Fluorodeoxyglucose F18 Positron Emission Tomography in Progressive Apraxia of Speech and Primary Progressive Aphasia Variants

Abstract

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. 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. Tertiary care medical center. Twenty-four patients with PAS or PPA and FDG-PET. Fluorodeoxyglucose F18 PET hypometabolic pattern. 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. Patterns of FDG-PET hypometabolism support the clinical categorizations of fluency, the distinction of apraxia of speech from progressive nonfluent aphasia, and the designation of a progressive fluent aphasia category.