Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Vespa, Paul; Miller, Chad M.; McArthur, David L.; Eliseo, Mathew; Etchepare, Maria; Hirt, Daniel; Glenn, Thomas C.; Martin, Neil A.; Hovda, David A.

doi:10.1097/00003246-200712000-00023

Cited by 154 publications

(114 citation statements)

References 20 publications

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“…Our observation of localized paroxysmal delta activity immediately following FPI in most rats is in agreement with data from posttraumatic patients. [34][35][36][37] This likely reflects nonspecific changes in the extracellular ionic and neurochemical milieu, leading to a transient suppression of synaptic activity and neuronal discharges 3,35,38 ; with no effect on subsequent epileptogenic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Pathologic electrographic changes after experimental traumatic brain injury

et al. 2016

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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.

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Section: Discussionmentioning

confidence: 99%

Pathologic electrographic changes after experimental traumatic brain injury

et al. 2016

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“…Existing evidence suggests that EPTS may reflect the severity of injury as well as contribute to secondary injury, with the potential to worsen long-term outcomes (Barlow et al, 2000;Keenan et al, 2007;Vespa et al, 2007aVespa et al, , 2010 and increase the risk for subsequent development of posttraumatic epilepsy (PTE) (Annegers & Coan, 2000). However, it has been shown that antiepileptic drugs (AEDs) do not prevent late PTE and are not without their own risk, particularly on the developing brain (Temkin et al, 1990;Bittigau et al, 1999;Olney et al, 2004;Young et al, 2004;Kaindl et al, 2006).…”

Section: Risk-benefit Of Prophylaxis For Pediatric Eptsmentioning

confidence: 99%

Subclinical early posttraumatic seizures detected by continuous EEG monitoring in a consecutive pediatric cohort

et al. 2013

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Summary Purpose Traumatic brain injury (TBI) is an important cause of morbidity and mortality in children and early post-traumatic seizures (EPTS) are a contributing factor to ongoing acute damage. Continuous video EEG monitoring (cEEG) was utilized to assess the burden of clinical and electrographic EPTS. Methods Eighty-seven consecutive, unselected (mild – severe), acute TBI patients requiring pediatric intensive care unit (PICU) admission at 2 academic centers were prospectively monitored with cEEG per established clinical TBI protocols. Clinical and subclinical seizures and status epilepticus (SE, clinical and subclinical) were assessed for their relation to clinical risk factors and short-term outcome measures. Key findings Of all patients, 42.5% (37/87) had seizures. Younger age (p=0.002) and mechanism (abusive head trauma - AHT, p<0.001) were significant risk factors. Subclinical seizures occurred in 16.1% (14/87), 6 of whom had only subclinical seizures. Risk factors for subclinical seizures included: younger age (p<0.001), AHT (p<0.001) and intraaxial bleed (p<0.001). Status Epilepticus (SE) occurred in 18.4% (16/87) with risk factors including: younger age (p<0.001), AHT (p<0.001), and intraaxial bleed (p=0.002). Subclinical SE was detected in 13.8% (12/87) with significant risk factors including: younger age (p<0.001), AHT (p=0.001), and intraaxial bleed (p=0.004). Subclinical seizures were associated with lower discharge KOSCHI score (p=0.002). SE and subclinical SE were associated with increased hospital length of stay (p=0.017 and p=0.041 respectively) and lower hospital discharge KOSCHI (p=0.007 and p=0.040 respectively). Significance cEEG monitoring significantly improves detection of seizures/SE and is the only way to detect subclinical seizures/SE. cEEG may be indicated after pediatric TBI, particularly in younger children, AHT cases, and those with intraaxial blood on CT.

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“…The rationale for continuous, multiday monitoring is primarily the evaluation of subclinical seizures as a possible etiology for altered mental status or coma, as well as belief that suppression of all early seizures, whether convulsive or nonconvulsive, may improve outcomes. 30,31 Seizures and spreading depolarizations often occur with interacting patterns in the same tissue, and depolarizations may enhance epileptic activity by suppression of inhibitory neurotransmission. [32][33][34] However, compared to seizures, spreading depolarizations have a 3-to 7-fold higher incidence in patients.…”

Section: Clinical Use Of Continuous Eegmentioning

confidence: 99%

Spreading depression in continuous electroencephalography of brain trauma

Hartings

Wilson

Hinzman

et al. 2014

Annals of Neurology

114

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Leão's spreading depression can be observed in clinically standard, continuous scalp EEG, and underlying depolarizations can spread widely across the injured cerebral hemisphere. These results open the possibility of monitoring noninvasively a neuronal pathophysiological mechanism in a wide range of disorders including ischemic stroke, subarachnoid hemorrhage, and brain trauma, and suggest a novel application for continuous EEG.

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Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Cited by 154 publications

References 20 publications

Pathologic electrographic changes after experimental traumatic brain injury

Pathologic electrographic changes after experimental traumatic brain injury

Subclinical early posttraumatic seizures detected by continuous EEG monitoring in a consecutive pediatric cohort

Spreading depression in continuous electroencephalography of brain trauma

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