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- All Subjects: TBI
- Creators: Alateeq, Halah
- Creators: Bjorklund, Reed
cognitive-communication deficits. In bilinguals, there are unique cognitive demands required to control and process two languages effectively. Surprisingly, little is known about the impact of mTBI on EF, communication, and language control in bilinguals. Therefore, the aim of this study was to examine the cognitive-communication abilities in bilinguals with a history of mTBI, identify any language control impairments, and explore the relationship between these language control impairments and domain-general cognitive control abilities. To this end, three-hundred and twenty-seven monolingual and bilingual college students with and without mTBI history participated in two experiments. In these experiments, EF, communication, and language control were examined using experimental and clinical tasks as well as self-rating scales. In Experiment 1, there was an interaction between mTBI history and language group (monolinguals vs. bilinguals) in how participants performed on a clinical measure of EF and a verbal fluency task. That is, only bilinguals with mTBI scored significantly lower on these tasks. In addition, there was a significant correlation between errors on a language switching task and performance on non-verbal EF tasks. In Experiment 2, a subgroup of bilinguals with persistent cognitive and behavioral symptoms reported greater everyday communication challenges in their first and second languages. Also, unbalanced bilinguals reported greater EF difficulties than monolinguals and balanced bilinguals regardless of mTBI history. In conclusion, bilinguals may face unique cognitive-communication challenges after mTBI. Factors related to the bilingual experience (e.g., language balance, daily language use) should be
considered in clinical evaluation and future research.
Traumatic brain injury (TBI) is defined as an injury to the head that disrupts normal brain function. TBI has been described as a disease process that can lead to an increased risk for developing chronic neurodegenerative diseases, like frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). A pathological hallmark of FTLD and a hallmark of ALS is the nuclear mislocalization of TAR DNA Binding Protein 43 (TDP-43). This project aims to explore neurodegenerative effects of TBI on cortical lesion area using immunohistochemical markers of TDP-43 proteinopathies. We analyzed the total percent of NEUN positive cells displaying TDP-43 nuclear mislocalization. We found that the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was significantly higher in cortical tissue following TBI when compared to the age-matched control brains. The cortical lesion area was analyzed for each injured brain sample, with respect to days post-injury (DPI), and it was found that there were no statistically significant differences between cortical lesion areas across time points. The percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was analyzed for each cortical tissue sample, with respect to cortical lesion area, and it was found that there were no statistically significant differences between the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization, with respect to cortical lesion area. In conclusion, we found no correlation between the percent of cortical NEUN positive cells displaying TDP-43 nuclear mislocalization with respect to the size of the cortical lesion area.