known or explorable brain mechanisms, one might argue that at this early stage of the work it would be more desirable to simply report the quantitative findings, leaving unanswerable questions about ultimate causality for later discussion (see below). The first EEG 4(+) was reported in a patient with epilepsy (Babloyantz and Destexhe, 1986) which was confirmed by others (lasemedia et al, 1988; Frank et all, 1990). An important study of simultaneous time series from 16 subdural electrodes placed in the right temporal cortex of a patient with a right medial temporal lobe epileptogenic focus demonstrated that a decrease in a single lead’s A(+) reliably anteceded and localized the first signs of the incipient seizure. The rest of the leads followed with similarly decreased positivity in their leading Lyapounov exponents associated with spatially coherent patterns of behavior. In addition, the averaged value of the leading Lyapounov exponents in the 16 leads increased post-ictally over the averaged values of 4(+)in the pre-ictal state (lasemidis et al, 1988,1990). These findings, including seizure anticipation for 25 minutes, were confirmed using intracranial recordings in 16 patients with temporal lobe epilepsy (Elger and Lehnertz, 1998). The para-ictal decrease and post-ictal increase in 4(+) found in patients with focal temporal lobe seizures was confirmed more generally in left and right pre-frontal-to-mastoid EEG recordings made before, during and after electroconvulsive shock treatment of psychiatric patients (Krystal and Weiner, 1991). Pre-ictal changes were also found six minutes before seizure onset from scalp EEG recordings in 17/19 patients with chronic focal epilepsy (Martinerie et al, 1998). The most exciting potential application of this approach is its use, in real time, for the prediction and prophylactic treatment of incipient seizures, minutes to hours before the event, in place of or augmenting long term drug management (lasemidis and Sackellares, 199