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Mov Disord. 2017 Jul;32(7):955-971. doi: 10.1002/mds.27038. Epub 2017 May 13.

Radiological biomarkers for diagnosis in PSP: Where are we and where do we need to be?

Author information

1
Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
2
Department of Neurology, Technische Universität München, Munich, Germany.
3
German Center for Neurodegenerative Diseases (DZNE), Germany.
4
Parkinson and Movement Disorder Unit, IRCCS Hospital San Camillo, Venice and Department of Neurosciences (DNS), Padova University, Padova, Italy.
5
Department of Neurology, University of California, Los Angeles, California, USA.
6
Memory and Aging Center, Department of Neurology, University of California, San Francisco, California, USA.
7
Department of Neurology, Santa Maria University Hospital, Terni, Italy.
8
Department of Nuclear Medicine, University of Cologne, Cologne, Germany.
9
Department of Neurology, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
10
Department of Neurology, University of Ulm, Ulm, Germany.
11
Psychiatrische Klinik, Ludwigs-Maximilians-Universität, München, Germany.
12
Department of Neurology, University of California, San Diego, California, USA.
13
Department of Neurology, John Hopkins University, Baltimore, Maryland, USA.
14
Deptartment of Nuclear Medicine, Ludwig-Maximilians-Universität München, Munich, Germany.
15
Department of Clinical Neurosciences, Cambridge University, Cambridge, UK.
16
Second Department of Neurology, Attikon University Hospital, University of Athens, Greece; Philipps University, Marburg, Germany; Movement Disorders Dept., HYGEIA Hospital, Athens, Greece.
17
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.

Abstract

PSP is a pathologically defined neurodegenerative tauopathy with a variety of clinical presentations including typical Richardson's syndrome and other variant PSP syndromes. A large body of neuroimaging research has been conducted over the past two decades, with many studies proposing different structural MRI and molecular PET/SPECT biomarkers for PSP. These include measures of brainstem, cortical and striatal atrophy, diffusion weighted and diffusion tensor imaging abnormalities, [18F] fluorodeoxyglucose PET hypometabolism, reductions in striatal dopamine imaging and, most recently, PET imaging with ligands that bind to tau. Our aim was to critically evaluate the degree to which structural and molecular neuroimaging metrics fulfill criteria for diagnostic biomarkers of PSP. We queried the PubMed, Cochrane, Medline, and PSYCInfo databases for original research articles published in English over the past 20 years using postmortem diagnosis or the NINDS-SPSP criteria as the diagnostic standard from 1996 to 2016. We define a five-level theoretical construct for the utility of neuroimaging biomarkers in PSP, with level 1 representing group-level findings, level 2 representing biomarkers with demonstrable individual-level diagnostic utility, level 3 representing biomarkers for early disease, level 4 representing surrogate biomarkers of PSP pathology, and level 5 representing definitive PSP biomarkers of PSP pathology. We discuss the degree to which each of the currently available biomarkers fit into this theoretical construct, consider the role of biomarkers in the diagnosis of Richardson's syndrome, variant PSP syndromes and autopsy confirmed PSP, and emphasize current shortfalls in the field. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

KEYWORDS:

diagnosis; magnetic resonance imaging; positron emission tomography; progressive supranuclear palsy; single-photon emission computed tomography

PMID:
28500751
PMCID:
PMC5511762
DOI:
10.1002/mds.27038
[Indexed for MEDLINE]
Free PMC Article

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