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Description
The increase of Traumatic Brain Injury (TBI) cases in recent war history has increased the urgency of research regarding how veterans are affected by TBIs. The purpose of this study was to evaluate the effects of TBI on speech recognition in noise. The AzBio Sentence Test was completed for signal-to-noise

The increase of Traumatic Brain Injury (TBI) cases in recent war history has increased the urgency of research regarding how veterans are affected by TBIs. The purpose of this study was to evaluate the effects of TBI on speech recognition in noise. The AzBio Sentence Test was completed for signal-to-noise ratios (S/N) from -10 dB to +15 dB for a control group of ten participants and one US military veteran with history of service-connected TBI. All participants had normal hearing sensitivity defined as thresholds of 20 dB or better at frequencies from 250-8000 Hz in addition to having tympanograms within normal limits. Comparison of the data collected on the control group versus the veteran suggested that the veteran performed worse than the majority of the control group on the AzBio Sentence Test. Further research with more participants would be beneficial to our understanding of how veterans with TBI perform on speech recognition tests in the presence of background noise.
ContributorsCorvasce, Erica Marie (Author) / Peterson, Kathleen (Thesis director) / Williams, Erica (Committee member) / Azuma, Tamiko (Committee member) / Barrett, The Honors College (Contributor) / Department of Speech and Hearing Science (Contributor)
Created2015-05
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Description
Neuroinflammation is an important secondary injury response occurring after traumatic brain injury (TBI). Anxiety-like disorders are commonly exacerbated after TBI and are mediated through the amygdala; however, the amygdala remains understudied despite its important contribution in processing emotional and stressful stimuli. Therefore, we wanted to study neuroinflammation after experimental TBI

Neuroinflammation is an important secondary injury response occurring after traumatic brain injury (TBI). Anxiety-like disorders are commonly exacerbated after TBI and are mediated through the amygdala; however, the amygdala remains understudied despite its important contribution in processing emotional and stressful stimuli. Therefore, we wanted to study neuroinflammation after experimental TBI using midline fluid percussion in rodent models. We assessed microglia morphology over time post-injury in two circuit related nuclei of the amygdala, the basolateral amygdala (BLA) and central amygdala of the nucleus (CeA), using skeletal analysis. We also looked at silver staining and glial fibrillary acidic protein (GFAP) to evaluate the role of neuropathology and astrocytosis to evaluate for neuroinflammation in the amygdala. We hypothesized that experimental diffuse TBI leads to microglial activation in the BLA-CeA circuitry over time post-injury due to changes in microglial morphology and increased astrocytosis in the absence of neuropathology. Microglial cell count was found to decrease in the BLA at 1 DPI before returning to sham levels by 28 DPI. No change was found in the CeA. Microglial ramification (process length/cell and endpoints/cell) was found to decrease at 1DPI compared to sham in the CeA, but not in the BLA. Silver staining and GFAP immunoreactivity did not find any evidence of neurodegeneration or activated astrocytes in the respectively. Together, these data indicate that diffuse TBI does not necessarily lead to the same microglial response in the amygdala nuclei, although an alternative mechanism for a neuroinflammatory response in the CeA likely contributes to the widespread neuronal and circuit dysfunction that occurs after TBI.
ContributorsHur, Yerin (Author) / Newbern, Jason (Thesis director) / Thomas, Theresa Currier (Committee member) / Beitchman, Joshua (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05