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Epilepsy and Seizures: Overview

Epilepsy and Seizures: Overview

Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...

Encephalitis l: Introduction

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...

Seizures l: Introduction

Seizures l: Introduction

Understanding seizures and epilepsy relies on key definitions that help in recognizing, classifying, and managing these disorders. These definitions provide a framework for recognizing, classifying, and managing seizure disorders.DefinitionsA seizure is a sudden, abnormal burst of electrical activity in the brain that can cause changes in awareness, movement, sensation, or behavior, depending on the area involved. Epilepsy is a chronic condition characterized by recurrent, unprovoked seizures,...

Encephalitis ll: Pathophysiology

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

Seizures: Classification

Seizures: Classification

Epilepsy is primarily characterized by unpredictable seizures, either provoked by an identifiable factor, such as injury or illness, or unprovoked, occurring spontaneously without apparent cause.
Seizures are typically classified into two main categories: focal and generalized seizures.
Focal Seizures
Focal seizures originate from specific regions of the brain. These seizures are further sub-classified into two types:

Epilepsy ll: Types

Epilepsy ll: Types

Recurrent seizures, stemming from abnormal electrical activity in the brain, are the defining characteristic of epilepsy, a chronic neurological condition. Because seizure features vary greatly, epilepsy is classified using two systems: by seizure type and by epilepsy syndromes. These classifications enable clinicians to describe seizure patterns and select suitable treatment strategies.I. Classification by Seizure Type1. Focal EpilepsyFocal epilepsy begins in one hemisphere of the brain.

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Related Experiment Video

Updated: May 28, 2026

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury

Published on: June 21, 2019

Epilepsy and brain inflammation.

Annamaria Vezzani¹, Eleonora Aronica, Andrey Mazarati

¹Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via G. La Masa 19, 20156 Milano, Italy. vezzani@marionegri.it

Experimental Neurology

|October 12, 2011

Summary

This summary is machine-generated.

Brain inflammation, driven by activated glial cells, contributes to seizures. Understanding these inflammatory mediators and glioneuronal interactions is key to developing new epilepsy treatments.

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Last Updated: May 28, 2026

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury

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Published on: June 21, 2019

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury

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Published on: February 10, 2020

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Area of Science:

Neuroscience
Neuroinflammation
Epileptology

Background:

Glial cells, including astrocytes and microglia, play a significant role in seizure precipitation and recurrence following brain injury.
Activated glial cells release proinflammatory mediators, initiating inflammatory cascades that alter neuronal excitability and glioneuronal communication.
These inflammatory changes can lower seizure thresholds and potentially compromise neuronal survival.

Purpose of the Study:

To review clinical observations in drug-resistant human epilepsies and experimental findings in rodents.
To link brain inflammation to the epileptic process in a causal and reciprocal manner.
To discuss the role of soluble inflammatory mediators in seizure etiopathogenesis and their effects on seizure threshold.

Main Methods:

Review of experimental research on glial cell activation in epilepsy.
Analysis of clinical data from drug-resistant human epilepsies.
Examination of findings from adult and immature rodent models of epilepsy.

Main Results:

Brain inflammation, mediated by glial cells, is causally linked to epilepsy.
Specific soluble inflammatory mediators contribute to seizure development and affect seizure threshold.
Inflammatory mediators may also contribute to epilepsy comorbidities.

Conclusions:

Understanding glioneuronal interactions and inflammatory mechanisms is crucial for epilepsy research.
Targeting inflammatory pathways offers potential therapeutic strategies for drug-resistant epilepsy and epileptogenesis prevention.