Evidence map›Paper›PMID 24715569›Full record

ReviewComprehensive Physiology2014

Dysautonomia in Parkinson disease.

David S Goldstein

Registry-linked trialAbstract readReview
In one paragraph

Review in Comprehensive Physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04251728 (Chronic Effects of Automated Mechanical Peripheral Stimulation on Cardiovascular and Functional Variables in Patients With Parkinson's Disease), which is not on this map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04251728 nacompletednot on this mapstarted 2022, after this paper: background citation

Chronic Effects of Automated Mechanical Peripheral Stimulation on Cardiovascular and Functional Variables in Patients With Parkinson's Disease

TypeinterventionalSponsorUniversidad Católica del MauleRan2022 to 2022Enrolled40ConditionsParkinson DiseaseArmsAutomated mechanical peripheral stimulation, Physical Exercise, SHAM
3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 137 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Sympathetic dysfunction as an early indicator of autonomic involvement in Parkinson's disease.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

David S GoldsteinClinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.
National Institutes of Health · US

Funding

Biomarkers of Parkinson Disease and Related DisordersZIANS003034 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GOLDSTEIN, DAVID · 2009 to 2025
$22.8M
Mechanisms of Parkinson Disease and Related DisordersZIANS003033 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GOLDSTEIN, DAVID · 2009 to 2022
$8.2M
Treatment of Catecholaminergic NeurodegenerationZIANS003125 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GOLDSTEIN, DAVID · 2011 to 2022
$3.2M
Intramural NIH HHS ZIA NS003033
6 · The paper itself

Abstract

Dysautonomias are conditions in which altered function of one or more components of the autonomic nervous system (ANS) adversely affects health. This review updates knowledge about dysautonomia in Parkinson disease (PD). Most PD patients have symptoms or signs of dysautonomia; occasionally, the abnormalities dominate the clinical picture. Components of the ANS include the sympathetic noradrenergic system (SNS), the parasympathetic nervous system (PNS), the sympathetic cholinergic system (SCS), the sympathetic adrenomedullary system (SAS), and the enteric nervous system (ENS). Dysfunction of each component system produces characteristic manifestations. In PD, it is cardiovascular dysautonomia that is best understood scientifically, mainly because of the variety of clinical laboratory tools available to assess functions of catecholamine systems. Most of this review focuses on this aspect of autonomic involvement in PD. PD features cardiac sympathetic denervation, which can precede the movement disorder. Loss of cardiac SNS innervation occurs independently of the loss of striatal dopaminergic innervation underlying the motor signs of PD and is associated with other nonmotor manifestations, including anosmia, REM behavior disorder, orthostatic hypotension (OH), and dementia. Autonomic dysfunction in PD is important not only in clinical management and in providing potential biomarkers but also for understanding disease mechanisms (e.g., autotoxicity exerted by catecholamine metabolites). Since Lewy bodies and Lewy neurites containing alpha-synuclein constitute neuropathologic hallmarks of the disease, and catecholamine depletion in the striatum and heart are characteristic neurochemical features, a key goal of future research is to understand better the link between alpha-synucleinopathy and loss of catecholamine neurons in PD.

Indexed as

HumansParkinson DiseasePrimary Dysautonomias

Identifiers

PMID24715569
PMCPMC4222515
OpenAlexW1598029032

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.