One sentence in this hard-to-understand abstract caught my eye: “Thus, in a clinically diagnosed and biomarker-confirmed cohort with early PSP, we demonstrate that neostriatal volume and shape are significantly reduced in vivo.”
I wondered what they meant by biomarker-confirmed PSP. There is something called the “penguin” or “hummingbird” sign, which is how the pons and atrophic midbrain appear on a mid-sagittal MRI. It is present in even mild to moderate PSP. I have never heard of anyone in our local support group having an MRI that shows the penguin sign or hummingbird sign. Years ago, I visited the Mayo Jax Brain Bank; one of the researchers there showed me the hummingbird sign on several MRIs.
The point of this study of 15 Swedish PSP patients is that there’s an anatomical basis for “the neuropsychiatric manifestations of PSP, such as the dysexecutive syndrome, gaze palsy, obsessive–compulsive phenomena and utilization behavior.” (I’m not sure how gaze palsy is a neuropsychiatric symptom but anyway…) Similarly, there is an anatomical basis for “the movement disorders of PSP, bradykinesia, gait disturbance and rigidity.”
Here’s the abstract, which is loaded with anatomical terms.
Psychiatry Research. 2011 Sep 5. [Epub ahead of print]
Morphometric analysis of subcortical structures in progressive supranuclear palsy: In vivo evidence of neostriatal and mesencephalic atrophy.
Looi JC, Macfarlane MD, Walterfang M, Styner M, Velakoulis D, Lätt J, van Westen D, Nilsson C.
Research Centre for the Neurosciences of Ageing, Academic Unit of Psychological Medicine, School of Clinical Medicine, Australian National University Medical School, Canberra, Australia.
Progressive supranuclear palsy (PSP) is a neurodegenerative disease characterized by gait and postural disturbance, gaze palsy, apathy, decreased verbal fluency and dysexecutive symptoms, with some of these clinical features potentially having origins in degeneration of frontostriatal circuits and the mesencephalon.
This hypothesis was investigated by manual segmentation of the caudate and putamen on MRI scans, using previously published protocols, in 15 subjects with PSP and 15 healthy age-matched controls.
Midbrain atrophy was assessed by measurement of mid-sagittal area of the midbrain and pons. Shape analysis of the caudate and putamen was performed using spherical harmonics (SPHARM-PDM, University of North Carolina).
The sagittal pons area/midbrain area ratio (P/M ratio) was significantly higher in the PSP group, consistent with previous findings. Significantly smaller striatal volumes were found in the PSP group – putamina were 10% smaller and caudate volumes were 17% smaller than in controls after controlling for age and intracranial volume. Shape analysis revealed significant shape deflation in PSP in the striatum, compared to controls; with regionally significant change relevant to frontostriatal and corticostriatal circuits in the caudate.
Thus, in a clinically diagnosed and biomarker-confirmed cohort with early PSP, we demonstrate that neostriatal volume and shape are significantly reduced in vivo.
The findings suggest a neostriatal and mesencephalic structural basis for the clinical features of PSP leading to frontostriatal and mesocortical-striatal circuit disruption.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
PubMed ID#: 21899988 (see pubmed.gov for this abstract only)