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EEG Biofeedback should play a major therapeutic role. In my opinion, if any medication had demonstrated such a wide spectrum of usefulness it would be universally accepted and widely used. There has not been a single report of harm. Frank Duffy, M.D., Associate Editor for Neurology Clinical EEG Vol 31 #1, Jan 2000

At a recent training course, a neurologist sat through the first three days and then exclaimed: "Incredible. Why is this course not full of neurologists?" What he was hearing was clearly of relevance to much of what concerns neurology: Epilepsy, traumatic brain injury, severe developmental delay, dementias, and brain-based disorders of various kinds.

It goes without saying that much of what neurologists deal with involves organic brain injury or in any case structural deficits of some kind. Yet the medications used to address the resulting behaviors do not address these structural deficits. Rather, they serve to stabilize the brain against recruitment of inappropriate neuronal firing patterns from neighboring healthy brain tissue. The critical frequencies in this regard appear to be the low frequencies (less than 30 Hz, and more particularly, less than 10 Hz) which are often elevated in epileptics, and which we now know to be involved in the regulation of physiological arousal. The intimate connection of seizures with arousal issues has been known since at least the 1930's. The majority of seizures are temporally correlated with the sleep-wake cycle, and in particular to the transitions in sleep stages when arousal is least stably managed.

It is now known that behavioral approaches can be successfully used to change the threshold of onset of seizures. These include the conventional behavioral approaches of self-monitoring one's arousal level, but they also include more neurologically relevant behavioral techniques: operant conditioning of EEG rhythms. It was discovered fortuitously in the late 1960's that operant conditioning of certain frequencies in the EEG (12-15 Hz) at the sensorimotor strip of the cat could effect an increase in threshold of seizure onset under hydrazine challenge. This work was replicated in primates. Subsequently, human subjects were successfully trained to raise their seizure threshold by similar means. This work was replicated ultimately in some twenty studies by a dozen different groups. A number of these studies were fully controlled designs.

Unfortunately, the interest of the neurosciences moved away from the level of organismic behavior to the level of molecular biochemistry, receptor site properties, ion channel, and membrane properties in the mid-1980's. Funding dried up for behavioral approaches, despite their high promise. The work was continued at a few centers with a clinical focus.

It is now time for clinically oriented as well as research neurologists to revisit this discipline. Much of what can be accomplished pharmacologically in terms of stabilization of brain function can similarly be accomplished with operant conditioning of the EEG at specific frequencies. Hence, the neurologist can add this modality to his arsenal, and thus achieve an improved quality of life for epileptic patients, a reduction from polypharmacotherapy to monotherapy in many cases, and potentially the avoidance of risky brain surgeries in certain cases.

Siegfried Othmer, Ph.D.