OBJECTIVE: To demonstrate the utility of Magnetoencephalography (MEG) in characterizing complex clinical presentation in patients with comorbid TBI and PTSD. BACKGROUND: Service members (SMs) with combat-related mild Traumatic Brain Injury (mTBI) and Posttraumatic Stress Disorder (PTSD) exhibit complex cognitive deficits to include language, memory, and attention impairment. While MEG has been effective in localizing electrophysiological disturbances associated with functional task, MEG patterns from brain injury identified by Speech-Language Pathology (SLP) testing have not been well described in combination with PTSD. DESIGN/METHODS: Results from SLP testing and MEG were compared in two SMs diagnosed with TBI and PTSD, one with and one without speech-language disturbances. Boston Naming Test and Rivermead Behavioral Memory Test were administered to assess cognition. MEG data were recorded while 80 common pictures (e.g. car, house) were presented. Patients were instructed to silently name pictures and then overtly name the pictures during the inter-trial Interval. Brain generators associated with peak activity in Wernicke’s and Broca’s areas were estimated using Dynamic Statistical Parametric Mapping. RESULTS: For the Boston Naming Test, patient 1 scored 6.1 below the mean for his age group and was classified as impaired. Patient 2 scored 3.2 above the mean for his age group and was classified as normal. For the RBMT-3 (average score = 100), patient 1 scored 81 while patient 2 scored 97. MEG results revealed that patient 1 had lower signal amplitude (normalized power 1.52 s.d. above baseline) and slower signal conduction (peak latency of 522 ms in Broca’s area) compared to patient 2 (normalized power 5.05 s.d. above the baseline and peak latency of 430 ms in Broca’s area). CONCLUSIONS: Suppression of activity and delay of peak onset in Broca’s area supports a TBI-related etiology, that includes axonal injury, not overtly confounded by PTSD. Results from this study demonstrate that MEG may be able to assist with the assessment of speech and language disorders in patients with comorbid disease. Disclosure: Dr. DeGraba has nothing to disclose. Dr. Merrifield has nothing to disclose. Dr. Mattingly has nothing to disclose. Dr. Mikola has nothing to disclose. Dr. Popescu has nothing to disclose. Dr. Popescu has nothing to disclose. Dr. Balbir has nothing to disclose. Dr. Balkin has nothing to disclose. Dr. Bleiberg has nothing to disclose. Dr. DeGraba has nothing to disclose.

Traumatic brain injury (TBI) causes severe disruption of cerebral electrical activity and electroencephalography (EEG) is emerging as a standard tool to monitor TBI patients in the acute period of risk for secondary injuries. However, animal studies of EEG pathology in the context of TBI are surprisingly sparse, largely because of the lack of real-time continuous EEG (cEEG) monitoring in animal TBI models. Here, we performed long-term EEG monitoring to study nonconvulsive seizures (NCS), periodic epileptiform discharges (PED), and EEG power spectra following three injury severity levels in a rat model of penetrating ballistic-like brain injury (PBBI). EEG signals were recorded continuously from bilateral hemispheres of freely behaving rats for 72 h and for 2 h on days 7 and 14 after the injury. We report that the incidence of NCS and PED positively correlated with the injury severity, where 13%, 39%, and 59% of the animals exhibited NCS, and 0%, 30%, and 65% of the animals exhibited PED following 5%, 10% and 12.5% PBBI, respectively. Similar correlations existed for the number of NCS and PED events and their duration. NCS and PED occurred either independently or in tandem. Longer NCS durations were associated with larger lesion volumes. Significant EEG slowing evidenced by the EEG power shift toward the δ frequency band (0.5-4 Hz) occurred within 2 h after PBBI, which resolved over time but persisted longer after greater injury severity. In contrast, decreases in higher frequency power (i.e., 30-35 Hz) remained depressed throughout 14 days. This is the first long-term cEEG study of the acute injury phase in a rat model of severe TBI, demonstrating common occurrences of clinically observed electrocortical pathology, such as NCS, PED, and cortical slowing. These EEG pathologies may serve as critical care biomarkers of brain injury, and offer clinically relevant metrics for studying acute therapeutic interventions.