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Book ChapterDOI

Neurodegeneration and Pathology in Epilepsy: Clinical and Basic Perspectives.

TLDR
While epilepsy has long and correctly been considered an electrical disorder, the vascular system likely plays an important causal role in the neurodegeneration and pathology that occur as a consequence of repeated seizures.
Abstract
Epilepsy is commonly associated with a number of neurodegenerative and pathological alterations in those areas of the brain that are involved in repeated electrographic seizures. These most prominently include neuron loss and an increase in astrocyte number and size but may also include enhanced blood–brain barrier permeability, the formation of new capillaries, axonal sprouting, and central inflammation. In animal models in which seizures are either repeatedly elicited or are self-generated, a similar set of neurodegenerative and pathological alterations in brain anatomy are observed. The primary causal agent responsible for these alterations may be the cascade of events that follow a seizure and lead to an hypoperfusion/hypoxic episode. While epilepsy has long and correctly been considered an electrical disorder, the vascular system likely plays an important causal role in the neurodegeneration and pathology that occur as a consequence of repeated seizures.

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Journal ArticleDOI

TRPV4-induced inflammatory response is involved in neuronal death in pilocarpine model of temporal lobe epilepsy in mice.

TL;DR: It is concluded that TRPV4-induced neuronal death is mediated at least partially by enhancing the neuroinflammatory response, and this action is involved in neuronal injury following status epilepticus.
Journal ArticleDOI

Small Vessels Are a Big Problem in Neurodegeneration and Neuroprotection

TL;DR: The up-to-date advances in understanding of the primary microcirculatory abnormalities that can result in neurodegenerative processes and the combined neurovascular protection approaches that can prevent acute as well as chronic Neurodegeneration are reviewed.
Journal ArticleDOI

Review: The past, present and future challenges in epilepsy‐related and sudden deaths and biobanking

TL;DR: The main neuropathology, cardiac and genetic findings inSUDEP are outlined, providing a framework for best practices, integration of clinical, pathological and molecular genetic investigations in SUDEP, and ultimately prevention.
Journal ArticleDOI

Bioenergetic Mechanisms of Seizure Control.

TL;DR: Current knowledge whether neurometabolic and neurovascular mechanisms are sufficient to cover the energy demand of hypersynchronous activity and whether a mismatch between energy need and supply could contribute to seizure control is summarized.
References
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Journal ArticleDOI

Modification of seizure activity by electrical stimulation. II. Motor seizure.

TL;DR: It was found that the development of motor seizures by stimulation of the amygdala resulted in an increased ability of the contralateral amygdala, and the septal area, but not of the hippocampus, to drive motor seizures when stimulated (“transfer”).
Journal ArticleDOI

A permanent change in brain function resulting from daily electrical stimulation.

TL;DR: High-intensity stimulation studies revealed that the development of convulsions was not based simply on threshold reduction, but involved complex reorganization of function.
Journal ArticleDOI

Epilepsy and Exacerbation of Brain Injury in Mice Lacking the Glutamate Transporter GLT-1

TL;DR: Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury, which can be attributed to elevated levels of residual glutamate in the brains of these mice.
Journal ArticleDOI

Inflammatory mechanisms in ischemic stroke: role of inflammatory cells.

TL;DR: An overview of the time‐dependent recruitment of different inflammatory cells following focal cerebral I/R is provided and certain recent findings and currently unanswered questions about inflammatory cells in the pathophysiology of ischemic stroke are highlighted.
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