Lentiform Nucleus Hyperechogenicity in Parkinsonian Syndromes: A Systematic Review and Meta-Analysis with Consideration of Molecular Pathology.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
18 12 2019
Historique:
received: 24 09 2019
revised: 03 12 2019
accepted: 14 12 2019
entrez: 22 12 2019
pubmed: 22 12 2019
medline: 19 8 2020
Statut: epublish

Résumé

The hyperechogenicity of the substania nigra (SN) has been established as a valid finding in patients with Parkinson´s disease (PD), probably caused by an increased tissue iron concentration in the SN. The application of transcranial sonography (TCS) has been investigated for further echogenic basal ganglia alterations in patients with extrapyramidal movement disorders. Compared to PD, a hyperechogenic nucleus lentiformis (LN) has been reported to appear more frequently in atypical parkinsonian syndromes (aPS) such as the parkinsonian phenotype of multiple system atrophy (MSA-P) or the progressive supranuclear palsy (PSP). As the evidence providing study sizes are small, we conduct the first meta-analysis of the prevalence of LN hyperechogenicity in PD and aPS. We search for available studies providing prevalence of LN hyperechogenicity in patients with PD and aPS (MSA-P and PSP) detected by TCS in MEDLINE and SCOPUS databases. We calculate the prevalence rates of LN hyperechogenicity detection in patients with clinical diagnosis of PD vs. aPS under the random-effects model. We include a total of 1330 patients, 1091 PD and 239 aPS (MSA-P and PSP). We find a significantly higher prevalence of LN hyperechogenicity in aPS (76%, 95% CI: 0.62-0.88) compared to PD (16%, 95% CI: 0.10-0.23). After proving a higher prevalence of LN hyperechogenicity in aPS compared to PD, its histopathological cause needs to be investigated. Furthermore, its full diagnostic accuracy and the qualification to serve as a risk factor for MSA-P and PSP should also be questioned in future studies.

Identifiants

pubmed: 31861253
pii: cells9010002
doi: 10.3390/cells9010002
pmc: PMC7016776
pii:
doi:

Types de publication

Comparative Study Journal Article Meta-Analysis Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Daniel Richter (D)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.

Aristeidis H Katsanos (AH)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.
nd Dept. of Neurology, National and Kapodistrian University of Athens, Athens 15344, Greece.

Christoph Schroeder (C)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.

Georgios Tsivgoulis (G)

nd Dept. of Neurology, National and Kapodistrian University of Athens, Athens 15344, Greece.
Dept. of Neurology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.

George P Paraskevas (GP)

st Dept. of Neurology, Cognitive and Movement Disorders Clinic and Unit of Neurochemistry and Biological Markers, School of Medicine, National and Kapodistrian University of Athens, Eginition Hospital, Athens 11528, Greece.

Thomas Müller (T)

Dept. of Neurology, Alexianer St. Joseph Berlin-Weißensee, Berlin 13088, Germany.

Andrei V Alexandrov (AV)

Dept. of Neurology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.

Ralf Gold (R)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.
Neurodegeneration Research, Protein Research Unit Ruhr (PURE), Ruhr University Bochum, Bochum 44791, Germany.

Lars Tönges (L)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.
Neurodegeneration Research, Protein Research Unit Ruhr (PURE), Ruhr University Bochum, Bochum 44791, Germany.

Christos Krogias (C)

Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum 44791, Germany.

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