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January 3, 2014

Comment: Why do nondopaminergic features in Parkinson disease matter?

February 4, 2014 issue
82 (5) 417

Abstract

Parkinson disease (PD) is a progressive multisystem disorder affecting both dopaminergic and nondopaminergic neurons. Whereas dopaminergic (mainly motor) symptoms are well-defined, the nondopaminergic symptoms (mainly nonmotor, such as depression, cognitive decline, anxiety, apathy, fatigue, sleep disorders, sensory symptoms, postural control deficits, orthostatic hypotension, and urogenital and gastrointestinal symptoms) are frequently missed or neglected during routine clinical visits; consequently, they are underinvestigated and undertreated. The neglect of nondopaminergic symptoms is surprising because 1) they occur in almost all patients with PD throughout the course of the disease1 and can even precede the occurrence of the classic motor symptoms; 2) they affect almost all aspects of daily life; and 3) they have a greater effect on health-related quality of life than dopaminergic symptoms.2 During the last decade, several initiatives have addressed this deficit with specific assessment procedures for application in clinical practice and research.1

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References

1.
Martinez-Martin P, Schapira AHV, Stocchi F, et al. Prevalence of nonmotor symptoms in Parkinson's disease in an international setting: study using nonmotor symptoms questionnaire in 545 patients. Mov Disord 2007;22:1623–1629.
2.
Visser M, van Rooden SM, Verbaan D, Marinus J, Stiggelbout AM, van Hilten JJ. A comprehensive model of health-related quality of life in Parkinson's disease. J Neurol 2008;255:1580–1587.
3.
van der Heeden JF, Marinus J, Martinez-Martin P, van Hilten JJ. Importance of nondopaminergic features in evaluating disease severity of Parkinson disease. Neurology 2014;82:412–418.

Information & Authors

Information

Published In

Neurology®
Volume 82Number 5February 4, 2014
Pages: 417
PubMed: 24391162

Publication History

Published online: January 3, 2014
Published in issue: February 4, 2014

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Funding Information

Study funding: No targeted funding reported.Disclosure: W. Maetzler receives funding from the European Union (SENSE-PARK, no. 288557, 2011–2014; Moving beyond, no. 316639, 2012–2016), from the Michael J. Fox Foundation, and the local University. He received funding from the Robert Bosch Foundation (2008–2011) and speaker honoraria from GlaxoSmithKline. Go to Neurology.org for full disclosures.

Authors

Affiliations & Disclosures

Walter Maetzler
From the Hertie Institute for Clinical Brain Research, Department of Neurodegeneration, Center of Neurology, University of Tübingen, and the German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
Movement Disorders Society, Annual Congress 2013, payment of travel-related expenses
Editorial Boards:
1.
Associate editor of the Journal of Alzheimer's Disease (2010-2013) Guest edtior of the International Journal of Alzheimer's Disease (2012)
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
GlaxoSmithKline (2011)
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
European Union (SENSE-PARK, no. 288557, 2011-2014; Scientific coordinator) European Union (Moving beyond, no. 316639, 2012-2016; Scientific coordinator)
Research Support, Academic Entities:
1.
University of T�bingen (doctoral student grants; 2006-2014; PI).
Research Support, Foundations and Societies:
1.
Michael J. Fox Foundation (Inflammatory Parkinson phenotype, 2013-2014; Co-PI) Robert Bosch Foundation (Geriatric aspects of Parkinson disease, 2008-2011; PI)
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE

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Cited By
  1. Serotonin and dopamine depletion in distinct brain regions may cause anxiety in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice as a model of early Parkinson’s disease, NeuroReport, 34, 11, (551-559), (2023).https://doi.org/10.1097/WNR.0000000000001922
    Crossref
  2. Voluntary exercise delays progressive deterioration of markers of metabolism and behavior in a mouse model of Parkinson’s disease, Brain Research, 1720, (146301), (2019).https://doi.org/10.1016/j.brainres.2019.146301
    Crossref
  3. Glucose-Dependent Insulinotropic Polypeptide Mitigates 6-OHDA-Induced Behavioral Impairments in Parkinsonian Rats, International Journal of Molecular Sciences, 19, 4, (1153), (2018).https://doi.org/10.3390/ijms19041153
    Crossref
  4. Exercise Ameliorates Motor Deficits and Improves Dopaminergic Functions in the Rat Hemi-Parkinson’s Model, Scientific Reports, 8, 1, (2018).https://doi.org/10.1038/s41598-018-22462-y
    Crossref
  5. Decreased Anti‐Parkinson's Therapy during Hospitalization due to Infectious Diseases is Associated with Worse Prognosis, CNS Neuroscience & Therapeutics, 22, 5, (423-425), (2016).https://doi.org/10.1111/cns.12545
    Crossref
  6. Decreased dopaminergic treatment of hospitalized Parkinson’s disease patients during infectious diseases is associated with poor outcomes, Journal of Clinical Neuroscience, 22, 8, (1272-1274), (2015).https://doi.org/10.1016/j.jocn.2015.02.010
    Crossref
  7. Effects of Progressive Resistance Exercise Training on the Motor and Nonmotor Features of Parkinson's Disease: A Review, Kinesiology Review, 4, 1, (11-27), (2015).https://doi.org/10.1123/kr.2014-0074
    Crossref
  8. A 'bird's Eye' View on the Current Status and Potential Benefits of Blood Biomarkers for Parkinson's Disease, Biomarkers in Medicine, 8, 2, (225-227), (2014).https://doi.org/10.2217/bmm.13.139
    Crossref
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