Periodic EEG: clinical settings, in vitro models, and potential mechanisms

Vollständiger Abstract

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Abstract Periodic complexes occur in the electroencephalogram (EEG) during a number of pathological conditions, often having a poor prognosis (Kuroiwa and Celesia 1980). The contexts in which periodic EEGs occur generally fall into three major categories: infections, sequelae to hypoxic/ischemic events, and metabolic disorders. In this review, we examine morphological and electrophysiological data from in vitro preparations. These data suggest several cellular mechanisms, which may underlie periodic EEGs, including altered excitation–inhibition relations, tonic activation of metabotropic glutamate receptors, altered neuromodulation, and electrical coupling of neurons by cell fusion or gap junctions. Some of the proposed mechanisms are empirically testable: for example, the occurrence of very fast oscillations (>∼70 Hz) superimposed on periodic complexes, and the occurrence of gamma oscillations (∼30 Hz–∼70 Hz) between complexes. The in vitro data further suggest an hypothesis concerning why some patients with periodic EEGs respond to anticonvulsant drugs (ACDs), while other patients do not: if the main cellular mechanism for neuronal synchrony involves excitatory chemical synapses, then a response to ACDs is possible; however, if a major factor in neuronal synchrony involves electrical coupling – as can occur with viral infections – then a response to ACDs would not be expected.