Fluorodeoxyglucose F18 positron emission tomography in progressive apraxia of speech and primary progressive aphasia variants

Objectives: To determine patterns of hypometabolism on fluorodeoxyglucose F18 positron emission tomography (FDG-PET) in patients with progressive apraxia of speech (PAS) and primary progressive aphasia (PPA) variants and to use these patterns to further refine current classification. Design: We identified all patients who had FDG-PET and PAS or PPA who were evaluated by an expert speech-language pathologist. Patterns of hypometabolism were independently classified by 2 raters blinded to clinical data. Three speech-language pathologists reclassified all patients into 1 of 7 operationally defined categories of PAS and PPA blinded to FDG-PET data. Setting: Tertiary care medical center. Patients: Twenty-four patients with PAS or PPA and FDG-PET. Main Outcome Measure: Fluorodeoxyglucose F18 PET hypometabolic pattern. Results: Of the 24 patients in the study, 9 had nonfluent speech output; 14, fluent speech; and 1 was unclassifiable. Twenty-one patients showed FDG hypometabolism; the remaining 3 did not. Among the patients showing hypometabolism, 8 had a prerolandic pattern of which 7 had nonfluent speech including progressive nonfluent aphasia (n=3), PAS (n=1), and mixed nonfluent aphasia/ apraxia of speech (n=3); the other patient had PPA unclassifiable. The remaining 13 had a postrolandic pattern, all with fluent speech (P<.001), including logopenic progressive aphasia (n=6), progressive fluent aphasia (n=6), and semantic dementia (n=1). Patterns of hypometabolism differed between the nonfluent variants and between the fluent variants, including progressive fluent aphasia. Conclusion: Patterns of FDG-PET hypometabolism support the clinical categorizations of fluency, the distinction of apraxia ofspeechfromprogressivenonfluentaphasia,and the designation of a progressive fluent aphasia category.