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.