Research Project
10330319
Characteristics and Treatment of lvPPA Subphonemic Errors Abstract Logopenic variant of primary progressive aphasia (i.e., lvPPA) is characterized by impaired single- word retrieval, impaired phrasal repetition, poor comprehension of complex sentences, and phonological speech errors (e.g., cap is said instead of tap). The phonological errors demonstrated by this population is thought to arise from a deficit of phonological working memory, due to atrophy of temporo-parietal regions. However, the characteristics and underlying pathology of the phonological errors made by lvPPA patients remain to be fully elucidated. Specifically, researchers have overlooked contributions of temporal lobe degeneration in the types of phonological errors that lvPPA patients make. Subphonemic representations for consonant place, manner, and voicing are stored in temporal regions and are activated during speech production. Temporal degeneration likely leads a systematic impairment of retrieval of subphonemic characteristics in lvPPA speech. Yet, no study to date has investigated this possibility. Targeting the subphonemic characteristics of lvPPA speech errors may be crucial for slowing the loss of speech due to this debilitating condition. Neuromodulation using transcranial direct-current stimulation (tDCS) of intact brain regions involved with phonological processes may be used to strengthen weakened connections to these subphonemic representations, and in turn, makes neuromodulation a promising treatment approach for lvPPA. Thus, the proposed study aims to specify the subphonemic characteristics of lvPPA speech errors (Aim 1), establish the neural correlates of these errors (Aim 2), and determine whether neuromodulation of intact regions involved with structuring these representations is an effective rehabilitative technique (Aim 3). Aim 1 will be accomplished by evaluating the frequency of different subphonemic error types among consonant productions made by lvPPA patients. Specifying the pattern of subphonemic errors made by lvPPA patients will allow clinicians to systematically target them during speech-language therapy. Aim 2 will be accomplished using anatomical imaging/measures of atrophy (magnetic resonance imaging [i.e., MRI]) of lvPPA individuals. Finally, Aim 3 will involve using tDCS to stimulate intact inferior frontal regions, which are implicated in facilitating and establishing phoneme categorization. By accomplishing this aim, we will determine whether stimulating intact regions improves phonological processing and thus proves a promising treatment strategy for treating individuals with lvPPA. More broadly, our proposed study will inform many future neuroimaging studies and intervention techniques by characterizing how subphonemic properties of lvPPA-characteristic speech and their corresponding neural properties are related to the behavioral outcomes observed among lvPPA individuals.
