Evidence map›Paper›PMID 34427338›Full record

ArticleMovement disorders : official journal of the Movement Disorder Society2021

Preexisting Bipolar Disorder Influences the Subsequent Phenotype of Parkinson's Disease.

Marco Onofrj, Angelo Di Iorio, Claudia Carrarini, Mirella Russo, Raffaella Franciotti, Alberto J Espay, Laura S Boylan, John-Paul Taylor, Massimo Di Giannantonio, Giovanni Martinotti and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Movement disorders : official journal of the Movement Disorder Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 13% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Bipolar Disorder as a Long-Term Risk Factor for Parkinson's Disease: A Nationwide Case-Control Study.Movement disorders : official journal of the Movement Disorder Society · 2026
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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

16 authors at 6 institutions in 3 countries.

Marco OnofrjDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.ORCID 0000-0002-0480-2495
Angelo Di IorioDepartment of Aging Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Claudia CarrariniDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Mirella RussoDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Raffaella FranciottiDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Alberto J EspayDepartment of Neurology, James J. and Joan A. Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati, Cincinnati, Ohio, USA.ORCID 0000-0002-3389-136X
Laura S BoylanDepartment of Neurology, Bellevue Hospital, New York University School of Medicine, New York, New York, USA.ORCID 0000-0003-3648-1531
John-Paul TaylorTranslational and Clinical Research Institute, Biomedical Research Building, Newcastle University, Newcastle upon Tyne, United Kingdom.
Massimo Di GiannantonioDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Giovanni MartinottiDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Enza M ValenteIRCCS Mondino Foundation and Department of Molecular Medicine, University of Pavia, Pavia, Italy.ORCID 0000-0002-0600-6820
Astrid ThomasDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Laura BonanniDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Stefano Delli PizziDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Fedele DonoDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
StefanoL SensiDepartment of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.ORCID 0000-0002-0710-2574
University of Chieti-Pescara · ITBellevue Hospital Center · USNIHR Newcastle Biomedical Research Centre · GBUniversity of California, Irvine · USUniversity of Cincinnati · USUniversity of Pavia · IT

Funding

Department of Health
6 · The paper itself

Abstract

backgroundPatients with bipolar spectrum disorders (BSDs) exhibit an increased risk of Parkinson's disease (PD).

objectiveThe aim is to investigate whether a previous diagnosis of BSDs influences the phenotype of PD.

methodsOf 2660 PD patients followed for at least 6 years (6-27), 250 (BSD-PD) had BSDs, 6-20 years before PD diagnosis; 48%-43% had a PD or BSD family history, and 34 carried glucocerebrosidase (GBA) and Parkin (PRKN) mutations. The cohort was split into a subset of 213 BSD-PD patients, compared with 426 matched PD patients without BSDs, and a subset of 34 BSD-PD and 79 PD patients carrying GBA or PRKN mutations. Carriers of mutations absent in BSD-PD patients and of synuclein triplication were excluded. Structured clinical interviews and mood disorder questionnaires assessed BSDs. Linear mixed models evaluated the assessment scales over time. Thirteen BSD-PD patients underwent subthalamic nucleus deep brain stimulation (STN-DBS) and were compared with 27 matched STN-DBS-treated PD patients.

resultsCompared to PD patients, BSD-PD showed (1) higher frequency of family history of PD (odds ratio [OR] 3.31; 2.32-4.71) and BSDs (OR 6.20; 4.11-9.35) 5); (2) higher incidence of impulse control disorders (hazard ratio [HR] 5.95, 3.89-9.09); (3) higher frequency of functional disorders occurring before PD therapy (HR, 5.67, 3.95-8.15); (4) earlier occurrence of delusions or mild dementia (HR, 7.70, 5.55-10.69; HR, 1.43, 1.16-1.75); and (5) earlier mortality (1.48; 1.11-1.97). Genetic BSD-PD subjects exhibited clinical features indistinguishable from nongenetic BSD-PD subjects. STN-DBS-treated BSD-PD patients showed no improvements in quality of life compared to the control group.

conclusionsBSDs as a prodrome to PD unfavorably shape their course and are associated with detrimental neuropsychiatric features and treatment outcomes. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Indexed as

Bipolar DisorderDeep Brain StimulationParkinson DiseaseHumansPhenotypeQuality of Lifebipolar spectrum disordersParkinson's disease; glucocerebrosidase mutation; parkin mutationsubthalamic nucleus deep brain stimulation

Identifiers

PMID34427338
PMCPMC9292484
OpenAlexW3196050234

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.