Cerebral perfusion and cortical thickness indicate cortical involvement in mild Parkinson's disease

Cortical dysfunction in Parkinson's disease (PD) may be caused by disruption to ascending systems or by intrinsic cortical neuropathology. We introduce and conduct a joint analysis of metabolism and atrophy capable of identifying whether metabolic disruption occurs in mild PD without cortical atrophy, to determine the extent and spatial pattern of cortical involvement in mild PD. The design was observational, studying 23 cognitively normal participants with mild PD (mean Hoehn & Yahr stage 2) and 21 healthy controls. Cortical thickness (obtained from analysis of structural magnetic resonance imaging [MRI] with FreeSurfer) and cerebral perfusion measures (obtained from arterial spin labeling [ASL]) analyzed independently and then together in a joint multiple factorial analysis to identify spatial patterns of perfusion and cortical thickness. We identify a pattern of changes in perfusion and cortical thickness characterized by symmetric parietal cortical thinning and reduced precuneus perfusion, with relative preservation of thickness and perfusion in the anterior cingulate cortex (ACC), right prefrontal gyrus, and medial frontal gyrus. The expression of this pattern is correlated with motor system symptoms and speed of processing. A spatial pattern of joint parietal cortical thinning and disproportionate reduction in perfusion occurs in our nondemented PD sample. We found no PD-related components of reduced perfusion without cortical thinning. This suggests that PD affects the cortex itself, even when symptoms are relatively mild.