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Cortical atrophy differentiates Richardson's syndrome from the parkinsonian form of progressive supranuclear palsy

Schofield, Emma C., Hodges, John R., Macdonald, Virginia, Cordato, Nicholas J., Kril, Jillian J., Halliday, Glenda M.·2011·Movement Disorders
DOI 10.1002/mds.23295
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Abstract

To determine whether brain atrophy differs between the two subtypes of progressive supranuclear palsy (PSP), Richardson's syndrome (PSP‐RS), and PSP parkinsonism (PSP‐P), and whether such atrophy directly relates to clinical deficits and the severity of tau deposition. We compared 24 pathologically confirmed PSP cases (17 PSP‐RS and 7 PSP‐P) with 22 controls from a Sydney brain donor program. Volume loss was analyzed in 29 anatomically discrete brain regions using a validated point‐counting technique, and tau–immunoreactive neurons, astrocytes and oligodendrocytes/threads semiquantified. Correlations between the two pathological measures and the presence or absence of cardinal PSP symptoms were investigated. Cortical atrophy was more severe in PSP‐RS than PSP‐P and affected more frontal lobe regions (frontal pole, inferior frontal gyrus). The supramarginal gyrus was atrophic in both subtypes. Additionally, atrophy of the internal globus pallidus, amygdala, and thalamus was more severe in PSP‐RS. As expected, more severe frontal lobe tau pathology differentiated PSP‐RS from PSP‐P. No correlations were found between the degree of atrophy and severity of tau pathology in any region assessed, or between the severity of atrophy or tau pathology and the presence or absence of cardinal PSP symptoms. Our study shows that thalamocortical atrophy is a defining feature of PSP‐RS, but this atrophy does not correlate with the presence of any specific cardinal clinical feature. Interestingly, there is a disassociation between tau pathology and atrophy in the brain regions affected in PSP‐RS that requires further investigation. © 2010 Movement Disorder Society

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  • The basal ganglia, insula, and amygdala are implicated in recognition of predominantly negative emotions, and these neuropsychological functions are abnormal in PSP.

    “Basal ganglia, insula and amygdala have been reported to be implicated in the recognition of predominately negative emotions, and these neuropsychological function is abnormal in PSP43,46.”

    From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [43]

  • The spatial distribution of the in vivo association between microglial activation and tau pathology in PSP mirrors previous findings that tau pathology affects both subcortical and cortical regions in PSP Richardson's syndrome.

    “The spatial distribution of this in vivo association between microglial activation and tau pathology in PSP mirrors previous findings showing that tau pathology affects not only subcortical but also cortical regions in PSP Richardson’s syndrome42,43.”

    From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [43]

  • The finding of tau and neuroinflammation co-localization in the cortex of PSP Richardson's syndrome patients is in keeping with previous post-mortem evidence showing tau pathology and atrophy in subcortical, limbic, and parietal regions.

    “Our finding of tau and neuroinflammation co-localization in the cortex of patients with PSP Richardson’s syndrome is in keeping with previous post-mortem evidence showing tau pathology and atrophy not only in subcortical and limbic regions, but also in the parietal lobe43.”

    From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [43]

  • The supramarginal gyrus has been described as the most affected brain region in two independent pathological cohorts of PSP Richardson's syndrome patients.

    “Specifically, the supramarginal gyrus has been described as the most affected brain region in two independent pathological cohorts of patients with PSP Richardson’s syndrome43.”

    From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [43]

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Authors
Schofield, E. C., Hodges, J. R., Macdonald, V., Cordato, N. J., Kril, J. J., & Halliday, G. M.
Affiliations
  • UNSW Sydney (AU)
  • The University of Sydney (AU)
Corresponding author
Halliday, Glenda M.
ORCID
Venue
Movement Disorders
Publisher
Wiley
Published
2010-12-13
Volume
26
Issue
2
Pages
256-263
ISSN
  • 0885-3185 (ISSN-L)
  • 1531-8257
DOI
10.1002/mds.23295
OpenAlex
W2036349916
Cited by
48
References
41
Citations by year
2025: 2 · 2024: 1 · 2023: 4 · 2022: 5 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 2 · 2014: 4 · 2013: 5 · 2012: 6
FWCI
2.85
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Movement Disorders (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Health and Medical Research Council of Australia (#282933)
  • Neuroscience Research Australia, and the University of New South Wales
  • Biomedical Postgraduate Research Scholar of the National Health and Medical Research Council of Australia (300672)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
Richardson's syndrome, progressive supranuclear palsy, cortical atrophy, brain atrophy, tau pathology, frontal lobe atrophy, supramarginal gyrus, globus pallidus internus, amygdala, thalamus, differential diagnosis
MeSH terms
Astrocytes, Atrophy, Cell Count, Cerebral Cortex, Diagnosis, Differential, Humans, Immunohistochemistry, Neurons, Oligodendroglia, Supranuclear Palsy, Progressive, Parkinsonian Disorders

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