Epilepsy after penetrating head injury. I. Clinical correlates

Salazar, Andrés M.; Jabbari, Bahman; Vance, Stephen C.; Grafman, Jordan; Amin, Dina; Dillon, J D

doi:10.1212/wnl.35.10.1406

Cited by 432 publications

(277 citation statements)

References 0 publications

Supporting

Mentioning

257

Contrasting

Unclassified

Order By: Relevance

“…Of head trauma survivors, 10 -15% develop post-traumatic epilepsy, and after penetrating injuries this number rises to 53% (Salazar et al, 1985;Salazar, 1992). Indeed, head injury is an important contributing etiology of remote symptomatic epilepsy (Annegers et al, 1980).…”

Section: Implications For Post-traumatic Epilepsymentioning

confidence: 99%

“…Hilar cells play a central role in the regulation of the input-output f unctions of the dentate gyrus (Amaral, 1978;Buzsáki et al, 1983), and the post-traumatic loss of these neurons is thought to be an important factor in the development of trauma-induced epilepsy, a disorder that affects a large percentage of head-injured patients (Annegers et al, 1980;Salazar et al, 1985). However, little is known about the precise nature of the functional defects that underlie trauma-induced hyperexcitability in the limbic system.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

et al. 1997

View full text Add to dashboard Cite

Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short-and longterm effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of traumainduced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)-and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV-and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer.These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.

show abstract

Section: Implications For Post-traumatic Epilepsymentioning

confidence: 99%

mentioning

confidence: 99%

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

et al. 1997

View full text Add to dashboard Cite

show abstract

“…This 1-4 week latent period ends with the subsequent emergence of spontaneous recurrent seizures which define epilepsy (Cavalheiro et al, 1991;Mello et al, 1993). A latent period also exists in human epilepsy, spanning months or years (Annegers et al, 1980;Salazar et al, 1985;Weiss et al, 1986). The synaptic changes during the latent period, especially with regards to inhibition, continue to be studied because they are likely fundamentally important to the development of chronic epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Disrupted Dentate Granule Cell Chloride Regulation Enhances Synaptic Excitability during Development of Temporal Lobe Epilepsy

Pathak

Weißinger²,

Terunuma³

et al. 2007

J. Neurosci.

246

254

View full text Add to dashboard Cite

GABA A receptor-mediated inhibition depends on the maintenance of intracellular ClϪ concentration ([Cl Ϫ ] in ) at low levels. In neurons in the developing CNS, [Cl Ϫ ] in is elevated, E GABA is depolarizing, and GABA consequently is excitatory. Depolarizing GABAergic synaptic responses may be recapitulated in various neuropathological conditions, including epilepsy. In the present study, rat hippocampal dentate granule cells were recorded using gramicidin perforated patch techniques at varying times (1-60 d) after an epileptogenic injury, pilocarpine-induced status epilepticus (STEP). In normal, non-epileptic animals, these strongly inhibited dentate granule cells act as a gate, regulating hippocampal excitation, controlling seizure initiation and/or propagation. For 2 weeks after STEP, we found that E GABA was positively shifted in granule cells. This shift in E GABA altered synaptic integration, increased granule cell excitability, and resulted in compromised "gate" function of the dentate gyrus. E GABA recovered to control values at longer latencies post-STEP (2-8 weeks), when animals had developed epilepsy. During this period of shifted E GABA , expression of the Cl Ϫ extruding K ϩ /Cl Ϫ cotransporter, KCC2 was decreased. Application of the KCC2 blocker, furosemide, to control neurons mimicked E GABA shifts evident in granule cells post-STEP. Furthermore, post-STEP and furosemide effects interacted occlusively, both on E GABA in granule cells, and on gatekeeper function of the dentate gyrus. This suggests a shared mechanism, reduced KCC2 function. These findings demonstrate that decreased expression of KCC2 persists for weeks after an epileptogenic injury, reducing inhibitory efficacy and enhancing dentate granule cell excitability. This pathophysiological process may constitute a significant mechanism linking injury to the subsequent development of epilepsy.

show abstract

“…In a different study, approximately twothirds of patients experienced at least one seizure within 1 year and approximately 80 percent within 2 years [3]. The incidence of PTE is highest after wartime penetrating head injuries, presumably because of their severity [4]. The Figure compares the cumulative probability from different studies of late unprovoked seizures after TBI.…”

Section: Risk Of Posttraumatic Epilepsy After Traumatic Brain Injurymentioning

confidence: 99%

“…In the Vietnam Head Injury Study, 53 percent of veterans with penetrating head injury developed at least one seizure [4]. In the Korean war, no treatment was provided to veterans, while in the Vietnam war, phenytoin (PHT) was given for 6 months to all veterans with penetrating TBI without any effort to monitor compliance.…”

Section: Risk Of Posttraumatic Epilepsy In Veterans With Traumatic Brmentioning

confidence: 99%

Posttraumatic epilepsy and treatment

Chen

Ruff

Eavey

et al. 2009

JRRD

View full text Add to dashboard Cite

Abstract-Posttraumatic epilepsy (PTE) is a major long-term complication of traumatic brain injury (TBI). PTE usually develops within 5 years of head injury. The risk for developing PTE varies with TBI type. Both Korean and Vietnam war veterans with penetrating TBI had a 53% risk of developing PTE. The risk of developing PTE is between 10% and 25% in combat-associated closed-head trauma with positive brain imaging and about 5% in moderately severe closed-head injury without imaging finding. We do not know the risk of PTE among Operation Iraqi Freedom/Operation Enduring Freedom veterans with minimal TBI because of blast exposure. Partial seizures may manifest with subtle behavioral alterations that can be mistaken for manifestations of posttraumatic stress disorder and improperly treated. Accidents and medical complications commonly occur during seizures. Sudden unexpected death in epilepsy is most frequent among 20-to 40-year-olds. Seizures increase the likelihood of refractory seizures years after TBI. Seizures are also a social stigma that compromise veterans' reintegration into society. People with uncontrolled epilepsy are not allowed to drive and have difficulty obtaining or maintaining employment. Optimal seizure control is essential to the physical and emotional health of veterans with TBI and to their ability to lead productive lives.

show abstract

Epilepsy after penetrating head injury. I. Clinical correlates

Cited by 432 publications

References 0 publications

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave-Transient Delivered to the Neocortex

Disrupted Dentate Granule Cell Chloride Regulation Enhances Synaptic Excitability during Development of Temporal Lobe Epilepsy

Posttraumatic epilepsy and treatment

Contact Info

Product

Resources

About