The Pathology of Post‐Traumatic Epilepsies

Payan, H; Toga, M; Berard-Badier, M

doi:10.1111/j.1528-1157.1970.tb03869.x

Cited by 68 publications

(19 citation statements)

References 2 publications

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“…Iron is liberated from hemoglobin and transferrin. Hemosiderin is deposited within the brains of patients with posttraumatic epilepsy [22]. Iron is critical to biological functions, but the two stable oxidation states and the redox properties of iron pose a biological hazard.…”

Section: Hemorrhage and Brain Injury Responsesmentioning

confidence: 99%

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Willmore

Ueda

2008

Neurochem Res

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Traumatic brain injury causes development of posttraumatic epilepsy. Bleeding within neuropil is followed by hemolysis and deposition of hemoglobin in neocortex. Iron from hemoglobin and transferring is deposited in brains of patients with posttraumatic epilepsy. Iron compounds form reactive free radical oxidants. Microinjection of ferric ions into rodent brain results in chronic recurrent seizures and liberation of glutamate into the neuropil, as is observed in humans with epilepsy. Termination of synaptic effects of glutamate is by removal via transporter proteins. EAAC-1 is within neurons while GLT-1 and GLAST are confined to glia. Persistent down regulation of GLAST production is present in hippocampal regions in chronic seizure models. Down regulation of GLAST may be fundamental to a sequence of free radical reactions initiated by brain injury with hemorrhage. Administration of antioxidants to animals causes interruption of the sequence of brain injury responses induced by hemorrhage, suggesting that such a strategy needs to be evaluated in patients with traumatic brain injury.

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Section: Hemorrhage and Brain Injury Responsesmentioning

confidence: 99%

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Willmore

Ueda

2008

Neurochem Res

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“…Altered cerebral vasomotor regulation leading to blood flow disturbances, intracranial pressure changes, and altered vascular permeability can potentially contribute to by increasing extracellular calcium, glutamate, and reactive oxygen species formation. Iron from hemoglobin and transferrin accumulates in the brain as hemosiderin enhances the formation of toxic free radicals (40, 42, 43). Disrupted fiber tracts results in anterograde transynaptic neuronal degeneration with the loss of inhibitory interneurons thus lower seizure threshold.…”

Section: Seizures and Epilepsy Following Traumatic Brain Injurymentioning

confidence: 99%

Blast TBI Models, Neuropathology, and Implications for Seizure Risk

2014

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Traumatic brain injury (TBI) due to explosive blast exposure is a leading combat casualty. It is also implicated as a key contributor to war related mental health diseases. A clinically important consequence of all types of TBI is a high risk for development of seizures and epilepsy. Seizures have been reported in patients who have suffered blast injuries in the Global War on Terror but the exact prevalence is unknown. The occurrence of seizures supports the contention that explosive blast leads to both cellular and structural brain pathology. Unfortunately, the exact mechanism by which explosions cause brain injury is unclear, which complicates development of meaningful therapies and mitigation strategies. To help improve understanding, detailed neuropathological analysis is needed. For this, histopathological techniques are extremely valuable and indispensable. In the following we will review the pathological results, including those from immunohistochemical and special staining approaches, from recent preclinical explosive blast studies.

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“…One hypothesis states that in the immediate peri-injury period, brain swelling, cerebral ischemia and the release of excitatory amino acids and other toxins precipitate neuronal damage (Agrawal et al 2006; Brodersen and Gjerris 1975). Comparatively, in the late post injury period, an excess of extracorpuscular hemoglobin facilitates the creation of cytotoxic hydroxyls, reactive oxygen species moieties and glutamate accumulation (Payan et al 1970). These compounds collectively promote neuronal damage propagating the creation of an epileptogenic nidus, and occasionally leading to status epilepticus (Willmore et al 1978; Rubin and Willmore 1980; Shaver et al 1996; Sahuquillo-Barris et al 1988; Becker 1986).…”

Section: Introductionmentioning

confidence: 99%

The epidemiology, risk factors, and impact on hospital mortality of status epilepticus after subdural hematoma in the United States

et al. 2014

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IntroductionSubdural hematoma (SDH) is a well described risk factor in the development of Status Epilepticus (SE), however the epidemiology of SE after SDH is unknown. In this study, we sought to determine the epidemiology of SE, the prevalence of risk factors, and impact on hospital mortality using a large administrative dataset.MethodsData was derived from the Nationwide Inpatient Sample from 1988 through 2011. We queried the NIS database for patients older than 18 years, with a diagnosis of SDH and SE. Diagnoses were defined by ICD 9 CM codes 432.1, 852.2, 852.3 and 345.3 for SE. Adjusted incidence rates of admission and prevalence proportions were calculated. Multivariate logistic models were then fitted to assess for the impact of status epilepticus on hospital mortality.ResultsOver the 23-year period, we identified more than 1,583,255 admissions with a diagnosis of SDH. The prevalence of SE in this cohort was 0.5% (7,421 admissions). The population adjusted incidence rate of admissions of SDH increased from 13/100,000 in 1988 to 38/100,000 in 2011. The prevalence of SE in SDH, increased from 0.5% in 1988 to 0.7% in 2011. In hospital mortality of patients with SDH and without SE decreased from 17.9% to 10.3% while in hospital mortality of patients with SDH and SE did not statistically change. Mortality increased over the same period (2.3/100,000 in 1988 to 3.9/100.000 in 2011) and the diagnosis of SE increased mortality in this cohort (OR 2.17, p < 0.0001). The risk of SE remained stable throughout the study period, but was higher among older patients, blacks, and in those with respiratory, metabolic, hematological, and renal system dysfunction.ConclusionOur study demonstrates that the incidence of admissions of SDH is increasing in the United States. Despite a decline in the overall SDH related mortality, SE increased the risk of in-hospital death in patients with a primary diagnosis of SDH.

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The Pathology of Post‐Traumatic Epilepsies

Cited by 68 publications

References 2 publications

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Blast TBI Models, Neuropathology, and Implications for Seizure Risk

The epidemiology, risk factors, and impact on hospital mortality of status epilepticus after subdural hematoma in the United States

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