Functional neuroanatomy of speech signal decoding in primary progressive aphasias

NEUROBIOLOGY OF AGING

卷:56

Article

Hardy, Chris J. D.¹  Agustus, Jennifer L.¹  Marshall, Charles R.¹  Clark, Camilla N.¹  Russell, Lucy L.¹  Brotherhood, Emilie V.¹  Bond, Rebecca L.¹  Fiford, Cassidy M.¹  Ondobaka, Sasha²  Thomas, David L.^1,3  Crutch, Sebastian J.¹  Rohrer, Jonathan D.¹  Warren, Jason D.¹ 

[1] UCL, UCL Inst Neurol, Dept Neurodegenerat Dis, Dementia Res Ctr, London, England

[2] Univ Coll London, UCL Inst Neurol, Wellcome Ctr Neuroimaging, London, ON, Canada

[3] Univ Coll London, UCL Inst Neurol, Leonard Wolfson Expt Neurol, London, ON, Canada

关键词: Frontotemporal dementia;    Primary progressive aphasia;    Semantic dementia;    Logopenic aphasia;    Progressive nonfluent aphasia;    Functional magnetic resonance imaging;   

DOI  :  10.1016/j.neurobiolaging.2017.04.026

来源: Elsevier

【 摘 要 】

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 3- 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 relatively 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 could index a generic physiological mechanism of reduced computational efficiency relevant to all these syndromes, with implications for development of new biomarkers and therapeutic interventions. (C) 2017 The Author(s). Published by Elsevier Inc.

【 授权许可】

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