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Research Article

Reemergence of the language network during recovery from severe traumatic brain injury: A pilot functional MRI study

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Pages 1552-1562 | Received 17 Nov 2020, Accepted 22 Aug 2021, Published online: 21 Sep 2021
 

ABSTRACT

Primary Objective

We hypothesized that, in patients with acute severe traumatic brain injury (TBI) who recover basic language function, speech-evoked blood-oxygen-level-dependent (BOLD) functional MRI (fMRI) responses within the canonical language network increase over the first 6 months post-injury.

Research Design

We conducted a prospective, longitudinal fMRI pilot study of adults with acute severe TBI admitted to the intensive care unit. We also enrolled age- and sex-matched healthy subjects.

Methods and Procedures

We evaluated BOLD signal in bilateral superior temporal gyrus (STG) and inferior frontal gyrus (IFG) regions of interest acutely and approximately 6 months post-injury. Given evidence that regions outside the canonical language network contribute to language processing, we also performed exploratory whole-brain analyses.

Main Outcomes and Results

Of the 16 patients enrolled, eight returned for follow-up fMRI, all of whom recovered basic language function. We observed speech-evoked longitudinal BOLD increases in the left STG, but not in the right STG, right IFG, or left IFG. Whole-brain analysis revealed increases in the right supramarginal and middle temporal gyri but no differences between patients and healthy subjects (n = 16).

Conclusion

This pilot study suggests that, in patients with severe TBI who recover language function, speech-evoked responses in bihemispheric language-processing cortex reemerge by 6 months post-injury.

Acknowledgments

We thank the nursing staff of the Massachusetts General Hospital Neurosciences ICU, Multidisciplinary ICU, and Surgical ICU. We also thank the Massachusetts General Hospital MRI technologists for assistance with data acquisition. We are grateful to the patients and families involved in this study for their participation and support.

Role of the funding sources

The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

This work was supported by the NIH Director’s Office (DP2HD101400), NIH National Institute of Neurological Disorders and Stroke (K23NS094538, R21NS109627, RF1NS115268), James S. McDonnell Foundation, Rappaport Foundation, and Tiny Blue Dot Foundation.

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