Excerpt from Epileptiform Discharges

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Background

Although no longer used for identification and localization of gross structural brain lesions, electroencephalography (EEG) remains the primary diagnostic test of brain function. Unlike relatively new functional imaging procedures, such as functional MRI (fMRI), single-photon emission computed tomography (SPECT), and positron emission tomography (PET), EEG provides a continuous measure of cortical function with excellent time resolution and is relatively inexpensive. EEG is especially valuable in investigation of patients with known or suspected seizures.

Seizures are infrequent events in the majority of patients, making recording of ictal EEG both time-consuming and expensive. The mainstay of diagnosis, therefore, remains detection of interictal (ie, between seizures, from the Latin icere, to strike) epileptiform discharges. Continuous video-EEG monitoring, developed over the last 20 years to facilitate recording of ictal events, also greatly increases the time available to detect interictal epileptiform discharges (IEDs). In the diagnosis of epilepsy and localization of seizure onset, these can be as useful as ictal recordings.

History

Interictal and ictal epileptiform EEG patterns were first identified in the 1930s, leading to distinction between partial and generalized seizures. The basic concepts developed by such pioneers as Fred and Erna Gibbs, William Lennox, and Herbert Jasper underlie our current understanding of the clinical neurophysiology of epilepsy; subsequent work has led mainly to improvements in detection and interpretation of findings they first noted decades ago.

Definition and classification of interictal discharges

The International Federation of Societies for Electroencephalography and Clinical Neurophysiology (IFSECN) describes interictal discharges as a subcategory of "epileptiform pattern," in turn defined as "distinctive waves or complexes, distinguished from background activity, and resembling those recorded in a proportion of human subjects suffering from epileptic disorders…." This somewhat circular definition makes clear that criteria must be verified empirically.

Interictal discharges may be divided morphologically into sharp waves, spikes, spike-wave complexes (also called spike-and-slow-wave complexes), and polyspike-wave complexes (also called multiple-spike-and-slow-wave-complexes). In practical terms, the morphological distinctions are less important than the certainty with which these entities can be distinguished from physiologic or nonspecific sharp transients. IEDs may occur in isolation or in brief bursts; bursts longer than a few seconds are likely to represent electrographic seizures rather than interictal discharges.

The following definitions are in use (IFSECN, 1974):

• Sharp wave - Transient, clearly distinguishable from background activity, with pointed peak at conventional paper speeds and a duration of 70-200 milliseconds (ms)

• Spike - Same as sharp wave, but with duration of 20 to less than 70 ms

• Spike-and-slow-wave complex - Pattern consisting of a spike followed by a slow wave (classically the slow wave being of higher amplitude than the spike)

• Multiple spike-and-slow-wave complex - Same as spike-and-slow-wave complex, but with 2 or more spikes associated with one or more slow waves

Pathophysiology

The underlying cellular pathophysiology of focal spikes is believed to be the "paroxysmal depolarization shift" (PDS). Several decades of studies using cortical application of penicillin or other excitatory agents have revealed a stereotyped neuronal correlate of the interictal spike as recorded at the cortical surface. Sustained neuronal depolarization mediated by an influx of calcium ions underlies a train of action potentials associated with sodium influx. Repolarization and usually hyperpolarization, mediated mainly by potassium, follow this sustained depolarization. The corresponding extracellular field, forming the basis of the surface EEG, shows a negative peak during calcium and sodium influx, falls back to and then below baseline during hyperpolarization, and finally returns gradually to baseline.

The PDS is a model based on intracellular and extracellular single-cell recording. In vivo, however, neuronal networks in hippocampus and neocortex are critical to production of both interictal and ictal discharges. A neuronal network involving thalamus as well as cortex is responsible for producing the generalized spike-wave complex that is the hallmark of idiopathic generalized epilepsies; this network is similar to that thought to be responsible for generating sleep spindles. A complex interaction of excitatory and inhibitory firing of thalamic reticular, thalamic relay, and neocortical pyramidal neurons generates the rhythmic burst firing underlying spike-wave complexes. The slow wave of the complex is thought to represent an inhibitory event, consistent with the major clinical manifestation of arrest of activity in generalized absence seizures (see Absence Seizures).

Simultaneous scalp and intracranial EEG recording has revealed that standard electrodes record only a relatively small proportion of spikes detectable at the cortical surface. Involvement of a relatively large cortical area, 6-10 cm², is required for spikes to be recorded at the scalp.

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