Literature DB >> 27012461

Pathologic electrographic changes after experimental traumatic brain injury.

Anatol Bragin1,2, Lin Li1, Joyel Almajano1, Catalina Alvarado-Rojas1, Aylin Y Reid1, Richard J Staba1, Jerome Engel1,2,3,4.   

Abstract

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. Wiley Periodicals, Inc.
© 2016 International League Against Epilepsy.

Entities:  

Keywords:  Electroencephalography; Epileptogenesis; Pathologic high frequency oscillations; Repetitive HFOs and spikes; Seizure; Spindles; Traumatic brain injury

Mesh:

Year:  2016        PMID: 27012461      PMCID: PMC5081251          DOI: 10.1111/epi.13359

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  37 in total

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2.  How and Why Study Posttraumatic Epileptogenesis in Animal Models?

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3.  Theta is the New Alpha.

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4.  Harmonization of the pipeline for seizure detection to phenotype post-traumatic epilepsy in a preclinical multicenter study on post-traumatic epileptogenesis.

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6.  Acute Non-Convulsive Status Epilepticus after Experimental Traumatic Brain Injury in Rats.

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Review 7.  Update on the mechanisms and roles of high-frequency oscillations in seizures and epileptic disorders.

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9.  Cortical Neuromodulation of Remote Regions after Experimental Traumatic Brain Injury Normalizes Forelimb Function but is Temporally Dependent.

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Review 10.  Converging early responses to brain injury pave the road to epileptogenesis.

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Journal:  J Neurosci Res       Date:  2017-11-29       Impact factor: 4.164

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