PURPOSE: No neurophysiological hypothesis currently exists addressing how and why periodic lateralized epileptiform discharges (PLEDs) arise in certain types of brain disease. Based on spectral analysis of clinical scalp EEG traces, the authors formulated a general mechanism for the emergence of PLEDs. METHODS: The authors retrospectively analyzed spectra of PLED time series and control EEG segments from the opposite hemisphere in 25 hospitalized neurological patients. The observations led to the development of a phenomenological model for PLED emergence. RESULTS: Similar to that observed in our previous work with afterdischarges, an analytic relationship is found between the spectrum of the baseline EEG and the PLED EEG, characterized by "condensation" of the main baseline spectral cluster, with variable inclusion of higher harmonics of the condensate. CONCLUSIONS: Periodic lateralized epileptiform discharges may arise by synchronization of preexisting local field potentials, through a variable combination of enhancement of excitatory neurotransmission and inactivation of inhibitory neurotransmission provoked by the PLED-associated disease process. Higher harmonics in the PLED spectrum may arise by recurrent feedback, possibly from entrained single units. A mechanism is suggested for PLED emergence in certain diseased brain states and the association of PLEDs with EEG seizures. The framework is a spatially extended version of that, which the authors proposed, underlies afterdischarge and analogous to the cooperative behavior seen in a variety of natural multi-oscillator systems.
PURPOSE: No neurophysiological hypothesis currently exists addressing how and why periodic lateralized epileptiform discharges (PLEDs) arise in certain types of brain disease. Based on spectral analysis of clinical scalp EEG traces, the authors formulated a general mechanism for the emergence of PLEDs. METHODS: The authors retrospectively analyzed spectra of PLED time series and control EEG segments from the opposite hemisphere in 25 hospitalized neurological patients. The observations led to the development of a phenomenological model for PLED emergence. RESULTS: Similar to that observed in our previous work with afterdischarges, an analytic relationship is found between the spectrum of the baseline EEG and the PLED EEG, characterized by "condensation" of the main baseline spectral cluster, with variable inclusion of higher harmonics of the condensate. CONCLUSIONS: Periodic lateralized epileptiform discharges may arise by synchronization of preexisting local field potentials, through a variable combination of enhancement of excitatory neurotransmission and inactivation of inhibitory neurotransmission provoked by the PLED-associated disease process. Higher harmonics in the PLED spectrum may arise by recurrent feedback, possibly from entrained single units. A mechanism is suggested for PLED emergence in certain diseased brain states and the association of PLEDs with EEG seizures. The framework is a spatially extended version of that, which the authors proposed, underlies afterdischarge and analogous to the cooperative behavior seen in a variety of natural multi-oscillator systems.
Authors: Irene García-Morales; M Teresa García; Lucia Galán-Dávila; Carlos Gómez-Escalonilla; Rosana Saiz-Díaz; Antonio Martínez-Salio; Pilar de la Peña; Julian A Tejerina Journal: J Clin Neurophysiol Date: 2002-04 Impact factor: 2.177
Authors: Catherine A Schevon; Sau K Ng; Joshua Cappell; Robert R Goodman; Guy McKhann; Allen Waziri; Almut Branner; Alexandre Sosunov; Charles E Schroeder; Ronald G Emerson Journal: J Clin Neurophysiol Date: 2008-12 Impact factor: 2.177