Since our initial reports of successful seizure reduction in drug-refractory epileptics through the application of EEG biofeedback techniques developed in cat research (Sterman & Friar, 1972; Sterman, Macdonald, & Stone, 1974), there have been abundant confirmations of this therapeutic effect in man (Finley, Smith, & Etherton, 1975; Seifert & Lubar, 1975; Ellertsen & Klove, 1976; Lubar & Bahler, 1976; Wyler, Lockard, Ward, & Finch, 1976; Wyler, Robbins, & Dodrill, 1979; Sterman & Macdonald, 1978; Kuhlman, 1978; Cott, Pavloski, & Black, 1979; Sterman & Shouse, 1981; Lubar, Shabsin, Natelson, Holder, Whitsett, Pamplin, & Krulikowski, 1981). Moreover, the questions immediately raised concerning the incorporation of adequate control procedures and the specificity of this effect have now been put to rest. What remains at issue, however, is an understanding of the mechanism responsible for the elevated seizure thresholds produced by this technique (see, for example, Wyler, Chapter 6). Also in question is the appropriate clinical utilization of EEG biofeedback therapy as an alternative to extended drug trials or neurosurgery for poorly controlled patients. This discussion will address both of these issues.