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Operant conditioning of epileptic neurons in monkeys and its theoretical application to EEG operant conditioning in humans.

This paper reviews a series of previous reports which summarize the physiology of chronic experimental epileptic foci in monkeys. It is shown that such monkeys can be trained to bidirectionally control the firing rates of normal and epileptic neurons which comprise the epileptic focus. As a result of this acquired operant performance, the monkeys show both a decrease in clinical seizures as well as a decrease in single unit epileptic activity. The EEG correlate of this change in single unit epileptic activity is generalized EEG desynchronization. The conclusion from these data would indicate epileptic neurons can be operantly controlled from and this control is not correlated with any specific EEG pattern. This brings to question the specificity of the SMR in EEG biofeedback paradigms which treat human epilepsy. This author feels that the result from such biofeedback studies are the result of the patient learning to manipulate electrical events within the CNS pathways through which the seizures propagates and is not contingent upon specific EEG frequencies.

Animals↗

Septal lesions facilitate the shift from conditioned escape to conditioned avoidance behavior in the rat.

Normal rats were given 1000 training trials in a discriminated lever-press avoidance task. Those animals which exhibited consistent escape behavior but minimal avoidance responding were subjected to either septal lesions or control operations. One week later they were retested in the avoidance apparatus for an additional 1000 trials. Rats with large septal lesions exhibited an immediate increase in avoidance performance relative to the control rats. This increase occurred without a concomitant increase in number of lever-press responses. The performance of 3 out of 4 rats with smaller more dorsal septal lesions was unaffected by the surgery.

Animals↗