Abstract

Approximately 10-15% of individuals diagnosed with mild traumatic brain injury (mTBI) continue to experience symptoms beyond 3 months post-injury. Although the underlying physiology of these prolonged symptoms remains unknown, numerous factors have been suggested to contribute to recovery from mild traumatic brain injury (mTBI). Among the most extensively studied is the influence of the Apoε4 allele. PURPOSE: The purpose of this study was to examine the potential influence of APOE genotype on neurophysiological recovery from mTBI in individuals with chronic symptoms. METHODS: Twenty seven participants provided a saliva sample for APOE genotyping and were categorized into one of two groups: (i) with history of mTBI and no remaining symptoms (n=21, Control), and (ii) with chronic symptoms from mTBI, lasting at least 3 months post-injury (n=6, Chronic). Measures of glutamate and GABA concentrations in the primary motor cortex were obtained using proton magnetic resonance spectroscopy (1H-MRS). Transcranial magnetic stimulation (TMS) was used to assess corticomotor excitability with the amplitude of the motor evoked potential (MEPamp), and intracortical inhibition through the duration of the cortical silent period (CSP). RESULTS: Glutamate (p=0.55) and GABA (p=0.73) concentrations in M1, as well as MEPamp (p=0.20) and CSP duration (p=0.47), did not differ between mTBI groups. There were no differences in these measures between ε4 carriers and non-carriers (p≥0.50) and no significant interactions between mTBI group and ε4 carrier status for any of the four measures (p≥0.07). CONCLUSION: The lack of differences in glutamate, GABA, and corticomotor excitability and inhibition across groups suggests that motor cortex function may not explain the physiology underlying differences in symptom recovery post-mTBI. While the apoε4 allele has been associated with differences in outcome following mTBI, it did not seem to affect the function of the human motor cortex in this group of participants.

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