Improved understanding of the interaction between state of vigilance (SOV) and seizure onset has therapeutic potential. Six rats received injections of tetanus toxin (TeTX) in the ventral hippocampus that resulted in chronic spontaneous seizures. The distribution of SOV before 486 seizures was analyzed for a total of 19 d of recording. Rapid eye movement sleep (REM) and exploratory wake, both of which express prominent hippocampal theta rhythm, preceded 47 and 34%, for a total of 81%, of all seizures. Nonrapid eye movement sleep (NREM) and nonexploratory wake, neither of which expresses prominent theta, preceded 6.8 and 13% of seizures. We demonstrate that identification of SOV yields significant differentiation of seizure susceptibilities, with the instantaneous seizure rate during REM nearly 10 times higher than baseline and the rate for NREM less than half of baseline. Survival analysis indicated a shorter duration of preseizure REM bouts, with a maximum transition to seizure at ϳ90 s after the onset of REM. This study provides the first analysis of a correlation between SOV and seizure onset in the TeTX model of temporal lobe epilepsy, as well as the first demonstration that hippocampal theta rhythms associated with natural behavioral states can serve a seizure-promoting role. Our findings are in contrast with previous studies suggesting that the correlations between SOV and seizures are primarily governed by circadian oscillations and the notion that hippocampal theta rhythms inhibit seizures. The documentation of significant SOV-dependent seizure susceptibilities indicates the potential utility of SOV and its time course in seizure prediction and control.

Design: Retrospective chart review using Mayo's Advanced Cohort Explorer (ACE) program. Setting: Tertiary care hospital. Participants: 120 subjects ages 18-60 with a history of depression who then went on to sustain a concussion were included in the study. 60 were on pharmacologic treatment of depression at the time of concussion and 60 were not on pharmacologic depression treatment at the time of concussion. Exclusion criteria included prior concussion, history of migraine, or intracranial bleed at time of head injury. Interventions: Not applicable. Main Outcome Measures: Number of clinician visits (physician, neuropsychologist, therapist) for post-concussion symptoms (symptoms not present prior to concussion) were counted via review of medical record and recorded at 3, 6, and 12 months. Results: In treated group, mean number of clinician visits for postconcussion symptoms was 1.91.5 at 3 months, 2.43.4 at 6 months, and 2.85.3 at 12 months. In untreated group, mean number of visits was 6.13.8 at 3 months, 10.811.3 at 6 months, and 15.818.8 at 12 months. The treated group had statistically significant (P<.001) fewer visits than the untreated group at 3, 6, and 12 months. Conclusions: In patients that have a history of depression and then sustain a concussion, pharmacologic treatment of depression at the time of concussion results in a significantly fewer clinician visits for post-concussion symptoms compared to depressed patients not pharmacologically treated for their depression at the time of sustaining a concussion. Furthermore, fewer clinician visits represents a decrease in healthcare utilization. A prospective study would be the next step to confirm this association and investigate role of starting pharmacologic treatment after concussion.