Functional neuroanatomy of speech signal decoding in primary progressive aphasias

Publication date: Available online 10 May 2017
Source:Neurobiology of Aging
Author(s): Chris J.D. Hardy, Jennifer L. Agustus, Charles R. Marshall, Camilla N. Clark, Lucy L. Russell, Emilie V. Brotherhood, Rebecca L. Bond, Cassidy M. Fiford, Sasha Ondobaka, David L. Thomas, Sebastian J. Crutch, Jonathan D. Rohrer, Jason D. Warren
The pathophysiology of primary progressive aphasias remains poorly understood. Here we addressed this issue using activation fMRI in a cohort of 27 patients with primary progressive aphasia (nonfluent, semantic, and logopenic variants) versus 15 healthy controls. Participants listened passively to sequences of spoken syllables in which we manipulated three key auditory speech signal characteristics: temporal regularity, phonemic spectral structure and pitch sequence entropy. Relative to healthy controls, nonfluent variant patients showed reduced activation of medial Heschl's gyrus in response to any auditory stimulation and reduced activation of anterior cingulate to temporal irregularity. Semantic variant patients had reduced activation of caudate and anterior cingulate in response to increased entropy. Logopenic variant patients showed reduced activation of posterior superior temporal cortex to phonemic spectral structure. Taken together, our findings suggest that impaired processing of core speech signal attributes may drive particular progressive aphasia syndromes and may index a generic physiological mechanism of reduced computational efficiency relevant to all these syndromes, with implications for development of new biomarkers and therapeutic interventions.



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