Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

Messori, Anna; Polonara, Gabriele; Carle, Flavia; Gesuita, Rosaria; Salvolini, U.

doi:10.1111/j.1528-1167.2005.34004.x

Cited by 49 publications

(27 citation statements)

References 43 publications

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“…Epilepsy is a relatively common complication of traumatic brain injury and may affect as many as 15-53% of patients after severe head injury, dependent on the severity of the hematoma (Annegers et al, 1998;Frey, 2003;Messori et al, 2005). Extravasation of red blood cells results in accumulation of heme and ferric/ ferrous compounds and production of reactive oxygen species within the brain parenchyma and increases the risk for development of posttraumatic epilepsy (Willmore et al, 1978(Willmore et al, , 1983Graham and Lantos, 1997;Annegers et al, 1998;Frey, 2003;Messori et al, 2005).…”

Section: Reactive Astrocytes In An Experimental Model Of Posttraumatimentioning

confidence: 99%

“…Extravasation of red blood cells results in accumulation of heme and ferric/ ferrous compounds and production of reactive oxygen species within the brain parenchyma and increases the risk for development of posttraumatic epilepsy (Willmore et al, 1978(Willmore et al, , 1983Graham and Lantos, 1997;Annegers et al, 1998;Frey, 2003;Messori et al, 2005). Intracortical injection of ferrous chloride recapitulates several key features of posttraumatic epilepsy, including physical injury and accumulation of ferric/ferrous compounds in the brain parenchyma (Willmore et al, 1978), and is associated with a high incidence of generalized recurrent seizures in rats, guinea pigs, cats, and Macaca mulatta monkeys (Willmore et al, 1978;Hammond et al, 1980;Lange et al, 1980;Reid and Sypert, 1980).…”

Section: Reactive Astrocytes In An Experimental Model Of Posttraumatimentioning

confidence: 99%

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Loss of Astrocytic Domain Organization in the Epileptic Brain

et al. 2008

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Gliosis is a pathological hallmark of posttraumatic epileptic foci, but little is known about these reactive astrocytes beyond their high glial fibrillary acidic protein (GFAP) expression. Using diolistic labeling, we show that cortical astrocytes lost their nonoverlapping domain organization in three mouse models of epilepsy: posttraumatic injury, genetic susceptibility, and systemic kainate exposure. Neighboring astrocytes in epileptic mice showed a 10-fold increase in overlap of processes. Concurrently, spine density was increased on dendrites of excitatory neurons. Suppression of seizures by the common antiepileptic, valproate, reduced the overlap of astrocytic processes. Astrocytic domain organization was also preserved in APP transgenic mice expressing a mutant variant of human amyloid precursor protein despite a marked upregulation of GFAP. Our data suggest that loss of astrocytic domains was not universally associated with gliosis, but restricted to seizure pathologies. Reorganization of astrocytes may, in concert with dendritic sprouting and new synapse formation, form the structural basis for recurrent excitation in the epileptic brain.

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Section: Reactive Astrocytes In An Experimental Model Of Posttraumatimentioning

confidence: 99%

Section: Reactive Astrocytes In An Experimental Model Of Posttraumatimentioning

confidence: 99%

Loss of Astrocytic Domain Organization in the Epileptic Brain

et al. 2008

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“…In some forms of trauma, a resulting hematoma can play a key role in posttraumatic epilepsy (D'Ambrosio et al 2004;Messori et al 2005). This is confirmed by the fact that injection of iron salts produces electrographic and behavioral seizures (Willmore et al 1978).…”

Section: Current Experimental Models Of Trauma-induced Epileptogenesimentioning

confidence: 91%

Injury Induced Epileptogenesis: Contribution of Active Inhibition, Disfacilitation and Deafferentation to Seizure Induction in Thalamocortical System

Timofeev

2010

Inhibitory Synaptic Plasticity

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Neocortical seizures are the seizures in which neocortex is the leading structure. They are characterized by spike-wave (SW) or spike-wave/polyspikewave (SW/PSW) complexes of 1.5-3 Hz, intermingled with episodes of fast runs at ~10-20 Hz. These seizures often develop during slow-wave sleep, transition from wake to slow-wave sleep or transition from slow-wave sleep to waking state. Intracellular studies on both anesthetized and non-anesthetized cats have shown that hyperpolarizing phase of the slow oscillation, a distinct feature of slow-wave sleep, is associated with disfacilitation, a temporal absence of synaptic activity in all cortical neurons. Periods of disfacilitation temporally increase network excitability. The hyperpolarizing components of SW-PSW complexes are mediated mainly by leak current (state similar to discfacilitation), Ca 2+ -and Na + -activated K + currents. It is proposed that prolonged periods of disfacilitation up-regulate neuronal excitability that contributes to the seizure generation. Once seizure has started, fast-spiking inhibitory interneurons fire multiple action potentials during paroxysmal depolarizing shifts (EEG spike components of SW/PSW complexes). During seizure a set of cellular processes induces a shift of reversal potential of GABA toward depolarization. Intense firing of GABAergic neurons and depolarizing GABA responses largely contribute to the generation of paroxysmal EEG spikes. Inhibition does not play a role in other components of neocortical seizures. Neocortical trauma, in particular penetrating wounds, produces partial deafferentation of a subset of neurons that decreases excitability of network. Cortical neurons display occasional periods of disfacilitation in deafferented cortex during all states of vigilance. As in the case of slow-wave sleep, periods of disfacilitation up-regulate neuronal excitability. Synaptic volleys originating from preserved axons impinge hyperexcitable neurons of deafferented cortex that trigger seizures.I. Timofeev (*)

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“…Furthermore, on T 1 -weighted magnetization transfer images, abnormalities extending beyond the T 2 changes or presence of gliosis surrounding hemosiderin deposits (especially when the gliosis wall is incomplete or shows a dynamic evolution in subsequent scans) are associated with higher risk for epilepsy [88,89]. Furthermore, hippocampal T 2 increased signal and atrophy have been shown to be strong indicators of seizure recurrence following AED withdrawal in seizure-free patients [90].…”

Section: Signal Changesmentioning

confidence: 99%

Neuroimaging the Epileptogenic Process

et al. 2014

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Epilepsy is one of the most common chronic neurological conditions worldwide. Anti-epileptic drugs (AEDs) can suppress seizures, but do not affect the underlying epileptic state, and many epilepsy patients are unable to attain seizure control with AEDs. To cure or prevent epilepsy, disease-modifying interventions that inhibit or reverse the disease process of epileptogenesis must be developed. A major limitation in the development and implementation of such an intervention is the current poor understanding, and the lack of reliable biomarkers, of the epileptogenic process. Neuroimaging represents a non-invasive medical and research tool with the ability to identify early pathophysiological changes involved in epileptogenesis, monitor disease progression, and assess the effectiveness of possible therapies. Here we will provide an overview of studies conducted in animal models and in patients with epilepsy that have utilized various neuroimaging modalities to investigate epileptogenesis.

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Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

Cited by 49 publications

References 43 publications

Loss of Astrocytic Domain Organization in the Epileptic Brain

Loss of Astrocytic Domain Organization in the Epileptic Brain

Injury Induced Epileptogenesis: Contribution of Active Inhibition, Disfacilitation and Deafferentation to Seizure Induction in Thalamocortical System

Neuroimaging the Epileptogenic Process

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