Traumatic brain injury (TBI) represents a significant global health burden and has the highest prevalence among neurological disorders. Even mild TBI can induce subtle, long-lasting changes that increase the risk of future neurodegeneration. Importantly, this can be challenging to detect through conventional neurological assessment. This underscores the need for more sensitive diagnostic tools, such as electroencephalography (EEG), to uncover opportunities for therapeutic intervention. Progress in the field has been hindered by a lack of studies linking mechanistic insights at the microscopic level from animal models to the macroscale phenotypes observed in clinical imaging. Our study addresses this gap by investigating a rat model of mild blast TBI using both immunohistochemical staining of inhibitory interneurons and translationally relevant EEG recordings. Although we observed no pronounced effects immediately post-injury, chronic timepoints revealed broadband hyperexcitability and increased connectivity, accompanied by decreased density of inhibitory interneurons. This pattern suggests a disruption in the balance between excitation and inhibition, providing a crucial link between cellular mechanisms and clinical hallmarks of injury. Our findings have significant implications for the diagnosis, monitoring, and treatment of TBI. The emergence of EEG abnormalities at chronic timepoints, despite the absence of immediate effects, highlights the importance of long-term monitoring in TBI patients. The observed decrease in inhibitory interneuron density offers a potential cellular mechanism underlying the EEG changes and may represent a target for therapeutic intervention. This study demonstrates the value of combining cellular-level analysis with macroscale neurophysiological recordings in animal models to elucidate the pathophysiology of TBI. Future research should focus on translating these findings to human studies and exploring potential therapeutic strategies targeting the excitation-inhibition imbalance in TBI.