OBJECTIVE: To explore the neuroanatomic basis of amnestic mild cognitive impairment (aMCI) in patients with Parkinson disease (PD; aMCI-PD(+)) and without PD (aMCI-PD(-)).
METHODS: A total of 119 patients with aMCI (aMCI-PD(-), n = 78, and aMCI-PD(+), n = 41) underwent T1-weighted MRI, and the image data were analyzed using voxel-based morphometry.
RESULTS: No significant differences in demographic characteristics or general cognition were found between patients with aMCI-PD(-) and aMCI-PD(+). Comparisons of neuropsychological tests between groups revealed that patients with aMCI-PD(-) had lower scores in delayed verbal and visual recognition memory, whereas visuospatial dysfunction was more severe in patients with aMCI-PD(+). Gray matter (GM) density in the right temporal and posterior cingular cortices was significantly lower in the aMCI-PD(-) group compared with controls. In contrast, GM density in the aMCI-PD(+) group was significantly lower in the precuneus and left prefrontal and primary motor areas relative to controls. A direct comparison between groups showed that decreased GM density in aMCI-PD(-) relative to aMCI-PD(+) was localized in the right temporal and anterior prefrontal areas, whereas decreased GM density in aMCI-PD(+) relative to aMCI-PD(-) was involved in the bilateral precuneus, left primary motor, and right parietal areas. Memory decline was correlated with temporal area atrophy in aMCI-PD(-) and with posterior cingulate cortex atrophy in aMCI-PD(+).
CONCLUSIONS: Our data suggest that different neuroanatomic systems underlie memory dysfunction in patients with aMCI-PD(-) and aMCI-PD(+).