Electroencephalographic Changes in Patients with Blast-Induced Concussion

Abstract

Purpose: Blast-induced concussion is classified as a mild traumatic brain injury (mTBI). It may elevated risk of developing epileptic seizures. The aim is to investigate electroencephalography (EEG) changes in patients in the chronic stage of blast-associated mTBI and to assess the potential of using EEG data for objective confirmation of brain injury. Method: The study included 32 male combatants aged 25–43 years with a diagnosis of “mTBI, chronic stage” (6 months to 3 years post-injury), and a control group of 15 healthy males. EEG was recorded in a soundproof room using a 19-channel NeuroCom EEG system (Ukraine) with a sampling rate of 400 Hz and 16-bit resolution. Electrodes were applied according to the international 10–20 system. EEG recordings were conducted during resting wakefulness for up to 30 minutes, including activation procedures: eye opening/closing, intermittent photic stimulation, and 3 minutes of hyperventilation. Both visual and spectral EEG analyses were performed. Spectral analysis was conducted on artifact-free, stationary segments (35–45 seconds) of resting-state EEG. Spectral analysis was conducted on artifact-free, stationary segments (35–45 seconds) of resting-state EEG. Results: Compared to controls, the mTBI group demonstrated decreased relative power in the alpha band and increased power in the beta, theta, and delta bands, predominantly in frontal and temporal regions. Visual analysis revealed frontal intermittent rhythmic delta activity (FIRDA) in 37.5% of cases, mild background slowing on the side of trauma in 87.5%, anterior temporal and frontal spikes in 21.9%, occipital spikes in 15.6%, and generalized spike-wave discharges in 6.3%. Conclusion: The EEG alterations identified in patients with chronic blast-induced mTBI suggest a general decrease in cortical functional activity. The presence of intermittent slow-wave activity in frontotemporal regions may reflect disruption in prefrontal-subcortical connectivity due to microscopic white matter damage. These findings may represent early electrophysiological markers of increased neuronal excitability and epileptogenesis.