We conclude that most TBIs are mild and most TBIs occur in males among the adult population. The incidence of TBI varies widely by ages and between countries. Despite being an important medical, economic, and social problem, the global epidemiology of TBI is still not well-characterized in the current literature. Understanding the incidence of TBI, particularly mild TBI, remains challenging because of nonstandardized reporting among neuroepidemiological studies.

SUMMARYPurpose: Assess the validity of ICD-9-CM and ICD-10 epilepsy coding from an emergency visit (ER) and a hospital discharge abstract database (DAD). Methods: Two separate sources of patient records were reviewed and validated. (1) Charts of patients admitted to our seizure monitoring unit over 2 years (n = 127, ICD-10 coded records) were reviewed. Sensitivity (Sn), specificity (Sp), and positive and negative predictive values (PPV and NPV) were calculated. (2) Random sample of charts for patients seen in the ER or admitted to hospital under any services, and whose charts were coded with epilepsy or an epilepsy-like condition, were reviewed. Two time-periods were selected to allow validation of both ICD-9-CM (n = 486) and ICD-10 coded (n = 454) records. Only PPV and NPV were calculated for these records. All charts were reviewed by two physicians to confirm the presence/ absence of epilepsy and compare to administrative coding. Results: Sample 1: Sn, Sp, PPV, and NPV of ICD-10 epilepsy coding from the seizure monitoring unit (SMU) chart review were 99%, 70%, 85%, and 97% respectively. Sample 2: The PPV and NPV for ICD-9-CM coding from the ER database were, respectively, 99% and 97% and from the DAD were 98% and 99%. The PPV and NPV for ICD-10 coding from the ER database were, respectively, 100% and 90% and from the DAD were 98% and 99%. The epilepsy subtypes grand mal status and partial epilepsy with complex partial seizures both had PPVs >75% (ICD-9-CM and ICD-10 data). Discussion: Administrative emergency and hospital discharge data have high epilepsy coding validity overall in our health region.

Peripheral inflammatory diseases are often associated with behavioral comorbidities including anxiety, depression, and cognitive dysfunction, but the mechanism for these is not well understood. Changes in the neuronal and synaptic functions associated with neuroinflammation may underlie these behavioral abnormalities. We have used a model of colonic inflammation induced by 2,4,6-trinitrobenzenesulfonic acid in Sprague Dawley rats to identify inflammation-induced changes in hippocampal synaptic transmission. Hippocampal slices obtained 4 d after the induction of inflammation revealed enhanced Schaffer collateral-induced excitatory field potentials in CA1 stratum radiatum. This was associated with larger-amplitude mEPSCs, but unchanged mEPSC frequencies and pairedpulse ratios, suggesting altered postsynaptic effects. Both AMPA-and NMDA-mediated synaptic currents were enhanced, and analysis of AMPA-mediated currents revealed increased contributions of GluR2-lacking receptors. In keeping with this, both transcripts and protein levels of the GluR2 subunit were reduced in hippocampus. Both long-term potentiation (LTP) and depression (LTD) were significantly reduced in hippocampal slices taken from inflamed animals. Chronic administration of the microglial/macrophage activation inhibitor minocycline to the inflamed animals both lowered the level of the cytokine tumor necrosis factor ␣ in the hippocampus and completely abolished the effect of peripheral inflammation on the field potentials and synaptic plasticity (LTP and LTD). Our results reveal profound synaptic changes caused by a mirror microglia-mediated inflammatory response in hippocampus during peripheral organ inflammation. These synaptic changes may underlie the behavioral comorbidities seen in patients.

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Summary Objective To investigate possible electroencephalography (EEG) correlates of epileptogenesis after traumatic brain injury (TBI) using the fluid percussion model. Methods Experiments were conducted on adult 2- to 4-month-old male Sprague-Dawley rats. Two groups of animals were studied: (1) the TBI group with depth and screw electrodes implanted immediately after the fluid percussion injury (FPI) procedure, and (2) a naive age-matched control group with the same electrode implantation montage. Pairs of tungsten microelectrodes (50 µm outer diameter) and screw electrodes were implanted in neocortex inside the TBI core, areas adjacent to TBI, and remote areas. EEG activity, recorded on the day of FPI, and continuously for 2 weeks, was analyzed for possible electrographic biomarkers of epileptogenesis. Video-EEG monitoring was also performed continuously in the TBI group to capture electrographic and behavioral seizures until the caps came off (28–189 days), and for 1 week, at 2, 3, and 6 months of age, in the control group. Results Pathologic high-frequency oscillations (pHFOs) with a central frequency between 100 and 600 Hz, were recorded from microelectrodes, beginning during the first two post-FPI weeks, in 7 of 12 animals in the TBI group (58%) and never in the controls. pHFOs only occurred in cortical areas within or adjacent to the TBI core. These were associated with synchronous multiunit discharges and popSpikes, duration 15–40 msec. Repetitive pHFOs and EEG spikes (rHFOSs) formed paroxysmal activity, with a unique arcuate pattern, in the frequency band 10–16 Hz in the same areas as isolated pHFOs, and these events were also recorded by screw electrodes. Although loss of caps prevented long-term recordings from all rats, pHFOs and rHFOSs occurred during the first 2 weeks in all four animals that later developed seizures, and none of the rats without these events developed late seizures. Significance pHFOs, similar to those associated with epileptogenesis in the status rat model of epilepsy, may also reflect epileptogenesis after FPI. rHFOSs could be noninvasive biomarkers of epileptogenesis.