Progression of nonmotor symptoms in subgroups of patients with non-dopamine-deficient Parkinsonism
2016; Wiley; Volume: 31; Issue: 3 Linguagem: Inglês
10.1002/mds.26456
ISSN1531-8257
AutoresStuart A. Taylor, Joseph Gafton, Bina Shah, Gennaro Pagano, К. Ray Chaudhuri, David J. Brooks, Nicola Pavese,
Tópico(s)Eating Disorders and Behaviors
ResumoMovement DisordersVolume 31, Issue 3 p. 344-351 Research Article Progression of nonmotor symptoms in subgroups of patients with non–dopamine-deficient Parkinsonism Stuart Taylor BSc, Stuart Taylor BSc Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorJoseph Gafton BSc, Joseph Gafton BSc Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorBina Shah MD, Bina Shah MD Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorGennaro Pagano MD, Gennaro Pagano MD Division of Brain Sciences, Imperial College London, UK Department of Medicine and Health Sciences, School of Medicine, University of Molise, Campobasso, ItalySearch for more papers by this authorK. Ray Chaudhuri MD FRCP, DSc, K. Ray Chaudhuri MD FRCP, DSc Kings' College London and Parkinson's Centre of Excellence, Kings College Hospital, London, UKSearch for more papers by this authorDavid J. Brooks MD, DSc, FRCP, FMedSci, David J. Brooks MD, DSc, FRCP, FMedSci Division of Brain Sciences, Imperial College London, UK Department of Clinical Medicine, Centre for Functionally Integrative Neuroscience University of Aarhus, DenmarkSearch for more papers by this authorNicola Pavese, Corresponding Author Nicola Pavese Division of Brain Sciences, Imperial College London, UK Department of Clinical Medicine, Centre for Functionally Integrative Neuroscience University of Aarhus, DenmarkCorrespondence to: Dr. Nicola Pavese, MD, PhD, Clinical Senior Lecturer & Consultant in Neurology, Neurology Imaging Unit (NIU), 1st Floor, B Block, Imperial College London, Division of Brain Sciences, Hammersmith Campus, DuCane Road, London W12 0NN, E-mail: nicola.pavese@imperial.ac.ukSearch for more papers by this author Stuart Taylor BSc, Stuart Taylor BSc Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorJoseph Gafton BSc, Joseph Gafton BSc Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorBina Shah MD, Bina Shah MD Division of Brain Sciences, Imperial College London, UKSearch for more papers by this authorGennaro Pagano MD, Gennaro Pagano MD Division of Brain Sciences, Imperial College London, UK Department of Medicine and Health Sciences, School of Medicine, University of Molise, Campobasso, ItalySearch for more papers by this authorK. Ray Chaudhuri MD FRCP, DSc, K. Ray Chaudhuri MD FRCP, DSc Kings' College London and Parkinson's Centre of Excellence, Kings College Hospital, London, UKSearch for more papers by this authorDavid J. Brooks MD, DSc, FRCP, FMedSci, David J. Brooks MD, DSc, FRCP, FMedSci Division of Brain Sciences, Imperial College London, UK Department of Clinical Medicine, Centre for Functionally Integrative Neuroscience University of Aarhus, DenmarkSearch for more papers by this authorNicola Pavese, Corresponding Author Nicola Pavese Division of Brain Sciences, Imperial College London, UK Department of Clinical Medicine, Centre for Functionally Integrative Neuroscience University of Aarhus, DenmarkCorrespondence to: Dr. Nicola Pavese, MD, PhD, Clinical Senior Lecturer & Consultant in Neurology, Neurology Imaging Unit (NIU), 1st Floor, B Block, Imperial College London, Division of Brain Sciences, Hammersmith Campus, DuCane Road, London W12 0NN, E-mail: nicola.pavese@imperial.ac.ukSearch for more papers by this author First published: 11 February 2016 https://doi.org/10.1002/mds.26456Citations: 21 Funding agencies: Part of the salary for N.P.'s research activity is paid for by the Medical Research Council UK. Relevant conflicts of interest/financial disclosures: The authors S.T., J.G., B.S., G.P., K.R.C., D.J.B., and N.P. have nothing to disclose in relation to this paper. Full financial disclosures and author roles may be found in the online version of this article. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract Background Ten to fifteen percent of Parkinson's disease (PD) patients recruited to clinical trials have scans without evidence of dopaminergic deficit, whose presence represents a heterogeneous patient population. Methods A cohort of 41 patients with parkinsonism and scans without evidence of dopaminergic deficit at baseline, were subdivided into groups according to their final clinical diagnoses and nigrostriatal dopamine function assessed after 2 years of study. At follow up, 23 patients had clinically probable PD or unclassified parkinsonism with normal nigrostriatal dopamine imaging ("true" scans without evidence of dopaminergic deficit), nine were diagnosed with another tremulous condition, five had psychogenic parkinsonism, and four had phenoconverted to PD with reduced nigrostriatal dopamine function. We analyzed nonmotor symptoms at baseline and follow-up in subgroups of patients with scans without evidence of dopaminergic deficit in comparison with a random sample of 62 PD patients and 195 healthy controls (HCs). All patients were enrolled in the Parkinson's Progressive Marker's Initiative. Results Patients who had true scans without evidence of dopaminergic deficit had more severe rapid eye movement sleep disorder, depression, anxiety, and autonomic dysfunction than HCs in addition to more frequent depressive symptoms and worse cardiovascular dysfunction than patients with PD (P = 0.038, P = 0.047, respectively). Patients with true scans without evidence of dopaminergic deficit had normal olfaction that was significantly better than that of patients with PD (P < 0.001). Subgroup analysis of the cohort with scans without evidence of dopaminergic deficit revealed that all patients shared similar nonmotor features irrespective of their final clinical diagnoses. Follow-up of subject groups showed stable nonmotor symptoms over 2 years of study. Conclusions At an early symptomatic stage, patients with scans without evidence of dopaminergic deficit and long-standing parkinsonism exhibit nonmotor features that differ from those of patients with PD on mood and cardiovascular and olfactory function, but remain similar to patients with scans without evidence of dopaminergic deficit with alternative final diagnoses. © 2016 International Parkinson and Movement Disorder Society Citing Literature Supporting Information Additional Supporting Information may be found in the online version of this article at the publisher's web-site. Filename Description mds26456-sup-0001-suppinfo01.jpg489.9 KB Supporting Information Figure 1 mds26456-sup-0002-suppinfo02.docx21.4 KB Supporting Information Table 1 Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. Volume31, Issue3March 2016Pages 344-351 RelatedInformation
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