These Australian researchers looked at the brains of 24 pathologically confirmed PSP cases. 17 cases had PSP-Richardson’s Syndrome and 7 cases had PSP-Parkinsonism — the two most common forms of PSP.
They found:
* “Cortical atrophy was more severe in PSP-RS than PSP-P and affected more frontal lobe regions.”
* “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.”
And, most interestingly, they found:
* “No correlations were found between the degree of atrophy and severity of tau pathology in any region assessed…”
* No correlations “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.”
Robin
Movement Disorders. 2010 Dec 13. [Epub ahead of print]
Cortical atrophy differentiates Richardson’s syndrome from the parkinsonian form of progressive supranuclear palsy.
Schofield EC, Hodges JR, Macdonald V, Cordato NJ, Kril JJ, Halliday GM.
Neuroscience Research Australia and the University of New South Wales, Sydney, New South Wales, Australia.
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.
PubMed ID#: 21154980 (see pubmed.gov for this abstract only)