Abstract
Progressive nonfluent aphasia (PNFA) is one of the language variants of frontotemporal dementia.1 Previously, PNFA, corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP) were regarded as separate disease entities because of their distinctive clinical features and different anatomic involvement: left perisylvian area in PNFA,2 basal ganglia and dorsal midbrain in PSP, and perirolandic area in CBD.3 However, recent studies show that the 3 disorders share tauopathy and clinical features such as language disturbance and parkinsonism in common.4 Furthermore, one disorder even evolves into others along the course of disease progression.5 One of the typical examples of this evolution is that PNFA can develop into CBD or PSP.6 Therefore, we hypothesized that the topography of glucose hypometabolism in patients with PNFA with parkinsonism (PNFA+P) would differ from those without parkinsonism (PNFA-P), even before evolving into PSP or CBD. That is, PNFA+P would have more glucose hypometabolism in the basal ganglia, midbrain, or perirolandic areas that are known to be affected in PSP or CBD. ### Methods. #### Subjects. We retrospectively found a total of 21 patients with PNFA who underwent clinical evaluations, including neuropsychological tests and [18F]fluoro-2-deoxy-d-glucose PET (FDG-PET) within a 3-month interval at a university-affiliated hospital. All patients fulfilled the diagnostic criteria for PNFA proposed …
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