Periodic lateralized epileptiform discharges (PLEDs) or lateralized periodic discharges (LPDs) are a well-known variant of pathological EEG activity. However, the mechanisms underpinning the appearance of this pattern are not completely understood. The heterogeneity of the features derived from LPDs patterns, and the wide range of pathological conditions in which they occur, raise a question about the unifying mechanisms underlying these phenomena. This paper reassesses the current opinion surrounding LPDs which considers glutamate excitotoxicity to be the primary pathophysiological basis, and the penumbral region to be the main morphological substrate. Arguments in favour of this hypothesis are presented, with interpretations supported by evidence from recent literature involving clinical and experimental data. Presently, no single hypothesis places considerable emphasis on the pathochemical properties of LPDs, which are implicitly meaningful towards better understanding of the clinical significance of this pattern.
Keywords: EEG; Excitotoxicity; Glutamate; LPDs; Mechanism; PLEDs; Penumbra; Periodic discharges.
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