A double-blind investigation of the relationship between seizure activity and the sleep EEG following EEG biofeedback training.

The sleep EEGs of eight medically refractory epileptic patients were examined as part of a double-blind, ABA crossover study designed to determine the effectiveness of EEG biofeedback for the control of seizures. The patients were initially reinforced for one of three EEG criteria recorded from electrodes placed over sensorimotor cortex: (a) suppression of 3- to 7-Hz activity, (b) enhancement of 12- to 15-Hz activity, or (c) simultaneous suppression of 3- to 7-Hz and enhancement of 11- to 19-Hz activity. Reinforcement contingencies were reversed during the second or B phase, and then reinstated in their original form during the final A' phase. All-night polysomnographic recordings were obtained at the end of each conditioning phase and were subjected to both visual and computer-based power spectral analyses. Four of the patients showed changes in their nocturnal paroxysmal activity that were either partially or totally consistent with the ABA' contingencies of the study. The spectral data proved difficult to interpret, though two trends emerged from the analyses. Decreases in nocturnal 4- to 7-Hz activity were correlated with decreases in seizure activity, and increases in 8- to 11-Hz activity were correlated with decreases in seizure activity. These findings were shown to strengthen the hypothesis that EEG biofeedback may produce changes in the sleep EEG that are related to seizure incidence.

EEG operant conditioning in intractable epileptics.

Eight epileptic patients with mixed seizures refractory to medical control participated in a double-blind crossover study to determine the effectiveness of operant conditioning of the EEG as an anticonvulsant procedure. Baseline levels of seizures were recorded for four months prior to the beginning of treatment. Participants then received false (noncontingent) feedback for two months followed by an ABA-patterned training program lasting a total of ten months. Subjects were assigned to three treatment groups based on different schedules of EEG feedback. They were first trained (A1 phase) either to suppress slow activity (3 to 8 Hz), to enhance 12- to 15-Hz activity, or to simultaneously suppress 3- to 8-Hz and enhance 11- to 19-Hz activity. This was followed by a B phase, in which patients were trained to enhance slow activity (3 to 8 Hz). In the final phase (A2), the initial training contingencies were reinstated. Neuropsychological tests were performed before and after training, and changes in EEG activity as determined by Fast Fourier spectral analyses were analyzed. Five of eight patients experienced a decrease in their mean monthly seizure rate at the completion of feedback training as compared with their initial baseline level.