Neuroglia: Gliosis and Focal Epilepsy

Pollen, Daniel A.; Trachtenberg, Michael C.

doi:10.1126/science.167.3922.1252

Cited by 201 publications

(61 citation statements)

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“…In late 1940s Penfield and co workers established that glial scar is a irritable source for the focal seizures, which develop either by anoxic or traumatic brain damage [16]. One patient in the present research had post gliotic seizures due to traumatic gliotic scar in the brain.…”

Section: Discussionmentioning

confidence: 62%

“…Fibrillary gliosis resulting from prior brain injury bordering the normal neuronal tissue can trigger epilepsy by impairing the homeostasis of extracellular potassium ions [16]. In late 1940s Penfield and co workers established that glial scar is a irritable source for the focal seizures, which develop either by anoxic or traumatic brain damage [16].…”

Section: Discussionmentioning

confidence: 99%

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Cross Sectional Imaging of Post Partum Headache and Seizures

Hiremath

Mundaganur

Sonwalkar

2014

JCDR

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Cross Sectional Imaging of Post Partum Headache and Seizures

Hiremath

Mundaganur

Sonwalkar

2014

JCDR

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“…Previous authors suggested that impaired glial regulation of extracellular potassium is important in the transition from the interictal to the ictal state (21)(22)(23)(24). More recently, evidence has accumulated that glia hold a role in neural information processing (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Differential Neuronal and Glial Relations with Parameters of Ictal Discharge in Mesial Temporal Lobe Epilepsy

et al. 1999

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Summary:Purpose: EEG recordings of spontaneous seizures should provide clues to epilepsy pathogenesis and pathology. We examined onset, propagation, and termination characteristics of spontaneous seizures recorded by intracranial EEG in temporal lobe (TL) epilepsy in relation to neuronal, glial, and synaptic changes in the same tissue.Methods: All of our patients with intracranial EEG recordings of spontaneous TL seizure onset, subsequent TL resection, and quantitative pathologic analysis of resected tissue were included. Seizure parameters were mean time to initial propagation, mean total electrical duration, uniformity of seizureonset distribution and location, and percentage of seizures with spiking onset per patient. Tissue was analyzed for glial and neuronal density in hippocampal fields and presence of sprouting. Outcome was classified as seizure free or not.Results: All seizures with onset in resected TL in 62 patients were analyzed. The percentage of each patient's seizures with spike onsets was significantly correlated with glial density in CA3 (p i 0.01). Initial propagation time was significantly and inversely correlated with neuronal density in CA4 (p < 0.02).Electrical seizure duration was significantly correlated with glial density in CA2 and CA3 (p < 0.02). Neuronal and glial density were significantly (and inversely) related to one another only in CAI (p < 0.001). Outcome was most significantly related to uniform hippocampal seizure onset. Presence or abhence of sprouting was not significantly related to outcome or any EEG measure.Conclusions: These results suggest both glia and neurons exert independent influences on the expression of ictal discharges in seizures of medial TL onset. Glial density influenced interictal-ictal transition, whereas neuronal density influenced seizure propagation. These findings may have implications for pathogenesis. Key Words: Neuronal changes-Glial changes-Temporal lobe.Mesial temporal lobe epilepsy is often medically refractory and may be treated successfully by surgical resection (1 -4). Quantifiable and predictable neuronal, glial, and synaptic changes accompany this epileptic process, which together define the entity called mesial temprovide clues to the meaning of those tissue changes and to the pathogenesis of mesial temporal lobe epilepsy.Some reports have described morphologic characteristics of ictal discharges as recorded from intracranial electrodes in mesial temporal lobe epilepsy (13-19). The poral sclerosis (MTS). Features that are consistently described include >50% neuronal loss in hippocampal fields CAI, CA3, and the dentate gyrus, accompanied by varying amounts of gliosis, and sprouting of fibers imrnunoreactive for neuropeptide Y, somatostatin, and dynorphin into the inner molecular layer of the dentate gyrus (5-12). The relation of these pathologic findings to the pathogenesis of mesial temporal lobe epilepsy remains uncertain. Correlations, therefore, of the pathologic alterations with specific EEG characteristics of the spontaneous seizures th...

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“…2,3 The almost invariable presence of gliotic scars in chronic focal epilepsy has led many to suggest a physiological role for glia in the disease. [4][5][6] Early studies on the role of astrocytes in epilepsy carried out mostly on gliotic scars induced by topical application of chemicals such as alumina or cobalt to the cortex of animal brains are reviewed by Tiffany-Castiglioni and Castiglioni. 7 In conclusion to their review, the authors write that "astrocytes can hypothetically contribute to epileptogenesis by any of three routes: (1) the initiation of neuronal hyperactivity in previously normal neurons, (2) the promotion of epileptic bursting in abnormal neurons, and (3) the failure to neutralize and arrest neuronal hyperactivity."…”

Section: Introductionmentioning

confidence: 99%

Astrocytes and Epilepsy

2010

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Summary: Astrocytes form a significant constituent of seizure foci in the human brain. For a long time it was believed that astrocytes play a significant role in the causation of seizures. With the increase in our understanding of the unique biology of these cells, their precise role in seizure foci is receiving renewed attention. This article reviews the information now available on the role of astrocytes in the hippocampal seizure focus in patients with temporal lobe epilepsy with hippocampal sclerosis. Our intent is to try to integrate the available data. Astrocytes at seizure foci seem to not be a homogeneous population of cells, and in addition to typical glial fibrillary acidic protein, positive reactive astrocytes also include a population of neuron glia-2-like cells The astrocytes in sclerotic hippocampi differ from those in nonsclerotic hippocampi in their membrane physiology, having elevated Naϩ channels and reduced inwardly rectifying potassium ion channels, and some having the capacity to generate action potentials. They also have reduced glutamine synthetase and increased glutamate dehydrogenase activity. The molecular interface between the astrocyte and microvasculature is also changed. The astrocytes are also associated with increased expression of many molecules normally concerned with immune and inflammatory functions. A speculative mechanism postulates that neuron glia-2-like cells may be involved in creating a high glutamate environment, whereas the function of more typical reactive astrocytes contribute to maintain high extracellular Kϩ levels; both factors contributing to the hyperexcitability of subicular neurons to generate epileptiform activity. The functions of the astrocyte vascular interface may be more critical to the processes involved in epileptogenesis.

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Neuroglia: Gliosis and Focal Epilepsy

Cited by 201 publications

References 12 publications

Cross Sectional Imaging of Post Partum Headache and Seizures

Cross Sectional Imaging of Post Partum Headache and Seizures

Differential Neuronal and Glial Relations with Parameters of Ictal Discharge in Mesial Temporal Lobe Epilepsy

Astrocytes and Epilepsy

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