The Neurobiology of Epileptiform Discharges

ABSTRACT.

Properly classifying epileptic seizures and epileptic syndromes is important for developing treatment strategies and determining prognoses for individual patients. Among the many factors important in such classification are the electrographic features of paroxysmal discharges. While many forms of paroxysmal discharges are described in the clinical and EEG literature, current understanding of the basic neurobiological events behind these discharges is limited to a few of them. In the review given below, three “prototypical” epileptiform events–interictal events, tonic-clonic electrographic seizures, and spike-wave seizures–are identified and the basic mechanisms by which they arise are discussed. The information provided considers functional anatomy in terms of major networks within the brain, a “fundamental local circuit” consisting of an excitatory neuron and the inhibitory neuron it is coupled to in a feedback circuit, and cellular processes of inhibition and excitation. The ways in which amino acid neurotransmitters exert excitatory synaptic events, via glutamate receptors, and inhibitory synaptic events, via gamma-aminobutyric acid (GABA) receptors are presented. In addition, key types of membrane potential-regulated ion channels in neurons are introduced. Details are then given as to how these basic neurobiological processes interact to produce the prototypical paroxysmal discharges. A distinct set of mechanisms is responsible for each of the discharges. Depending on the type of discharge, certain mechanisms are shared between types of discharges while others are not. With the information covered, one can gain an understanding of how common and important EEG paroxysms originate at the cellular and synaptic level.

KEY WORDS.:

• Electroencephalogram
• epilepsy
• GABA
• glutamate
• seizure
• spike-wave
• tonic-clonic