Pathogenesis and significance of abnormal nonepileptiform rhythms in the EEG

Abstract

In this article the present state of knowledge of physiological mechanisms underlying nonepileptiform EEG abnormalities is reviewed. Focal and widespread slow waves, background activity abnormalities, and bursts of rhythmic slow activity are discussed. Clinical and experimental data accumulated over the past four decades suggest that polymorphic slow activity is generated in cerebral cortex by layers of pyramidal cells and is probably due to partial deafferentation from subcortical areas. Unilateral background activity changes are probably due to thalamic dysfunction, and bilateral paroxysmal slow activity is due to abnormal thalamocortical circuits combined with cortical pathology. The fact that pathologic slow-wave phenomena are longer in duration than the average postsynaptic potential is also discussed.