·Curr Neurol Neurosci Rep · Pubmed #28324303.

ABSTRACT: Parkinson's disease is a widely heterogeneous disorder with a broad list of motor and nonmotor manifestations. Identifying subtypes of Parkinson's disease is one of the top clinical and research priorities. This review aims to summarize the most valid conventional and recent subtyping solutions that have been introduced so far and to update our current knowledge with recent discoveries on the association between subtypes and disease progression. We also discuss the challenges of subtyping in the context of Parkinson's disease, stability of the subtypes over time, and potential clinical implications. Sophisticated evidence show that there are distinct subtypes of Parkinson's disease with diverging trends of progression. A more holistic view of subtyping to merge traditional motor features with key nonmotor manifestations is a promising approach to identify subgroups with different prognosis. Subtyping could improve further by adding continuing to add data from imaging, CSF, and genetic biomarkers.

24 Review Deep Brain Stimulation Target Selection for Parkinson's Disease. 2017

Honey, Christopher R / Hamani, Clement / Kalia, Suneil K / Sankar, Tejas / Picillo, Marina / Munhoz, Renato P / Fasano, Alfonso / Panisset, Michel. ·1Division of Neurosurgery,University of British Columbia,Vancouver,British Columbia. · 2Research Imaging Centre,Centre for Addiction and Mental Health,Toronto. · 3Department of Surgery,Division of Neurosurgery,University of Toronto. · 5Division of Neurosurgery,Walter C. MacKenzie Health Sciences Centre,University of Alberta,Edmonton,Alberta. · 4Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease,Toronto Western Hospital,University Health Network,Toronto,Ontario. · 6Division of Neurology,Department of Medicine,Hôpital Notre-Dame,University of Montreal Health Centre,Montréal,Québec,Canada. ·Can J Neurol Sci · Pubmed #26976064.

ABSTRACT: During the "DBS Canada Day" symposium held in Toronto July 4-5, 2014, the scientific committee invited experts to discuss three main questions on target selection for deep brain stimulation (DBS) of patients with Parkinson's disease (PD). First, is the subthalamic nucleus (STN) or the globus pallidus internus (GPi) the ideal target? In summary, both targets are equally effective in improving the motor symptoms of PD. STN allows a greater medications reduction, while GPi exerts a direct antidyskinetic effect. Second, are there further potential targets? Ventral intermediate nucleus DBS has significant long-term benefit for tremor control but insufficiently addresses other motor features of PD. DBS in the posterior subthalamic area also reduces tremor. The pedunculopontine nucleus remains an investigational target. Third, should DBS for PD be performed unilaterally, bilaterally or staged? Unilateral STN DBS can be proposed to asymmetric patients. There is no evidence that a staged bilateral approach reduces the incidence of DBS-related adverse events.

25 Review Advances in markers of prodromal Parkinson disease. 2016

Postuma, Ronald B / Berg, Daniela. ·Department of Neurology, L7-305 Montreal General Hospital, 1650 Cedar Avenue, Montreal H3G1A4, Canada. · Department of Neurology, Christian-Albrechts-University of Kiel, Arnold-Heller-Straße 3, 24105 Kiel, Germany. · Department of neurodegeneration, Hertie Institute of Clinical Brain Research, Hoppe, Seyler-Straße 3, 72076 Tübingen, Germany. ·Nat Rev Neurol · Pubmed #27786242.

ABSTRACT: Efforts to develop neuroprotective therapy for Parkinson disease (PD) are focusing on the early stages of disease, which offer the best opportunity to intervene. Early PD can be divided into preclinical, prodromal and clinical stages; in this Review, we focus on the prodromal stage and markers that can be used to identify prodromal PD. We consider the necessary properties of a marker, before providing an overview of the proven and potential markers of prodromal PD, including clinical nonmotor markers, clinical motor markers, neuroimaging markers and tissue biomarkers. Markers for which the ability to predict conversion to PD is supported by the strongest evidence include olfactory loss, REM sleep behaviour disorder and constipation. Markers with the highest diagnostic strength include REM sleep behaviour disorder, dopaminergic imaging and subtle motor parkinsonism. The lead time - the period between the appearance of a marker and conversion to PD - is highly variable between markers, ranging from 5 years for impaired motor performance to >20 years for autonomic symptoms. The cost of screening for these markers also varies dramatically: some require just questionnaires, whereas others require sophisticated scanning techniques. Finally, we summarize how prodromal and risk markers can be combined to estimate the probability that an individual has prodromal PD, with a focus on the International Parkinson Disease and Movement Disorders Society (MDS) Prodromal Parkinson Criteria.