Monitoring the Impact of Traumatic Brain Injury: A Review and Update

Waxweiler, Richard J.; Thurman, David J.; Sniezek, Joseph E.; Sosin, Daniel M.; O'Neil, J.

doi:10.1089/neu.1995.12.509

Cited by 104 publications

(48 citation statements)

References 11 publications

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“…Introduction P ost-traumatic epilepsy (PTE), cognitive impairment, and dementia are long-term medically intractable complications of TBI (Sosin et al, 1996;Waxweiler et al, 1995). More than 20% of adults have a spontaneous seizure within 2 years of TBI associated with intracranial hematoma, depressed skull fracture, cortical contusion, or penetration of the brain (Weiss et al, 1983).…”

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confidence: 99%

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Chrzaszcz

Venkatesan

Dragisic

et al. 2010

Journal of Neurotrauma

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The mechanisms linking traumatic brain injury (TBI) to post-traumatic epilepsy (PTE) are not known and no therapy for prevention of PTE is available. We used a mouse closed-skull midline impact model to test the hypotheses that TBI increases susceptibility to seizures in a ''two-hit'' injury model, and that suppression of cytokine upregulation after the first hit will attenuate the increased susceptibility to the second neurological insult. Adult male CD-1 mice underwent midline closed skull pneumatic impact. At 3 and 6 h after impact or sham procedure, the mice were injected IP with either Minozac (Mzc), a suppressor of proinflammatory cytokine upregulation, or vehicle (saline). On day 7 after sham operation or TBI, seizures were induced using electroconvulsive shock (ECS), and susceptibility to seizures was measured by the current required for seizure induction. Activation of glia, neuronal injury, and metallothionein-immunoreactive cells were quantified in the hippocampus by immunohistochemical methods. Neurobehavioral function over 14-day recovery was quantified using the Barnes maze. Following TBI there was a significant increase in susceptibility to seizures induced by ECS, and this susceptibility was prevented by suppression of cytokine upregulation with Mzc. Astrocyte activation, metallothionein expression, and neurobehavioral impairment were also increased in the two-hit group subjected to combined TBI and ECS. These enhanced responses in the two-hit group were also prevented by suppression of proinflammatory cytokine upregulation with Mzc. These data implicate glial activation in the mechanisms of epileptogenesis after TBI, and identify a potential therapeutic approach to attenuate the delayed neurological sequelae of TBI.

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confidence: 99%

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Chrzaszcz

Venkatesan

Dragisic

et al. 2010

Journal of Neurotrauma

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“…H ead trauma is a leading cause of mortality and morbidity among young people in the western world (1). Traumatic and ischemic brain injury triggers a large, transient increase in excitatory amino acid transmitter efflux in the brain of experimental animals and human subjects (2)(3)(4)(5)(6).…”

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confidence: 99%

Dynamic changes in N -methyl- d -aspartate receptors after closed head injury in mice: Implications for treatment of neurological and cognitive deficits

Biegon

Fry

Paden

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

220

164

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Traumatic brain injury is a leading cause of mortality and morbidity among young people. For the last couple of decades, it was believed that excess stimulation of brain receptors for the excitatory neurotransmitter glutamate was a major cause of delayed neuronal death after head injury, and several major clinical trials in severely head injured patients used blockers of the glutamate N-methyl-D-aspartate (NMDA) receptor. All of these trials failed to show efficacy. Using a mouse model of traumatic brain injury and quantitative autoradiography of the activity-dependent NMDA receptor antagonist MK801, we show that hyperactivation of glutamate NMDA receptors after injury is short-lived (<1 h) and is followed by a profound and long-lasting (>7 days) loss of function. Furthermore, stimulation of NMDA receptors by NMDA 24 and 48 h postinjury produced a significant attenuation of neurological deficits (blocked by coadministration of MK801) and restored cognitive performance 14 days postinjury. These results provide the underlying mechanism for the well known but heretofore unexplained short therapeutic window of glutamate antagonists after brain injury and support a pharmacological intervention with a relatively long (>24 h) time window easily attainable for treatment of human accidental head injury.H ead trauma is a leading cause of mortality and morbidity among young people in the western world (1). Traumatic and ischemic brain injury triggers a large, transient increase in excitatory amino acid transmitter efflux in the brain of experimental animals and human subjects (2-6). Glutamate activation of the N-methyl-D-aspartate (NMDA) receptor (NMDAR), which is a ligand-gated ion (calcium and sodium) channel, results in channel opening and ion influx into the cell. It has been suggested that this process mediates delayed excitotoxic neuronal death after brain ischemia and trauma (7,8), although the concept is not universally accepted (9, 10). Support for the involvement of NMDAR activation in neuronal death after brain injury has come from numerous studies showing that NMDAR antagonists reduce cell death and improve outcome in animal models of traumatic brain injury (TBI) and stroke. NMDAR antagonists appear to be most efficacious when given before or immediately after the insult and lose efficacy if administered Ͼ30-60 min postinjury (11)(12)(13)(14)(15).Microdialysis studies of extracellular glutamate in human TBI and stroke patients suggested that the increase in glutamate in humans is more sustained [6 h to several days (7, 8)] than in rodents, where it only lasts minutes (2-6). This result may have contributed to a decision to administer NMDAR antagonists in clinical trials of head injury for several days rather than once after severe nonpenetrating injury. All clinical trials of NMDAR antagonists to date failed to show efficacy. Furthermore, some of these trials had to be stopped prematurely because of increases in mortality and morbidity in the drug arm of the stroke trials (16-18), suggesting that prolonged bloc...

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“…3 Few studies have specifically analyzed the presentation of TBI to emergency departments (EDs). Most have relied on hospital admission data, 4 although one study conducted in Minnesota included ED visits and outpatient examinations involving residents in a single county. 5 Diamond reviewed data from the Virginia Brain Injury Central Registry for 1988-1993, which included ED visits, and found the incidence highest for children less than 6 (237 per 100,000) and lowest for ages 40-69 (56 per 100,000).…”

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confidence: 99%

Traumatic Brain Injuries Evaluated in U.S. Emergency Departments, 1992‐1994

Jager

Weiss

Coben

et al. 2000

Academic Emergency Medicine

292

169

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Abstract. Objective: To describe the incidence and patient characteristics of traumatic brain injuries (TBIs) treated in U.S. emergency departments (EDs). Methods: A secondary analysis was performed on data from the National Hospital Ambulatory Medical Care Survey administered from 1992 to 1994. An ED visit was determined to represent a case of TBI if the case record contained ICD-9-CM codes of 800.0-801.9, 803.0-804.9, or 850.0-854.1. Results: The average annual estimate of new TBI treated in U.S. EDs was 1,144,807, equaling 444 per 100,000 persons (95% CI = 390 to 498), which represents approximately 3,136 new cases of TBI per day and accounts for 1.3% of all ED visits. Males were 1.6 times as likely as females to suffer TBI until the age of 65 years, when the female rate exceeded the male. The rate for blacks was 35% higher than that for whites.

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Monitoring the Impact of Traumatic Brain Injury: A Review and Update

Cited by 104 publications

References 11 publications

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Dynamic changes in N -methyl- d -aspartate receptors after closed head injury in mice: Implications for treatment of neurological and cognitive deficits

Traumatic Brain Injuries Evaluated in U.S. Emergency Departments, 1992‐1994

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