Button to scroll to the top of the page.
Henry, Maya

Maya L Henry

Associate Professor, Assistant Professor of Neurology
Department of Communication Sciences and Disorders, Department of Neurology



maya.henry@austin.utexas.edu


Office Location
HDB

Postal Address
2504 A WHITIS AVE
AUSTIN, TX 78712

Dr. Henry is a speech-language pathologist by training. She did her master’s and doctoral work at the University of Arizona, in the lab of Dr. Pelagie Beeson. Subsequently, she completed postdoctoral training in the lab of Dr. Maria Luisa Gorno-Tempini at the UCSF Memory and Aging Center. Her research interests lie in the nature and treatment of aphasia and related neurogenic communication disorders, with a special focus on primary progressive aphasia.

The Aphasia Research and Treatment Lab (ARTlab), under the direction of Maya Henry, PhD, CCC-SLP, is housed in the Department of Communication Sciences and Disorders, in the Moody College of Communication at the University of Texas at Austin. Research in the lab is directed at improving our understanding of how the brain supports speech and language processes and how targeted treatment programs may improve communication impairments caused by stroke or neurodegenerative disease. The lab utilizes current approaches in cognitive neuroscience, neuroimaging, and cognitive rehabilitation to address these issues.

 

Projects

Rehabilitation of speech and language in aphasia caused by stroke and neurodegenerative disease (primary progressive aphasia)

The goal of this study is to develop optimized treatment methods for rehabilitation of speech and language deficits in the three variants of primary progressive aphasia (nonfluent, semantic, and logopenic PPA) and to compare outcomes in individuals with aphasia caused by stroke. Specifically, we are exploring dose modifications, novel treatments for speech production, and neural bases of treatment efficacy.

Treatments for language and memory in progressive aphasia, mild dementia, and MCI

Whereas memory deficits are clinically recognized and more commonly treated features of dementia and MCI, language impairments are diagnosed and treated far less reliably. In this study, we are addressing word-finding difficulty in individuals with mild forms of dementia and MCI who have naming deficits as a primary feature. We are implementing a proven, tailored treatment approach for naming in these individuals and combining this approach with another method designed to improve retention of newly learned information. This project aims to provide evidence regarding the utility of these treatment methodologies as well as neuroimaging predictors of response to treatment in mild dementia and MCI.

Neural bases of speech and language impairments in progressive aphasia and stroke 

The goal of this study is to collect comprehensive behavioral data documenting speech, language, and cognitive deficits in individuals with aphasia caused by stroke and neurodegenerative disease. In conjunction with multimodal imaging data (structural MRI, diffusion tensor imaging (DTI), and resting state functional imaging) we are examining brain-behavior relations for various speech and language domains, including phonological processing, written language, naming, and motor planning for speech.

 

Binney, R. J., Henry, M.L., Babiak, M., Pressman, P. S., Santos, M. A., Narvid, J., ... & Rosen, H. J. (2016). Reading words and other people: a comparison of exception word, familiar face and affect processing in the left and right temporal variants of primary progressive aphasia. 

Santos, M.A.,  Mandelli, M.L., Binney, R.J., Ogar, J. , Wilson, S.M., Henry, M.L., Hubbard, H.I., Meese, M, Attygalle, S., Rosenberg, L., Pakvasa, M., Trojanowski, J.Q. , Grinberg, L.T, Rosen, H.J., Boxer, A.L., Miller, B.L., Seeley, W.W., Gorno-Tempini, M.L. (2016). Cross-sectional and longitudinal features of non-fluent/agrammatic primary progressive aphasia with underlying corticobasal degeneration or progressive supranuclear palsy pathology. JAMA Neurology, 1;73(6)733-742.

Henry, M.L., Wilson, S.M., Babiak, M.C., Mandelli, M.L., Beeson, P.M., Miller, Z.A., & Gorno-Tempini, M.L. (2016). Phonological processing in primary progressive aphasia. Journal of Cognitive Neuroscience, 28(2), 210-222.

Mandelli, M. L., Vitali, P., Santos, M., Henry, M.L., Gola, K., Rosenberg, L., ... & Gorno-Tempini, M. L. (2016). Two insular regions are differentially involved in behavioral variant FTD and nonfluent/agrammatic variant PPA. Cortex, 74, 149-157.

Henry, M.L., Wilson, S.M., Ogar, J.M., Sidhu, M., Rankin, K.P, Miller, B.L., Gorno-Tempini, M.L., & Seeley, W.W. (2014). Neuropsychological, behavioral and anatomical evolution in right temporal variant frontotemporal dementia: A longitudinal and post-mortem single case analysis. Neurocase, 20(1), 100-109.
Review abstract: here

Wilson, S. M., Brandt, T. H., Henry, M. L., Babiak, M., Ogar, J. M., Salli, C., ... & Gorno-Tempini, M. L. (2014). Inflectional morphology in primary progressive aphasia: An elicited production study. Brain and Language, 136, 58-68.

Mandelli, M. L., Caverzasi, E., Binney, R. J., Henry, M. L., Lobach, I., Block, N., ... & Gorno-Tempini, M. L. (2014). Frontal White Matter Tracts Sustaining Speech Production in Primary Progressive Aphasia. The Journal of Neuroscience, 34(29), 9754-9767.

Sánchez-Juan, P., Ghosh, P. M., Hagen, J., Gesierich, B., Henry, M.L., Grinberg, L. T., … & Rabinovici, G. D. (2014). Practical utility of amyloid and FDG-PET in an academic dementia center. Neurology, 82(3), 230-238.               Review abstract: here.

Wilson, S. M., DeMarco, A. T., Henry, M. L., Gesierich, B., Babiak, M., Mandelli, M. L., … & Gorno-Tempini, M. L. (2014). What Role Does the Anterior Temporal Lobe Play in Sentence-level Processing? Neural Correlates of Syntactic Processing in Semantic Variant Primary Progressive Aphasia. Journal of Cognitive Neuroscience, 26(5), 970-985.
Review abstract: here

Caso, F., Mandelli, M. L., Henry, M.L., Gesierich, B., Bettcher, B. M., Ogar, J., … & Gorno-Tempini, M. L. (2014) In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology. Neurology, 82(3), 239-247.
Review abstract: here.