The neurological disorder known as epilepsy, a recurrent seizure, is caused by abnormal electrical discharge of nerve cells in the brain.

Referred to as an episode, the seizure is a direct consequence of the exquisite regulation of neuronal excitation in the human brain. Simply, epilepsy can occur with the body's inability to maintain physiologic regulation. This regulation is essential to the complex functions of the

evolved brain. There are, unfortunately, a number of factors that can tip the balance of excitability toward abnormal neuronal discharge. In a given individual, the occurrence of a single seizure can result from a variety of influences or triggering factors, including traumatic head injury, excess sensory stimulation, acute systemic metabolic disturbance, excessive loss of sleep, substance abuse or a combination of these factors.

Epilepsy is one of the most common neurological disorders. Approximately 7 percent of the American population, or more than 15 million people, will experience at least one convulsion, or epileptic seizure in their lifetime. Recurrent seizures, which is the criterion for a diagnosis of epilepsy, have been estimated to occur in approximately two percent of the human population. Genetic factors are responsible for an increased risk in siblings and offspring of individuals with non-traumatic epilepsy. Whether or not such events will lead to epilepsy depends upon the predisposition to this disorder in a given individual. However, severe or chronic metabolic disturbances of brain insult from head injury or tumors can also lead to the eventual development of epilepsy, with or without this genetic influence.

There are many seizure types and varying degrees of severity of affliction in the epileptic population. The categories are determined by clinical manifestation and EEG discharge. They range from generalized epilepsy with clinical manifestations involving the entire individual to several categories of partial epilepsy, of which the most common are partial-complex seizures, and simple motor seizures. The site and spread of abnormal discharge will determine the behavioral expression of this disorder, a fact that results in a diversity of epileptic manifestations. For example, in a more severe form of epilepsy, such as grand mal seizure, the individual suddenly loses consciousness with little warning, experiences generalized stiffness with muscle spasm followed by relaxation of some muscles thus producing jerking of the limbs, accompanied by sweating, rapid heart rate, rise in blood pressure, dilation of pupils and biting of the tongue from jaw clenching .In contrast, in a less severe form of epilepsy, such as a petit mal seizure (commonly referred to as "absence"), the individual experiences a cessation of activity, momentary disturbance of consciousness, slight movement, resuming activity without awareness of interruption.

Since epilepsy arises from an excitatory threshold disturbance in the brain, any factor that can, alter the excitatory regulation of the brain can influence the probability of seizure occurrence. Traditionally, medical efforts to influence this excitatory threshold have relied on the neurochemical effects of anticonvulsant drugs. Unfortunately, however, these drugs are nonspecific, and can produce changes in the brain or other body tissues leading to undesirable and even dangerous side effects.

Some 25 year ago researchers at UCLA found that cats and monkeys could learn to voluntarily change their brain wave patterns (electroencephalogram or EEG) when food rewards were provided for these changes. This process is called "operant conditioning" and is used to increase the occurrence of selected responses in behavioral research. In this application it was used to increase an EEG pattern called the sensorimotor rhythm, or SMR, which is associated with the suppression of movements. Because these same animals were being used in studies of seizure induction, it was accidentally discovered that this training produced resistance to seizures elicited by convulsive drugs. In untrained animals these drugs increased motor excitability and suppressed the SMR pattern in the EEG, while in trained animals this effect was delayed and in some instances completely blocked. A series of studies focusing on the physiology of the SMR shows that this EEG pattern was, indeed, related to a reduction in motor excitability, both at the level of the brain and along the conduction pathways between muscles and the brain. Since epileptics with motor seizures show reduced and/or disrupted SMR patterns, presumably related to abnormal motor excitability, it was suggested that normalization of these EEG patterns through feedback training might reduce this excitability and raise the threshold for seizures in human beings.

Several decades of both animal and human research have established clearly that EEG feedback training can produce functional changes in the brain which can alter susceptibility to seizures. The first attempt at SMR feedback training in a human epileptic by Sterman's group in 1972 achieved significant enhancement of the SMR pattern together with a dramatic reduction in major-motor seizures. With extended training this patient's seizures were sufficiently controlled to warrant issuance of a California drivers license. This work was followed by expanded studies in many laboratories that include "placebo" conditions and added training for the suppression of abnormal EEG frequencies as well as enhancement of the SMR. Normalization of the EEG and significant seizure reduction were associated exclusively with non-placebo EEG feedback training.

Today, advances in computerized EEG technology have made delivery of this adjunctive therapy for epilepsy both easier and more effective. Sophisticated software programs provide comprehensive EEG analysis for the clinician and flexible training strategies for self-regulation of electrical activity of the brain by the individual. Further, these concepts and methods have been extended to the treatment of other neurological disorders where abnormal EEG patterns can be identified and manipulated.

                      Lantz, D. and Sterman, M.B. (1988). Neuropsychological assessment of subjects with uncontrolled epilepsy: Effects of EEG    

                       feedback training. Epilepsia, 29(2), 163-171.

                       Tozzo, C.A., Elfner, L.F., & May, J.G., Jr. (1988). EEG biofeedback and relaxation training in the control of epileptic .