Brain Advance Access originally published online on April 20, 2005
Brain 2005 128(6):1259-1266; doi:10.1093/brain/awh508
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Clinical deficits correlate with regional cerebral atrophy in progressive supranuclear palsy
1 Department of Geriatric Medicine, Westmead Hospital and the University of Sydney, 2 Department of Neurology, Westmead Hospital, Westmead, NSW, 3 Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, NSW and 4 Melbourne Neuropsychiatry Centre, The University of Melbourne, Royal Melbourne and Sunshine Hospitals, Victoria Australia
Correspondence to: Dr N. J. Cordato, Department of Geriatric Medicine, Westmead Hospital, Westmead, NSW 2145, Australia E-mail: Nicholas_Cordato{at}wsahs.nsw.gov.au
Most cerebral imaging studies of patients with progressive supranuclear palsy (PSP) have noted subtle atrophy, although the full extent of atrophy and any correlates to clinical features have not been determined. We used voxel-based morphometry analysis of grey matter, white matter and CSF on MRI brain scans to map the statistical probability of regional tissue atrophy in 21 patients with PSP, 17 patients with Parkinson's disease and 23 controls. PSP and Parkinson's disease cohorts were selected to approximate the mid-stages of their respective disease courses. Where regions of significant tissue atrophy were identified in a disease group relative to controls, the probability of tissue loss within those regions was correlated with global indices of motor disability, and behavioural and cognitive disturbance for that disease group. Minimal regional atrophy was observed in Parkinson's disease. PSP could be distinguished from both controls and Parkinson's disease by symmetrical tissue loss in the frontal cortex (maximal in the orbitofrontal and medial frontal cortices), subcortical nuclei (midbrain, caudate and thalamic) as well as periventricular white matter. For PSP, motor deficits correlated with atrophy of the caudate and motor cingulate, while behavioural changes related to atrophy in the orbitofrontal cortex and midbrain. These data suggest that intrinsic neurodegeneration of specific subcortical nuclei and frontal cortical subregions together contribute to motor and behavioural disturbances in PSP and differentiate this disorder from Parkinson's disease within 2–4 years of symptom onset.
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