To determine how frequently features of posterior cortical atrophy (PCA) occur in patients with logopenic progressive aphasia (LPA) and determine the neuroimaging correlates of these features.
LPA and PCA are two atypical clinical variants of Alzheimer’s disease. Overlap can be observed clinically between phenotypes, although it is unclear how frequently patients meeting criteria for LPA develop clinical PCA features, and whether these features are associated with neuroanatomical overlap with PCA.
Thirty-six LPA patients recruited by the Neurodegenerative Research Group underwent extensive neuropsychological testing, MRI and [18F] flortaucipir PET. All patients were evaluated for PCA features including simultanagnosia, Gerstmann syndromes, ideomotor apraxia, and visuospatial and visuoperceptual function, with cut-points used to define abnormality. Patients were classified as Pure-LPA (having no PCA feature), LPA+ (impairment on one test) or LPA-PCA (impairment on 2+ tests). Neuroimaging profiles in each of the three LPA groups were compared to 14 matched healthy controls and 14 matched typical PCA patients using multiple regression analysis in SPM12.
Eleven patients (31%) were classified as pure-LPA, 16 (44%) as LPA+ and 9 (25%) as LPA-PCA. There were no differences in disease duration, naming, or sentence repetition across groups. The LPA+ group showed worse simultanagnosia (29%), ideomotor apraxia and Gerstmann syndrome (34%) compared to Pure-LPA group. The LPA-PCA group showed further worsening in simultanagnosia (89%), and visuospatial and visuoperceptual impairment compared to LPA+ group. All three LPA groups showed greater left temporoparietal volume loss and flortaucipir uptake compared to controls and PCA, with greater flortaucipir uptake occurring in the occipital and frontal lobes in LPA+ and LPA-PCA compared to Pure-LPA.
Our results demonstrate that LPA patients can develop features of PCA related to spread of tau into occipito-frontal regions, highlighting syndromic and anatomical overlap between atypical variants of AD.